Skip to content

Advertisement

  • Poster presentation
  • Open Access

Thrombopenia and/or splenomegaly in HIV/HCV co-infected patients with mild liver fibrosis alerts for the risk of portal hepatopathy

  • 1,
  • 1,
  • 1,
  • 1 and
  • 1
Journal of the International AIDS Society200811 (Suppl 1) :P286

https://doi.org/10.1186/1758-2652-11-S1-P286

  • Published:

Keywords

  • Portal Hypertension
  • Liver Fibrosis
  • Didanosine
  • Variceal Bleeding
  • Advanced Liver Fibrosis

Background

Non-cirrhotic portal hypertension has recently emerged as a new entity in HIV-infected patients. Histological findings often reveal different hepatic portal perivascular abnormalities. In most cases it was related to previous didanosine exposure. Although its recognition could be more difficult, this drug-induced vascular damage in the liver might also appear in HIV/HCV co-infected patients.

Clinical cases

Three HIV individuals with chronic hepatitis C presented with complicated portal hypertension as oesophageal variceal bleeding. Liver fibrosis measured by transient elastometry did not reveal advanced liver fibrosis. Liver function tests were completely normal. All subjects presented previous clinical signs of portal hypertension, thrombopenia and splenomegaly, lasting on average 4 and 2 years, respectively. They had been exposed to didanosine for long periods in the past. (Table 1.)

Table 1

 

Case 1

Case 2

Case 3

Age (years)

41

49

42

Gender

Male

Female

Male

Race

Caucasian

Caucasian

Caucasian

Risk group

IDU

IDU

IDU

On HAART

Yes

Yes

Yes

Prior didanosine exposure (months)

64

30

44

CD4 count (cells/mm3)

351

168

324

Plasma HIV-RNA (copies/ml)

<50

<50

<50

Platelet count/ul

78,000

57,000

81,000

Liver fibrosis stage (Metavir, stiffness KPa)

F2 (9)

F3 (11.5)

F4 (15)

Splenomegaly

Yes

Yes

Yes

Discussion

Primary hepatic vascular damage induced by didanosine might result in non-cirrhotic portal hypertension. This condition may appear in HIV patients without any known cause of liver disease, as well as superimposed to other hepatic illnesses, as chronic hepatitis C. The recognition of clinical classical signs of portal hypertension (e.g. thrombopenia, splenomegaly) in the absence of a significant liver fibrosis or synthetic function compromise may alert to the possibility of this condition.

Authors’ Affiliations

(1)
Hospital Carlos III, Madrid, Spain

Copyright

© Vispo et al; licensee BioMed Central Ltd. 2008

This article is published under license to BioMed Central Ltd.

Advertisement