Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diclofenac sodium, a phenylacetic acid-derived nonsteroidal anti-inflammatory drug (NSAID) recently released in the United States, was associated with the development of significant hepatitis in seven patients, with one associated death. Signs and symptoms developed within several weeks of initiation of drug use and generally resolved 4 to 6 weeks following discontinuation of use of the drug. The only patient rechallenged with the drug developed a recurrence of her hepatic abnormalities. In one patient, fatal, fulminant hepatitis developed despite early withdrawal of the drug. Review of the European literature disclosed three additional fatalities associated with diclofenac therapy. It is unclear whether the incidence of hepatotoxicity is higher with this drug compared with other nonsteroidal anti-inflammatory drugs. Careful patient monitoring is advised, and prompt discontinuation of the drug is suggested when signs or symptoms of liver disease develop.
JAMA 1990 Nov 28
PMID:Diclofenac-associated hepatotoxicity. 223 46

Niacin (nicotinic acid) is available in several forms, including crystalline preparations and various types of sustained-release preparations. Evidence exists that sustained-release niacin, with respect to both dosage and severity, is more hepatotoxic than crystalline niacin. Three patients who developed hepatitis during treatment with sustained-release niacin were rechallenged with equivalent or higher doses of crystalline niacin, with no evidence of recurring hepatocellular damage. Although the mechanism for niacin-induced hepatitis is unknown, these cases support previous observations that crystalline niacin may be less hepatotoxic than sustained-release preparations in certain patients.
JAMA 1990 Jul 11
PMID:Rechallenge with crystalline niacin after drug-induced hepatitis from sustained-release niacin. 235 46

Certain RNA molecules can mediate their own cleavage or splicing or act as enzymes to promote reactions on substrate RNA molecules. Thus, RNA is not restricted to being a passive carrier of genetic information but can have an active role in directing cellular biochemistry. These findings suggest the possibility that other cellular RNAs, including the RNA components of small nuclear ribonucleoproteins, of the ribosome, and of various ribonucleoprotein enzymes, are catalysts. RNA enzymes (ribozymes) can be used as sequence-specific RNA cleavage agents in vitro, providing useful tools for biochemical studies of RNA. On a more speculative note, ribozymes directed against viral RNAs have the potential of serving as therapeutic agents. Finally, some infectious agents, including hepatitis delta virus and perhaps poliovirus and rhinoviruses, are themselves ribozymes, providing potential targets for pharmaceuticals.
JAMA 1988 Nov 25
PMID:Ribozymes and their medical implications. 246 Jun 49

To identify previously unrecognized sources for acquiring acute hepatitis B and non-A, non-B (NANB) hepatitis, we interviewed patients with these types of hepatitis who were reported to two county health departments in the United States and matched control subjects for known and potential risk factors for acquiring hepatitis. Of 218 patients with hepatitis B and 140 patients with NANB hepatitis, 46% and 53%, respectively, had no commonly recognized source for infection. When these patients were compared with control subjects, significantly more patients with hepatitis B had multiple heterosexual partners, accounting for 14% of all hepatitis B infections; more patients with NANB hepatitis either had sexual or household contact with a person who had hepatitis in the past or had multiple heterosexual partners, accounting for 11% of all NANB infections. This is the first study to suggest that heterosexual transmission may play an important role in the spread of NANB hepatitis.
JAMA 1989 Sep 01
PMID:Importance of heterosexual activity in the transmission of hepatitis B and non-A, non-B hepatitis. 229 22

In 1981, a hepatitis B virus vaccine demonstration project was conducted in 1630 Yupik Eskimos in southwest Alaska. Levels of antibody to hepatitis B surface antigen and markers for hepatitis B virus infection in vaccinees were monitored yearly for 5 years. After 5 years of follow-up, 19% of those who initially had an immune response to vaccine of 10 sample ratio units or greater subsequently had levels of antibody to hepatitis B surface antigen lower than 10 sample ratio units. During the 5 years after the first dose of vaccine, in three responders and one person with an antibody to hepatitis B surface antigen response lower than 10 sample ratio units, antibody to hepatitis B core antigen developed, and the level of antibody to hepatitis B surface antigen was boosted. Hepatitis B surface antigen did not develop in any subjects, and none had clinical hepatitis. In the 5 years following the demonstration project, the annual incidence of hepatitis B virus infection decreased from 50 cases per 1000 population before the vaccine trial to 0.45 per 1000.
JAMA 1989 Apr 28
PMID:Duration of immunogenicity and efficacy of hepatitis B vaccine in a Yupik Eskimo population. 252 2

