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Basal Cell Carcinoma Arising from an Epidermal Naevus

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Abstrak (In MALAY language): 

Epidermal naevus adalah hamartoma kulit kongenital yang benigna. Kami mengetengahkan kes yang jarang ditemui iaitu epidermis naevus dengan transformasi malignan untuk karsinoma sel basal. Seorang lelaki berusia 79 tahun telah dibiopsi untuk nodul kulit berukuran 2 x 4 cm yang timbul di dalam lesi papular linear berukuran 2 x 4 cm di sebelah kiri lehernya. Nodul itu kemudiannya disahkan sebagai karsinoma sel basal yang timbul daripada epidermal naevus. Mutasi gen PIK3CA mutasi dikaitkan dengan karsinoma sel basal, yang menunjukkan komponen sel karsinoma basal adalah bebas daripada komponen epidermis naevus. Doktor klinikal dan pakar patologi perlu sedar kemungkinan perubahan malignan yang mungkin timbul dalam epidermal naevus.

Correspondance Address: 
Fazarina Mohammed. Department of Pathology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +603-91459482 Fax: 03-91459485 E-mail: fazarina.m@gmail.com.
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INTRODUCTION

Epidermal naevus is a congenital cutaneous lesion which is composed of epidermal overgrowth. It arises from Blashko’s lines, which corresponds to the patterns of epidermal migration during embryogenesis. Epidermal naevus usually presents as a flat tan linear lesion at the trunk or limbs during infancy or early childhood (Brandling-Bennett & Morel 2010). As the patient ages, the lesion may be thickened and appear warty. Histologically the lesion presents as proliferation of keratinocytes and skin appendages. Epidermal naevus follows a benign course even when left untreated. Medical treatment such as topical calcitriol is prescribed to reduce the thickness of the lesion if necessary (Zvulunov et al. 1997).

Rarely, epidermal naevus may undergo malignant transformation. Basal cell carcinoma arising within epidermal naevus is even more infrequent, as documented by previous case reports. In this report, we highlight a rare case of epidermal naevus with concurrent basal cell carcinoma.

CASE REPORT

A 79-year-old male presented with several papular lesions in a linear distribution at the left side of his neck measuring 2 x 4 cm. The papular lesions had been present since childhood, but later coalesced and gradually enlarged and thickened. Within the past few months the papular lesions were pruritic with contact bleeding and became ulcerated with crust formation (Figure 1). Based on the history and clinical examination, the initial clinical impression was linear epidermal naevus with malignant transformation. A skin biopsy was performed to rule out malignancy.

Section from the skin biopsy showed proliferation of basaloid malignant cells arising from the epidermis forming sheets, small nests and trabeculae and infiltrating into the dermis (Figure 2). Peripheral palisading and retraction artefact were also present. These malignant cells were surrounded by parakeratosis, acanthosis and mild spongiosis of the epidermis, which were consistent with features of epidermal naevus (Figure 3). The diagnosis was finalized as basal cell carcinoma arising from an epidermal naevus.

Further follow-up was scheduled for the patient to monitor for recurrence of the malignancy. However, the patient did not attend further appointment and his outcome was unknown.

DISCUSSION

To date, few cases have been reported regarding this rare entity of basal cell carcinoma in association with epidermal naevus (De et al. 2007; Zheng et al. 2013; Mordovtseva 2015; Viana et al. 2015). Presentation of basal cell carcinoma within an epidermal naevus is similar to classical presentation of basal cell carcinoma of the skin.

Similar to our case, the basal cell carcinoma component may present as an ulcerating foci with rolled edges within the naevus (De et al. 2007; Mordovtseva 2015). The basal cell carcinoma component in an epidermal naevus may also present as a pearly shiny papule within the epidermal naevus (Viana et al. 2015). Ulceration and shiny papule with rolled edges are classical presentations of basal cell carcinoma. Other than usual examination of the skin lesion, dermoscopy may also be performed.

Dermoscopy is a non-invasive method that can be used to distinguish between the epidermal naevus component and basal cell carcinoma component. Dermoscopy is a skin surface microscopy that can be performed by the dermatologist before doing a biopsy. Different lesions usually produce different patterns on dermoscopy. Verrucous epidermal naevus shows a characteristic appearance of dark brown circles on dermoscopy (Carbotti et al. 2016). Meanwhile, basal cell carcinoma appears hypopigmented on dermoscopy with presence of at least one criterias as listed: blue-gray globules, blue-ovoid nests, maple-leaf like arrangement, arborizing vessels and spoke wheel arrangement (Puig et al. 2012).

Excision of the lesion is the mainstay of treatment for these patients. Based on other case reports, the treatment for basal cell carcinoma in association with epidermal naevus is mainly excision of the entire lesion with adequate skin margin 3 - 5 mm with closure of skin flap if necessary (De et al. 2007; Zheng et al. 2013). All of the cases reported no recurrence during follow-up.

There are different theories on how basal cell carcinoma may arise from epidermal naevus. Malignant transformation of epithelial germ cells within epidermal naevus was thought to be a possible cause (Crowson 2006). However, a molecular study showed that the basal cell carcinoma component and the epidermal naevus component may be a part of a collision tumour. A collision tumour is the presence of two independent tumours within the same lesion.

A molecular study was done on one lesion of basal cell carcinoma within epidermal naevus to determine whether the epidermal naevus and the basal cell carcinoma components are clonally related (Hafner et al. 2009). The results showed a PIK3CA mutation that was present in the basal cell carcinoma component but not in the epidermal naevus component. This suggests that the basal cell carcinoma component and the epidermal naevus component are a part of collision tumour. However, in view of the limited sample tested for molecular study, the possibility of a relationship between these two entities in the same lesion cannot be excluded. Hence, a more extensive study to include more samples must be done to prove that these two entities are indeed collision tumour.

CONCLUSION

In conclusion, basal cell carcinoma arising from epidermal naevus is a rare occurrence. Despite its benign course, clinicians must be vigilant in observing changes in an epidermal naevus for the possibility of malignancy. Any new lesions within an epidermal naevus should be biopsied. Pathologists must also be aware of possible malignant lesion within an epidermal naevus. The histology of the lesion must be scrutinized to exclude possibility of malignancy.

References: 
Brandling-Bennett, H.A., Morel, K.D. 2010. Epidermal nevi. Pediatr Clin North Am 57(5): 1177-98. Carbotti, M., Coppola, R., Graziano, A., Verona Rinati, M., Paolili, F.L., Zanframundo, S., Panasiti, V. 2016. Dermoscopy of verrucous epidermal nevus: large brown circles as a novel feature for diagnosis. Int J Dermatol 55(6): 653-6. Crowson, A.N. 2006. Basal cell carcinoma: biology, morphology and clinical implications. 2006. Mod Pathol 19 (Suppl 2): S127-47. De, D., Kanwar, A.J., Radotra, B.D. 2007. Basal cell carcinoma developing in verrucous epidermal nevus. Indian J Dermatol Venereol Leprol 73(2): 127-8. Hafner, C., Klein, A., Landthaler, M., Vogt, T. 2009. Clonality of basal cell carcinoma arising in an epidermal nevus: new insights provided by molecular analysis. Dermatology 218(3): 278-81. Mordovtseva, V. 2015. Multifocal basal cell carcinoma arising within a linear epidermal nevus. 2015. Indian Dermatol Online J 6(1): 37-8. Puig, S., Cecilia, N., Malvehy, J. 2012. Dermoscopic criteria and basal cell carcinoma. G Ital Dermatol Venereol 147(2): 135-40. Viana, A., Aguinaga, F., Marinho, F., Rodrigues, R.. Cuzzi, T., Ramos-E-Silva, M. 2015. Basal cell carcinoma arising on a verrucous epidermal nevus: a case report. Case Rep Dermatol 7(1): 20-4. Zheng, L.Q., Huang, Y., Qu, Y.J., Zhang, Y.H., Han, X.C. 2013. Multiple basal cell carcinomas arising in a verrucous epidermal nevus. J Dermatol 40(6): 482–3. Zvulunov, A., Grunwald, M.H., Halvy, S. 1997. Topical calcipotriol for treatment of inflammatory linear verrucous epidermal nevus. Arch Dermatol 133(5): 567-8.

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A Rare Case of Scrotal Basal Cell Carcinoma in the Presence of Metastatic Squamous Cell Carcinoma of the External Auditory Meatus and its Management Strategy

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Abstrak (In MALAY language): 

Penyakit kanser sel basal (KSB) di bahagian skrotum jarang ditemui dan punca ia berlaku tidak difahami dengan baik. KSB yang tumbuh di skrotum ini dikatakan lebih agresif dan mempunyai kebolehan merebak yang lebih tinggi daripada KSB kawasan-kawasan lain. Rawatan utama untuk KSB peringkat awal di skrotum adalah pembedahan, manakala untuk peringkat lanjut di mana penyakit telah merebak, ia perlu dikawal dengan rawatan kemoterapi. Satu keadaan klinikal yang luar biasa di mana KSB skrotum berlaku serentak dengan kanser yang lain tidak pernah dilaporkan. Kes ini mengisahkan cabaran diagnostik dan rawatan kerana KSB skrotum dan kanser sel squamous (KSS) berlaku pada waktu yang sama. Seorang lelaki berusia 70 tahun mengadu wujudnya ulser di skrotum beliau yang tidak sembuh selama lebih setahun. Pada ketika itu, beliau sedang disiasat kerana mengalami penyakit KSS di telinga yang berada di peringkat lanjut. Ulser di skrotum itu pada mulanya dianggap sebagai KSS yang telah merebak ke situ. Ia kemudiannya didapati penyakit KSB dengan biopsi dan pemeriksaan histopatologi. Beliau menjalani pembedahan untuk membuang ulser di skrotum dan diikuti dengan kemoterapi paliatif menggunakan cisplatin dan radioterapi ke atas kumpulan-kumpulan limpa yang dijangkiti KSS. Enam bulan selepas tamatnya rawatan paliatif, beliau kekal sihat dan tidak mempunyai apa-apa kesan KSB berulang di skrotum. Rawatan pembedahan bersama dengan kemoterapi dan radioterapi paliatif dapat memberi kualiti hidup yang baik untuk pesakit yang ditimpa KSB skrotum dan KSS peringkat lanjut.

Correspondance Address: 
Tan Guan Hee, Urology Unit, Department of Surgery, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +60391456202 Fax: +60391456684 E-mail: drtan.guanhee@gmail.com
Full text: 

INTRODUCTION

Basal cell carcinoma (BCC) is a skin malignancy that commonly affects sun-exposed areas of the body such as the head and neck region (Jeon et al. 2006; Wang et al. 2010). However, BCC of the scrotum quite uncommon (Dai et al. 2012; Jeon et al. 2006; Kinoshita et al. 2005) and its pathogenesis is not well understood (Jeon et al. 2006). It is thought to be more aggressive and metastasizes earlier than BCC of other parts of the body (Kinoshita et al. 2005). Localized scrotal BCC is usually treated with wide local excision (Delto et al. 2016; Jeon et al. 2006; Ribuffo et al. 2002; Wang et al. 2010) but metastatic disease may require systemic chemotherapy for disease control (Cieplinski 1984; Jeon et al. 2006). To our knowledge, scrotal BCC occurring concurrently with another metastatic carcinoma has never been reported. We encountered a rare case of scrotal BCC in the presence of metastatic squamous cell carcinoma (SCC) of the ear canal. This case illustrates the challenges encountered in diagnosing and treatment. It also highlights a palliative strategy that provides the patient with a good quality of life.

CASE REPORT

A 70-year-old male complained of having a chronic and non-healing ulcer on his left hemiscrotum for two yrs. He used to work as a supervisor at a chemical factory for over 20 yrs. The job involved exposure and close contact with various chemicals including magnesium sulphate, nitric oxide, ammonia, paraquat, liquid hydrogen, chlorine gas and sulphur compounds. The scrotal lesion was made known to us while he was undergoing investigation for SCC of his right external auditory meatus. The SCC was found to have metastasized to the liver and lymph nodes in the abdomen and pelvis. The concomitant presence of this metastatic SCC raised the suspicion that the scrotal lesion could be a metastatic secondary. On physical examination, the lesion was located at the inferior part of the scrotum. It measured 3cm x 4cm in size, and had pearly irregular borders and central ulceration (Figure 1). It had a hard consistency but it did not feel adherent to the underlying tunica vaginalis and testes. The clinical appearance of this scrotal lesion was uncharacteristic of SCC. His inguinal lymph nodes were also found to be enlarged bilaterally. A wedge biopsy of the scrotal lesion unexpectedly diagnosed it to be BCC instead of metastatic SCC (Figure 2).

He underwent wide local excision (WLE) of the scrotal lesion with the intention for local disease control. Intraoperatively, the tumour was resected with at least 1 cm macroscopic margin. However, the histopathological examination (HPE) showed nodular, infiltrative pattern BCC of the scrotum with inadequate resection margin. Meanwhile, he developed a new satellite scrotal sinus just near the base of penis. He subsequently underwent further excision of the scrotal scar and sinus. While the scrotal scar HPE showed good clearance margin this time, the scrotal sinus was found to harbour even more BCC. After surgery, he was treated with palliative chemoradiation consisting of 6 cycles of cisplatin 30mg/m2, and 70 Gy in 35 fractions of radiotherapy to the metastatic neck and abdominal lymph nodes. He remained well six month after completing palliative treatment and there was no local recurrence of the scrotal BCC.

DISCUSSION

Basal cell carcinoma is the commonest skin cancer in most parts of the world (Lomas et al. 2012). It is widely accepted that excessive exposure to ultraviolet (UV) radiation is a major risk factor for developing BCC (Wang et al. 2010). Therefore, most BCC occur on parts of the skin that are usually exposed to sun (Jeon et al. 2006), and BCC of the scrotum is understandably quite uncommon (Dai et al. 2012; Jeon et al. 2006; Kinoshita et al. 2005). Unlike SCC of the scrotum that has several established risk factors, scrotal BCC does not have any clear relations with carcinogen exposure. (Jeon et al. 2006). Indeed, its pathogenesis still remains unclear and few postulations were proposed. These include impaired immune surveillance, genetic mutation and even chronic irritation (Jeon et al. 2006; Ouchi & Sugiura 2008; Wang et al. 2010).

Scrotal BCC is also thought to behave more aggressively than its counterpart located elsewhere on the body. Metastatic scrotal BCC is known to occur much earlier, at around 2-3 yrs after the initial diagnosis; in contrast, BCC on other sites that metastasize at an average time of 11 yrs after being diagnosed (Kinoshita et al. 2005). The commonest sites of metastasis are lymph nodes, lungs and bones (Kinoshita et al. 2005). Nevertheless, there was a single case report of scrotal BCC that remained dormant for over 50 yrs (Wang et al. 2010). Unfortunately, we were unable to predict which patient would have metastasis sooner than others. Previous attempts at using histological features to predict metastatic potential have been largely unsuccessful (Kinoshita et al. 2005). Therefore, we must remain vigilant for the possibility of early distant spread in all cases of scrotal BCC.

The present case was a diagnostic challenge to us because while the patient was being investigated for metastatic SCC of the external auditory meatus, he alerted us about an ulcerating lesion on his scrotum. The initial impression was that the scrotal lesion should also be squamous cell in origin and treatment would follow the course for SCC. However, a biopsy of the lesion found it to be BCC. This then posed a question of whether to wide local excision of the scrotal was appropriate in the presence of widespread metastatic SCC from his ear. Furthermore, we also faced a dilemma in deciding the systematic therapy that he should receive in this unusual situation.

Most authors agree that surgery is the mainstay of treatment for localized scrotal BCC (Delto et al. 2016; Jeon et al. 2006; Ribuffo et al. 2002; Wang et al. 2010). A clear surgical margin of > 6 mm reduces the risk of disease relapse (Delto et al. 2016). Other authors advocate greater clear surgical margin of 2-3cm for complete resection of the local disease (Hernández-Aragüés & Baniandrés-Rodríguez 2016). In cases where metastases occurred, systemic chemotherapy should be administered (Cieplinski 1984; Jeon et al. 2006) and a cisplatin-based combination seems to produce acceptable results (Cieplinski 1984). Of particular note, metastatic scrotal SCC can also be treated with cisplatin in combination with methotrexate and bleomycin (Vyas et al. 2014).

We offered the patient wide local excision of his scrotal BCC as a means for local control and also to free him from the constant discomfort of an ulcerating lesion. This was followed by palliative systemic treatment with cisplatin chemotherapy, and radiotherapy to the metastatic lymph nodes at his neck and abdomen. This treatment strategy gave him a good quality of life at 6 months, post-chemoradiation.

CONCLUSION

In conclusion, a patient with scrotal BCC presenting concurrently with metastatic SCC of the ear is rare and can be a challenge to manage. A careful and individualized treatment plan, combining surgery, chemotherapy and radiotherapy can provide excellent palliative outcome in this clinical scenario.

