Two cases of adult varicella accompanied by hepatic dysfunction.

Varicella is a typical acute exanthematous viral infection caused by varicella-zoster virus (VZV). In recently years, as far as hepatic dysfunction caused by viruses other than the hepatitis virus is concerned, there have been a few reports on hepatic dysfunction accompanying varicella following organ transplantation of Europe and America and another report on an immunocompromized adult following treatment for Systemic lupus erythematosis (SLE) in Japan. Nonetheless, we searched the MEDLINE and J MEDICINE listing the publications between 1986 and 1996 and found one report on healthy adults with varicella accompanied by hepatic dysfunction in Europe and America and two reports in Japan. Only Noguchi et al. dealt with the findings of liver biopsy. We examined two healthy adults with varicella and mild-to-moderate hepatic dysfunction, and referred to the results of their liver biopsies. The present paper discusses this issue, citing some references.

Detection of serum HBV DNA and anti-HCV antibody in HBsAg seronegative patients with hepatocellular carcinoma in Japan.

One hundred eight patients with hepatocellular carcinoma (HCC) underwent serologic testing for HBsAg, antibodies to HBs (anti-HBs), HBc (anti-HBc) and HCV (anti-HCV), and an assay for hepatitis B virus (HBV) DNA by the polymerase chain reaction (PCR). Ten (9.3%) of the 108 patients were positive for HBsAg and 96 (88.8%) were positive for anti-HCV. Both HBsAg and anti-HCV were present in 4 (3.7%) of the 108 patients. HBV DNA was detected in the serum of all patients who were positive for HBsAg and 9 (9.2%) of the 98 patients who were HBsAg-negative. Anti-HBc was positive and anti-HBs was negative in 8 of these 9 HBsAg negative patients with HBV DNA. HBsAg, HBV DNA and anti-HCV were negative in 6 (5.5%) of the 108 patients. These results suggest that HCV is highly associated with HCC and that HBV is occasionally associated with HCC even when HBsAg is negative.

Thyroid dysfunction induced by interferon therapy for the treatment of hepatitis type C. A report of 4 cases.

We describe 4 patients with onset or aggravation of thyroid dysfunction induced by interferon (IFN) treatment of hepatitis type C. All 4 patients were females; 2 had hyperthyroidism and 2 had hypothyroidism during or after IFN therapy. The onset or aggravation of thyroid dysfunction occurred during administration of IFN in 1 patient and 4 weeks after the end of IFN therapy in the remaining 3 patients. The 2 patients who demonstrated hyperthyroidism were euthyroid and negative for thyroid autoantibodies before receiving IFN therapy. The remaining 2 patients who demonstrated hypothyroidism were positive for thyroid autoantibodies before IFN therapy. One of these patients had a slight decrease in thyroid function before IFN therapy. Anti-thyroid stimulating hormone (TSH) receptor antibodies became positive in all 4 patients. Since there may have been a causal relationship between IFN therapy and the onset or aggravation of thyroid dysfunction, IFN therapy should be administered with caution.

Clinical significance of serum HBVDNA detected by the PCR method.

Changes in serum HBVDNA and their relationship to the prognosis following interferon (IFN) therapy were examined by the polymerase chain reaction (PCR) in 4 patients with chronic hepatitis B infection undergoing IFN therapy. The disappearance of HBVDNA was confirmed by the PCR methods in 3 out of 4 patients who showed favorable subsequent courses. The remaining patient was positive for HBVDNA despite the disappearance of the HBe antigen. In this patient, the hepatitis recurred, and was accompanied by a persistent hepatic disorder. The PCR assay was also carried out to clarify the involvement of the hepatitis B virus in 12 patients who were positive for the HBe antibody and who showed fluctuating transaminase levels. The PCR method revealed that all 12 patients were positive for HBVDNA. These findings indicate the clinical usefulness of the PCR assay for hepatitis B virus infection.

Evaluation of first- and second-generation assays for detection of antibody to hepatitis C virus in non-A, non-B chronic liver diseases--evaluation of 1st and 2nd-generation assays in NANBH.

