Hepatitis C virus infection in sporadic fulminant viral hepatitis in NorthIndia: cause or co-factor?

Introduction The role of hepatitis C virus (HCV) infection in fulminant hep atitis (FH) is poorly understood and the available data are conflicting. We have examined the aetiological role of HCV in 50 consecutive patients with sporadic FH by employing serology and reverse transcription - polymerase c hain reaction (RT - PCR). Materials and methods A total of 50 consecutive patients with sporadic FH w ere included. After an initial clinical and biochemical assessment, tests w ere performed for detection of HBsAg, IgM anti-HBc, IgM anti-HAV, IgM anti- HEV and anti-HCV. RT-PCR was carried out for detection of HCV RNA in sera o f all the patients and in post mortem liver biopsy tissue of 20 subjects, u sing primers selected from the conserved 5' non-coding region of the HCV ge nome. Results Hepatitis E virus (HEV) was found to be the most common viral infec tion (21/50; 42%) followed by HBV (14/50; 28%), HCV (7/50; 14%) and HAV (2/ 50; 4%). No viral markers could be detected in nine patients (18%) and mult iple infections were seen in seven (14%). Of the seven subjects who tested positive for HCV-related markers, two had both anti-HCV and HCV RNA, three had HCV RNA alone and the remaining two had anti-HCV alone. Interestingly, all the HCV-infected subjects were coinfected with other hepatotropic virus es and the most common co-infecting agent was found to be HBV (5/7). Liver tissue was available in 20 cases and HCV RNA was detected in three of them. All of these patients were also positive for the viral genome in their ser um samples. Comparison of the biological attributes of HCV-positive and HCV -negative cases revealed that haemorrhagic symptomatology (haematemesis, me laena and purpurae) was significantly more common, prothrombin time more de ranged and mortality was much higher in the former group. The overall morta lity was 68% and the most common cause of death was cerebral oedema (70.6%) . No significant correlation was observed between mortality and the duratio n of the icterus- encephalopathy interval. The study included a total of 21 pregnant females; HEV infection was found to be significantly greater in t his group and was associated with a higher mortality rate. Conclusions The results clearly suggest that HCV is not an important aetiol ogical factor for FH in North India. However, it may act as a co-factor in the development of FH leading to a higher mortality. HEV appears to contrib ute substantially to the causation of sporadic FH in India and advanced sta ge pregnancy is a potential risk factor for HEV-induced FH and high rate of mortality. Our study also suggests that the length of the icterus- encepha lopathy period may not have significant prognostic implications in Indian p atients with FH. Eur J Gastroenterol Hepatol 11:1231-1237 (C) 1999 Lippinco tt Williams & Wilkins.