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Letters to the Editor
Arvind Krishnamurthy, Urmila Majhi1
taken for a radical surgery which entailed a lateral temporal bone excision and an elective neck dissection. The resultant defect was bridged by an anterolateral thigh microvascular flap [Figure 3a- d]. The patient is disease free for a year following surgery. MCC has traditionally been described as a skin cancer that lacks distinguishing clinical features. Heath et al.[5] in a study of 195 patients of MCC defined clinical features that may serve as clues in the diagnosis of MCC. They summarized the most significant features in an acronym: AEIOU (asymptomatic/lack of tenderness, expanding rapidly, immune suppression, older than 50 years, and ultraviolet ray exposure). Our patient had only two of the above criteria, he was very young with a slow growing recurrent swelling and there was no evidence of any immunosuppression. MCC in the HIV-positive patients occurs at a significantly younger age with a possible association with Merkel cell polyoma virus;[6] our patient did not have any underlying disease or predisposing risk factor. The histogenesis of MCC is controversial. The possible cells of origin include the epidermal Merkel cell, a dermal Merkel cell equivalent or a neural-crest-derived cell of the amine precursor uptake. The diagnosis in most cases of MCC is made on the basis of histopathologic features aided by immunohistochemistry, the latter is essential to differentiate MCC from metastatic small cell lung carcinoma and other small round blue cell tumors.[7] The treatment of the MCC is surgery, which normally consists of an excision with wide margins or micrographic surgery and preferably with adjuvant radiotherapy.[8,9] Some studies have suggested that elective lymph node dissection decreases the chance of local recurrences and improves survival. The use of adjuvant chemotherapy has been shown to be toxic and with no survival benefit and is hence not routinely recommended. [10] Since immunological factors have been implicated with the occurrence of MCC, their manipulation may possibly offer additional therapeutic options in the future.
Departments of Surgical Oncology, and 1Pathology, Cancer Institute (WIA), 36, Sardar Patel Rd, Adyar, Chennai - 600020, India For correspondence: Dr. Arvind Krishnamurthy, Department of Surgical Oncology, Cancer Institute (WIA), 36, Sardar Patel Rd, Adyar, Chennai - 600020, India. E-mail:
[email protected]
REFERENCES 1.
Medina-Franco H, Urist MM, Fiveash J, Heslin MJ, Bland KI, Beenken SW. Multimodality treatment of Merkel cell carcinoma: case series and literature review of 1024 cases. Ann Surg Oncol 2001;8:204- 8. 2. Boersma GA, van Raalte JA, Botke G, de Vogel PL, Marck KW. Merkel cell carcinoma: A treacherous skin tumor. Ned Tijdschr Geneeskd 1989;133:1933-5. 3. Karapantzos I, Tsaroucha A, Polychronidis A, Simopoulos C, Simasko N. Merkel cell carcinoma: report of seven cases. ORL J Otorhinolaryngol Relat Spec 2003;65:370-4. 4. Rockville Merkel Cell Carcinoma Group. Merkel cell carcinoma: recent progress and current priorities on etiology, pathogenesis, and clinical management. J Clin Oncol 2009;20:4021-5. 5. Heath M, Jaimes N, Lemos B, Mostaghimi A, Wang LC, Peñas PF, et al. Clinical Characteristics of Merkel Cell Carcinoma at Diagnosis in 195 Patients: The AEIOU Features. J Am Acad Dermatol 2008;58:375- 81. 6. Feng H, Shuda M, Chang Y, Moore PS. Clonal integration of a polyomavirus in human Merkel cell carcinoma. Science 2008;319:1096- 100. 7. Bobos M, Hytiroglou P, Kostopoulos I, Karkavelas G, Papadimitriou CS. Immunohistochemical distinction between merkel cell carcinoma and small cell carcinoma of the lung. Am J Dermatopathol 2006; 28:99-104. 8. Allen PJ, Bowne WB, Jaques DP, Brennan MF, Busam K, Coit DG. Merkel cell carcinoma: Prognosis and treatment of patients from a single institution. J Clin Oncol 2005;23:2300-9. 9. Lewis KG, Weinstock MA, Weaver AL, Otley CC. Adjuvant local irradiation for Merkel cell carcinoma. Arch Dermatol 2006;142:693- 700. 10. Poulsen MG, Rischin D, Porter I, Walpole E, Harvey J, Hamilton C, et al. Does chemotherapy improve survival in high-risk stage I and II Merkel cell carcinoma of the skin? Int J Radiat Oncol Biol Phys 2006;64:114-9.
