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Little information is available in the literature on acute exacerbation of chronic hepatitis C (r-CHC).1–5 In Taiwan, Sheen et al estimated an annual incidence rate of 11.9%.3 In this study, 40.2% of 78 patients experienced at least one episode of reactivation during a mean observation period of six years and a total of 151 episodes of reactivation were observed, 45% of them symptomatic. The paper by Rumi et al from Milan (Gut 2005;54:402–6) on r-CHC in relation to hepatitis C virus (HCV) genotyping described it as frequent in patients with genotype 2c (39% of 100 patients) and infrequent in those with genotype 1b (7.5% of 106 patients), with a rate×1000 persons/year of 55.6 and 15.0, respectively. From January 2002 to the present, we have enrolled 49 consecutive patients with acute hepatitis C (AHC group) and 57 consecutive patients with r-CHC (r-CHC group) in a prospective follow up study. All patients were hospitalised at our ward because the illness was symptomatic.
The criteria for a diagnosis of AHC were: (a) negative serum anti-HCV and normal serum alanine aminotransferase (ALT) levels in the four months preceding the onset of symptoms; and (b) positive anti-HCV/HCV-RNA and increased ALT (>5 times the highest value of normal) during the acute stage of the illness. The diagnosis of r-CHC was made for patients with: (a) positive serum anti-HCV and plasma HCV-RNA during the six months before the onset of symptoms and on admission; and (b) ALT increase >5 times the mean of the ALT values observed during the previous six months. As a control group for patients in the r-CHC group, 57 hepatitis B virus surface antigen (HBsAg) negative, symptom free, untreated patients with chronic hepatitis C (CHC group), hospitalised in the same period for their first liver biopsy, were pair matched by age (±5 years), sex, and risk factors for acquisition of parenteral infection.
All patients in the AHC and r-CHC groups lacked serum HBsAg, antibodies to hepatitis B core antigen (anti-HBc) IgM, anti-hepatitis D virus (HDV) and anti-hepatitis A virus IgM, and IgM to the herpes viruses. Excluded were patients treated with interferon and ribavirin in the last 24 months, anti-human immunodeficiency virus (HIV) positive subjects, those with a history of alcohol abuse, and those treated with potentially hepatotoxic drugs. Plasma HCV-RNA was determined by qualitative reverse transcriptase-polymerase chain reaction (HEPA-Check-C; Nuclear Laser Medicine) and HCV genotyping by Line-Probe- Assay (INNO-LIPA HCV II; Innogenetics). Anti-HCV, anti-HIV, HBV, and HDV serum markers were determined using a commercial immunoenzymatic assay. Statistical analysis of the results was made applying the χ2 test with Yates’ correction. A p value <0.05 was considered statistically significant.
HCV genotype 2 was found more frequently in patients in the r-CHC group (35.1%) than in those in the AHC group (8.2%, p<0.005) or the CHC group (14%, p<0.05). Conversely, HCV genotype 1 was detected less frequently in the r-CHC group (49.1%) than in the AHC (67.3%) or CHC (65%) group (p>0.1). The observation that patients with symptomatic acute exacerbation of chronic hepatitis C harbour HCV genotype 2 more frequently than asymptomatic chronic hepatitis patients and patients with acute hepatitis C is in good agreement with the more frequent occurrence described by Rumi et al of r-CHC (mostly asymptomatic) in patients with HCV genotype 2c compared with those with HCV genotype 1b. The available data seem to indicate that whether the clinical presentation is symptomatic or asymptomatic, acute exacerbation of chronic hepatitis C is associated with HCV genotype 2 chronic infection. However, a multicentre prospective study is needed to obtain more conclusive data.
This study was supported by a grant from Ministero della Salute, D Leg vo 229/99, EF 2000; MIUR, Cofinanziamento 2003.
Conflict of interest: None declared.
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