We identified 15 patients with acute hepatitis C (AHC) among 29 healthy volunteers participating in 2 consecutive pharmacokinetics studies. Molecular techniques were used to determine the relatedness of viral strains, whereas clinical and virologic follow-up was started to establish the course and outcome of the acute infection. After presentation, serum liver enzymes and HCV RNA were monitored weekly for 4 months, then monthly for at least 12 months. Liver biopsy was performed 6 to 12 months after AHC diagnosis. Phylogenetic analysis of coding regions for the envelope glycoproteins E1 and E2 was performed. At presentation, all 15 patients tested HCV RNA-positive and had HCV genotype 2c. Phylogenetic analysis indicated a common source of infection. Fourteen patients agreed to be followed prospectively. Infection resolved spontaneously in 8 patients, HCV RNA becoming undetectable by 4 to 5 months after the presumed time of infection in 5 of them and by 8, 13, and 24 months in the remaining 3. Six patients developed chronic infection. Liver biopsies performed in 9 subjects who were HCV RNA-positive 6 months after AHC diagnosis revealed that the prevalent histologic finding was lobular inflammation. In conclusion, our homogeneous cohort showed a wide spectrum of clinical, virologic and histologic features, and, more importantly, short-term outcome differed noticeably despite the common source of infection.

Experimental and clinical observations suggest that patients with primary biliary cirrhosis (PBC) have endothelial dysfunction. Postischemic digital blood flow, nailfold capillaroscopy, von Willebrand factor (vWf) and tissue-type plasminogen activator (t-PA) plasma levels were examined in 59 PBC patients. Fourty-six subjects (15 with liver diseases other than PBC, 11 hypercholesterolemics, 20 healthy subjects) served as controls. PBC had hyperemic blood flow significantly reduced (p < 0.01 or less). Capillaroscopy was altered in 42% of patients. vWf and t-PA were increased in PBC versus healthy controls (209.8 ± 1.4% and 16.54 ± 1.44 ng/ml vs. 120.2 ± 1.4% and 9.91 ± 1.49 ng/ml; p < 0.001) and related to bilirubin (r = 0.38, p < 0.02; r = 0.47, p < 0.0005, respectively). vWf was also increased in other liver diseases (249.9 ± 1.7%; p < 0.001) and related to bilirubin (r = 0.59, p < 0.05). Postischemic finger blood flow negatively correlated with vWf (p < 0.05 or less). Our data indicate that PBC patients have microvascular disease. Whether vessels other than those of the fingers were involved remained unclear. vWf and t-PA might reflect a dysfunction of the hepatic vascular endothelium.

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