Pericardial effusion and the unsuspected culprit Access this article online Website: www.cancerjournal.net www.cancerjournal.net DOI: 10.4103/0973-1482.103538
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Sir, A seven-year-old boy, a case of T-cell lymphoblastic lymphoma, was subjected to chemotherapy with BFM protocol. After the first cycle of high dose methotrexate in M phase, he presented with chest discomfort and low-grade fever. Chest X-ray was normal except for mild cardiomegaly and the subsequent 2D-echocardiogram revealed pericardial effusion. Since the effusion was minimal, it could not be drained. Mantoux was
Journal of Cancer Research and Therapeutics - July-September 2012 - Volume 8 - Issue 3
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Letters to the Editor
negative. Anti-inflammatory agents were initiated and he was put on close follow up. The child became asymptomatic with serial echocardiogram showing gradual resolution of effusion. Before the second cycle of high dose methotrexate, chest X-ray and 2D-echocardiogram were repeated and they showed no effusion. Hence it was decided to proceed with the second cycle. However, during the leucovorin rescue phase, he again developed the same symptoms. Chest X-ray showed significant cardiomegaly [Figure 1] and 2D-echocardiogram confirmed a significant pericardial effusion with impending tamponade. A pig-tail catheter was inserted and approximately 400 ml of serous fluid was removed. Fluid was paucicellular with scattered inflammatory cells, and showed a glucose level of 107.6 mg/dl, protein level of 6.27 g/dl and adenosine deaminase level of 25 U/L. The fluid was negative for malignant cells, and culture and polymerase chain reaction for tuberculosis. In view of the temporal relationship between methotrexate administration and onset of pericardial effusion as well as the negative results for other possible etiologies, methotrexateinduced pericarditis was attributed to the development of pericardial effusion in our patient. Methotrexate is a commonly used drug in oncology. Its dose varies depending on the type of malignancy and route of administration (from 12.5 mg for intrathecal methotrexate to 12 g/m2, for highdose methotrexate). The route of administration can be oral, intramuscular, intravenous or intrathecal. The most commonly encountered toxicities following methotrexate administration are nausea, vomiting and mucositis. Methotrexate-induced pleurisy and pneumonitis with or without pericardial involvement are very rare,[1] where the pathologic mechanism is thought to be immune-mediated serositis.[2] Isolated pericardial effusion as a toxic effect of methotrexate is extremely rare. Only two cases have been reported in the literature. The first reported case was in a 22-year-old woman with hydatidiform mole who received low-dose methotrexate (total dose over nine courses was 1.8 g)[3] and the second patient was a case of psoriasis treated with very small dose of methotrexate (dose ranges from 7.5 to 25 mg per week).[4] Our patient experienced the toxicity following high-dose methotrexate for malignancy (5 g/m2 per cycle). We believe it to be immune-mediated as the fluid was protein-rich, paucicellular with inflammatory cells, and negative for malignancy and tuberculosis. Even in a country where tuberculosis is common,
Figure 1: Chest X-ray showing pericardial effusion
the possibility of drug-induced pericardial effusion should be considered in patients receiving methotrexate. Boben Thomas, Palaniappan Muthu, Archana Karichala, Pavithran Keechilat Department of Medical Oncology, Cancer Institute, Amrita Institute of Medical Sciences, AIMS Ponekkara post, Edappally, Kochi, Kerala, India. For correspondence: Dr. Palaniappan M, Department of Medical Oncology, Cancer Institute, Amrita Institute of Medical Sciences, AIMS Ponekkara post, Edappally, Kochi - 682041, Kerala, India. E-mail:
[email protected]
REFERENCES 1.
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Journal of Cancer Research and Therapeutics - July-September 2012 - Volume 8 - Issue 3
Sheridan E, Hancock B, Smith S, Dorreen M, Neal F, Pennington G, et al. Gestational trophoblastic disease: experience of the Sheffield (United Kingdom) supraregional screening and treatment service (Review). Int J Oncol 1993;3:149-55. Akoun GM, Mayaud CM, Touboul JL, Denis MF, Milleron BJ, Perrot JY. Use of bronchoalveolar lavage in the evaluation of methotrexate lung disease. Thorax 1987;42:652-5. Forbat LN, Hancock BW, Gershlick AH. Methotrexate-induced pericarditis and pericardial effusion; first reported case. Postgrad Med J 1995;71:244-5. Palungwachira P, Palungwachira P, Laohathai P. Methotrexate induced pericarditis and pericardial effusion in psoriatic patient. J Med Assoc Thai 1998;81:141-5.
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