References: 
Cieplinski, W. 1984. Combination chemotherapy for the treatment of metastatic basal cell carcinoma of the scrotum. A case report. Clin Oncol 10(3): 267-72. Dai, B., Kong, Y.Y., Ye, D.W., Xu, X.W., Yao, X.D., Zhang, S.L. 2012. Basal cell carcinoma of the scrotum: clinicopathologic analysis of 10 cases. Dermatol Surg 38(5): 783-90. Delto, J.C., Garces, S., Sidhu, A.S., Ghaffaripour, T., Omarzai, Y., Nieder, A.M. 2016. Giant Fungating Basal Cell Carcinoma of the Scrotum. Urology 91: e1-2. Hernández-Aragüés, I., Baniandrés-Rodríguez, O. 2016. Basal cell carcinoma of the scrotum. Actas Urol Esp 40(9): 592-3. Jeon, J., Song, H.J., Oh, C.H. 2006. Basal Cell Carcinoma of the scrotum. Ann Dermatol 18(2): 97-9. Kinoshita, R., Yamamoto, O., Yasuda, H., Tokura, Y. 2005. Basal cell carcinoma of the scrotum with lymph node metastasis: report of a case and review of the literature. Int J Dermatol 44(1): 54-6. Lomas, A., Leonardi-Bee, J., Bath-Hextall, F. 2012. A systematic review of worldwide incidence of nonmelanoma skin cancer. Br J Dermatol 166(5): 1069-80. Ouchi, T., Sugiura, M. 2008. Polypoid basal cell carcinoma on the scrotum. J Dermatol 35(12): 804-5. Ribuffo, D., Alfano, C., Ferrazzoli, P.S., Scuderi, N. 2002. Basal cell carcinoma of the penis and scrotum with cutaneous metastases. Scand J Plast Reconstr Surg Hand Surg 36(3): 180-2. Vyas, R., Zargar, H., Trolio, R.D., Di Lorenzo, G., Autorino, R. 2014. Squamous cell carcinoma of the scrotum: A look beyond the chimneystacks. World J Clin Cases 2(11): 654-60. Wang, J.W., Man, L.B., He, F., Huang, G.L., Li, G.Z., Wang, H.D. 2010. Images for diagnosis . Basal cell carcinoma of the scrotum: report of a case and review of the literature. Chin Med J (Engl) 123(19): 2748-9.
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Urethral Masson’s Tumour: A Rare and Puzzling Entity

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Abstrak (In MALAY language): 

Intravascular papillary endothelial hyperplasia (IPEH) atau Masson’s tumor merupakan sejenis proliferasi vaskular yang berkelakuan lebih kurang sama dengan tumor vaskular malignan yang lain. Sehingga kini, laporan kes ini merupakan kes tumor Masson uretra yang keempat yang pernah dilaporkan. Seorang wanita yang berusia 65, para 2 datang dengan pendarahan dari vagina selepas menopos. Satu ketumbuhan bersaiz 4x3x3 cm dijumpai di uretra meatus sewaktu pemeriksaan fizikal. Pesakit telah menjalani pemeriksaan di bawah bius dan ketumbuhan tersebut telah dibedah siasat. Tumor Masson telah dikenalpasti melalui pemeriksaan histopatologi. Diagnosis dan pengendalian kes luar biasa ini akan dibincang dalam laporan kes ini.

Correspondance Address: 
Lim Pei Shan, Department of Obstetrics &Gynaecology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +603-91455949 Fax: +603-91456672 E-mail: peishan9900@yahoo.com
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INTRODUCTION

Intravascular papillary endothelial hyperplasia (IPEH) is a unique clinical entity i.e. a non-neoplastic intravascular lesion. This lesion was first described by Pierre Masson in 1923 (Masson 1923) then was termed IPEH (Clearkin & Enzinger 1976). So far, various researchers have struggled to define this unique condition with various terminologies such as Masson’s tumour, vegetating hemangioendothelioma, intravascular angiomatosis etc. This lesion should be differentiated from other malignant vascular neoplasm like angiosarcoma. We report an extremely rare case of IPEH that occurred in female urethra.

CASE REPORT

A 65-year-old Para 2, post-menopausal for 10 yrs not on hormone replacement therapy, presented with vaginal bleeding for one-week duration. There was no abnormal vaginal discharge or urinary symptoms. Her last Pap smear was 10 yrs ago. She was diagnosed to have hypertension and dyslipidaemia on treatment. Her aunt suffered from breast carcinoma.

Upon presentation, her blood pressure was 126/64mm Hg with pulse rate of 86 beats/min. There was no mass palpable abdominally. Perineal inspection revealed an atrophic vulva and vagina. There was a 3.0 x 3.0 x 4.0 cm growth seen surrounding the urethral meatus. Punch biopsy was taken and sent for histo-pathological examination (HPE).

HPE of the biopsy showed few segments of brownish tissue with aggregate diameter of 18 mm, macroscopically. Microscopically, there were few segments of haemorrhagic and oedematous fibrous stromal tissue. The stroma was hypocellular and oedematous, composed of multiple thombosed vessels with some of them displayed intravascular papillary endothelial cells proliferation (Figure 1). The endothelial cells expressed CD34 (Figure 2). There was no dysplasia or evidence of malignancy. The HPE was consistent with intravascular papillary epithelial cell proliferation (Masson’s tumour). She subsequently underwent examination under anaesthesia and full excision of the remaining lesion (Figure 3).

DISCUSSION

To date, the pathogenesis of IPEH remained poorly understood. Possible mechanisms include papillary proliferation of endothelial cell that subsequently degenerates and necrosis in the vascular lumen. Hashimoto et al. (1983) classified IPEH into 3 types. Type I IPEH (primary or pure form) occurs within the vascular spaces, where as, Type II is mixed form that occurs at pre-existing vascular lesion such as haemangioma, arteriovenous malformation or pyogenic granuloma. Lastly, Type III, the least common type, is found in extravascular space. All these lesions were closely associated with thrombus and thrombotic material (Pegado et al. 2015).

Most IPEH developed in head and neck, extremities and trunk (Hashimoto et al. 1983). It was rarely found in the genitourinary area especially urethra. Clinically, IPEH elsewhere usually presented as a firm tender mass overlying the skin or mucous membrane where as urethral IPEH presented with vaginal bleeding. To date, there are only four reports of urethral IPEH (Nevin et al. 2006; Barua & Munday 1983; Fernandes-Flores et al. 2003) (Table 1). All reported cases were post-menopausal women who were above 60 yrs.

Due to its non-specific clinical presentation; it poses a significant diagnostic challenge as malignant vascular neoplasm like angiosarcoma needs to be ruled out especially in elderly patient. Histopathologically, IPEH is associated with thrombi in an expanded vessel without evidence of mitotic activity, atypia or necrosis. The cells do not invade the perivascular spaces compared to angiosacrcoma. Immunochemically, IPEH reacts with various substances such as MSA, SMA, CD31 and CD34. Fortunately, angiosacrcoma can be differentiated with CD 105 staining as this molecule only overexpressed in angiosarcoma associated endothelial cells (Soares et al. 2008; Akdur et al. 2013).

The prognosis of IPEH is very good. Treatment includes local excision. Recurrence is extremely rare, though, it might occur at the site of previous vascular lesion or if the lesion is incompletely excised (Inaioz et al. 2001). The present patient presented with post-menopausal bleeding secondary to urethral IPEH. There was no evidence of recurrence after one year of excision.

IPEH at female urethra is an extremely rare occurrence. The lesion must be differentiated from other malignant vascular neoplasm. Surgical excision is warranted for histopathological examination as incorrect diagnosis may lead to over aggressive treatment.

References: 
Akdur, N.C., Donmez, M., Gozel, S., Ustun, H., Hucumenoglu, S. 2013. Intravascular papillary endothelial hyperplasia: histomorphological and immunohistochemical features. Diagn Pathol 8: 167. Barua, R., Munday, R.N. 1983. Intravsacular angiomatosis in female urethral mass. Masson intravascular hemangioendothelioma. Urology 21(2): 191-3. Clearkin, K.P., Enzinger, F.M. 1976. Intravascular papillary endothelial hyperplasia. Arch Pathol Lab Med 100(8): 441-4. Fernandez-Flores, A., Merino-Sanchez, J.M., Del-Barrio, M., Bouso, M., Alonso-Ortiz, J. 2003. Intravascular papillary endothelial hyperplasia in a female urethral mass. BJU Int 92(Suppl 3): e58-e59. Hashimoto, H., Daimaru, Y., Enjoji, M. 1983. Intravascular papillary endothelial hyperplasia. A clinicopathologic study of 91 cases. Am J Dermatopathol 5(6): 539-46. Inaioz, H.S., Patel, G., Knight, AG. 2001. Recurrent intravascular papillary endothelial hyperplasia developing from a pyogenic granuloma. J Eur Acad Dermatol Venereol 15(2): 156-8. Masson, P. 1923. Hemangioendothelioma vegetant intra-vasculae. Bull Soc Anat 93: 517-23. Nevin, D.T., Palazzo, J., Petersen, R. 2006. A urethral mass in a 67-year-old woman. Papillary endothelial hyperplasia (Masson tumour). Arch Pathol Lab Med 130(4): 561-2. Pegado, P.F., Ordi, Q.C., Roche, S., Rivas, A.G., Domiguez, R.O. 2015. Intravascular papillary endothelial hyperplasia (Masson tumour) mimicking a sarcoma and developing from an arteriovenous hemodialysis fistula. Skeletal Radio 44(6): 859-62. Soares, A.B., Altemani, A., Furuse, C., Demasi, A.P., Gati, C., Nunes, N., de Araujo, V.C. 2008. Intravascular papillary endothelial hyperplasia: report of 2 cases and immunohistochemical study. Oral Surg Oral Med Oral Pathol Oral Radio and Endod 106(5): 708-11.
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Allergic Cutaneous and Visceral Angioedema Secondary to Clozapine: A Case Report

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Abstrak (In MALAY language): 

Laporan ini menerangkan kejadian tindak balas ubat clozapine yang jarang berlaku, iaitu alahan kutaneus dan angioedema visera, pada seorang pesakit skizofrenia yang tidak menunjukkan kesan terhadap rawatan ubat-ubatan yang biasa. Kami melaporkan seorang pesakit skizofrenia rintang-rawatan yang mengalami masalah alahan pada kulit dan sistem gastro-usus sejurus beliau menerima rawatan ubat clozapine. Beliau kemudiannya dirawat dengan kombinasi beberapa ubat-ubatan, namun masih mengalami gejala-gejala residual. Manifestasi alahan kepada ubat clozapine and strategi perawatan dibincangkan di dalam laporan kes ini. Terdapat keperluan yang mendesak bagi penghasilan ubat psikotropik yang setanding clozapine untuk merawat pesakit, memandangkan masalah alahan ubat seperti laporan kes ini.

Correspondance Address: 
Chia Lip Choy Department of Psychiatry, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +603-9145 6143/6142 Fax: +603 9145 6681 E-mail: chialipchoy@gmail.com
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INTRODUCTION

Clozapine was once withdrawn from the market in 1978 due to its life-threatening adverse reaction (Wahlbeck et al. 2000). However, it was reintroduced back in 1990 for individuals with schizophrenia who were resistant to typical neuroleptics (Warnez & Alessi-Severini 2014). Generally, clozapine is proven to be superior to other anti-psychotics (Leucht et al. 2009) and its role is also found in other psychiatric disorders, possibly mania (Ng et al. 2013). Clozapine is well accepted and tolerated in most individuals (Leucht et al. 2013), except few adverse reactions which limits its use (McIlwain et al. 2011; Warnez & Alessi-Severini 2014). To date, clozapine is the only drug licensed for for the treatment of treatment-resistant schizophrenia (TRS) (Kane & Corell 2016).

Angioedema, a systemic allergic reaction to clozapine has not been reported widely. We aim to report a case of allergic angioedema involving skin and gastrointestinal system secondary to clozapine in an individual with treatment resistant schizophrenia (TRS). We highlight the need to develop an alternative drug which is as effective as clozapine in treating this group of patients.

CASE REPORT

SF, a 22-year-old lady who was diagnosed with schizophrenia 3 yrs earlier, was hospitalized in February 2014 due to relapse of her illness with symptoms of auditory hallucination, persecutory delusion, insomnia, 126irritability and aggression, despite being on antipsychotic treatment. Since the onset of her illness, she had never achieved full symptom remission despite being treated with adequate dosage and duration of a few anti-psychotics. She had frequent relapses with aggression as the main presenting symptom which typically required hospitalization. Her first medication was the oral risperidone up to 4mg daily. Due to persisting symptoms and possibility of non-adherence to medication, intramuscular (IM) depot flupenthixol 20 mg was subsequently introduced monthly at first and later fortnightly as symptom control was still not adequate with monthly injection. She who was not known to have any drug allergy in the past.

The diagnosis was revised to treatment-resistant schizophrenia and clozapine was initiated. Her symptoms improved significantly and she was discharged following her parent’s request with a dose of 50 mg twice daily. She developed urticaria in the next few days which waxed and waned, and it was not reported to the attending doctor on her subsequent follow up. Clozapine dose was further increased another 25 mg during this visit. She developed mild fever without other symptoms of infections. She visited a general practitioner and she was given tablet paracetamol. Subsequently, she developed periorbital oedema, generalized itchy rashes, loss of appetite, abdominal pain, vomiting and lethargy. She had no respiratory failure. She was admitted to the medical ward. Eosinophilia (10.6%) was detected 3 days after hospitalization. She was diagnosed with angioedema secondary to clozapine. Her family members objected to the suggestion for a skin prick test for clozapine to confirm the diagnosis. She was successfully treated with regular intravenous hydrocortisone and oral loratadine. She was discharged medically after 3 days.

Then clozapine was withheld and she was started on Tablet Haloperidol. Subsequently she was tried on quetiapine 800 mg daily with combination of haloperidol 5 mg daily and IM flupenthixol 40 mg 3 weekly. Haloperidol was switched later to tablet risperidone and titrated up to 4 mg daily. She reported residual symptoms all the times despite optimization with augmentation and compliance was assured.

DISCUSSION

Clozapine is the only drug licensed for the treatment of TRS (O’Brien 2004). Despite 30-50% significant clinical response to clozapine for patients with TRS (Chakos et al. 2001), the efficacy of clozapine is limited by certain life-threatening adverse effects, e.g. hypersensitivity, which impose challenges in the management in these group of patients. There are reports on allergic asthmatic reactions (Stoppe et al. 1992), allergic vasculitis (Penaskovic et al. 2005), angioneurotic edema (Mishra et al. 2007) and a case of late-onset angioedema (Tatar et al. 2014) secondary to clozapine.

The understanding of immunological mechanism of allergic reactions to clozapine is based on the hapten hypothesis which involves the hypersensitivity to the autologous protein from the chemically reactive metabolites of the drug (Park et al. 2001). This is a type I hypersensitivity reaction which is mediated by Ig E antibodies (Lamer et al. 2010). The reaction can be systemic or local. The local reactions can be manifested by cutaneous swelling, nasal or conjunctival discharge, bronchial asthma and gastroenteritis. The systemic reaction can present with anaphylaxis and drug rash with eosinophilia and systemic symptoms (DRESS) syndrome (Warrington & Silviu-Dan 2011). In this case, she developed recurrent episodes of angioedema involving the swelling of skin and possibly mucosal of gastrointestinal system (as there was no objective investigation e.g. colonoscopy, biopsy, done to her).

Sensitization to clozapine is required before a series of reactions to take place. Following sensitization, the initial response will occur within seconds and subsequently subsides within an hour, while a late phase takes 8 to 12 hrs to develop (Murphy et al. 2008). The patient had developed transient urticaria following clozapine administration in ward. However, the presentation was subtle and went unreported. She had an exacerbation of allergic symptoms after clozapine dose was increased a week later.

Both phases involve powerful primary and secondary mediators which are responsible in the production of the clinical symptoms. The IL-1β, TNF-ααand GM-CSF regulate the activation, maturation and migration of professional antigen presenting cells (APC), e.g. epidermal Langerhan’s cells, and mast cells. The activated APCs and helper T cells in turn produce cytokines, e.g. IL-12 and IL-4 to regulate the activation, proliferation and differentiation of drug hapten specific T-lymphocytes, which the latter elicit an inflammatory reaction. Histamine and leukotrienes released from mast cells play important roles in Ig E mediated hypersensitivity reaction. The late recruitment of eosinophils which directly activate mast cells and sustain the immunological reaction (Park et al. 2000).

Rechallenge of clozapine has been reported in the case of clozapine-induced leucopenia (Dunk et al. 2006; Stanulovic et al. 2013). However, there is no literature which discussed rechallenging clozapine in the case of allergic reaction. The general principle of management of drug allergy is to withhold the offending medication (Frew 2011). Only when there is definite medical need for the particular medication, there is a strategy of induction desensitization or graded challenge (Castells 2006). The strategy of induction desensitization is discussed in hypersensitivity to antibiotics (Gruchalla 1998) and aspirin (Wong et al. 2000) but was never discussed in case of clozapine.

Among other strategies in clozapine intolerant schizophrenic patients, there is combination or augmentation of various psychotropics and electroconvulsive therapy (Porcelli et al. 2012). There are reports on high-dose aripiprazole (Tripathi et al. 2015) and high-dose quetiapine (Chandrappa & Ho 2012) in cases of TRS intolerant of clozapine. In this case, she was subsequently maintained on high-dose quetiapine which controlled her illness but few psychotic symptoms still remained.

Allergy to clozapine in TRS renders psychiatrist no equivalent choice in subsequent management. There is a dire need for new development of pharmacological agent which has similar efficacy to clozapine.