Between April 1, 1984, and Feb 1, 1985, nine cases of hepatitis B occurred in the patients of a dentist practicing in a rural Indiana county (population, 35,000). This was over 20 times the mean annual incidence for the county in the previous decade. All of the patients had been treated by the dentist two to five months before illness. Although the dentist had never had hepatitis symptoms, his serum was positive for hepatitis B surface antigen and hepatitis B e antigen and negative for anti-hepatitis B core IgM antibody, indicating that he was probably a hepatitis B carrier. Two patients (22%) died of fulminant hepatitis; the case-fatality ratio was over ten times the reported US mean for hepatitis B. Using a case definition based on anti-hepatitis B core IgM antibody positivity and exposure to the dentist during a defined time period, a serosurvey of the dentist's patients identified 15 asymptomatic cases (overall attack rate, 3.2%). Infection risk was related to the amount of trauma involved in the cases' dental procedures. No cause was found for the unusual lethality of the outbreak.
JAMA 1986 Jun 20
PMID:Lethal outbreak of hepatitis B in a dental practice. 287 42

Clinical and biochemical data collected during the Holy Cross College football team hepatitis A outbreak in 1969 suggested that 32 team members had icteric hepatitis, 58 had anicteric illness, and only seven were not infected. Using a currently available radioimmunoassay, we tested stored serum samples obtained during the outbreak for IgM antibody to hepatitis A virus (IgM anti-HAV). Only individuals with icteric hepatitis were found to have IgM anti-HAV in serum; those with presumed anicteric illness were shown not to be infected with hepatitis A virus. The attack rate was thus only 34%, not 93% as originally reported, and the incidence of icteric illness in those infected was 100%, not 33%. This serological analysis of a classic outbreak of hepatitis A illustrates the utility and importance of IgM anti-HAV testing in seroepidemiologic investigations of hepatitis outbreaks.
JAMA 1985 Aug 09
PMID:Revisiting the Holy Cross football team hepatitis outbreak (1969) by serological analysis. 298 69

Over a 5 1/2-year period, 22 of 262 children receiving liver transplants developed adenoviral infections. Five had adenoviral hepatitis in the allograft, caused by serotype 5. All five were treated for rejection, either just before or at the time of infection. Liver biopsy specimens had characteristic histological appearance, and diagnosis of adenoviral infection was confirmed with monoclonal antiadenoviral antibodies, electron microscopy, and by culture of liver tissue. In the remaining 17 patients, adenovirus was isolated from urine, stool, throat secretions, and/or blood samples, but none had any detectable visceral infection. Serotypes 1 and 2 predominated, similar to children not receiving transplants during the same time period. Three of the patients with hepatitis are alive and well; two died of liver failure. Adenoviral hepatitis did not recur in the second allograft of a patient who underwent retransplantation for combined rejection and adenoviral hepatitis, and appears, therefore, not to be a contraindication to retransplantation when liver failure ensues.
JAMA
PMID:Adenoviral infections in pediatric liver transplant recipients. 303 28

Thirty patients with ocular melanoma metastatic to the liver were treated by hepatic arterial chemoembolization using an admixture of cisplatin and polyvinyl sponge. Tumor regression was complete in one patient and partial (greater than 50%) in 13 patients. The total response rate was 46%. The median survival for the entire group was 11 months (95% confidence interval, nine to 18 months). Treatment-related morbidity was short-lived and included primarily severe upper right quadrant abdominal pain, transient paralytic ileus, and nonicteric hepatitis. Hepatic arterial chemoembolization provided effective palliation, with good-quality survival among 46% of patients with ocular melanoma metastatic to the liver.
JAMA 1988 Aug 19
PMID:Regression of ocular melanoma metastatic to the liver after hepatic arterial chemoembolization with cisplatin and polyvinyl sponge. 339 2

To define more exactly the epidemiology of delta virus infection and confirm its role in causing fulminant Labrea hepatitis in the Amazon Basin, we studied the prevalence of delta virus infection among persons with acute and chronic hepatitis B virus infection in the Boca do Acre district of the southern Amazon Basin. Delta virus infection was found in 24% of asymptomatic hepatitis B virus carriers, 29% of acute nonfulminant hepatitis B cases, 74% of fulminant hepatitis B cases, and 100% of chronic hepatitis B cases. Chronic delta virus infection occurred primarily in older children and adults, while acute and fulminant delta virus infection occurred in young children as well. In fulminant hepatitis cases, delta virus superinfection of hepatitis B virus carriers was the most common serological pattern; histopathologic examination showed features identical to those described in fulminant hepatitis cases of similar etiology in Colombia and Venezuela. Delta virus infection is highly endemic in the southern Amazon Basin and is the principal cause of Labrea hepatitis.
JAMA
PMID:Hepatitis delta virus infection and Labrea hepatitis. Prevalence and role in fulminant hepatitis in the Amazon Basin. 359 43


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