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CORRESPONDENCE
Year : 2009  |  Volume : 27  |  Issue : 1  |  Page : 85-86
 

Visceral leishmaniasis simulating chronic liver disease: Successful treatment with miltefosine


Department of Medicine, University College of Medical Sciences (University of Delhi) and GTB Hospital, Delhi-110 095, India

Date of Submission10-Mar-2008
Date of Acceptance11-May-2008

Correspondence Address:
S C Chaudhary
Department of Medicine, University College of Medical Sciences (University of Delhi) and GTB Hospital, Delhi-110 095
India
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Source of Support: None, Conflict of Interest: None


PMID: 19172077

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How to cite this article:
Avasthi R, Chaudhary S C, Khanna S. Visceral leishmaniasis simulating chronic liver disease: Successful treatment with miltefosine. Indian J Med Microbiol 2009;27:85-6

How to cite this URL:
Avasthi R, Chaudhary S C, Khanna S. Visceral leishmaniasis simulating chronic liver disease: Successful treatment with miltefosine. Indian J Med Microbiol [serial online] 2009 [cited 2020 Jan 27];27:85-6. Available from: http://www.ijmm.org/text.asp?2009/27/1/85/45186


Dear Editor,

A 45-year-old non-alcoholic male resident of Bihar, an Indian state endemic for Kala-azar, was admitted with high-grade fever associated with chills and rigor, pain in the left upper abdomen, anorexia and weight loss for 1 months. He had severe pallor, bilateral pedal oedema, non-tender hepatosplenomegaly and ascites. Investigations revealed haemoglobin of 5.5 g/dL, total leukocyte count 1.4x10 3 /mm 3 , platelet count 60x10 3 /mm 3 , ESR 78 mm/h and peripheral smear suggestive of pancytopenia. Bone marrow smear showed plasma cells and Leishman donovan (LD) bodies. Indirect immunofluorescent antibody test (IFAT) for Kala-azar was positive (titre 1:1600). Serum bilirubin was 1.2 mg/dL, serum alanine aminotransferase 20 U/L, serum aspartate aminotransferase 16 U/L, serum alkaline phosphatase 240 U/L and total serum protein 10.7 g/dL (albumin 1.44 g/dL). Prothrombin time (PT) was 25 (13 s) and activated partial thromboplastin time (aPTT) was 50 (28 s). Protein electrophoresis was suggestive of chronic inflammation and hypoalbuminaemia without any M-spike. Urine examination revealed albumin +++, Bence-Jones protein negative and 24-h urinary protein was 1312 mg. Hepatitis B surface antigen, antihepatitis C virus and enzyme-linked immunosorbent assay for human immunodeficiency virus were negative. Ultrasound of the abdomen showed hepatomegaly (14 cm), massive splenomegaly (> 19 cm), borderline portal hypertension (portal vein size 13 mm) and ascites. Ascitic fluid was transudative in nature. Upper gastrointestinal endoscopy was normal. Liver and renal biopsies could not be performed as patient refused to consent. The patient was put on tablet Miltefosine 50 mg BD for 4 weeks. He responded well to treatment and became afebrile after 10 days, with marked regression in the size of the liver and spleen. Repeat investigations performed after 8 weeks showed near normal haemogram, normal liver function tests and normal size portal vein on ultrasound and the bone marrow smear became negative for LD bodies. IFAT titre (1:400) and proteinuria (476 mg/24 h) decreased significantly.

Our patient had evidence suggestive of significant liver disease in view of hepatosplenomegaly, elevated serum alkaline phosphatase, marked hypoalbuminaemia, impaired PT/aPTT, transudative ascites and ultrasonographic evidence of hepatosplenomegaly, ascites and borderline portal hypertension along with definitive evidence of Kala-azar. Most of these findings did revert after successful treatment with oral miltefosine.

Although liver involvement is not unusual in Kala-azar, presentation as cirrhosis, portal hypertension and chronic liver disease is always a curiosity. Extensive literature search revealed only one case report with visceral leishmaniasis along with histological evidence of leishmanial hepatitis and portal hypertension. [1] On the contrary, a series of 60 Kala-azar cases did not have any case of chronic liver disease, although one quarter of the patients had biochemical evidence of hepatitis. [2] Our patient also had non-nephrotic range proteinuria at the time of diagnosis, which is a common finding usually reported as a late complication. [3]

The Indian subcontinent has been plagued by resistance to classical antileishmanial drugs and the approval of miltefosine in this regard has been a significant milestone in the treatment due to ease of administration, few toxic effects and excellent cure rate. [4],[5]

 
 ~ References Top

1.Prakash A, Singh NP, Sridhara G, Malhotra V, Makhija A, Garg D, et al . Visceral leishmaniasis masquerading as chronic liver disease. J Assoc Physicians India 2006;54:893-4.  Back to cited text no. 1  [PUBMED]  
2.Aggarwal P, Wali JP, Chopra P. Liver in kala-azar. Indian J Gastroenterol 1990;9:135-6.  Back to cited text no. 2    
3.Salgado Filho N, Ferreira TM, Costa JM. Involvement of the renal function in patients with visceral leishmaniasis (kala azar). Rev Soc Bras Med Trop 2003;36:217-21.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Sundar S, Jha TK, Thakur CP, Engel J, Sindermann H, Fischer C, et al . Oral miltefosine for Indian visceral leishmaniasis. N Engl J Med 2002;347:1739-46.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Bhattacharya SK, Sinha PK, Sundar S, Thakur CP, Jha TK, Pandey K, et al . Phase 4 trial of miltifosine for the treatment of Indian visceral leishmaniasis. J Infect Dis 2007;196:591-8.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]




 

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