References: 
Castells, M. 2006. Desensitization for drug allergy. Curr Opin Allergy Clin Immunol 6(6): 476-81. Chakos, M., Lieberman, J., Hoffman, E., Bradford, D., Sheitman, B. 2001. Effectiveness of second-generation antipsychotics in patients with treatment-resistant schizophrenia: a review and meta-analysis of randomized trials. Am J Psychiatry 158(4): 518-26. Chandrappa, P., Ho, L. 2012. Case reports of patients with treatment-resistant schizophrenia and related psychotic disorders intolerant to clozapine responding to high doses of quetiapine. Ther Adv Psychopharmacol 2(5): 207-9. Dunk, L.R., Annan, L.J., Andrews, C.D. 2006. Rechallenge with clozapine following leucopenia or neutropenia during previous therapy. Br J Psychiatry 188: 255-63. Frew, A. 2011. General principles of investigating and managing drug allergy. Br J Clin Pharmacol 71(5): 642-6. Gruchalla, R.S. 1998. Acute drug desensitization. Clin Exp Allergy 28 Suppl 4: 63-4. Kane, J.M., Corell, C.,U. 2016. The Role of Clozapine in Treatment-Resistant Schizophrennia. JAMA Psychiatry 73(3): 187-8. Lamer, V., Lipozencic, J., Turcic, P. 2010. Adverse cutaneous reactions to psychopharmaceuticals. Acta Dermatovenerol Croat 18(1): 56-67. Leucht, S., Cipriani, A., Spineli, L., Mavridis, D., Orey, D., Richter, F., Samara, M., Barbui, C., Engel, R.R., Geddes, J.R., Kissling, W., Stapf, M.P., Lässig, B., Salanti, G., Davis, J.M. 2013. Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: a multiple-treatments meta-analysis. Lancet 382(9896): 951-62. Leucht, S., Corves, C., Arbter, D., Engel, R.R., Li, C., Davis, J.M. 2009. Second-generation versus first-generation antipsychotic drugs for schizophrenia: a meta-analysis. Lancet 373(9657): 31-41. McIlwain, M.E., Harrison, J., Wheeler, A.J., Russell, B.R. 2011. Pharmacotherapy for treatment-resistant schizophrenia. Neuropsychiatr Dis Treat 7: 135-49. Mishra, B., Sahoo, S., Sarkar, S., Akhtar, S. 2007. Clozapine-induced angioneurotic edema. Gen Hosp Psychiatry 29(1): 78-80. Murphy, K., Travers P., Walport, M. 2008. Chapter 13: Allergy and Hypersensitivity. In Janeway’s Immunobiology. 7th edition. New York: Garland Science; 555-97. Ng, Y.P., Kassim, S.M., Maniam, T. 2013. Treatment-Emergent Hypomania or Bipolar Disorder? A Case Report. ASEAN Journal of Psychiatry 14(2): 157-60. O’Brien, A. 2004. Starting clozapine in the community: a UK perspective. CNS Drugs 18(13): 845-52. Park, B.K., Kitteringham, N.R., Powell, H., Pirmohamed, M. 2000. Advances in molecular toxicology-towards understanding idiosyncratic drug toxicity. Toxicology 153(1-3): 39-60. Park, B.K., Naisbitt, D.J., Gordon, S.F., Kitteringham, N.R., Pirmohamed, M. 2001. Metabolic activation in drug allergies. Toxicology 158(1-2): 11-23. Penaskovic, K.M., Annamraju, S., Kraus, J.E. 2005. Clozapine-induced allergic vasculitis. Am J Psychiatry 162(8): 1543. Porcelli, S., Balzarro, B., Serretti, A. 2012. Clozapine resistance: augmentation strategies. Eur Neuropsychopharmacol 22(3): 165-82. Stanulovic, V., Venegoni, M., Edwards, B. 2013. Intentional rechallenge: does the benefit outweigh the risk? Drug Saf 36(3): 155-61. Stoppe, G., Muller, P., Fuchs, T., Ruther, E. 1992. Life-threatening allergic reaction to clozapine. Br J Psychiatry 161: 259-61. Tatar, Z.B., Oflaz, S., Baran, B. 2014. A case of late-onset angioedema associated with clozapine and redevelopment of angioedema with olanzapine. J Clin Psychopharmacol 34(4): 523-5. Tripathi, P., Goyal, P., Kumar, D., Prakash, O. 2015. High doses of aripiprazole therapy for a patient with treatment-resistant schizophrenia responsive to, but intolerant of, clozapine. Aust N Z J Psychiatry 49(2): 185. Wahlbeck, K., Cheine, M., Essali, M.A. 2000. Clozapine versus typical neuroleptic medication for schizophrenia. Cochrane Database Syst Rev (2): CD000059. Warnez, S., Alessi-Severini, S. 2014. Clozapine: a review of clinical practice guidelines and prescribing trends. BMC Psychiatry 14: 102. Warrington, R., Silviu-Dan, F. 2011. Drug allergy. Allergy Asthma Clin Immunol 7 Suppl 1: S10. Wong, J.T., Nagy, C.S., Krinzman, S.J., Maclean, J.A., Bloch, K.J. 2000. Rapid oral challenge-desensitization for patients with aspirin-related urticaria-angioedema. J Allergy Clin Immunol 105(5): 997-1001.

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A Case of Missed Thoracic Fracture Masquerading as Intra-Abdominal Injury

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Abstrak (In MALAY language): 

Keadaan status mental yang rendah di dalam politrauma merupakan cabaran kepada pasukan kecemasan dalam pengurusan pesakit. Kecenderungan untuk terlepas penemuan positif dalam keadaan ini meningkat beberapa kali ganda kerana pelbagai faktor seperti kemurungan/kemabukan, kehadiran kecederaan yang mengganggu dan kecederaan yang mengancam nyawa serentak, menyebabkan perlunya memberi perhatian yang lebih mendesak. Memandangkan keadaan ini, kriteria NEXUS (Kajian Penggunaan X-Radiografi Kecemasan Nasional) untuk memeriksa tulang belakang servikal telah diterima pakai dan digunakan di seluruh dunia. Walau bagaimanapun, tiada kata sepakat untuk memeriksa bahagian lain tulang belakang. Kes ini melaporkan seorang lelaki berusia 18 tahun dengan status mental berubah, sakit dan luka di bahagian muka akibat kemalangan jalan raya. Kepatahan di bahagian muka disahkan dan dia dibernarkan keluar dari hospital. Tiga hari kemudian dia kembali dengan sakit epigastrik yang teruk. Sakit pada bahagian belakang mendorong imbasan CT dilakukan. Beberapa vertebra toraks didapati patah. Sebagai kesimpulan, pemeriksaan primer dan sekunder yang menyeluruh perlu dilakukan pada pesakit yang telah sedar semula sebelum dibenarkan pulang.

Correspondance Address: 
Nik Azlan Nik Muhamad, Urology Unit, Department of Emergency Medicine, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +603-91455703 Fax: +603-91456577 E-mail: nikazlanmuhamad@hotmail.com
Full text: 

INTRODUCTION

Fracture of thoracolumbar spine may occur following high impact accidents. Cooper and colleagues stated that the incidence of thoracolumbar spinal fracture can be as high as 50% in blunt traumas (Cooper et al. 1995). Hsu and colleagues proposed radio imaging of the thoracolumbar spine in all victims of high impact accidents in the presence of midline tenderness, local signs of thoracolumbar injury, abnormal neurological signs, cervical spine fracture, GCS < 15, major distracting injury, and alcohol or drug intoxication (Hsu et al. 2003).

This was a case of an 18-yrs-old male, who presented with altered mental status and multiple abrasions wound over the face following a motor vehicle accident. Thoracolumbar spine fracture was missed during the first admission. This can be avoided by thorough primary and secondary examination followed by required radiological examination.

CASE REPORT

A previously well, 18-yrs-old male was involved in a motor vehicle vertebraaccident. He could not recall the exact mechanism of his injury. His Glasgow coma scale (GCS) was 14/15. He suffered multiple abrasion wounds over the maxillary area. Face computed tomography (CT) showed facial bone fracture with no intracranial bleeding. Following complete recovery of his GCS, he was discharged 6 hrs, later. Three days later, he presented to emergency department with severe epigastric pain. The pain was described as pricking in nature and radiated to the back. He was still able to walk, had no vomiting, chest pain or fever. Vital signs were stable. Tenderness was felt over T6-T8 vertebrae. There were no neurological abnormalities. Focussed Assessment using Sonography in Trauma (FAST) showed no positive findings. Due to raised suspicion of thoracic injury CT spine was done and showed burst fracture of T7 vertebral body with compression fracture of T6 and T8 (Figure 1). He was referred to orthopedic team and was admitted for surgical intervention. The patient underwent posterior instrumentation and fusion from level of T6-T10 four days after admission. Post-operative physiotherapy was done and he was able to self ambulate prior to discharge.

DISCUSSION

There are few case reports describing thoracic injury presenting as abdominal pain. Xiong et al. (2001) described a young lady who presented with abdominal pain and found to have a thoracolumbar fracture. We need to bear in mind that abdominal pain is an atypical presentation of thoracic injury. This should be suspected in patients complaining of abdominal pain where intra abdominal injury has been ruled out. The presentation of thoracic injury was similar to a previous case report in which radiculopathic pain resulted from nerve root compression (Xiong et al. 2001). Nerve root compression can produce poorly localized pain which may present as a non specific abdominal pain. Pain may be intermittent or constant and is usually described as electric, burning, or shooting in nature. As a result from dermatomal distribution, any compressing fracture between T7 and L1 can present as referred abdominal pain.

There are number of factors that contribute to delay in diagnosis. Substance intoxication, multiple injuries, altered level of consciousness and two level spinal cord injuries are among factors reported to cause delay in diagnosis (Reid et al. 1987). A trauma patient with concurrent low GCS and persistent complaint of abdominal pain should be suspected to have a possible thoracolumbar fracture if intra-abdominal injury has been ruled out. A screening criteria or tools similar as the NEXUS criteria in cervical spine clearance should be used in order to determine patients that require a CT of the thoracolumbar spine.

CONCLUSION

Thoracolumbar spinal injury may easily be missed in a trauma patient with altered mental status and distracting painful injury. Currently, there is no established guideline in ruling out thoracolumbar spine injury such as NEXUS or Canadian CT rule for cervical spine injury. We would advocate a thoracolumbar CT for any abdominal pain following trauma with normal abdomen CT.

References: 
Cooper, C., Dunham, C.M., Rodrigues, A. 1995. Falls and major injuries are risk factors for thoracolumbar fractures: cognitive impairment and multiple injuries impede the detection of back pain and tenderness. J Trauma 38(5): 692–6. Hsu, J.M., Joseph, T., Ellis, A.M. 2003. Thoracolumbar fracture in blunt trauma patient: guidelines for diagnosis and imaging. Injury 34(6): 426-33. Reid, D.C., Henderson, R., Saboe, L., Miller, J.D. 1987. Etiology and clinical course of missed spine fractures. J Trauma 27(9): 980-6. Xiong, Y., Lachmann, E., Marini, S., Nagler, W. 2001. Thoracic disk herniation presenting as abdominal and pelvic pain: a case report. Arch Phys Med Rehabil 82(8) : 1142-4.
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Fatal Pulmonary Haemorrhage in Co-infection with Dengue and Leptospirosis

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Abstrak (In MALAY language): 

Leptospirosis merupakan penyakit berjangkit yang semakin banyak dilaporkan di serata dunia. Simptom-simptom penyakit ini adalah tidak spesifik dan hampir menyerupai simptom jangkitan lain seperti deman denggi, malaria, hepatits dan deman kepialu, terutamanya di negara-negara tropika di mana penyakit-penyakit tersebut adalah endemik. Demam denggi pula adalah penyakit berjangkit yang dilihat sebagai krisis kesihatan awam disebabkan kadar jangkitan sedunia yang tinggi. Dalam laporan kes ini, kami melaporkan satu kes berkenaan seorang pesakit yang menghidapi demam denggi yang juga disahkan positif dengan jangkitan leptospirosis melalui ujian serologi. Koinfeksi antara demam denggi dan leptospirosis boleh menimbulkan kerumitan pada peringkat diagnosis kerana simptom-simptom bagi kedua-dua jangkitan tersebut hampir serupa. Oleh itu, pakar klinikal harus mempunyai indeks wasangka yang tinggi,khususnya di kawasan di mana kedua-dua penyakit ini adalah endemik. Penggunaan ujian diagnosis yang berasaskan antigen adalah amat penting bagi membantu pakar klinikal dalam membuat diagnosis yang tepat secepat mungkin agar rawatan yang sewajarnya dapat diberikan

Correspondance Address: 
Zyneelia Husain, Department of Emergency Medicine, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +60391455555 Fax: +60391456577 E-mail: zyneelia.husain@gmail.com
Full text: 

INTRODUCTION

Dengue and leptospirosis, commonly found in humid tropical and subtropical areas, are infectious diseases of global importance. Mixed infections of these two pathogens which are associated with high mortality, are typically seen in areas of high endemicity, especially in Malaysia.

Dengue is the fastest spreading vector-borne disease in the world that is transmitted by mosquitoes Aedes aegypti and Aedes albopictus. The incidence of dengue infection continues to rise with growing geographic expansion to new countries for the past half-century, and a 30-fold increase has been reported for that period (World Health Organization 2009). In fact, the number of reported cases in Malaysia has notably increased over the previous decade; from 32 cases per 100,000 to 361 cases per 100,000 in 2014 (MOH 2015). This mosquito-borne viral illness places 2.5 million people in more than 100 countries at risk with an annual estimation of 50 million cases of dengue infections occur worldwide (World Health Organization 2009).

Leptospirosis is a bacterial infection caused by the spirochete leptospiraceae and is the most common zoonosis worldwide. According to WHO, the yearly incidence of leptospirosis ranges from 0.1–1.0/100,000 in temperate climates to 10–100/100,000 in the humid tropics (World Health Organization 2003). In addition, the incidence may reach over 100 per 100,000 during out breaks particularly in five high-exposure risk groups (World Health Organization 2003).

The clinical manifestation of both infectious diseases at early stages of illness consists of an ample array of non-specific signs and symptoms such as high-grade fever, anorexia, generalised body ache, arthralgia, myalgia, nausea, and vomiting (Libraty et al. 2007; Flannery et al. 2001). Libraty et al. (2007) reported that the presence of petechial rash was significantly higher in dengue patients compared to those with leptospirosis. Another study conducted in Brazil by Flannery et al. (2001) showed that a greater proportion of patients develop jaundice in leptospirosis infection compared to those with dengue. However, both of the aforementioned symptoms present at the late stage of the diseases. Because their clinical manifestations at early stages are similar, it may complicate the diagnosis and management of such patients with acute fever. We report a fatal case of a patient who presented with acute febrile illness (AFI) and was positive for dengue virus DENV-3 and leptospiral spp.

CASE REPORT

A 43-yrs-old farmer presented to a district hospital in Sarawak, East Malaysia with a history of high grade fever, generalised bodyache as well as haemoptysis for three days. He was previously well. He denied abdominal pain, nausea or vomiting. Neither chest discomfort nor shortness of breath was reported. The initial blood investigation showed leukopenia and thrombocytopenia, which prompted his referral to the nearest tertiary centre for further management.

On examination, the patient was conscious and orientated with good hydration status. His blood pressure was 107/59 mmHg and the pulse rate was 85 beat/min which was regular and of good volume. He was not tachypnoeic with a respiratory rate of 20 breaths/min. Documented temperature in the Emergency Department was 39.9°°C. Examination of the abdomen showed enlarged liver 3 cm below the right costal margin with neither tenderness nor guarding. In addition, there was no jaundice or rash. Other systemic examinations were unremarkable.

Repeated blood investigations showed bicytopenia with deranged renal and liver function tests (Table 1). The initial chest radiograph was normal. The diagnosis of dengue fever with warning signs was initially made based on his presenting features and a positive dengue NS-1 antigen test. The patient’s serum was also tested for dengue specific IgM antibodies using enzyme-linked immunosorbent assay (ELISA) which came out to be positive. He was managed with appropriate supportive therapy and hydration with crystalloid fluids according to the established guidelines for dengue. However, four hours later, his condition drastically deteriorated. He developed fulminant pulmonary haemorrhage which required invasive ventilation. Intravenous (IV) Ceftriaxone was promptly started based on strong clinical suspicion of leptospirosis despite pending confirmatory serology. The leptospirosis IgM rapid test was then reported to be positive and was further confirmed with a positive microscopic agglutination test (MAT) as shown in Table 1. Reverse transcriptase polymerase chain reaction (RT-PCR) was also performed and dengue virus type 3 (DENV-3) infection was identified.

Throughout his admission in the intensive care unit, his condition did not improve despite aggressive medical regimes as well as escalation of antibiotics. Ventilation became increasingly difficult and required high ventilator settings due to persistent pulmonary haemorrhage with Type ll respiratory failure and was further compounded by ventilator-acquired pneumonia. There was worsening of diffuse opacity over bilateral lung fields, as evidenced in the serial chest X-rays in Figure 1. In addition to that, severe thrombocytopenia persisted despite multiple blood product transfusions (Table 1). On day 23 of hospital admission, the patient, unfortunately succumbed to death.

DISCUSSION

Both dengue and leptospirosis are among the many medical conditions that cause AFI in humid tropical and subtropical areas. Because the clinical manifestations are similar, both dengue and leptospirosis are often indistinguishable at the early stages of illness. Hence, this can complicate the diagnosis of a patient presented with AFI especially in high endemic areas. In addition, co-infection cases are not uncommon. A study conducted in Jamaica showed that 2.5% of the 314 dengue IgM positive samples were also positive for leptospirosis infection (Brown et al. 2010). In another study conducted by Kumar et al. (2012), co-infection of dengue and leptospirosis was confirmed in 1.3% of 1,309 cases where both dengue and leptospirosis were investigated. Similar report is also found in a study done in India by with result of mixed infection of leptospirosis and dengue at 17.5% (Deodar & John 2011).

Our patient was initially presented with symptoms of viral-like illness with evidence of bleeding tendency. The positive dengue NS-1 antigen result together with leucopenia, thrombocytopenia and raised haematocrit level prompted us to treat him as dengue fever with warning signs as he came from a high endemic area for dengue. It is a common practice that if a patient with acute fever is confirmed to be dengue positive, dengue infection is assumed as the sole cause of the fever. Such assumption has caused leptospirosis, “The Great Mimicker”, to be overlooked and under-diagnosed. Due to the overlapping symptoms and signs, it remains difficult to diagnose without serologic test and this problem is proven in a recent cross-sectional study conducted among 10 healthcare facilities done in Northeastern Malaysia. Only 31% of confirmed leptospirosis cases were diagnosed as leptospirosis at the time of hospital discharge while another 38% were wrongly diagnosed as dengue fever or dengue hemorrhagic fever (Rafizah et al. 2012). A study in Thailand by Libraty et al. (2007) also reported that 19% of the children with confirmed leptospirosis were not diagnosed correctly on discharge from hospital. Because the specific treatment differs for both infectious diseases, the availability of antigen-based rapid diagnostic tests is essential to aid the clinicians to make timely and accurate diagnosis as well as to start appropriate treatment regimes, which is even more important in co-infection cases.

