Serum anti-cholesterol antibodies in chronic hepatitis-C patients during IFN-alpha-2b treatment.
Previously we detected more than 3 times higher anti-cholesterol antibody (ACHA) levels in HIV positive patients compared to healthy individuals, however, this level significantly decreased during highly active anti-retroviral therapy (HAART). In our present study we examined whether these findings could also be detected in patients with chronic hepatitis C (CHC). We calculated the correlation between the ACHA levels and the C5b-9 complement activation product. 39 patients with CHC were treated with IFN-alpha-2b (Schering-Plough) 5 MU daily for 6 weeks, followed by 5 MU TIW. Serum levels of ACHA and complement activation products were measured with ELISA. Serum HCV RNA was measured by a highly sensitive branched DNA technique before and 3, 6 and 12 months after the beginning of IFN-alpha-2b therapy. 52 healthy persons served as controls. At the onset of treatment ACHA level was significantly (p = 0.0062) higher in patients (40 (24-69) AU/ml) (median (interquartile range)) than in control sera (26 (20-35) AU/ml). In the 26 responder patients ACHA levels decreased to the normal level during the therapy, but no change was observed in the 13 non-responders. In patients with a sustained response ACHA levels remained low till the end of the 12 months IFN treatment. ACHA levels were significantly (p = 0.0422) higher in the patients with low (< 4.0 mmol/l) than in those with normal (> or = 4.0 mmol/l) cholesterol concentrations. The ACHA level before the therapy strongly correlated (r = 0.5499, p = 0.0014) with C5b-9 serum levels. ACHA levels are elevated in CHC, but this elevation is not as high as in HIV. Decrease of viral load by IFN-alpha-2b treatment in the responders results in normalization of ACHA concentration. High ACHA levels in patients with low serum cholesterol concentration suggest that high ACHA levels may contribute to the decrease in cholesterol levels. The correlation between the ACHA and C5b-9 levels indicate, that the ACHA may play a role in the complement activation in CHC.
Biró
Adrienn
A
3rd Department of Medicine, Semmelweis University, Budapest, Hungary.
Horváth
Anna
A
Varga
Lilian
L
Nemesánszky
Elemér
E
Csepregi
Antal
A
Dávid
Károly
K
Tolvaj
Gyula
G
Ibrányi
Endre
E
Telegdy
László
L
Pár
Alajos
A
Romics
László
L
Karádi
István
I
Horányi
Margit
M
Gervain
Judit
J
Ribiczey
Pál
P
Csöndes
Mihály
M
Füst
George
G
D000328:Adult; D000888:Antibodies, Anti-Idiotypic; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood / Q000276:immunology*; D003167:Complement Activation; D015938:Complement Membrane Attack Complex / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D016174:Hepacivirus / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000097:blood* / Q000628:therapy*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D011994:Recombinant Proteins; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
D000888:Antibodies, Anti-Idiotypic; D015938:Complement Membrane Attack Complex; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; D014280:Triglycerides; D002784:Cholesterol