The positive rates of the second-generation enzyme-linked immunoassay (2nd-generation assay), and two first-generation immunoassays (C100-3 and KCL-163 assay) to test for anti-HCV antibodies in the serum of patients with non-A, non-B chronic liver disease were determined. The clinical usefulness of these assays was also evaluated. The group positive for the 2nd-generation assay alone was compared with that positive for the 2nd-generation and C100-3 assays with respect to the serum GPT levels determined simultaneously with the antibodies. The latter group showed slightly higher GPT levels. These findings suggest that the 2nd-generation assay is useful for the diagnosis of hepatitis C, and that C100-3 and KCL-163 assays are useful indicators of the activity of hepatic disorders.

Incidence of antibodies to hepatitis C virus in patients undergoing chronic dialysis and CAPD.

We measured antibodies to hepatitis C virus (anti-HCV) in patients who were receiving hemodialysis or continuous ambulatory peritoneal dialysis (CAPD). Sixty seven patients (28%) were anti-HCV positive. The anti-HCV positive frequency increased with the time of treatment with dialysis, the frequency being 50% with a dialysis period > or = 10 years. The frequency of anti-HCV positivity was similar in patients with a history of blood transfusion (48/152, 32%) and in those without this history (19/89, 21%, p > 0.05). Therefore, in addition to blood transfusion, there may be other routes of HCV infection associated with long-term dialysis. Chronic liver disease was observed in 31% (21/67) of the patients positive for anti-HCV but in only 6% (11/174) of the negative patients (p < 0.01). HCV seems to be important as a cause of chronic liver disease in dialysis patients.

[Clinical study on relationship between hepatocellular carcinoma and hepatitis C virus infection in patients with chronic liver disease].

The relationship between hepatocellular carcinoma (HCC) and hepatitis C virus (HCV) infection was investigated. Antibody to hepatitis C virus was detected in 88.8% and 87.0% of 240 patients with hepatocellular carcinoma and liver cirrhosis, respectively. A history of blood transfusion was shown in only 21.8% (21/96) of the HCV antibody positive HCC patients. Of 196 patients with chronic hepatitis type C and the HCV antibody positive liver cirrhosis, 10 developed HCC during the follow-up period of two years. A high prevalence of HCV antibody was also shown among 83 patients with alcoholic liver cirrhosis and HCC associated with alcoholic liver cirrhosis. HCV-RNA was detected in all patients with alcoholic HCC. These data support a causal association between hepatitis C virus and hepatocellular carcinoma.

Effectiveness of 6-month intermittent administration of natural human interferon-alpha against non-A non-B chronic hepatitis.

Interferon (IFN) was administered intermittently for 6 months to the patients with non-A non-B chronic hepatitis (CHNANB), and the effectiveness of the treatment for improving the hepatic function was evaluated. Of 26 patients with CHNANB, 16 received intermittent IFN therapy (IFN group), and 10 were treated by conventional therapies without IFN (non-IFN group). All patients were observed for 1 year. IFN was administered once a day at 3 MU in principle (1 MU in some patients and 6 MU in 1 patient) daily for 1 week immediately after the beginning of the therapy and 3 times a week for the subsequent 6 months at the outpatient clinic. The patients were followed up for at least 6 months after completion of the treatment. In the IFN group, the serum GPT level normalized in 11 (68.8%) of the 16 patients 1 year after the beginning of the treatment. In these 11 patients (normalized group), HCV-RNA was negative or became negative in 3 of the 6 patients in whom the serum HCV-RNA could be examined. Histological grades of inflammation in the liver were also markedly alleviated in the normalized group. The hepatic function did not normalize in any of the 10 patients in the non-IFN group. These findings indicate that IFN therapy is useful for CHNANB.

[A study on hepatic dysfunction associated with rubella infection].

We had 11 patients with rubella infection accompanied by hepatic dysfunction from 1979 through 1989. The elevations of sGOT were moderate, but sLDH levels were high. Extra hepatic manifestations were suspected by analysis of LDH isozymes. In 9 out of 11 patients, the sGPT levels returned to normal within 8 weeks. But prolonged courses of abnormal transaminase levels were observed in 2 patients. One was accompanied by underlying chronic hepatitis type non-A, non-B, and the other was supposed to have a prolonged rubella infection. Liver biopsy specimen taken from one patient in the acute phase demonstrated a non-specific reactive hepatitis. These observations suggest that rubella infection should be taken into consideration in making the diagnosis of sporadic hepatitis type non-A, non-B.