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)

While no unanimity of opinion exists regarding the risk to physical health from smoking marihuana, we have seen four cases that demonstrate clearly that intravenous usage is hazardous. The severity of the multisystemic involvement is dose-related. On initial examination, signs of most severe overdosage included fulminant gastroenteritis, hypoalbuminemia, toxic hepatitis confirmed by serial biopsy, acute renal failure, electrolyte disturbances, leukocytosis, anemia, and a relative thrombocytopenia. In three patients who shared a common needle, gingivostomatitis also developed.
JAMA 1975 Jul 28
PMID:The toxicity of intravenously used marihuana. 117 50

Liver function tests were performed in 500 young servicemen with a history of drug abuse. Serum glutamic oxaloacetic transaminase (SGOT) level was abnormal in 66% of 68 patients with a history of parenteral drug abuse. Forty-one percent of 432 patients with a history of only nonparenteral drug abuse also had elevated SGOT levels. A high incidence of liver disease in parenteral drug abusers is well established; however, to our knowledge, the magnitude of the problem in nonparenteral drug abusers has not been noted previously. Liver biopsy specimens in 34 of our patients showed either a classic viral hepatitis or a mild nonspecific hepatitis. Limited follow-up suggested a slowly resolving process. We conclude that hepatitis may be a common sequel to epidemic nonparenteral drug abuse.
JAMA 1975 Sep 01
PMID:Liver disease in nonparenteral drug abusers. 117 17

Serum creatine phosphokinase (CPK) and serum glutamic oxaloacetic and pyruvic transaminase (SGOT, SGPT) levels were determined in 61 patients with leptospirosis and 16 with viral hepatitis during the acute phase of illness. The CPK value was elevated in 29 leptospirosis patients and normal in all 16 hepatitis patients. Conversely, mean SGOT and SGPT levels were lower in leptospirosis patients. The CPK determination is a simple test that may provide diagnostic information in a jaundiced patient, particularly when characteristic manifestations of leptospirosis are absent. The pattern of greatly elevated CPK levels with only modest elevations in transaminase values in an acutely jaundiced patient should strongly suggest a diagnosis of leptospirosis.
JAMA 1975 Sep 01
PMID:Serum creatine phosphokinase in leptospirosis. 117 21

Four patients who had received silicone injections had the following complications: migration, hepatic disease manifested as granulomatous hepatitis (previously undescribed, to our knowledge), hypopigmentation, and death. Silicone should now be considered as a possible cause of hepatic granulomas in an appropriate host.
JAMA 1975 Oct 20
PMID:Injectable fluid silicone therapy. Human morbidity and mortality. 117 44

Beginning in 1971, acute viral hepatitis was epidemic among US soldiers stationed in Europe, with a total of over 8,700 cases reported between 1971 and 1974. Hepatitis B surface antigen (HBsAg) determinations suggest a predominance of hepatitis B. In the Nuremberg area, primary association was with the illicit use of drugs. This association was demonstrated by a chronologic relationship between measurable community drug use and the number of hepatitis admissions three to six months later and by a case-control study. Parenteral drug use and, to a lesser degree, cannabis smoking appeared to be factors in disease transmission. Sharing of illicit drugs with a hepatitis contact, whether parenterally or orally, was associated with increased risk of contracting the disease.
JAMA 1975 Dec 01
PMID:Hepatitis B in Nuremberg, Germany. Epidemiology of a drug-associated epidemic. Among US Army soldiers. 124 90

Thirty-one Japanese nonresponders to subcutaneous hepatitis B vaccination and 15 medical personnel who were accidentally exposed to specimens positive for hepatitis B e antigen and were given hepatitis B immunoglobulin were intradermally immunized with 5 micrograms of plasma-derived hepatitis B vaccine every 2 weeks until delayed type hypersensitivity skin reaction to hepatitis B surface antigen became positive. Thirty (97%) of the 31 nonresponders developed delayed type hypersensitivity skin reactions to hepatitis B surface antigen after 2.3 +/- 1.2 (mean +/- SD) revaccinations. Twenty-nine (94%) of the 31 nonresponders had anti-hepatitis B surface antigen antibody levels greater than 10 IU/L. The immunoglobulin subclass of the antibody to hepatitis B surface antigen was mainly IgG1. After 1 year, 23 (74%) of the 31 nonresponders continued to have anti-hepatitis B surface antigen antibody levels greater than 10 IU/L. Persons accidentally exposed to specimens positive for hepatitis B e antigen developed delayed type hypersensitivity skin reactions to hepatitis B surface antigen following 3.1 +/- 1.1 revaccinations. None developed clinical hepatitis. There was no production of anti-hepatitis B core antigen antibody 1 year after exposure, indicating that protection was 100%. Intradermal hepatitis B vaccination is useful in reversing nonresponsiveness to hepatitis B surface antigen and for prophylaxis after exposure.
JAMA
PMID:Reversal of nonresponders and postexposure prophylaxis by intradermal hepatitis B vaccination in Japanese medical personnel. 182 67

