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Insulin Resistance in HBV, HCV & Non-Virus Related Chronic Hepatitis (liver enzymes)
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...HBV therapy appeared to have protective effect regarding insulin resistance.
Reported by Jules Levin
EASL, April 2007, Barcelona, Spain
M. Montagnani 1, F. Lodato 1, F. Azzaroli 1, M.R. Tame 1, A. Colecchia 1, P. Cecinato 1, R. Muratori 1, D. Festi 1, G. Mazzella 1
1 Department Of Internal Medicine And Gastroenterology, University Of Bologna, Bologna, Italy
Background/Aims: Insulin resistance (IR) is the background of many cryptogenetic liver diseases. In genotype 1 and 2 HCV chronic hepatitis (CH-C) the virus seems to induce insulin resistance (IR). In HBV chronic hepatitis (CH-B) the virus role in steatosis and IR is to be clarified. The aim of our study is to evaluate IR and the relationship with disease severity, in patients with CH-C, CH-B or with non-virus related hypertransaminasemia, elevated ALT/AST (NV-H).
Methods: Twenty-eight outpatients with NV-H and 50 outpatients in follow-up for CH-B (n=23) or CH-C (n=27) were consecutively enrolled between January and May 2006. Patients with alcohol consumption >10 grams/day were excluded. Abdominal circumference (AC), BMI, fasting blood glucose (FBG) insulinemia, OGTT, HOMA-r and liver ultrasonography were evaluated. ANOVA, Mann-Whithney test and c2 were used for statistical analysis. Data are expressed as mean±SE.
Results
Groups were comparable for age, BMI, AC and FBG; males were prevalent in CH-B (M:F 21:2 vs CH-C:17:10 and NV-H:12:16, p=0.001).
Steatosis was present in 75, 52 and 82% respectively for NV-H, CH-B and CH-C (p=ns).
Cirrhosis was present in 18% in NV-H, 48% in CH-B and 52% in CH-C (p=0.02).
Insulin was higher in CH-C than NV-H (16.3±1.6 vs 10.8±1.2, p=0.016), and in cirrhosis vs non-cirrhosis [17.4±2.7, 16,4±1.2 and 18.7±2.7 ng/ml vs 9.4±1.1 (p<0.013), 10.3±1.3 (p<0.003) and 13.6±1.6 (ns) respectively for NV-H, CH-B & CH-C].
HOMA-r was 2.5±0.33, 2.9±0.32 and 4.2±0.41 respectively for NV-H, CH-B and CH-C (p=0.01).
Cirrhosis had higher HOMA-r respect to non-cirrhosis in all groups [4.5±0.8, 3.9±0.47, and 4.9±0.7 2.1±0.3 (p<0.012), 1.95±0.21 (p<0.003) and 3.2±0.42 (p<0.05)].
Treatment with nucleos(t)ide analogues (HBV therapy) was related to significant reduction in HOMA-r in CH-B (2.5±0.4 vs 3.6±0.5, p=0.05). At multivariate analysis HOMA-r was associated with age, BMI, AC and steatosis and independently related to abdominal circumference (AC) in NV-H, to cirrhosis and antiviral treatment in CH-B, to AC and cirrhosis in CH-C.
Discussion: IR is associated with cirrhosis regardless of underlying disease when evaluated by HOMA-r. In CH-B, inhibition of viral replication by necleos(t)ide analogues seems to protect from IR, possibly through: 1) reduction in liver inflammation; 2) inhibition of viral replication; 3) direct metabolic effect.
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