[On the risk of hepatitis infection in forensic dentistry].
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During the last two decades an economic boom has occurred in Taiwan, a region where the prevalence of both hepatitis A and B virus infection was formerly very high. To examine the impact of socioeconomic developments on the secular trend and geographical variation in hepatitis A and B virus infection, 875 adolescents selected randomly from 20 junior high schools were studied. Serum samples collected from the subjects were tested for hepatitis A antibody (anti-HAV) and hepatitis B surface antigen (HBsAg) by enzyme immunoassay using commercial reagents. The anti-HAV prevalence increased from northern through central to southern Taiwan; the prevalence was highest in aboriginal townships and lowest in metropolitan precincts. This striking variation in anti-HAV prevalence in different geographical locations and at different urbanization levels remained significant in multiple logistic regression analysis. The HBsAg prevalence was significantly higher in aboriginal townships than in rural and urban townships and metropolitan precincts. In addition, HBsAg prevalence was related inversely to the number of physicians per 1,000 population. The prevalence of both anti-HAV and HBsAg declined significantly during the last decade in Taipei City and County. The decrease in anti-HAV prevalence may be due to improvements in environmental hygiene, water supply, and food sanitation, while the decline in the HBsAg carrier rate may result from the use of disposable needles and syringes as well as screening for HBsAg in blood banks.
There is a paucity of data on occurrence of delta hepatitis in India. We here present our preliminary data showing that delta coinfection and superinfection occur quite frequently in our set up. The coinfection rate was found to be 15% and superinfection rate 26.6% in the initial screening of 69 patients of acute and chronic liver disease.
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Liver cysts are commonly observed, but infection of a liver cyst is a rare complication. Although patients have clinical symptoms, such as a high-grade fever and abdominal pain, diagnosing an infected cyst by abdominal ultrasonography, computed tomography (CT) with contrast medium and magnetic resonance imagings (MRI) is not always easy. We experienced an unusual case who had only clinical symptoms, such as high-grade fever and a right quadrant abdominal pain, but no imaging findings when admitted. Careful observation using ultrasonography once a week revealed signs of an infected cyst containing echogenic fluid 32 days after admission. We performed percutaneous transhepatic cystic drainage. When a patient has liver cysts and complains of high-grade fever and abdominal pain, liver cysts should be considered as a focus of sepsis, and we recommend repeat use of ultrasonography or CT, even if no typical findings occur the first time.
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Donor shortage has led to the use of hepatitis B core antibody (anti-HBc)--positive (anti-HBc(+)) liver allografts for patients in need of relatively urgent orthotopic liver transplantation (OLT). Because anti-HBc(+) allografts transmit hepatitis B virus (HBV) infection at a high rate, effective prophylaxis is required. We assessed the effectiveness of lamivudine in preventing HBV transmission by anti-HBc(+) allografts. Between March 1996 and March 2000 at Cedars-Sinai Medical Center (Los Angeles, CA), 15 of 169 patients (8.9%) received liver allografts from anti-HBc(+) donors. Six patients were hepatitis B surface antigen (HBsAg)(+) (group 1), and 9 patients were HBsAg negative (HBsAg(-); group 2) before OLT. All patients were administered lamivudine, 100 or 150 mg/d, orally after OLT. Patients who were HBsAg(+) before OLT also were administered hepatitis B immunoglobulin (HBIG) prophylaxis. Hepatitis B serological tests were performed on all patients, and HBV DNA was determined in liver tissues in 10 patients. All 15 patients remained HBsAg(-) at their last follow-up 2 to 40 months (mean, 17 months) post-OLT. All patients in group 1 had antibody to HBsAg (anti-HBs) titers greater than 250 mIU/mL post-OLT (mean follow-up, 20 months; range, 7 to 40 months). Of the 2 patients in group 1 who underwent liver biopsy after OLT, 1 patient had detectable hepatic HBV DNA despite being anti-HBs(+) and HBsAg(-). Among the patients in group 2, none acquired anti-HBc or HBsAg. Hepatic HBV DNA was undetectable in the 7 patients in group 2 who underwent liver biopsy after OLT. Anti-HBc(+) allografts can be safely used in patients who undergo OLT for chronic hepatitis B and susceptible transplant recipients if prophylaxis with combination HBIG and lamivudine or lamividine alone is administered after OLT, respectively. However, more data are needed to determine the efficacy of lamivudine monotherapy in preventing transmission of HBV infection from anti-HBc(+) liver allografts to susceptible recipients.
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Thyroid function, the occurrence of goiter, and ultrasonically determined thyroid gland volume were investigated in 23 consecutive nonalcoholic patients with acute viral hepatitis during and six months after recovery, and compared with data obtained from 23 matched controls. Seven patients had clinically detectable goiter during disease, but only one after recovery (P less than 0.05). Median thyroid volume was 28 mL (range 15 to 42 mL) compared with 18 mL (range 12 to 27 mL) after recovery (P less than 0.001), and 17 mL (range 11 to 24 mL) in the controls (P less than 0.001). During acute hepatitis, serum levels of thyroxine, thyroxine binding globulin, and free thyroxine index were significantly increased while triiodothyronine and thyrotropin levels were unaltered and triiodothyronine resin uptake and free triiodothyronine index levels were decreased. After recovery all thyroid variables were normalized. In conclusion, acute liver disease was associated with a marked increase in thyroid volume, but the study did not clarify the mechanism underlying thyroid enlargement.
OBJECTIVE: To assess the clinical significance of cases who were negative for hepatitis B serological markers but were found incidently to be HBV carriers with HBV replicative infection. METHODS: In 12 out of the 50 biopsy proved cases, the hepatitis B serological markers and anti-HCV were all negative and ALT level also normal in repeated assays. Serum HBV DNA and HCV RNA of all the cases were analysed by PCR. Liver specimens were examined by immunohistochemistory for HBsAg and HBcAg. The pathological changes were classified into 4 grades and 4 stages, and Knodell HAI was also recorded. RESULTS: Five cases initially diagnosed as HBV carriers showed high viral replication (4 cases had loads of 10(4) approximately 10(5) copies/ml, the other 1 had < 10(4) copies/ml). The periportal and/or intralobular inflammation and fibrosis were G1 and S1. The virus load of the 4 cases initially suspected of chronic hepatitis were even higher (2 case > 10(6) copies/ml, 2 case > 10(5) copies/ml). On the contrary, 3 cases initially suspected of liver cirrhosis showed low replication (all less than 10(4) copies/ml), but their histologic changes were more advanced, 2 cases of G4 and S4, 1 case of G3 and S4. Their HAI were 17, 17 and 11, respectively. CONCLUSIONS: HBV carriers with normal level of ALT and negative serological HBV markers are not very uncommon. They often have a high replicative infection. Some of the chronic hepatitis patients with normal ALT and negative serological HBV markers have more active viral replication. The clinical significance of this kind of patients should not be underestimated. It may be the cause of some cases of cryptogenic cirrhosis and hepatocellular carcinoma of unknown etiology.
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