The mechanisms causing the increased vascular permeability in severe dengue are not well defined yet. Many theories have been postulated about the pathogenesis of severe dengue infection. Among all, the most studied one is about the development of imbalance immune response. Expression of cytokine, chemokines, and adhesion molecules as well activation of T-lymphocytes and complement system are responsible for the endothelial dysfunction (World Health Organization 2009). In addition, dengue virus infection can affect megakaryocytopoieses, leading to platelet dysfunction and thrombocytopenia (World Health Organization 2009). Similarly, the development of endothelial dysfunction in severe leptospirosis is due to activation of immune mediators (Maciel et al. 2006; Yang & Hsu 2005). Hence, in our case, we believe that the synergistic actions of both organisms lead to generalized endothelial damage, thrombocytopenia as well as platelet dysfunction, resulting in fulminant pulmonary haemorrhage. Mixed infection of dengue and leptospirosis is associated with a higher mortality rate as reported by Kumar et al. (2012) The mortality rate was reported at 29.6% (5/17) in co-infected cases, followed by leptospirosis 14.6% (42/287) and dengue 3.7% (9/239). Sharma et al. (2012) also reported that highest mortality of 12.69% (5/63) in co-infected cases followed by leptospirosis 1.91% (27/63) and dengue 0.425% (6/63).

Co-infection with dengue and leptospirosis requires a variation of treatment modalities. Transfusion of blood products such as fresh packed red cells or fresh whole blood is mandatory in severe dengue with haemorrhagic complication (World Health Organization 2009). To date, the use of antibiotics in leptospirosis remains controversial. However, a Cochrane systemic review showed that antibiotic treatment might shorten the duration of illness (Brett-Major & Coldren 2012). Few studies have advocated the use of glucocorticoids in haemorrhagic pulmonary leptospirosis (Trivedi et al. 2001; Ittyachen et al. 2005; Shenoy et al. 2006). The role of glucocorticoids is imminently significant, particularly within the first 12 hrs of respiratory involvement (Shenoy et al. 2006). It reduces the need for mechanical ventilation and the mortality rate in severe leptospirosis (Shenoy et al. 2006; Kularatne et al. 2011). In addition, other immunomodulation approaches such as plasmapheresis and immunoglobulin may also be helpful (Meaudre et al. 2008). Some novel approaches such as desmopressin, inhaled nitric oxide, activated Protein C and activated Factor VII were also proven beneficial in severe leptospirosis when conventional therapy ceases to work (Gulati & Gulati 2008). However, the potential of such treatments in co-infection with dengue and leptospirosis still remain unclear.

CONCLUSION

Infection of dengue and leptospirosis may co-exist, especially in high endemic areas. Hence, a high index of suspicion is necessary to diagnose a co-infection as most clinicians are used to linking every symptom and sign to a single pathology. In addition, the optimal usage of rapid diagnostic laboratory investigation plays a crucial role in determining the management of undifferentiated AFI, particularly in mixed infection cases. Co-infection with dengue and leptospirosis, as depicted in the case report, warrants a variation of treatment regimes that has to be initiated the earliest possible in order to reduce its severity and, ultimately leading to the favourable outcome of this condition.

References: 
Brett-Major, D.M., Coldren, R. 2012. Antibiotics for leptospirosis. Cochrane Database Syst Rev (2): CD008264. Brown, M.G.,Vickers, I.E., Salas, R.A., Smickle, M.F. 2010. Leptospirosis in suspected cases of dengue in Jamaica, 2002-2007. Trop Doct 40(2): 92-4. Deodhar, D., John, M. 2011. Leptospirosis: experience at a tertiary care hospital in northern India. Natl Med J India 24(2): 78-80. Flannery, B., Pereira, M.M., Velloso, L. de. F., Carvalho, C. de. C., De Codes, L.G., Orrico, G. de. S,, Dourado, C.M., Riley, L.W., Reis, M.G., Ko, A.l. 2001. Referral pattern of leptospirosis cases during a large urban epidemic of dengue. Am J Trop Med Hyg 65(5): 657–63. Gulati, S., Gulati, A. 2012. Pulmonary manifestations of leptospirosis. Lung India 29(4): 347–53. Ittyachen, A., Lakshmanakumar, V.K., Eapen, C.K., Joseph, M.R. 2005. Methylprednisolone as adjuvant in treatment of acute respiratory distress syndrome owing to leptospirosis - a pilot study. Indian J Crit Care Med 9(3): 133–6. Kularatne, S.A., Budagoda, B.D., de Alwis, V.K., Wickramasinghe, W.M., Bandara, J.M., Pathirage, L.P., Gamlath, G.R., Wijethunga, T.J., Jayalath, W.A., Jayasinghe, C., Pinto, V., Somaratne, P., Kumarasiri, P.V. 2011. High efficacy of bolus methylprednisolone in severe leptospirosis: a descriptive study in Sri Lanka. Postgrad Medl J 87(1023): 13-7. Kumar, A., Balachandran, V., Dominic, A., Dinesh, K.R., Karim, S., Rao, G. 2012. Serological evidence of leptospirosis and dengue coinfection in an endemic region in South India. Ann Trop Med Public Health 5(4): 286-90. Libraty, D.H., Myint, K.S., Murray, C.K., Gibbons, R.V., Mammen, M.P., Endy, T.P., Li, W., Vaughn, D.W., Nisalak, A., Kalayanarooj, S., Hospenthal, D.R., Green, S., Rothman, A.L., Ennis, F.A. 2007. A comparative study of leptospirosis and dengue in Thai children. PLoS Negl Trop Dis 1(3): 1-7. Maciel, E.A., Athanazio, D.A., Reis, E.A., Cunha, F.Q., Queiroz, A., Almeida, D., McBride, A.J., Ko, A.l., Reis, M.G. 2006. High serum nitric oxide levels in patients with severe leptospirosis. Acta Trop 100(3): 256-60. Meaudre, E., Asencio, Y., Montcriol, A., Martinaud, C., Graffin, B., Palmier, B., Goutorbe, P. 2008. Immunomodulation in severe leptospirosis with multiple organ failure: Plasma exchange, Intravenous immunoglobulin or corticosteroids? Ann Fr Anesth Reanim 27(2): 172–6. Ministry of Health Malaysia, (MOH). 2015. Clinical Practical Guidelines: Management of Dengue Infection in Adults. Putrajaya; Ministry of Health Malaysia; 1-75. Rafizah, A.A.N., Aziah, B.D., Azwany, Y.N., Imran, M.K., Rusli, A.M., Nazri, S.M., Nikman, A.M., Nabilah, I., Asma,’ H.S., Zahiruddin, W.M., Zaliha, I. 2012. Leptospirosis in Northeastern Malaysia: misdiagnosed or coinfection? Int J Collab Res Intern Med Public Health 4(7): 1419-27. Sharma, K.K., Latha, P.M., Kalawat, U. 2012. Coinfection of leptospirosis and dengue fever at a tertiary care centre in South India. Scho Res J 2(1): 12-6. Shenoy, V.V., Nagar, V.S., Chowdhury, A.A., Bhalgat, P.S., Juvale, N.I. 2006. Pulmonary leptospirosis: An excellent response to bolus methyl prednisolone. Postgrad Med J 82(971): 602–6. Trivedi, S.V., Chavda, R.K., Wadia, P.Z., Sheth, V., Bhagade, P.N., Trivedi, S.P., Clerk, A.M., Mevawala, D.M. 2001. The role of glucocorticoid pulse therapy in pulmonary involvement in leptospirosis. J Assoc Physicians India 49(1): 901–3. World Health Organisation. 2009. Dengue: Guidelines for Diagnosis, Treatment, Prevention and Control: New edition. Geneva: World Health Organization; 1-160. World Health Organization. 2003. Human Leptospirosis: Guidance for Diagnosis, Surveillance and Control. Geneva: World Health Organization; 1-109. Yang, G.G., Hsu, Y.H. 2005. Nitric oxide production and immunoglobulin deposition in leptospiral hemorrhagic respiratory failure. J Formos Med Assoc 104(10): 759-63.
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An Unusual Variant of the Sphenopalatine Foramen and Artery with an Absent Crista Ethmoidalis: An Intra-Operative Challenge

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Abstrak (In MALAY language): 

Ligasi arteri sphenopalatine merupakan satu terapi pembedahan untuk masalah hidung berdarah. Prosedur ini memerlukan pengetahuan yang luas mengenai variasi anatomi hidung. Walaubagaimanapun, petanda yang biasanya dipercayai seperti crista ethmoidalis mungkin tidak dijumpai atau tiada langsung. Variasi tersebut adalah penting dan boleh menentukan keberkesanan prosedur ini. Kami memaparkan satu kes variasi foramen dan arteri sphenopalatine yang tiada crista ethmoidalis. Foramen sphenopalatine dijumpai di bahagian atas meatus superior melepasi lamella concha superior di bahagian horizontalnya. Hanya satu cabang arteri yang ditemui keluar daripada foramen sphenopalatine. Foramen sphenopalatine diukur daripada bahagian depan hidung. Ia berukuran 69 mm dari “nasal sill” dan 54 mm dari limen nasi.

Correspondance Address: 
Fahrin Zara Nasseri, Department of Otorhinolaryngology Head and Neck Surgery, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +60391456599 Fax: +60391456675 E-mail: zaranasseriwork@gmail.com
Full text: 

INTRODUCTION

Endoscopic sphenopalatine artery ligation is a known successful approach to alleviating severe epistaxis. The procedure may rather prove to be tricky with so many anatomical variants. Intimate knowledge of all the possible anatomical variants is vital in performing SPA ligations to achieve excellent surgical outcome. A surgeon with familiarity with the variants should find this a straightforward procedure. (Simmen et al. 2006). We present a peculiar case of a postero-superiorly located variant of the sphenopalatine foramen and artery with an absent crista ethmoidalis. The absent crista ethmoidalis is a significant landmark for the search of the sphenopalatine foramen and its artery (Lee et al. 2002). Furthermore, the location of the sphenopalatine foramen and its number of vessel appearing from it may complicate the outcome and aim of the surgery.

CASE REPORT

We report on a 56-years-old male who presented with left-sided unilateral epistaxis. He was previously well and his epistaxis failed to stop despite conservative methods. It started two days prior to admission and was estimated at 200 ml each day. Upon arrival in the emergency department, he was found to be hypertensive at 200/110 mmHg which was successfully treated with anti-hypertensive medication. Rigid 0 degree nasal endoscopy was done which revealed blood trickling from the right ostiomeatal complex (OMC). The epicenter was not as yet visible. The epistaxis was so severe that he had blood trickling out of his anterior nares bilaterally as well as posteriorly into his oropharynx. Anterior and posterior nasal packing was done and he was admitted for close observation. A repeat full blood count 24 hrs later revealed a drop of hemoglobin level of 5g/dL from 14g/dL to 9g/dL. The steep fall of hemoglobin level and failure of nasal packing prompted surgical intervention. He underwent an endoscopic sphenopalatine artery ligation under general anaesthesia 24 hrs after admission.

Intra-operatively, fresh blood with old clotted blood was seen in the left nasal cavity with some overspill noted in the right nasal cavity. Once both nasal cavities were suctioned, we found the right side to be normal, with fresh blood oozing from left lateral wall. A right middle meatalantrostomy was performed. The posterior wall of the maxillary sinus was identified. A mucoperichondrial flap was made postero-superiorly and postero-inferiorly to identify the crista ethmoidalis. This was found to be absent which made locating the sphenopalatine foramen a challenge as it was not immediately visible. The sphenopalatine foramen was found superiorly at the superior meatus beyond the horizontal part of the lamella of the superior concha (Figure 1). Only one trunk was seen exiting the sphenopalatine foramen. The sphenopalatine foramen was measured from the anterior part of the nose. It was 69 mm from the nasal sill and 54 mm limen nasi. The trunk of the sphenopalatine artery was successfully cauterized and bleeding stopped (Figure 2). Anterior nasal packing was done at the end of the procedure.

The patient was well with no epistaxis, post-operatively. The anterior nasal packing was removed the next day. He was discharged well following two days of observation.

DISCUSSION

The present patient with epistaxis was initially subjected to anterior and posterior packing as per local protocol. When this failed to check the epistaxis, he underwent endoscopic sphenopalatine artery ligation. Numerous reports recommend this technique as it has a high success rate (Graz-Cabrerizo et al. 2014; Abdelkader et al. 2007). The intimate knowledge of the multiple variants of the sphenopalatine foramen and its artery is essential to a successful outcome.

Studies had been done revealing the commonest location of the sphenopalatine foramen (SPF). According to Lee et al., 90% is located within the superior meatus, between the middle turbinate and the posterior horizontal end of the lamella of the superior turbinate, attaching to the lateral nasal wall while in 10%, the foramen extended superiorly beyond the posterior horizontal portion of the lamella of the superior turbinate (Lee et al. 2002). In this case, in terms of its location it is consistent with the report i.e. located at the superior meatus beyond the horizontal part of the lamella of the superior turbinate. However, the measurements 69 mm from the nasal sill and 54 mm limen nasi were deviated from a study 59.4 ± 4.2 mm and 49.1 ± 3.7 mm (Lee et al. 2002).

The crista ethmoidalis (CE) is a vital anatomical landmark which unfortunately was absent in our patient. Bolger et al., observed 95.5% of the cadavers had the SPF posterior to the crista ethmoidalis (Bolger et al. 1999). The presence of the (CE) in 96.4% is highlighted by Rezende et al. (2012). Its absence is a rare phenomenon and priovides a difficult intra-operative challenge in the search for the sphenopalatine foramen and artery, especially in an acutely bleeding patient.

Much has been documented on the number of branches of the SPA (Table 1). Lee et al. reported SPA divided into two branches 76%, three branches 22%, four branches 2% (Lee et al. 2002). Simmen et al. (2006) reported a range from 1 to 10 branches branched from the SPA. Two or three branches are the commonest at 32% and 31%. More recently, Padua & Voegels (2008) and Gras-Cabrerizo et al. (2014) contradicted that the single trunk is the commoner finding with incidence of 67% (Pádua & Voegels 2008), and 63% (Gras-Cabrerizo et al. 2014). The number of branches vary depending on the authors finding the branches before and after crossing the SPF. All branches had to be ligated to logically to avoid failure in endoscopic SPA ligation. In our patient, only one branch was found. This single branch of the SPA was cauterized and it successfully checked the epistaxis.

CONCLUSION

The anatomy of the lateral nasal wall varies significantly. Intimate knowledge of all the possible anatomical variants is vital in performing SPA ligations to achieve excellent surgical outcome.

References: 
Abdelkader, M., Leong, S.C., White, P.S. 2007.Endoscopic control of the sphenopalatine artery for epistaxis: long-term results. J Laryngol Otol 121(8):759-62. Bolger, W.E., Borgie, R.C., Melder, P. 1999. The role of the crista ethmoidalis in endoscopic sphenopalatine artery ligation. Am J Rhinol 13(2): 81-6. Gras-Cabrerizo, J.R., Ademá-Alcover, J.M., Gras-Albert, J.R., Kolanczak, K., Montserrat-Gili, J.R., Mirapeix-Lucas, R., Del Campo, F.S., Massegur-Solench, H. 2014. Anatomical and surgical study of the sphenopalatine artery branches. Eur Arch Otorhinolaryngol 271(7): 1947-51. Lee, H.Y., Kim, H.U., Kim, S.S., Son, E.J., Kim, J.W., Cho, N.H., Kim, K.S., Lee, J.G., Chung, I.H., Yoon, J.H. 2002. Surgical anatomy of the sphenopalatine artery in lateral nasal wall. Laryngoscope 112(10): 1813-8. Pádua, F.G., Voegels, R.L. 2008. Severe posterior epistaxis–endoscopic surgical anatomy. Laryngoscope 118(1): 156-61. Rezende, G.L., Soares, V.Y., Moraes, W.C., Oliveira, C.A., Nakanishi, M. 2012. The sphenopalatine artery: a surgical challenge in epistaxis. Braz J Otorhinolaryngol 78(4): 42-7. Simmen, D.B., Raghavan, U., Briner, H.R., Manestar, M., Groscurth, P., Jones, N.S. 2006. The anatomy of the sphenopalatine artery for the endoscopic sinus surgeon. Am J Rhinol 20(5): 502-5.
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Single Incision Laparoscopic Bariatric Surgery: Challenging the Conventional

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Abstrak (In MALAY language): 

Pembedahan 'sleeve gastrectomy' semakin popular kebelakangan ini dan kebiasaannya dijalankan menggunakan kaedah laparoskopi yang memerlukan beberapa potongan kecil di atas kulit. Kehadiran pembedahan laparoskopik insisi tunggal telah membolehkan pembedahan 'sleeve gastrectomy' kini dilakukan menerusi satu luka kecil yang lebih kosmetik justeru meningkatkan kepuasan pesakit. Menerusi artikel ini, kami cuba untuk menerangkan sejarah, kekangan teknikal, cadangan untuk mengatasi cabaran-cabaran yang mungkin timbul dalam pembedahan bariatrik laparoskopik insisi tunggal dan teknik pilihan kami sewaktu menjalankan pembedahan laparoskopik insisi tunggal 'sleeve gastrectomy' secara eksklusif melalui hanya satu alat akses ke rongga peritoneal.

