Z Gastroenterol 2006; 44 - A122
DOI: 10.1055/s-2006-943488

Anti-cholesterol antibody levels in chronic hepatitis c. high titers in patients with genotype 3 and 4, but not in genotype 1B

F Szalay 1, T Csak 1, A Biro 2, T Scherzer 3, A Folhoffer 1, A Horvath 1, J Osztovits 1, PL Lakatos 1, I Karádi 2, G Füst 2, P Ferenci 3
  • 11st Dept. of Medicine, Semmelweis University, Budapest
  • 23rd Dept. of Medicine, Semmelweis university; Budapest
  • 34th Dept of Medicine of University Vienna

Background and Aims: Anti-cholesterol antibodies (ACHA) are natural antibodies against the 3beta-OH group of free cholesterol. High level of ACHA was reported in HIV and hepatitis C infected patients. Association was reported between HCV infection and lipid disorders. Steatosis is more common in HCV genotype 3 infection.

We aimed to compare the ACHA level in patients with chronic hepatitis C of different HCV genotypes. Correlation between ACHA and BMI, lipid levels, viral load, transaminases and HCV genotypes were also investigated.

Methods: 29 patients with HCV genotype 1b (age: 55.6±12.6 years), 27 patients with HCV genotype 3 (age: 37±9.3) and 25 patients with HCV genotype 4 (age: 41.7±7.7, each with obesity and fatty liver) infection were investigated. None of the patients were treated previously. Age-matched healthy persons served as controls for each group. ACHA was measured in sera by solid phase enzyme immunoassay as described. Serum total-, LDL- and HDL-cholesterol, triglyceride, bilirubin, AST, ALT, GGT, ALP, albumin, CRP, immunoglobulin, AFP, viral load and BMI were measured.

Results: Higher serum ACHA level was found in patients infected with HCV genotype 3 and 4 (63.1±39 AU/ml and 64±46.6 AU/ml) compared to both healthy controls (28.7±15 AU/ml, p=0.00005 and p=0.0008) and genotype 1b (24±15.5 AU/ml, p=0.000009 and p=0.00024) infected patients. We did not found difference in the ACHA level between the HCV genotype 1b infected patients and healthy controls. There was no correlation between the ACHA levels and BMI, viral load, any liver function tests, CRP, immunoglobulin or any lipid parameters in HCV infected patients. In healthy controls negative correlation was found between serum ACHA and total cholesterol level indicating the reactivity of ACHA to free cholesterol.

Conclusion: Our novel finding of elevated serum ACHA in HCV genotype 3 infected patients compared to HCV genotype 1b infected patients is in concordance with published data on the particular role of HCV genotype 3 in the genesis of hepatic steatosis. Results might stimulate further research to clarify the clinical significance of ACHA.