Virchows Archiv

, Volume 458, Issue 2, pp 231–235

The development of hepatoportal sclerosis and portal hypertension due to didanosine use in HIV

  • Thomas D. Schiano
  • Alison Uriel
  • Douglas T. Dieterich
  • M. Isabel Fiel
Original Article

DOI: 10.1007/s00428-010-1004-7

Cite this article as:
Schiano, T.D., Uriel, A., Dieterich, D.T. et al. Virchows Arch (2011) 458: 231. doi:10.1007/s00428-010-1004-7

Abstract

Hepatoportal sclerosis (HPS) is one of several entities known to cause noncirrhotic portal hypertension. To date, its etiology is unknown. There have been increasing reports of HPS occurring in patients with human immunodeficiency virus (HIV), and the US Food and Drug Administration (FDA) recently issued an advisory regarding the development of noncirrhotic portal hypertension in association with didanosine (ddI) use. We report on a patient with HIV who had taken ddI for 4 years and who developed portal hypertension. Histopathological review of paired liver biopsies showed an initial drug hepatotoxicity, microvascular liver injury, and the presence of HPS. Despite cessation of ddI, the latter biopsy showed resolution of the drug-induced injury, but it also showed progression of the HPS. The patient’s portal hypertension also progressed suggestive of an unremitting vascular injury. This case demonstrates the development of HPS resulting from a drug-induced microvascular injury. The paired biopsies demonstrate that the initial vascular injury may disappear but that the portal hypertension and HPS progress.

Keywords

HIV Noncirrhotic portal hypertension Hepatoportal sclerosis Nodular regenerative hyperplasia Didanosine Antiretroviral therapy 

Copyright information

© Springer-Verlag 2010

Authors and Affiliations

  • Thomas D. Schiano
    • 1
  • Alison Uriel
    • 1
  • Douglas T. Dieterich
    • 1
  • M. Isabel Fiel
    • 2
  1. 1.Division of Liver Diseases, Department of MedicineThe Mount Sinai Medical CenterNew YorkUSA
  2. 2.Department of PathologyThe Mount Sinai Medical CenterNew YorkUSA

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