Correspondance Address: 
Reynu Rajan, Minimally Invasive, Upper Gastrointestinal and Bariatric Surgery Unit, Department of Surgery, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +603 91456201 Fax: +603- 91456684 E-mail: dr.reynu@gmail.com
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Single incision laparoscopic surgery has become increasingly popular among surgeons and the medical-device industry, with some even calling it the Holy Grail of Minimal Access Surgery with its near-scarless effect. The cosmetic advantage, familiarity of laparoscopic view observed with this technique and the freedom to convert single incision laparoscopic surgery to a conventional laparoscopic surgery has made this approach irresistible to modern day surgeons despite being technically demanding. Single incision laparoscopic surgery has been referred to by many names such as Single Port Access (SPA), Embryonic Natural Orifice Transumbilical Endoscopic Surgery (E-NOTES), Single Incision Multi Port Laparo-Endoscopic Surgery (SIMPLE) and Single Port Surgery (SPS) just to name a few. This is largely due to the absence of consensus among surgeons to adopt a standardized nomenclature. In 2008, a multidisciplinary consortium of surgeons also known as the Laparo-Endoscopic Single Site Surgery Consortium for Assessment and Research (LESSCAR) attempted to put an end to this confusion and suggested the name Laparo-Endoscopic Single Site Surgery or “LESS Surgery” to be applied when describing a procedure through a single site of access – a decision that has yet to garner undivided support from the global bariatric surgery community at large.

EVOLUTION OF SINGLE INCISION LAPAROSCOPIC BARIATRIC SURGERY

Despite the new found fan-fare, single incision laparoscopic surgery is no “New Kid on the Block”. Gynecologists have been performing single incision laparoscopic tubal ligation since the 70s (Bailer & Rauskolb 1975). In 1992, the first single incision laparoscopic supracervical hysterectomy was reported in the Journal of Reproductive Medicine (Pelosi & Pelosi 1992). This approach further expanded in general surgery to perform single incision laparoscopic cholecystectomy (Navarra et al. 1997). Later, the use of single incision laparoscopic appendectomy was performed successfully in children (Esposito et al. 2007). But it was not until 2008 that the surgical fraternity would read about a single incision laparoscopic bariatric surgery (SILBS), the year that the first single incision laparoscopic adjustable gastric banding was reported (Nguyen et al. 2008). The same year, report of the first single incision laparoscopic sleeve gastrectomy was published (Saber et al. 2008). A year later in 2009, Saber and team reported the first single port access laparoscopic Roux-en-Y gastric bypass surgery and since then has gone on to publish numerous scientific papers on the feasibility and safety of single incision laparoscopic bariatric procedures in varying class of obesity (Saber et al. 2009). The first wave of this near-scarless bariatric surgery revolution arrived on the shores of Asia circa 2009-2011 (Huang et al. 2009; Lakdawala et al. 2011).

SITE OF INCISION

SILBS can be performed through a horizontal incision in the upper abdomen (single incision transabdominal or SITA) in patients with a xiphoid-umbilicus distance of more than 25cm. In patients with xiphoid-umbilicus distance of 25cm or less, SILBS can be performed through a hidden transumbilical incision (single incision transumbilical or SITU). SITU has been associated with increased patient satisfaction, improved cosmesis and less pain compared to its transabdominal counterpart. Circum-umbilical incision and Omega incision have also been reported and can be applied as an alternative to the incision used in the SITU approach. Once the incision has been made, laparoscopic instruments are introduced into the abdominal cavity either through a single access device such as SILS™ Port (Medtronic) and GelPort® (Applied Medical) or alternatively by introducing 3-4 laparoscopic trocars directly through the abdominal wall via different facial planes i.e. single incision-multiport laparoendoscopic technique (SIMPLE).

LIVER RETRACTION

Good liver retraction facilitates creation of adequate working space for laparoscopic upper gastrointestinal procedures to be performed. By lifting the hypertrophied left liver lobe, the surgeon is able to better visualize the Angle of His, thus reducing the risk of possible injury to this area during dissection or gastric stapling. The additional space also enables the surgeon to perform complete mobilization of the posterior fundus during surgery. Various liver retractions techniques have been reported over the years from application of a regular Nathanson liver retractor to the more cosmetically appeasing methods described by various surgeons (Sakaguchi et al. 2008), (Huang 2011) and (Tacchino et al. 2010).

TECHNICAL CHALLENGES WITH SILBS

SILBS did have its own teething problems in the beginning which were quickly overcome by a timely influx of advanced laparoendoscopic gadgetry and innovative modification to existing technology. Among the challenges of performing SILBS were the loss of triangulation, “sword-fighting” between laparoscopic instruments, friction between the internal and external components of laparoscopic trocars, the risk of port site hernia, difficulty in maintaining pneumoperitoneum due to leakage of gas, inadequate exposure of vital structures, clash between the bulky camera head and the surgeon’s hand and risk of direct damage to the telescope itself. Existing anatomical features in obese individuals such as hepatomegaly or hypertrophied left lobe of liver, visceral adiposity and torque of the thick abdominal wall adds to the list of potential challenges. If not for technical improvisation by an innovative breed of surgeons, and the race to produce single incision friendly laparoscopic devices by corporate giants in the med-tech field, it would have not been possible for SILBS to grow and evolve at its current rate (Table 1).

BARIATRIC SURGERY IN MALAYSIA

Malaysia’s footprint in bariatric surgery began in 1996 with the first open vertical gastroplasty. Since then there has been 2009 bariatric procedures performed up till December 2016. Interestingly, approximately 1787 of those cases were performed over a short span of 7 years from 2010 to 2016. In 2016 alone, 463 cases carried out throughout the country, a steep jump from merely 158 cases in 2010. The positive growth of bariatric surgery in Malaysia over the years is a testament to the courage, drive and commitment shown by local pioneers in the field. Their passion for improving patient outcome and increasing training opportunities for surgeons have paved the way for a whole new generation of surgeons to step in and be a part of this exiting time in bariatric surgery – one that has seen the Malaysian bariatric scene transitioning from open surgery to laparoscopic surgery to reduced incision laparoscopic surgery and now single incision laparoscopic surgery.

FIRST SILBS IN MALAYSIA

Our first experience with single incision laparoscopic sleeve gastrectomy at UKMMC and Malaysia, dates back to the year 2016. The surgery was carried out through the SITU approach using SILS™ Port (Medtronic) and straight laparoscopic instruments. The left lobe of liver was elevated using the right crux transfixion technique with a single Vicryl 2-0 suture. We then went on to successfully complete Malaysia’s first pure single incision laparoscopic sleeve gastrectomy in 2017. The surgery was carried out in a similar fashion as before but with one exception – there was no additional incision at the epigastrium for an ancillary trocar, needlescopic instruments or puppeteering sutures to retract the liver (Figure 1). The only incision on the body was a single hidden transumbilical incision measuring 3 cm in length (Figure 2). Intra-operative visualisation of the Angle of His was achieved by neatly packing 4 pieces of gauze beneath the left lobe of liver in order to elevate it (Figure 3). The stomach was separated from the omentum along the greater curvature using LigaSure™ Maryland jaw 44 cm long (Medtronic). The gastric tube was created using iDrive™ Ultra Powered Stapling Device with 60mm Tri-Staple™ cartridge (Medtronic).The stapler line was then reinforced with V-Loc™ wound closure device (Medtronic) along its entire length. The resected specimen was then delivered through the transumbilical incision (Figure 4). Patient was allowed clear fluids the next day and discharged on post-operative day 2. This method resulted in greater patient satisfaction, improved cosmesis and less pain compared to the conventional method of performing laparoscopic sleeve gastrectomy which involves making 5 separate incisions over the anterior abdominal wall (Figure 5). From extensive literature review, we do believe that this is the first descriptive account of Malaysia’s involvement, history and progress in the field of Bariatric surgery as well as the first report of a successful pure single incision laparoscopic sleeve gastrectomy in Malaysia.

FUTURE DIRECTION OF SILBS IN MALAYSIA

Despite the positive trend of volume of bariatric cases in Malaysia, acceptance of SILBS among local surgeons has been somewhat lukewarm. In the era of cost-effectiveness, the large amount of investment needed to purchase single incision specific laparoscopic equipment, the added cost in the form of procedural fee that a patient would have to endure for purchase of the SILBS access device and the lack of training opportunities in SILBS are among plausible factors that have restricted the popularity of SILBS. However, with record number of industry players showing interest in the this “scarless revolution”, operational cost for the surgeon or institution and procedural cost for the patient is expected to reduce, increasing the reach and feasibility of SILBS in Malaysia.

References: 
Bailer, P., Rauskolb, R. 1975. Gynaecological laparoscopy. Geburtshilfe Frauenheilkd 35(10): 747–53. Esposito, C., Borzi, P., Valla, J.S., Mekki, M., Nouri, A., Becmeur, F., Allal, H., Settimi, A., Shier, F., Sabin, M.G., Mastroianni, L. 2007. Laparoscopic versus open appendectomy in children; a retrospective comparative study of 2332 case. World J Surg 31(4): 750–5. Huang, C.K., Houng, J.Y., Chiang, C.J., Chen, Y.S., Lee, P.H. 2009. Single incision transumbilical laparoscopic Roux-en-Y gastric bypass: a first case report. Obes Surg 19(12): 1711-5. Huang, C.K. 2011. Single-incision laparoscopic bariatric surgery. J Minim Access Surg 7(1): 99–103. Lakdawala, M.A., Muda, N.H., Goel, S., Bhasker, A. 2011. Single-incision sleeve gastrectomy versus conventional laparoscopic sleeve gastrectomy--a randomised pilot study. Obes Surg 21(11): 1664–70. Navarra, G., Pozza, E., Occhionorelli, S., Carcoforo, P., Donini, I. 1997. One-wound laparoscopic cholecystectomy. Br J Surg 84(5): 695. Nguyen, N.T., Hinojosa, M.W., Smith, B.R., Reavis, K.M. 2008. Single laparoscopic incision transabdominal (SLIT) surgery-adjustable gastric banding: A novel minimally invasive surgical approach. Obes Surg 18(12): 1628–31. Pelosi, M.A., Pelosi, M.A. 1992. Laparoscopic supracervical hysterectomy using a single-umbilical puncture (minilaparoscopy). J Reprod Med 37(9): 777–84. Saber, A.A., Elgamal, M.H., Itawi, E.A., Rao, A.J. 2008. Single incision laparoscopic sleeve gastrectomy (SILS): a novel technique. Obes Surg 18(10): 1338–42. Saber, A.A., El-Ghazaly, T.H., Minnick, D.B. 2009. Single port access transumbilical laparoscopic Roux-en-Y gastric bypass using the SILS Port: first reported case. Surg Innov 16(4): 343–7. Sakaguchi, Y., Ikeda, O., Toh, Y., Aoki, Y., Harimoto, N., Taomoto, J., Masuda, T., Ohga, T., Adachi, E., Okamura, T. 2008. New technique for the retraction of the liver in laparoscopic gastrectomy. Surg Endosc 22(11): 2532-4. Tacchino, R.M., Greco, F., Matera, D. 2010. Laparoscopic gastric banding without visible scar: A short series with infraumbilical SILS. Obes Surg 20(2): 236–9.
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Do Pathogens from Corneal Scraping Show Their True Colours Better in Bactec Bottles?

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Abstrak (In MALAY language): 

Pengenalpastian jenis organisma dalam kes jangkitan ulser kornea adalah sangat penting supaya rawatan antibiotik yang sesuai dapat diberikan kepada pesakit. Kaedah konvensional dengan menggunakan kultur plat tidak memberi hasil kajian yang memberangsangkan. Percubaan kami dengan teknik yang diubahsuai menggunakan campuran cecair BACTEC untuk mengenal pasti organisma dalam tiga kes jangkitan ulser kornea memberi keputusan cemerlang 100%.

Correspondance Address: 
Aida Zairani Mohd. Zahidin. Department of Ophthalmology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +603-91455981 Fax: +603-9145 6733 E-mail: aidazahidin@gmail.com
Full text: 

Microbial keratitis (infectious keratitis) is a serious sight-threatening ocular infection. Prompt-targeted treatment and subsequent tailoring is needed to check the disease process. This can limit the progression of corneal scarring and severe loss of vision (Thomas & Geraldine 2007). Identification of the causative organisms and its sensitivity to antibiotics only can be determined by carrying out microbiological lab test (Wilhelmus & Schlech 2004). However, even if a specimen of the corneal infiltrate is obtained for microbiological investigation using traditional method, subsequent growth and identification of pathogens occurs only in average of 50.47% cases (Kratz et al. 2006). The traditional method involves the use of multiple specimens scraping with direct inoculation onto enriched solid culture agar plates (Kaye et al. 2003). Studies were conducted to study the suitability of other transport medium and commercially available broth culture medium to increase positive yields (Kratz et al. 2006; Kaye et al. 2003).

In Universiti Kebangsaan Malaysia Medicla Centre (UKMMC), the routinely performed laboratory investigation for corneal scrape specimen are microscopic examination with gram stain and potassium hydroxide (KOH), followed by inoculation onto conventional culture media like blood, chocolate, MacConkey and sabouraud dextrose agar (Fisher Scientific Sdn Bhd Malaysia, part of Thermo Fisher Scientific). Unfortunately, as reported in the previous study (Kratz et al. 2006), our pathogen recovery from this traditional method is not that encouraging. Thus, we decided to improve culture positive rate for microbial keratitis by adding a new technique using BD BACTEC Peds Plus/F broth (Becton, Dickinson and Company, USA).

Three cases of clinically suspected infectious keratitis in post penetrating keratoplasty eyes, which presented to Ophthalmology Clinic, UKMMC in the month of May 2016 were tested for microbial identification in BD BACTEC Peds Plus/F culture vial. Specimens for the routine microscopic examination of gram stain and potassium hydroxide (KOH); and culture & sensitivity on culture agar plates (blood, chocolate, Mac’conkey and Sabouraud agar) were taken first then followed by our additional method using corneal scrape specimens into BACTEC vial.

Corneal scrape procedures were carried out under aseptic technique following the instillation of topical anaesthesia (proparacaine hydrochloride 0.5%). Sterile surgical blades sized 15 were used for Gramstain, KOH and conventional culture agar plates (blood, chocolate, MacConkey and sabouraud). Each scraping was carried out with fresh new blade. The base and leading edges of the ulcer was scraped. The scraped material was smeared on two glass slides, one for potassium hydroxide (KOH) wet mount preparation and the other for Gramstain. For, conventional culture method, scrape material was inoculated directly in rows of C-shaped streaks onto room temperature culture plates. For the additional BACTEC method, scraped specimen using 21G sterile needle, which were already connected to 5ml empty syringe, was used to withdraw and reintroduce liquid broth from and into BACTEC vial (Figure 1 & Figure 2). All the collected specimens were sent to UKMMC Microbiology laboratory as soon as possible in order to incubate according to standard procedure.

The first case was a specimen from a 7-year-old girl which showed positive growth of Moraxella lacunata in broth and no growth with the culture plate. 

In the second case involving a 66-year-old lady, both methods yielded positive for Enterobacter spp. Last case from a 56-year-old male eventually yielded only in the broth method and not on culture plates. The organism identified was coagulase negative Staphylococcus (Table 1). We tailored our antibiotic treatment according to culture sensitivity results for all three patients. All three patients eventually recovered without any serious complication such as corneal perforation.

According to the National Eye Survey conducted in 1996, microbial keratitis accounted as the fourth major cause of blindness in Malaysia (Zainal et al. 2002). Identification of causative organisms plays an important role in reducing the morbidity caused by microbial keratitis (Norina et al. 2008). This is because successful targeted treatment can only be given if pathogen is known or else we have to depend on broad spectrum antibiotic which eventually may increase the drug resistance.

Although some keratitis clinically have distinctive appearances, it is not easy to identify the likely causative organisms based on slit lamp examination of the corneal lesion alone. Microbiological laboratory analysis is therefore required for the identification of causative organism (Garg & Rao 1999). As pathogen recovery is poor through conventional method, considerations need to be taken in order to increase positive culture rate in those analysis by adding new technique.

BD BACTEC Peds Plus/F (Becton, Dickinson and Company, USA) is a type of broth culture medium commonly used in peadiatric practice to isolate microorganisms from small volume sample of about 3 ml blood or body fluids (Kratz et al. 2006). The medium contains 20ml of an enriched soybean-casein digest broth and an optimal amount of sodium polyanethole sulfonate, which enhance the detection of sodium polyanethole sulfonate susceptible organisms. Each vial also contains resins to neutralize antibiotics (Welby et al. 1992). It has been successfully used to recover not only aerobic and anaerobic bacteria but also fungi.

This commercial broth media has been studied in the work-up of microbial keratitis to elucidate whether the BACTEC Peds Plus F could be used for corneal cultures (Kratz et al. 2006). Kratz and associates found this method yields 73.33% positive cultures combined with conventional method together. In their methodology, specimens were inserted to a regular sterile Eppi 40 tube (Eppendorf International) previously filled with 1.5 ml of sterile saline 0.9%. The diluted specimen with sterile saline was then drawn using a regular 2.5 ml syringe, and inserted into regular BACTEC Peds Plus F broth. In our method, BACTEC system was also used, however scraped specimens were directly inoculated into BACTEC vial using sterile needle without diluting it in the sterile saline 0.9%.

As portrayed by these three cases, this modified technique using BD BACTEC Peds Plus/F culture vial to increase positive yields for microbial keratitis at our centre has showed promising results. Thus, in conclusion BACTEC Peds PLUS/F broth can be used successfully as a valuable adjunct to conventional method of agar plates for organisms' identification in the work-up of clinically suspected microbial keratitis in our country. Larger sample sized-study using this method may be beneficial in the future.

ACKNOWLEDGEMENT

The authors thank Mr. Hairul Nizam Harun for image editing.

