Indian J Sex Transm Dis Indian J Sex Transm Dis
Official Publication of the Indian Association for the Study of Sexually Transmitted Diseases
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Year : 2009  |  Volume : 30  |  Issue : 1  |  Page : 57-58

Recurrent venous thromboses in HIV-2 patient

Yashodhan Hospital, Extension Area, Station Road, Miraj - 416 410, Sangli, Maharashtra, India

Date of Web Publication5-Sep-2009

Correspondence Address:
Uday Arun Phatak
Yashodhan Hospital, Extension Area, Station Road, Miraj - 416 410, Sangli, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0253-7184.55480

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How to cite this article:
Phatak UA. Recurrent venous thromboses in HIV-2 patient. Indian J Sex Transm Dis 2009;30:57-8

How to cite this URL:
Phatak UA. Recurrent venous thromboses in HIV-2 patient. Indian J Sex Transm Dis [serial online] 2009 [cited 2020 Aug 11];30:57-8. Available from:


The real incidence of HIV-2 infection in Indian patients is not known. Different studies have reported 0.22 to 0.8% prevalence of HIV-2 infection in different States of India. [1] Venous thrombosis is a rare complication of HIV-1 or mixed (HIV-1 and 2) infection in 1.52% of patients. [2] There are very few reports on venous thrombosis in HIV-2 patients [3] and no case studies from India. We present a case of recurrent venous thromboses in HIV-2 infection in an Indian patient.

The patient, a 42-year-old male, presented with per-rectal bleeding and progressively increasing swelling of the neck and left arm, with edema of the arm and forearm. Routine investigations revealed hemoglobin 12.4 Gm/dL, normal white blood cell (WBC) count with differential count. Erythrocyte sedimentation rate (ESR) was 110 mm at the end of first hour. Urine examination was normal. Biochemical investigations were normal. X-ray chest Normal. Tridot test showed only HIV-2 infection confirmed with Western blot test. CD4 count was 168/ mm 3 and CD8 count was 890/mm 3 . HIV-1 RNA was undetectable. HIV-2 viral load could not be performed. Ultrasound with Doppler study of the neck showed thrombosis of the internal jugular vein. There were multiple matted glands in the neck region. Fine needle aspiration showed acid fast bacilli. Patient was treated with low molecular weight heparin followed by warfarin and anti-tuberculosis drugs. Later, Patient discontinued warfarin after two months. He was re admitted with thrombosis of the left femoral vein and swelling, confirmed by a Doppler study and treated with low molecular weight heparin. Coagulation profile was normal except raised homocysteine level was 50µmol/L. (normal is less than 15 µmol/L).

This patient had jugular and deep vein thrombosis due to raised homocysteine level. Venous thrombosis in HIV infection is a multifactorial process. It may be due to hypercoagulable state induced by HIV infection per se or could be due to raised levels of antiphospholipid antibody, fibrinogen or homocysteine or protein C and S deficiency while idiopathic in significant number of patients.[2] Bouchard reported portal vein thrombosis in HIV-2 patient due to high antiphospholipid level [3] while Soman and Kanekar reported a case of venous thrombosis in HIV patient due to raised homocysteine level. [4]

Hyperhomocysteinemia is a marker of endothelial dysfunction and is associated with premature atherosclerosis. There could be higher incidence of myocardial infarction, stroke, arterial and venous thromboses. High levels of homocysteine could be due to genetic deficiencies of certain enzymes or some co-factor deficiencies such as dietary deficiency of vitamin B12 folic acid. It may be associated with systemic diseases like renal failure, thyroid diseases or malignancies or certain infections. Risk of venous thrombosis is significant when homocystine levels increase by five per cent and above [2] the impact of antiretroviral therapy on homocysteine level and venous thrombosis has not been not fully understood. Soentjens et al . reported development of portal venous thrombosis due to hyperhomocysteinemia, protein S deficiency and elevated factor VIII coagulant activity. It was postulated that protease inhibitor might have played a role in increasing the thromboembolic risk. [5]

   References Top

1.Arora U, Jindal N, Chopra S. Seroprevalence of human immunodeficiency virus-2 in and around Amritsar. Indian J Pathol Microbiol 2007;50:926-7.  Back to cited text no. 1  [PUBMED]  Medknow Journal
2.Laing RB, Brettle RP, Leen CL. Venous thrombosis in HIV infection. Int J STD and AIDS. 1996;7:82-85.  Back to cited text no. 2    
3.Bouchard O, Bosseray A, Leclercq P, Micoud M. Portal thrombosis and anticardiolipin antibodies association in an HIV-2 infected patient. Presse Med 1998;27:965.  Back to cited text no. 3    
4.Soman R, Kanekar A. Jugular venous thrombosis in HIV-seropositive man. J Assoc Physicians India 2002;50:595.  Back to cited text no. 4    
5.Soentjens P, Ostyn B, Van Outryve S, Ysebaert D, Vekemans M, Colebunders R. Portal vein thrombosis in a patient with HIV treated with a protease inhibitor-containing regimen. Acta Clin Belg 2006;61:24-9.  Back to cited text no. 5    

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