Hepatic steatosis in patients with HIV-Hepatitis C Virus coinfection: is it associated with antiretroviral therapy and more advanced hepatic fibrosis?
BMC Research Notes
Short Report Hepatic steatosis in patients with HIV-Hepatitis C Virus coinfection: is it associated with antiretroviral therapy and more advanced hepatic fibrosis?
Sumita Verma 1
Robert D Goldin 0
Janice Main 1
0 Department of Cellular Pathology, Imperial College at St Mary's Hospital , London , UK
1 Hepatology Section, Department of Medicine, Imperial College at St Mary's Hospital , London , UK
Background and aims: Patients with HIV and hepatitis C virus (HCV) coinfection are at increased risk of developing hepatic steatosis. The aims of this study were to assess the prevalence of steatosis in a cohort with HIV-HCV coinfection, and to determine an association, if any, between steatosis, antiretroviral therapy (ART), and advanced hepatic fibrosis. Patients and methods: HIV-HCV coinfected patients were retrospectively identified from the HIV clinic. ART was classified as none, nucleoside reverse transcriptase inhibitors (NRTIs) only, highly active antiretroviral therapy (HAART) only, and sequential therapy (initial NRTIs followed by HAART). Fibrosis stage and necroinflammation grade were assessed by the modified HAI (Ishak) scoring method. Steatosis was graded as 0-3. Results: Sixty patients were identified. The overall prevalence of hepatic steatosis was 58%. Those that received HAART only had a lower prevalence of steatosis (41%) compared to those on NRTIs only (70%) or sequential therapy (82%). Independent predictors of hepatic steatosis were absence of HAART only therapy, OR 2.9, p = 0.09, and presence of cirrhosis, OR 4.6, p = 0.044. Forty five percent of the patients had advanced fibrosis (fibrosis stage ≥ 3). NI grade (OR 1.9, p = 0.030), and steatosis grade (OR 3.6, p = 0.045), were independent predictors of advanced fibrosis. Conclusion: Hepatic steatosis is associated with more advanced hepatic fibrosis in the HIV-HCV coinfected population. HAART only therapy (rather than NRTIs only or sequential therapy) appears to be associated with a lower prevalence of hepatic steatosis. This may be one of the mechanisms by which HAART could attenuate hepatic fibrosis in such a cohort.
Introduction
Highly active antiretroviral therapy (HAART) has
significantly improved survival in patients with human
immunodeficiency virus (HIV) infection [1]. Increasing attention
is now being focused on co infection with other viruses
like hepatitis C (HCV). Because of similar routes of
transmission, approximately 25–30% of patients with HIV are
also coinfected with HCV [2]. Factors associated with
more advanced hepatic fibrosis in HCV infection include
HIV coinfection [3] and hepatic steatosis, (prevalence of 47%–79%) [4-6].
Patients with HIV are also at increased risk of developing
hepatic steatosis due to multiple factors including
antiretroviral therapy (ART), obesity, hyperglycemia,
lipodystrophy, and coinfection with HCV [
2,7-11
]. In HIV-HCV
coinfection prevalence of hepatic steatosis varies between
40–72.1% [
9-13
]. In the coinfected population, the
association between ART and steatosis, and whether steatosis
is associated with advanced fibrosis remains controversial
[
9-11
]. The aims of this study were therefore to assess
whether in those with HIV-HCV coinfection
1. Use of ART is associated with hepatic steatosis
2. Hepatic steatosis is an independent predictor of advanced hepatic fibrosis
3. Hepatic steatosis is associated with fibrosis progression in serial liver biopsies
Patients and methods
The study period was from 1990–2005. Patients with HIV
HCV coinfection were identified from the Pathology and
HIV database after which, their charts and computerised
chemical pathology and histology databases reviewed. To
be included in the study the patients had to be
1. HCV antibody and or HCV PCR (qualitative) positive
2. HIV antibody positive
3. Have had a liver biopsy.
The indications for a liver biopsy in most patients were
abnormal liver tests. All the liver biopsies had been
reviewed by RG who was blinded to the clinical
information. The fibrosis stage (0–6) and necroinflammatory (NI)
grade (0–18) were assessed by the modified HAI (Ishak)
scoring system [
14
]. Steatosis was graded, (depending on
% of hepatocytes containing fat), into grade 0 (< 5%),
grade 1 (<33%), grade 2 (33%–66%), and grade 3
(>66%).
HCV disease duration and fibrosis progression were
calculated as before [
15
]. Lipoatrophy was stated to be present
if mentioned in the patient records. Diabetes mellitus
(DM) was defined by presence of one or more of the
following: fasting blood glucose > 7 mmol/l, being on anti
diabetic medications, and/or a note in the patient record
stating that there was a history of DM.
Anti-HCV antibody testing, HCV RNA and HIV RNA quantification and HCV genotyping were performed in the hospital virology laboratory using standard commercial kits (Abbott, Bayer, Roche).
Alcohol abuse was defined as either consumption of > 3
units of alcohol/day (approximately 40 gms/day), an (...truncated)