References: 
Garg, P., Rao, G.N. 1999. Corneal ulcer: diagnosis and management. Community Eye Health 12(30): 21-3. Kaye, S.B., Rao, P.G., Smith, G., Scott, J.A., Hoyles, S., Morton, C.E., Willoughby, C., Batterbury, M., Harvey, G. 2003. Simplifying collection of corneal specimens in cases of suspected bacterial keratitis. J Clin Microbiol 41(7): 3192-7. Kratz, A., Levy, J., Klemperer, I., Lifshitz, T. 2006. Broth cultures yield vs traditional approach in the workup of infectious keratitis. Eye (Lond) 20(2): 215-20. Norina, T.J., Raihan, S., Bakiah, S., Ezanee, M., Liza-Sharmini, A.T., Wan Hazzabah, W.H. 2008. Microbial keratitis: aetiological diagnosis and clinical features in patients admitted to Hospital Universiti Sains Malaysia. Singapore Med J 49(1): 67-71. Thomas, P.A., Geraldine, P. 2007. Infectious keratitis. Curr Opin Infect Dis 20(2): 129-41. Welby, P.L., Zusag, T.M., Storch, G.A. 1992. Comparison of the Bactec Peds Plus pediatric blood culture vial with Roche pediatric Septi-Chek for blood cultures from pediatric patients. J Clin Microbiol 30(5): 1361-2. Wilhelmus, K. R., & Schlech, B. A. 2004. Clinical and epidemiological advantages of culturing bacterial keratitis. Cornea 23(1); 38-42. Zainal, M., Ismail, S.M., Ropilah, A.R., Elias, H., Arumugam, G., Alias, D., Fathilah, J., Lim, T.O., Ding, L.M., Goh, P.P. 2002. Prevalence of blindness and low vision in Malaysian population: results from the National Eye
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Left Facial Tumour. What Is It?

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Correspondance Address: 
Hardip S Gendeh. Department of Surgery, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +6-03-91456202 Fax: +6-03-91456684 E-mail: hardip88@hotmail.com
Full text: 

QUESTION

A 30-year Malay gentleman (South-East Asian) ethnicity has been suffering from a left facial tumour, progressively increasing in size since birth. The tumour exits from the left orbital cavity and has displaced his left eye globe inferior posteriorly (Figure 1). Left eye vision has been progressively deteriorating in his left eye with the ability to only perceive bright light. He is of a short stature with multiple facial nodules. Spot the diagnosis and what other symptoms the patient might exhibit?

ANSWER

The diagnosis is left Plexiform Neurofibromata, easily mistaken with an optic glioma. The tumour has protruded through his left orbital socket over his left cheek in a progressive manner, with multiple neurofibromatosis nodules throughout his torso and four limbs. The overlying skin is non-tender with normal tactile sensation.

Plexiform Neurofibromata is a subset of neurofibromatosis type 1. Other symptoms include café-au-lait spots, axillary or inguinal freckles, Lisch nodules (pigmented hamartomatous nodules in the iris), sphenoid dysplasia with a strong genetic preponderance. There is no cure, a routine follow-up to monitor complications is recommended. Cosmetic tumour resection can be considered but they have high rates of recurrence.

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Proximal Stability Assessment of Knee Osteoarthritis Patients

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Abstrak (In MALAY language): 

Kestabilan proksimal yang terdiri daripada kestabilan otot teras dan pinggul, memainkan peranan penting dalam menyokong berat badan dalam keadaan statik dan bergerak. Seterusnya, kestabilan proksimal boleh menyumbang kepada osteoarthritis lutut. Justeru, kajian ini dilaksanakan untuk menentukan kestabilan teras dan pinggul pesakit osteoarthritis lutut (OA lutut). Seramai 32 orang wanita berumur antara 45 hingga 60 tahun yang terdiri daripada 16 orang pesakit OA lutut dan 16 orang normal telah bersetuju menyertai projek kajian ini. Kestabilan pinggul diuji menggunakan ujian “Hip Crossover” dan kestabilan otot teras dinilai menggunakan ujian daya tahan otot teras, ujian kekuatan otot teras dan ujian kelenturan otot teras. Data kestabilan pinggul, kekuatan dan kelenturan otot teras dianalisa menggunakan ujian chi-square; dan daya tahan otot teras dianalisis menggunakan ujian-t tidak bersandar. Kajian ini mendapati pesakit OA lutut mempunyai pinggul yang kurang stabil [Hip Crossover Test (λ=0.500, p=0.033)] dan kestabilan otot teras yang lebih rendah berbanding dengan subjek normal. Kestabilan otot teras dinilai berdasarkan kepada kekuatan otot teras [abdominal muscles (χ=12.157, p<0.001); quadriceps and gluteal muscles (χ=13.364, p<0.001); hip muscles (χ=17.936, p<0.001); latissimus dorsi and quadriceps (χ=15.906, p<0.001)]; daya tahan otot teras [plank endurance (t=4.719, p<0.001); trunk flexion (t=2.824, p=0.008); trunk extension (t=1.364, p=0.193)]; dan kelenturan otot teras [Ely’s test (λ=0.438, p=0.010)]. Kestabilan proksimal pesakit OA lutut jelas lebih lemah berbanding subjek normal. Oleh itu, latihan untuk meningkatkan kestabilan pinggul dan otot teras perlu dipertimbangkan dalam program rehabilitasi OA lutut, bukan sahaja bagi mengurangkan symptom OA lutut, tetapi juga memperbaiki pergerakan berfungsi pesakit OA lutut.

Correspondance Address: 
D. Maryama binti AG. Daud. Physical Fitness Rehab Centre, Faculty Psychology and Education, Universiti Malaysia Sabah, Kota Kinabalu, 88400 Sabah, Malaysia. Tel: +6010-9310913 Email: dmaryama@ums.edu.my
References: 
Alnahdi, A.H., Zeni, J.A., Snyder-Mackler, L. 2012. Muscle Impairments in Patients with Knee Osteoarthritis. Sports Health 4(4): 284-92. Behm, D.G., Drinkwater, E.J., Willardson, J.M., Cowley, P.M. 2010. The use of instability to train the core musculature. Appl Physiol Nutr Metab 35(1): 91-108. Kivlan, B.R., Carcia, C.R., Clemente, F.R., Phelps, A.L., Martin, R.L. 2013. Reliability and validity of functional performance test in dancers with hip dysfunction. Int J Sports Phys Ther 8(4): 360- 9. Bennell, K.L., Hunt, M.A., Wrigley, T.V., Lim, B.- W., Hinman, R.S. 2008. Role of muscle in the genesis and management of knee osteoarthritis. Rheum Dis Clin North Am 34(3): 731-54. Bennell, K.L., Wrigley, T.V., Hunt, M.A., Lim, B.-W., Hinman, R.S. 2013. Update on the Role of muscle in the genesis and management of knee osteoarthritis. Rheum Dis Clin North Am 39(1): 145-76. Bertrand, J., Cromme, C., Umlauf, D., Frank, S., Pap, T. 2010. Molecular mechanisms of cartilage remodelling in osteoarthritis. Int J Biochem Cell Biol 42(10): 1594-601. Biabanimoghadam, M., Motealleh, A., Cowan, S.M. 2016. Core muscle recruitment pattern during voluntary heel raises is different between patients with patellofemoral pain and healthy individuals. Knee 23(3): 382-6. Bliss, L.S., Teeple, P. 2005. Core stability: the centerpiece of any training program. Curr Sports Med Rep 4(3): 179-83. Bodine, S.C. 2013. Disuse-induced muscle wasting. Int J Biochem Cell Biol 45(10): 2200-8. Borghuis, J., Hof, A.L., Lemmink, K.A. 2008. The importance of sensory-motor control in providing core stability. Sports Med 38(11): 893- 916. Chang, A., Hayes, K., Dunlop, D., Song, J., Hurwitz, D., Cahue, S., Sharma, L. 2005. Hip abduction moment and protection against medial tibiofemoral osteoarthritis progression. Arthritis Rheum 52(11): 3515-9. Chuter, V.H., Janse de Jonge, X.A. 2012. Proximal and distal contributions to lower extremity injury: a review of the literature. Gait Posture 36(1): 7-15. Colston, M.A. 2012. Core stability, part 2: the coreextremity link. International Journal of Athletic Therapy and Training 17(2): 10-15. Costa, R.A., Oliveira, L.M.d., Watanabe, S.H., Jones, A., Natour, J. 2010. Isokinetic assessment of the hip muscles in patients with osteoarthritis of the knee. Clinics 65(12): 1253-9. Creps, J.M. 2014. An Investigation of simulated core muscle activation during running and its effect on knee loading and lower extremity muscle activation using opensim. PhD thesis. The Ohio State University Hagio, S., Nagata, K., Kouzaki, M. 2012. Region specificity of rectus femoris muscle for force vectors in vivo. J Biomech 45(1): 179-82. Hame, S., Alexander, R. 2013. Knee osteoarthritis in Women. Curr Rev Musculoskelet Med 6(2): 182-7. Hu, H., Meijer, O.G., Hodges, P.W., Bruijn, S.M., Strijers, R.L., Nanayakkara, P.W., van Royen, B.J., Wu, W.H., Xia, C., van Dieën, J.H. 2012. Control of the lateral abdominal muscles during walking. Hum Mov Sci 31(4): 880-96. Inchai, C., Mahakkanukrauh, P. 2017. Biological markers associated osteoarthritis. Med & Health 12(1): 18-26. Kean, C.O., Hinman, R.S., Wrigley, T.V., Lim, B.W., Bennell, K.L. 2017. Impact loading following quadriceps strength training in individuals with medial knee osteoarthritis and varus alignment. Clin Biomech 42: 20-4. Kibler, W.B., Press, J., Sciascia, A. 2006. The role of core stability in athletic function. Sports Med 36(3): 189-98. Litwic, A., Edwards, M.H., Dennison, E.M., Cooper, C. 2013. Epidemiology and burden of osteoarthritis. Br Med Bull (105): 185-99. Liikavainio, T., Isolehto, J., Helminen, H.J., Perttunen, J., Lepola, V., Kiviranta, I., Arokoski, J.P., Komi, P.V. 2007. Loading and gait symmetry during level and stair walking in asymptomatic subjects with knee osteoarthritis: importance of quadriceps femoris in reducing impact force during heel strike? Knee 14(3): 231-8. Mayer, J.M., Nuzzo, J.L., Chen, R., Quillen, W.S., Verna, J.L., Miro, R., Dagenais, S. 2012. The impact of obesity on back and core muscular endurance in firefighters. J Obes 2012: 729283. Mbada, C.E., Ayanniyi, O., Adedoyin, R.A. 2008. Influence of relative adiposity on static back extensor muscle endurance in apparently healthy adults. Hong Kong Physiotherapy Journal 26(1): 2-8. Mbada, C.E., Ayanniyi, O., Adedoyin, R.A. 2009. Reference values of static back extensor muscle endurance in healthy nigerian adults. Med Princ Pract 18(5): 345-50. Mikesky, A.E., Meyer, A., Thompson, K.L. 2000. Relationship between quadriceps strength and rate of loading during gait in women. J Orthop Res 18(2): 171-5. Mizner, R.L. 2004. Quadriceps femoris weakness and functional outcome in individuals with end-stage knee osteoarthritis. http://search. ebscohost.com/login.aspx?direct=true&db=c8h&AN=109844558&site=ehost-live [7 July 2018]. Mündermann, A., Dyrby, C.O., Andriacchi, T.P. 2005. Secondary gait changes in patients with medial compartment knee osteoarthritis: increased load at the ankle, knee, and hip during walking. Arthritis Rheum 52(9): 2835-44. Palmer, T.G. 2012. Effects of proximal stability training on sport performance and proximal stability measures. ProQuest Dissertations and Theses, 168. Pandy, M.G., Andriacchi, T.P. 2010. Muscle and joint function in human locomotion. Annu Rev Biomed Eng. 12: 401-33. Panjabi, M.M. 2003. Clinical spinal instability and low back pain. J Electromyogr Kinesiol 13(4): 371-9. Rice, D.A., McNair, P.J., Lewis, G.N. 2011. Mechanisms of quadriceps muscle weakness in knee joint osteoarthritis: the effects of prolonged vibration on torque and muscle activation in osteoarthritic and healthy control subjects. Arthritis Res Ther 13(5): R151. Sasaki, K., Neptune, R.R. 2010. Individual muscle contributions to the axial knee joint contact force during normal walking. J Biomech 43(14): 2780-4. Segal, N.A., Glass, N.A. 2011. Is quadriceps muscle weakness a risk factor for incident or progressive knee osteoarthritis? Phys Sportsmed 39(4): 44- 50. Segal, N.A., Glass, N.A., Torner, J., Yang, M., Felson, D.T., Sharma, L., Nevitt, M., Lewis, C.E. 2010. Quadriceps weakness predicts risk for knee joint space narrowing in women in the most cohort. Osteoarthritis Cartilage 18(6): 769-75. Silverwood, V., Blagojevic-Bucknall, M., Jinks, C., evidence on risk factors for knee osteoarthritis in older adults: a systematic review and metaanalysis. Osteoarthritis Cartilage 23(4): 507-15. Sritharan, P., Lin, Y.C., Pandy, M.G. 2012. Muscles that do not cross the knee contribute to the knee adduction moment and tibiofemoral compartment loading during gait. J Orthop Res 30(10): 1586-95. Waldhelm, A. 2011. Assessment of core stability: developing practical models. PhD thesis. Louisiana State University Waldhelm, A., Li, L. 2012. Endurance tests are the most reliable core stability related measurements. Journal of Sport and Health Science 1(2): 121-8. Winters, J.D., Rudolph, K.S. 2014. Quadriceps rate of force development affects gait and function in people with knee osteoarthritis. Eur J Appl Physiol 114(2): 273-84.

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A Case of Secondary Choroidal Neovascularization in Inactive Choroidal Tuberculoma

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Abstrak (In MALAY language): 

tuberculosis (TB). Sebanyak 5-10% kes keradangan okular disebabkan oleh TB okular. Spektrum TB okular adalah berbeza-beza, menjejaskan mana-mana bahagian adnexa, lapisan dan struktur bola mata yang berlainan, kandungan orbit, saraf optik pada bahagian belakang orbit. Ia boleh dikaitkan dengan/atau tanpa manifestasi sistemik. Uveitis posterior adalah manifestasi tuberkulosis okular yang paling biasa. Perdarahan subretinal sekunder yang disebabkan oleh ‘neovascularization’ choroidal adalah komplikasi yang jarang berlaku dalam tuberkulosis ocular. Kami melaporkan satu kes yang jarang ditemui iaitu ‘neovascularization’ choroidal sekunder pada kanak-kanak lelaki berusia 9 tahun yang dijangkiti ‘choroidal tuberculoma’ pada kedua-dua mata disebabkan oleh tuberkulosis miliari. Dia dirawat dengan suntikan ranibizumab intravitreal dan suntikan plasminogen activator rekombinan intravitreal (r-TPA). Walaupun perdarahan subretinal pulih, namun penglihatan adalah terhad disebabkan oleh fovea atropik.

Correspondance Address: 
Department of Ophthalmology, Hospital Kuala Lumpur, Jalan Pahang, 50586 Kuala Lumpur. Tel: +603-26155555 E-mail: farhana_189@ yahoo.com
References: 
Handwerger, B.A., Blodi, B.A., Chandra, S.R., Olsen, T.W., Steven, T.S. 2001. Treatment of submacular hemorrhage with low dose intravitreal tissue plasminogen activator injection and pneumatic displacement. Arch Ophthalmology 119: 28-32. Sharkachi, F.I. 2015. Ocular tuberculosis: current perspectives. Clinical Ophthalmology 9: 2223- 7. Kok, H.S., Tara, M.G., Mae-Lynn, C.B., Muhaya, H.M. 2006. Two cases of retinal vasculitis in ocular tuberculosis involving different parts of the vascular system. Med & Health 1(1): 91-3. Koushik, T., Rohan, C., Yog, R.S. 2016. Intravitreal bevacizumab for choroidal neovascular membrane at the edge of a healed choroidal tuberculoma. Ocul Immunol Inflamm 26(2): 239-41. Bansal, R., Nikhil, B., Aman, S., Amod, G. 2013. Intravitreal bevacizumab as an adjunct in the management of vascular choroidal granuloma. BMJ case Rep 2013: bcr2013200255. Thayil, S.M., Albini, T.A., Nazari, H., Moshfeghi, A.A., Parel, J-MA., Rao, N.A. 2011. Local ischemia and increases expression of vascular endothelial growth factor following ocular dissemination of Mycobacterium tuberculosis. PLoS ONE 6(12) Shahidatul-Adha, M., Zunaina, E., Liza-Sharmini, A.T., Wan-Hazabbah, W.H., Shatriah, I., Mohtar, I., Azhany, Y., Adil, H. 2017. Ocular tuberculosis in Hospital Universiti Sains Malaysia – a case series. Ann Med Surg 24: 25-30

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Morphological Variant of Pronator Quadratus Muscle: A Case Report

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Abstrak (In MALAY language): 

Dibentangkan di sini adalah satu kes anomali morfologi berbeza bagi otot pronator quadratus (PQ). Di sini, bentuk PQ tidak sama dengan morfologi normal otot tersebut di mana otot PQ kelihatan berbentuk segi tiga dan bukan bentuk segi empat. Di samping itu, bentuk segi tiga ini terdapat di dua tempat, iaitu proksimal dan distal. Dengan ketara, otot PQ ini terdiri daripada dua serat-serat merah berisi dan aponeurosis putih. Bahagian proksimal mempunyai asas yang luas dan puncak yang lebih sempit. Asas yang lebih besar itu tersisip dengan tulang ulna dan membentuk serat merah berisi yang berkumpul di sisi dan berterusan dengan aponeurosis berakhir pada tulang radius. Sebaliknya, bahagian segi tiga distal mempunyai serat berisi dilampirkan dengan tulang radius dan tertumpu di bahagian medial menjadi berterusan dengan bahagian aponeurotik pada tulang ulna tersebut. Setiap bahagian dirujuk sebagai pronator triangularis proximalis dan pronator triangularis distalis. Perbezaan-perbezaan ini mungkin memberi kesan kepada kes-kes atipikal pronasi lengan. Maklumat variasi ini adalah penting dalam pembedahan tangan dan memberi pengetahuan tambahan kepada hubungan antara morfologi otot PQ dan had atau kekuatan dalam tindakannya.