In a survey carried out from 1985 through 1986, volunteer blood donors to The Greater New York Blood Program were tested for two surrogate markers for non-A, non-B hepatitis--elevation of alanine aminotransferase level and presence of antibody to hepatitis B core antigen. Stored serum samples from selected donors were also recently tested for antibody to hepatitis C virus (anti-HCV). Anti-HCV was detected in 0.9% to 1.4% of donors and was higher in black and Hispanic donors than in white donors. Anti-HCV prevalence increased with increasing age through the fourth decade of life, but decreased thereafter, possibly reflecting the disappearance of detectable antibody with time. Anti-HCV correlated with both alanine aminotransferase level and the presence or absence of antibody to hepatitis B core antigen. These associations suggest that donor screening for elevation of alanine aminotransferase level and presence of antibody to hepatitis B core antigen was, as expected, at least partially effective in preventing transfusion-associated non-A, non-B hepatitis. The detection of anti-HCV in donors who have neither an elevation of alanine aminotransferase level nor presence of antibody to hepatitis B core antigen suggests that donor screening for anti-HCV will further reduce the risk of transfusion-associated hepatitis.
JAMA 1990 Jan 05
PMID:Epidemiology of hepatitis C virus. A preliminary study in volunteer blood donors. 210 48

Stored serum samples from the Transfusion-transmitted Viruses Study in the 1970s were tested for the presence of antibody to hepatitis C virus (anti-HCV). Single specimens from five control subjects who did not receive transfusions tested negative for anti-HCV. Of four control subjects who did not receive transfusions and who developed non-A, non-B (NANB) hepatitis after hospitalization, three remained anti-HCV negative; the fourth person with postoperative NANB hepatitis tested anti-HCV positive before the operation. Five transfusion recipients with posttransfusion hepatitis B virus infection remained seronegative; a sixth with NANB hepatitis as well as hepatitis B virus infection had seroconversion for anti-HCV. Five of nine transfusion recipients with NANB hepatitis had anti-HCV seroconversion. These results show that present anti-HCV testing demonstrates an etiologic basis for approximately half of the cases of transfusion-associated NANB hepatitis, particularly those that develop chronicity. Although cases of NANB hepatitis without seroconversion may be explained otherwise, they may be caused by another, presently unidentified, virus.
JAMA 1990 Jan 05
PMID:Non-A, non-B hepatitis and antibody to hepatitis C virus. 210 49

Outbreaks of acute hepatitis occurred in Huitzililla and Telixtac, two rural villages 70 miles south of Mexico City, Mexico, in late 1986. The first outbreak began in Huitzililla in June of that year, 1 month after the start of the rainy season. A census revealed 94 icteric case subjects, for an attack rate of 5%; two women died. Attack rates were higher for persons older than 15 years (10%) than for younger persons. A case-control study showed that illness was highly associated with water-related factors. The second outbreak began in August 1986 in Telixtac. There were 129 case subjects, for an attack rate of 6%; one woman died. Epidemiologic findings were similar to those in Huitzililla, except that most disease transmission was not linked to unsafe water sources. None of 62 case subjects in Huitzililla and only 2 of 53 case subjects in Telixtac tested had serological evidence for recent infection with hepatitis A or B. Two of eight stool samples from Huitzililla and one of the eight stool samples from Telixtac were positive by immune electron microscopy for 32- to 34-nm viruslike particles similar to those seen in cases of enterically transmitted non-A, non-B hepatitis from Asia. To our knowledge, these investigations document for the first time the epidemic transmission of enterically transmitted non-A, non-B hepatitis virus in the Americas.
JAMA 1990 Jun 27
PMID:Epidemic transmission of enterically transmitted non-A, non-B hepatitis in Mexico, 1986-1987. 211 4

The Centers for Disease Control conducted intensive surveillance for acute non-A, non-B hepatitis in four sentinel counties over a 7-year period. Testing for antibody to hepatitis C virus was performed with the newly developed enzyme immunoassay. The incidence of non-A, non-B hepatitis remained relatively stable (average, 7.1 cases per 100,000, but there were significant changes in disease transmission patterns. The proportion of patients with a history of blood transfusion declined from 17% to 6%, but the proportion with a history of parenteral drug use increased from 21% to 42%. The proportion of patients with histories of sexual exposure (6%), household exposure (3%), occupational exposure to blood (2%), or hemodialysis (0.6%) did not change over time. Antibody to hepatitis C virus was found in 45% of patients within 6 weeks of onset of illness and in 68% of patients followed up for at least 6 months. Patients with no history of transfusions were just as likely to be positive for antibody to hepatitis C virus as patients with transfusion-associated hepatitis, indicating that hepatitis C virus is the major causative agent of all non-A, non-B hepatitis in the United States.
JAMA 1990 Nov 07
PMID:Risk factors for acute non-A, non-B hepatitis in the United States and association with hepatitis C virus infection. 217 Jul 2


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