Correspondance Address: 
Dr. Syed Baharom Syed Ahmad Fuad. Department of Anatomy, Faculty of Medicine, Universiti Teknologi MARA, Jalan Hosital, Sungai Buloh, 47000 Selangor, Malaysia. Tel: +603-61267297 Email: syedbaharom@salam.uitm.edu.my
References: 
Choung, P.W., Kim, M.Y., Im, H.S., Kim, K.H., Rhyu, I.J., Park, B.K., Kim, D.H. 2016. Anatomic characteristics of pronator quadratus muscle: a cadaver study. Ann Rehabil Med 40(3): 496- 501. Haugstvedt, J.R., Langer, M.F., Berger, R.A. 2017. Distal radioulnar joint: functional anatomy, including pathomechanics. J Hand Surg Eur 42(4): 338-45. Hollinshead. 1962. Second edition Text book of Anatomy. Oxford and IBH publishing company. Jadhav, S.D., Gosavi, S.N., Zambare, B.R. 2014. Morphology of pronator quadratus muscle: a cadaveric study. International Journal of Medical Research & Health Sciences 3(4): 876-9. Kapoor, S.K., Tiwari, A., Kumar, A., Bhatia, R., Tantuway, V., Kapoor, S. 2008. Clinical relevance of palmaris longus agenesis: Common anatomical aberration. Anat Sci Int 83(1): 45-8. Lee, W.P., Idler, R.S. 1996. Functional transfer of pronator quadratus free flap for thenar muscle loss. J Reconstr Microsurg 12(2): 77-80. Loukas, M., Merbs, W., Tubb, R.S., Curry, B., Jordan, R. 2008. Levator glanduleae muscle with three slips. Anat Sci Int 83(4): 273-6. Mochizuki, Y., Sawaizumi, T., Tsunoda, R., Horiguchi, G., Matsui, S., Takai, S. 2013. A case of rotational restriction of the forearm due to abnormal configuration of pronator quadratus muscle. Hand Surg 18(2): 247-50. Mosconi, T., Kamath, S. 2003. Bilateral asymmetric deficiency of the pectoralis major muscle. Clin Anat 16(4): 346-9. Moore, K.L., Dally A.F. 2006. Clinically Oriented Anatomy. Fifth edition. Lippincott Williams& Wilkins: 30-31. O’rahilly, R. 1986. Basic Human Anatomy: A Regional Study of Human Structure. Fifth edition. WB Saunders Co: 24. Standring, S. 2005. Gray’s Anatomy, 39th edition: The Anatomical Basis of Clinical Practice. Elsever Churchill Livingstone: 878. Tuttle, R.H., Hollowed, J.R., Basmajian, J.V. 1992. Electromyography of pronators and supinators in great apes. Am J Phys Anthropol 87(2): 215- 26. Wang, Y., Zhu, S., Zhang, B. 1997. Anatomical study and clinical application of transfer of pronator quadratus branch of anterior interosseous nerve in the repair of thenar branch of median nerve and deep branch of ulnar nerve. Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi 11(6):335-7. Zar Chi T., Ahmad Ruzain S., Mohammad Johari I., Syed Baharom S.A.F. 2017. Anomalous third head of biceps brachii muscle and its variant insertion compresses surrounding neurovascular structure: a rare case report. Med & Health 12(2): 368-74.

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Delay in Ludwig Angina Diagnosis is Fatal

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Abstrak (In MALAY language): 

‘Ludwig Angina’ adalah penyakit yang merbahaya. Sekiranya penyakit tersebut tidak dikesan dari peringkat awal ataupun dirawat, kadar kematian adalah sebanyak 50%. Kami ingin memaparkan satu kes klinikal yang melibatkan seorang pesakit lelaki yang berumur 43 tahun yang mempunyai simptom dan tanda-tanda ‘Ludwig angina’ selama dua hari. Beliau telah menjalani prosedur cabutan gigi sebelum itu. Walaupun pesakit menunjukkan simptom dan tanda-tanda yang klasik untuk ‘Ludwig angina’, diagnosa tersebut tidak dapat dikesan pada rawatan yang pertama. Penyakit ‘Ludwig angina’ hanya boleh dikesan sekiranya doktor mempunyai indeks kecurigaan yang tinggi terhadap penyakit tersebut. Penangguhan dalam pengesanan penyakit tersebut akan menyebabkan saluran pernafasan tersumbat kerana kebengkakan pada saluran pernafasan.

Correspondance Address: 
Siti Nidzwani Mohamad Mahdi. Department of Anesthesiology and Intensive Care, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +6012-4210670 E-mail: nidzwani@yahoo.com
References: 
Britt, J.C., Josephson, G.D., Gross, C.W. 2000. Ludwig’s angina in the pediatric population: Report of a case and review of the literature. Int J Pediatr Otorhinolaryngol 52(1): 79-87. Fischmann, G.E., Graham, B.S. 1985. Ludwig’s angina resulting from the infection of an oral malignancy. J Oral Maxillofac Surg 43(10): 795- 6. Hasan, W., Leonard, D., Russell, J. 2011. Ludwig’s angina - a controversial Surgical Emergency: How we do it. Int J Otolaryngol 2011: 231816. Kurien, M., Mathew, J., Job, A., Zachariah, N. 1997. Ludwig’s angina. Clin Otolaryngol Allied Sci 22(3): 263-5. Lemonick, D.M. 2002. Ludwig’s angina: diagnosis and treatment. Hospital Physician 38: 31-7. Quinn, F.B. 1999. Ludwig angina. Arc Otolaryngol Head Neck Surg 125(5): 599. Spitalnic, S. J., Sucov, A. 1995. Ludwig’s angina: case report and review. J Emerg Med 13(4): 499-503.

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‘Boating’ Out Migrated Dexamethasone Implant; Surgical Management of Removal of Anterior Chamber Migrated Dexamethasone Intravitreal Implant: A Case Report

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Abstrak (In MALAY language): 

Biasanya, implant Ozurdex® jarang bergerak dari ruang vitreus ke depan melalui anak mata. Fenomena ini lebih kerap dijumpai dalam pesakit yang tiada kanta mata (aphakic) atau mereka yang telah mengalami operasi katarak tetapi dengan pemegang kanta mata yang longgar (zonular dehiscence). Kami melaporkan satu kes yang mempunyai bengkak di bahagian macula disebabkan kencing manis yang tidak terkawal dan mengalami penghijrahan implant Ozurdex® ke depan mata. Penghijrahan implant Ozurdex® ke ruang depan kanta mata (anterior chamber) boleh dirawat sama ada dengan meletakkan semula implant itu ke lokasi yang asal, iaitu ruang vitreus, atau mengeluarkannya dari mata pesakit melalui bukaan kecil di bahagian kornea untuk mengelakkan komplikasi yang bakal berlaku. Walau bagaimanapun, implant ini adalah rapuh terutamanya setelah beberapa minggu berada di dalam mata pesakit. Oleh itu, cubaan untuk memegang atau menyentuh implant Ozurdex® boleh menyebabkan ia patah kepada cebisan yang lagi halus, menyebarkannya dan lagi mencabar untuk mengeluarkannya. Laporan ini menujukkan teknik yang mudah, cepat dan efisien untuk mengeluarkan implant Ozurdex® yang berada di bahagian anterior chamber dengan menggunakan brannula yang telah diubahsuai.

Correspondance Address: 
Mushawiahti Mustapha. Department of Ophthalmology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +603-91455981 E-mail: drmusha@gmail.com
References: 
Bansal, R., Bansal, P., Kulkarni, P., Gupta, V., Sharma, A., Gupta, A. 2012. Wandering Ozurdex(®) implant. J Ophthalmic Inflamm Infect 2(1): 1-5. Haller, J.A., Bandello, F., Belfort, R., Blumenkranz, M. 179 'Boating' Out Migrated Dexamethasone Implant Med & Health Dec 2018;13(2): 175-179 S., Gillies, M., Heier, J., Loewenstein, A., Yoon, Y.H., Jacques, M.L., Jiao, J., Li, X.Y., Whitcup, S.M., Ozurdex GENEVA Study Group. 2011. Dexamethasone intravitreal implant in patients with macular edema related to branch retinal vein occulusion twelve-month study results. Ophthalmology 118(12): 2453-60. Khurana, R.N., Appa, S.N., McCannel, C.A., Elman, M.J., Wittenberg, S.E., Parks, D.J., Ahmad, S., Yeh, S. 2014. Dexamethasone implant anterior chamber migration: risk factors, complications, and management strategies. Ophthalmology 121(1): 67-71. Pardo-López, D., Francés-Muñoz, E., Gallego-Pinazo, R., Díaz-Llopis, M. 2012. Anterior chamber migration of dexamethasone intravitreal implant (Ozurdex®). Graefes Arch Clin Exp Ophthalmol 250(11): 1703-4. Pitcher, J.D. III. 2014. A no-touch technique for removal of a dexamethasone implant 3rd edition. Retina Today, USA. 36-8.

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Biochemical Derangement in Twin Pregnancy: Complete Hydatidiform Mole and Viable Foetus

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Abstrak (In MALAY language): 

Kes kehamilan kembar molar bersama dengan kehamilan intrauterin yang normal adalah sangat jarang berlaku. Insiden kehamilan tersebut adalah sangat rendah dengan kadar satu kes di dalam 20,000 – 100,000 kelahiran. Kehamilan tersebut dikaitkan dengan risiko keguguran, kelahiran pramatang, kematian janin didalam rahim, pendarahan, pre-eklampsia, dan persistence trophoblastic disease (PTD). Kehamilan ini juga boleh mengakibatkan perubahan paras ujian biokimia di dalam ibu hamil dan mengakibatkan manifestasi gejala kepada ibu. Terdapat beberapa kes yang sama telah dilaporkan di kalangan penduduk Asia dengan dilema pengurusan klinikal yang signifikan kepada ibu dan janin. Di sini, kami laporkan kes seorang wanita muda dengan sejarah obstetrik yang kompleks hadir dengan masalah pendarahan per vagina di awal kehamilan. Beliau mempunyai kehamilan kembar molar hydatidiform lengkap dengan janin yang normal. Keadaan ini mengakibatkan paras ujian biokimia human chorionic gonadotrophin (hCG) yang sangat tinggi. Beliau juga mengalami hipertiroid. Selepas proses kelahiran, nilai hCG masih tinggi dan beliau didiagnosakan sebagai ‘Gestational Trophoblastic Neoplasm’.

Correspondance Address: 
Dr. Munirah Md Mansor. Chemical Pathology Unit, Department of Pathology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +603-91459507 Email: munirah.md.mansor@ppukm.ukm.edu.my
References: 
Aguilera, M., Rauk, P., Ghebre, R., Ramin, K. 2012. Complete hydatidiform mole presenting as a placenta accrete in a twin pregnancy with a coexisting normal fetus: case report. Case Rep Obstet Gynecol 2012: 405085. Berkowitz, R.S., Goldstein, D.P., Horowitz, N.S. 2018. Hydatidiform mole: Epidemiology, Clinical Features, and Diagnosis. http://www. uptodate.com [5 September 2018] Guideline No 38: The Management of Gestational Trophoblastic Disease. 2010. http://www.rcog. org.uk [4 September 2018] Lin, L.H., Maesta, I., Braga, A., Sun, S.Y., Fushida, K., Francisco, R.P.V., Elias, K.M.,Horowitz, N., Goldstein, D.P., Berkowitz, R.S. 2017. Multiple pregnancies with complete mole and coexisting normal fetus in North and South America: A retrospective multicenter cohort and literature review. Gynecol Oncol 145(1): 1-8. Montes-de-Oca-Valero, F., Macar, L., Shaker, A. 1999. Twin pregnancy with a complete hydatidiform mole and co-existing fetus following in-vitro fertilization. Hum Reprod 14(11): 2905-7. Newland, E.S. 2003. Presentation and management of persistent gestational trophoblastic disease and gestational trophoblastic tumour in the UK. In Gestational Trophoblastic Disease. 3rd edition. Edited by Hancock, B.W., Newland, E.S., Berkowitz, R.S., Cole, L.A.London: International Society for the Study of Trophoblastic Disease 3: 277-98. Niemann, I., Sunde, L., Petersen, L.K. 2007. Evaluation of the risk of persistent trophoblastic disease after twin pregnancy with diploid hydatidiform mole and coexisting normal fetus. Am J Obstet Gynaecol 197(1): 45.e1-5. Pisal, N., Tidy, J., Hancock, B. 2004. Gestational trophoblastic disease: Is intensive follow up essential in all women? BJOG 111(2): 1449-51. Sebire, N.J., Foskett, M., Short, D., Savage, P., Stewart, W., Thomson, M., Seckel, M.J. 2007. Shortened duration of human chorionic gonadotrophin surveillance following complete or partial hydatididform mole: evidence for revised protocol of a UK regional trophoblastic disease unit. BJOG 114(6): 760-2. Sharma, D., Usha, M.G., Gaikwad, R. 2013. Twin pregnancy with complete hydatidiform mole and coexisting live fetus complicated with HELLP syndrome. Int J Reprod Contracept Obstet Gynecol 2(1): 92-4. Shazly, S.A.E.M., Ali, M.K., Abdel Badee, A.Y., Alsokkary, A.B.A., Khodary, M.M., Mostafa, N.A.E. 2012. Twin pregnancy with complete hydatidiform mole and coexisting fetus following ovulation induction with nonprescribed clomiphene citrate regimen. A case report. J Med Case Reports 6: 95. Swaminathan, S., James, R.A., Chandran, R., Joshi, R. 2017. Anaesthetic implications of severe hyperthyroidism secondary to molar pregnancy: A case report and review of literature. Anesth Essays Res 11(4): 1115-7. Vimercati, A., de Gennaro, A.C., Cobuzzi, I., Grasso, S., Abruzzese, M., Fascilla, F.D., Cormio, G., Selvaggi, L. 2013. Two cases of complete hydatidiform mole and coexistent live fetus. J Prenat Med 7(1): 1-4. Virmani, S., Srinivas, S.B., Bhat, R., Rao, R.,Kudva, R. 2017. Case report: Transient Thyrotoxicosis in Molar Pregnancy. J Clin Diagn Res 11(7): QD01 - QD02.

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Intraspinal Epidural Hematoma in a Warfarinized Patient Presenting with Back Pain: A Case Report

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Abstrak (In MALAY language): 

Warfarin adalah ubat mencairkan darah beku yang sering digunakan untuk mencegah daripada pembekuan darah kepada pesakit yang berisiko tinggi untuk mengalami peristiwa thrombo-embolik. Penggunaan warfarin diketahui umum boleh menyebabkan pendarahan kerana kesannya dalam mencairkan darah. Walaupun, bahagian yang paling kerap berlaku pendarahan adalah saluran pencernaan makanan dan saluran kencing, ia juga boleh berlaku di bahagian yang kurang dijangkakan. Kami melaporkan satu kes yang jarang berlaku melibatkan penekanan kepada saraf tunjang disebabkan oleh pendarahan pada bahagian lapisan luar saraf tunjang akibat pencairan darah berlebihan pada seorang pesakit yang pernah menjalani pemindahan hati. Beliau telah menjalani pembedahan serta-merta untuk meringankan kesan tekanan kepada lapisan saraf tunjang dan membuang darah beku setelah kesan pencairan darah cair dibalikkan kepada tahap normal.

Correspondance Address: 
Dazlin Masdiana Sabardin. Department of Emergency Medicine, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +6013-8863961 E-mail: dazlinms926@yahoo.com
References: 
Ageno, W., Gallus, A.S., Wittkowsky, A., Crowther, M., Hylek, E.M., Palareti, G. 2012. Oral anticoagulant therapy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American 194 Med & Health Dec 2018;13(2): 188-194 Jolina W.N. et al. College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 141(2 Suppl): e44S-e88S. Algarni, A.A., Mourad, M.M., Bramhall, S.R. 2015. Anticoagulation and antiplatelets as prophylaxis for hepatic artery thrombosis after liver transplantation. World J Hepatol 7(9):1238-43. Groen, R.J., Ponssen, H. 1990. The spontaneous spinal epidural hematoma: a study of the etiology. J Neurol Sci 98: 121-38. Harik, S.I., Raichle, M.E., Reis, D.J. 1971. Spontaneously remitting spinal epidural hematoma in a patient on anticoagulants. N Engl J Med 284(24): 1355-7. Heppner, P.A., Monteith S.J., Law, A.J. 2004. Spontaneous spinal hematomas and lowmolecular- weight heparin. Report of four cases and review of the literature. J Neurosurg Spine 1(2): 232-6. Inamasu, J., Ito, K., Hattori, N., Hirose, Y. 2016. Warfarin-associated intrasponal haematoma. Keio J Med 65(4): 74-7. Leep Hunderfund, A.N., Wijdicks, E.F. 2009. Intramedullary spinal cord Hemorrhage (Hematomyelia ). Rev Neurol Dis 6(2): E54-E61. Lisman, T., Bakhtiari, K., Pereboom, I.T., Hendriks, H.G., Meijers, J.C., Porte, R.J. 2010. Normal to increased thrombin generation in patients undergoing liver transplantation despite prolonged conventional coagulation tests. J Hepatol 52(3): 355-61. Lo, C.C., Chen, J.Y., Lo, Y.K., Lai, P.H., Lin, Y.T. 2012. Spontaneous spinal epidural hematoma: a case report and review of the literatures. Acta Neurol Taiwan 21(1): 31-4. Makris, M., van Veen, J.J., Maclean, R. 2010. Warfarin anticoagulation reversal: management of the asymptomatic and bleeding patient. J Thromb Thrombolysis 29(2): 171-81. Mukerji, N., Todd, N. 2013. Spinal epidural haematoma; factors influencing outcome. British J Neurosurg 27(6): 712-7. Pagano, M.B., Chandler, W.L. 2012. Bleeding risks and response to therapy in patients with INR higher than 9. Am J Clin Pathol 138: 546-50. Palareti, G., Leali, N., Coccheri, S., Poggi, M., Manotti, C., D’Angelo, A., Pengo, V., Erba, N., Moia, M., Ciavarella, N., Devoto, G., Berrettini, M., Musolesi, S. 1996. Bleeding complications of oral anticoagulant treatment : an inceptioncohort, prospective collaborative study ( ISCOAT). Italian Study on Complications of Oral Anticoagulant Therapy. Lancet 348(9025): 423-8. Patrono, C., Rocca, B. 2007. Drug Insight: aspirin resistance-fact or fashion ? Nat Clin Pract Cardiovas Med 4(1): 42-50. Pullarkat, V. A., Kalapura, T., Pincus, M., Baskharoun, R. 2000. Intraspinal hemorrhage complicating oral anticoagulant therapy: an unusual case of cervical hematomyelia and a review of the literature. Arch Intern Med 160(2): 237-40. Stahl, R.L., Duncan, A., Hooks, M.A., Henderson, J.M., Milikan, J.W., Warren, W.D. 1990. A hypercoagulable state follows orthotopic liver transplantation. Hepatology 12: 553-8. Yu, J.X., Liu, J., He, C., Sun, L.Y., Xiang, S.S., Ma, Y.J., Bian, L.S., Hong, T.J., Tao, P.Y., Li, J.W., Li G.L., Ling, F., Zhang, H.Q. 2016. Spontaneous spinal epidural hematoma:a study of 55 cases focused on the etiology and treatment strategy. World Neurosurg 98: 546-54.

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Acute Pancreatitis with Electrocardiographic Changes Mimicking Acute Coronary Syndrome: A Diagnostic Conundrum.

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Abstrak (In MALAY language): 

Elektrocardiogram yang tidak normal boleh dikaitkan dengan radang pancreas akut. Tetapi malangnya punca-punca penyebab penyakit ini masih belum diketahui. Terdapat banyak laporan kes terdahulu manyatakan bahawa perubahan corak yang tidak normal pada ST dan T pada elektrokardiogram berkaitan dengan pankreas akut tetapi jarang sekali berlaku peningkatan enzim jantung. Kami membincangkan kes seorang wanita 70 tahun dengan masalah ini. Pesakit kami pada mulanya di rawat sebagai keradangan pancreas tetepi terdapat perubahan elektrokardiogram dan peningkatan enzim jantung. Selepas rawatan untuk pankreas akut diberikan, didapati elektrokardiogram pesakit kembali kepada normal. Ini membuktikan penyakit ini boleh menyebabkan perubahan biokimia dan elektrik yang menyerupi penyakit jantung. Oleh itu, pakar perubatan kecemasan perlu mengambil kira elektrokardiogram yang tidak normal adalah disebabkan oleh radang pancreas akut.

Correspondance Address: 
Dr. Shamala Nair. Department of Emergency Medicine, Faculty of Medicine, Universiti Kebangsaan Malaysia, Jalan Yaacob Latiff, Bandar Tun Razak, 56000, Cheras, Kuala Lumpur. Malaysia. Tel: +6016-3635092 Email: sham_128@outlook.com
References: 
Antonio, V., Francesca, C., Giulia, G., Riccardo, B., Paola, S. 2017. Acute pancreatitis mimicking myocardial ischemia: A case report and a review of the literature. Journal of Health and Social Sciences 2(2): 209-14. Buch, J., Buch, A., Schmidt, A. 1980. Transient ECG changes during acute attacks of pancreatitis. Acta Cardiol 35(5): 381-90. Kellner, A., Robertson, T. 1953. Selective necrosis of cardiac and skeletal muscle induced experimentally by means of proteolytic enzyme solutions given intravenously. J Exp Med 99(4): 387-404. Khairy, P., Marsolais, P. 2001. Pancreatitis with electrocardiographic changes mimicking acute myocardial infarction. Can J Gastroenterol 15(8): 522-6 Khan, R., Chang, H.L., Lavi, S. 2014. Acute pancreatitis mimicking the electromechanical manifestations of ST-segment elevation myocardial infarction. Curr Res Cardiol 1(2): 117-19. Patel, J., Movahed, A., Reeves, W.C. 1994. Electrocardiographic and segmental wall motion abnormalities in pancreatitis mimicking myocardial infarction. Clin Cardiol 17(9): 505-9. Patel, K., Chang, N.L., Shulik, O., DePasquale, J., Shamoon, F. 2015. Small bowel obstruction mimicking acute ST-elevation myocardial infarction. Case Rep Surg 2015: 739147 Phadke, M.S., Punjabi, P., Sharma, S., Kide, S., Nawale, J., Chaurasia, A. 2013. Acute pancreatitis complicated by ST-elevation myocardial infarction. J Emerg Med 44(5): 932-5. Rubio-Tapia, A., Garcia-Leiva, J., Asensio-Lafuente, E., Robles-Diaz, G., Vargas-Vorackova, F. 2005. Electrocardio-graphic abnormalities in patients with acute pancreatitis. J Clin Gastroenterol 39(9): 815-8. Shamma’a, M.H., Rubeiz, G.H. 1962. Acute pancreatitis with electrocardiographic findings of myocardial infarction. Am J Med 32: 827-30. Yaylaci, S., Kocayigit, I., Genc, A.B., Cakar, M.A., Tamer, A., Uslan, M.I. 2015. Electrocardiographic changes in patients with acute pancreatitis. Med J DY Patil Univ 8: 196-8. Yegneswaran, B., Kostis, J.B., Pitchumoni, C.S. 2011. Cardiovascular manifestations of acute pancreatitis. J Crit Care 26(2): 225e11-18.

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Antenatal Traumatic Brain Injury Secondary to Maternal Motor Vehicle Accident

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Abstrak (In MALAY language): 

Trauma merumitkan 1 daripada 12 kehamilan. Rawatan perubatan wanita mengandung agak berbeza kerana kandungan boleh mengubah fisiologi si ibu. Tambahan pula, janinnya mempunyai potensi untuk menjadi mangsa kedua kejadian. Di Jabatan Kecemasan, rawatan yang diberi perlu memfokus kepada diagnosis kecederaan yang dialami oleh janin dan prognosisnya untuk masa hadapan. Kecederaan otak janin berpunca dari kemalangan si ibu boleh berlaku tetapi agak jarang. Kes kami melibatkan seorang wanita mengandung yang berumur 22-tahun dan terlibat dalam kemalangan jalan raya. Rawatan awal tidak mengesan sebarang kecederaan janin tetapi selepas kelahiran pre-matang mendapati ianya mengalami kecederaan otak akibat kemalangan tersebut. Diagnosis melalui gelombang ultrasonik dan tempoh pemerhatian mengunakan alat pemantauan janin boleh meningkatkan pengesanan dan rawatan kecemasan boleh diberi pada kes-kes sebegini.

Correspondance Address: 
Dr. Shamala Nair. Department of Emergency Medicine, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Jalan Yaacob Latif, Bandar Tun Razak, 56000 Cheras, Kuala Lumpur, Malaysia. Tel: +6016-3635092 E-mail: sham_128@outlook.com
References: 
Achiron, R., Pinchas, O.H., Reichman, B., Heyman, Z., Schimmel, M., Eidelman, A., Mashiach, S. 1993. Fetal intracranial hemorrhage: clinical significance of in utero ultrasonographic diagnosis. Br J Obstet Gynaecol 100(11): 995-9. American College of Obstetricians and Gynecologists. 1999. ACOG educational bulletin. Obstetric aspects of trauma management. Number 251, September 1998. Int J Gynaecol Obstet 64(1): 87-94. Catanzarite, V.A., Schrimmer, D.B., Maida, C., Mendoza, A. 1995. Prenatal sonographic diagnosis of intracranial haemorrhage: Report of a case with a sinusoidal fetal heart rate tracing, and review of the literature. Prenat Diag 15(3): 229-35. Esposito, T.J., Gens, D.R., Smith, L.G., Scorpio, R., Buchman, T. 1991. Trauma during pregnancy. A review of 79 cases. Arch Surg 126(9): 1073-8. Ghi, T., Simonazzi, G., Perolo, A., Savelli, L., Sandri, F., Bernardi, B., Santini, D., Bovicelli, L., Pilu, G. 2003. Outcome of antenatally diagnosed intracranial hemorrhage: case series and review of the literature. Ultrasound Obstet Gynecol 22(2): 121-30. Grossman, N.B. 2004. Blunt trauma in pregnancy. Am Fam Physician 70(7): 1303-10. Jain, V., Chari, R., Maslovitz, S., Farine, D., Maternal Fetal Medicine Committee., Bujold, E., Gagnon, R., Basso, M., Bos, H., Brown, R., Cooper, S., Gouin, K., McLeod, N.L., Menticoglou, S., Mundle, W., Pylypjuk, C., Roggensack, A., Sanderson, F. 2015. Guideline for the management of a pregnant trauma patient. J Obstet Gynaecol 37(6): 553-74. Khor, C.C., Tan, T.L. 2017. Morel-lavallee lesion: a forgotten cause of bleeding in trauma. Med & Health 12(2): 363-7. Kuehn, B. 2018. Lasting effects of childhood TBI. JAMA 319(14): 1428. Kurland, D., Hong, C., Aarabi, B., Gerzanich, V., Simard, J.M. 2012. Hemorrhagic Progression of a contusion after traumatic brain injury: a review article. J Neurotrauma 29(1): 19-31. Mendez-Figueroa, H., Dahlke, J.D., Vrees, R.A., Rouse, D.J. 2013. Trauma in pregnancy: an updated systemic review. Am J Obstet Gynecol 209(1): 1-10. Mirza, F.G., Devine, P.C., Gaddipati, S. 2010. Trauma in pregnancy: a systematic approach. Am J Perinatol 27: 579-86. Nelson, C.G., Elta, T., Bannister, J., Dzandu, J., Mangram, A., Zach, V. 2016. Severe Traumatic Brain Injury: A Case Report. Am J Case Rep 17: 186-91. Piastra, M., Pietrini, D., Massimi, L., Caldarelli, M., De Luca, D., Del Lungo,L.M., De Carolis,M.P., Di Rocco, C., Conti, G., Zecca, E. 2009. Severe subdural hemorrhage due to minimal prenatal trauma. J Neurosurg Pediatr 4(6): 543-6. Rogers, F.B., Rozycki, G.S., Osler, T.M., Shackford, S.R, Jalbert, J., Kirton, O., Scalea, T., Morris, J., Ross, S., Cipolle, M., Fildes, J., Cogbill, T., Bergstein, J., Clark, D., Frankel, H., Bell, R., Gens, D., Cullinane, D., Kauder, D., Bynoe, R.P. 1999. MDA multi-institutional study of factors associated with fetal death in injured pregnant. Arch Surg 134(11): 1274-7. Shy, K.K., Luthy, D.A., Bennett, F.C., Whitfield, M., Larson, E.B., van Belle, G., Hughes, J.P., Wilson, J.A., Stenchever, M.A. 1990. Effects of electronic fetal-heart-rate monitoring, as compared with periodic auscultation the neurologic development of prematureInfants. N Engl J Med 322(9): 588-93.

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Idiopathic Hypereosinophilic Syndrome with Unusual Presentation: Two Case Reports And Review of Literature

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Abstrak (In MALAY language): 

Sindrom hipereosinofil idiopatik (HES) boleh mengakibatkan morbiditi dan mortaliti yang ketara. Pesakit biasanya mempunyai bilangan darah putih eosinofil yang tinggi untuk jangka masa yang berpanjangan dan menyebabkan tanda-tanda kerosakan organ dalaman. Protein yang merosakkan yang terhasil oleh granul eosinofilik bertanggungjawab terhadap kerosakan tisu dan sistem organ. Kami laporkan dua kes sindrom hipereosinofil idiopatik dan cabaran luar biasa yang ditimbulkan oleh penyakit ini yang jarang berlaku. Kedua-dua pesakit itu adalah wanita muda yang mengalami demam gred tinggi dan gejala bersamaan. Penemuan makmal menunjukkan sel darah putih periferi yang tinggi dengan neutrofilia dan eosinofilia yang dominan. Diagnosis idiopatik HES dibuat selepas tiada punca sekunder eosinofilia dijumpai. Walau bagaimanapun, keadaan pesakit pertama dirumitkan dengan beberapa trombosis vena. Rawatan heparin intravena dimulakan dan kemudiannya ditukar kepada subkutaneus heparin molekul rendah (LMWH). Pesakit kemudian mengalami efusi pleura. Rawatan diteruskan dengan intravena Tazoscin, tablet Prednisolone dan tablet Hydroxyurea dan pesakit beransur pulih. Namun, dua minggu kemudian, tiba-tiba keadaan pesakit kembali parah dan meninggal dunia. Di sisi lain, pesakit kedua mengalami demam, trombositopenia, anemia hemolitik, kegagalan buah pinggang akut dan defisit neurologi yang merupakan sebahagian daripada Trombotik Trombositopenik Purpura (TTP). Pertukaran plasma telah dimulakan dan keadaan pesakit beransur baik. Walau bagaimanapun, beberapa episod hipoksia yang dialami telah mengakibatkan kecederaan otak kekal yang memerlukan trakeostomi untuk bantuan ventilasi yang berpanjangan. Tujuan utama rawatan HES adalah untuk meminimumkan kerosakan tisu yang boleh disebabkan oleh hypereosinofilia. Oleh itu, diagnosis dan rawatan awal adalah penting untuk mencegah penyebaran penyakit dan kerosakan organ.

Correspondance Address: 
Dr. Suria Abdul Aziz. Department of Pathology, Faculty of Medicine, Universiti Kebangsaan Malaysia, Jalan Yaacob Latif, Bandar Tun Razak, 56000, Cheras, Kuala Lumpur. Malaysia. Tel: +603-91455443 Email: suria.abdulaziz@gmail.com
References: 
Al Aly, Z., Philoctete Ashley, J.M., Gellens, M.E., Gonzalez, E.A. 2005. Thrombotic thrombocytopenic purpura in a patient treated with imatinib mesylate: true association or mere coincidence? Am J Kidney Dis 45: 762-8. Buyuktas, D., Eskazan, A.E., Borekci, S., Umut, S., Ongen, Z., Tuzuner N., Soysal T. 2012. Hypereosinophilic syndrome associated with simultaneous intracardiac thrombi, cerebral thromboembolism, and pulmonary embolism. Internal Medicine 51(3): 309-13. Gao, S., Wei, W., Chen, J., Tan, Y., Yu, C., Litzow, M.R., Liu, Q. 2016. Hypereosinophilic syndrome presenting with multiple organ infiltration and deep venous thrombosis, A case report and literature review. Medicine 95: 35 (e4658). Gotlib, J. 2015. World Health Organization-defined eosinophilic disorders: 2015 update on diagnosis, risk stratification, and management. Am J Hematol 90(11): 1077-89. Hafiza, A., Azura, A.H., Azma, R.Z., Azlin, I., Zarina, A.L., Hamidah, N.H. 2011. Early lineage switch from T-acute lymphoblastic leukaemia to common B-ALL. Med & Health 6(2): 131-8. Leon-Ferre, R.A., Weiler, C.R., Halfdanarson, T.R. 2013. Hypereosinophilic syndrome presenting as an unusual triad of eosinophilia, severe thrombocytopenia, and diffuse arterial thromboses, with good response to mepolizumab. Clinical Advances in Hematology & Oncology 11(5): 317-9. Liapis, H., Ho, A.K., Brown, D., Mindel, G., Gleich, G. 2005. Thrombotic microangiopathy associated with the hypereosinophilic syndrome. Kidney Int 67: 1806-11. Narayan, S., Ezughah, F., Standen, G.R., Pawade, J., Kennedy, C.T. 2003. Idiopathic hypereosinophilic syndrome associated with cutaneous infarction and deep venous thrombosis. Br J Dermatol 148: 817-20. Narisa, S.S., Shanti, P., Jeevinesh, N.A., Sakthiswary, R. 2013. Eosinophilic gastroenteritis as the initial manifestation of hypereosinophilic syndrome. Med & Health 8(2): 94-9. Ohguchi, H., Sugawara, T., Harigae, H. 2009. Thrombotic thrombocytopenic purpura complicated with hypereosinophilic syndrome. Inter Med 48: 1687-90. Rick, M.E., Austin, H., Leitman, S.F., Krizek, D.M., Aronson, D.L. 2004. Clinical usefulness of a functional assay for the von Willebrand factor cleaving protease (ADAMTS 13) and its inhibitor in a patient with thrombotic thrombocytopenic purpura. Am J Hematol 75(2): 96-100. Scully, M., Yarranton, H., Liesner, R., Cavenagh, J., Hunt, B., Benjamin, S., Bevan, D., Mackie, I., Machin, S. 2008. Regional UK TTP registry: correlation with laboratory ADAMTS 13 analysis and clinical features. British Journal of Haematology 142: 819-26. Simon, H.U, Klion, A. 2012. Therapeutic approaches to patients with hypereosinophilic syndromes. Semin Hematol 49(2): 160-70. Sui, T., Li, Q., Geng, L., Xu, X., Li, Y. 2013. A case of hypereosinophilic syndrome presenting with multiorgan thromboses associated with intestinal obstruction. Turk J Hematol 30: 311-4. Swerdlow, S.H., Campo, E., Harris, N.L., Jaffe, E.S., Pileri, S.A., Stein, H., Thiele, J., Vardiman, J.W. Chronic eosinophilic leukaemia, not otherwise specified. 2008. In WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues 4th edition. Lyon: International Agency for research on Cancer; 51-53.

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