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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

History of oral-contraceptive use was compared between 68 women with a hospital-discharge diagnosis of acute hepatitis and 1142 women who had been admitted for other reasons to the same hospitals during the same period. The risk of admission to hospital for hepatitis for users of oral contraceptives was estimated to be 3-3 times that for non-users (95% confidence interval, 1-8--6-3). This overall association was almost entirely attributable to a strong association among women under 25 years of age. Among users of oral contraceptives, duration of use tended to be shorter for hepatitis patients than for controls.
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PMID:Oral contraceptives and hepatitis. A report from the Boston Collaborative Drug Surveillance Program, Boston University Medical Center. 6 36

The prognostic significance of in-vitro complement fixation (V.C.F.) by hepatitis-B core antigen/antibody immunocomplexes in hepatitis-B surface antigen (HBsAg) positive liver biopsy specimens was prospectively evaluated in 47 patients presenting with acute viral hepatitis type B. 34 of 37 V.C.F.-negative patients made an uneventful recovery and became HBsAg negative; in all patients with a V.C.F.-positive test chronic hepatitis and persistent antigenaemia developed. The V.C.F. test is a simple and reliable prognostic indicator of persistent infection and of progression of apparently acute hepatitis to a chronic liver disorder.
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PMID:Prognostic significance of in-vitro complement fixation in liver biopsy specimens from patients with acute viral hepatitis type B. 7 41

Plasma or serum from 4 patients with acute or chronic non-A, non-B post-transfusion hepatitis (P.T.H.) and from a blood-donor implicated in two cases of P.T.H. was inoculated into 5 chimpanzees. Biochemical and histological evidence of hepatitis developed in these 5 chimpanzees but not in a control animal. The mean incubation period in the chimpanzees was 13.4 weeks, compared with 7.7 weeks in the 4 patients with P.T.H. The peak alanine aminotransferase (A.L.T.) levels in the 5 chimpanzees were 265, 212, 219, 70, and 62 I.U./l. Histological changes ranged from mild to conspicuous hepatitis and generally correlated with the degree of A.L.T. elevation. There was no evidence of clinical disease and all animals went on to biochemical and histological recovery. There was no serological evidence of type A or type B hepatitis. Hepatitis was transmitted by serum derived from patients with chronic as well as acute hepatitis, strongly suggesting a chronic carrier state for the agent responsible for non-A, non-B hepatitis. Non-A, non-B hepatitis thus seems to be due to a transmissible agent which can persist and remain infectious for long periods.
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PMID:Transmissible agent in non-A, non-B hepatitis. 7 17

Serum samples from 94 Finnish hospital patients with hepatitis B were investigated for subtypes of HBsAg. Subtype ay predominated in patients with acute hepatitis (77%). All drug abusers had the ay subtype. Of 11 patients with chronic liver disease, 10 (91%) had the ad subtype. Five of 7 hepatitis cases associated with blood transfusion had subtype ay, although this determinant has not been detected among Finnish non-paid blood donors. These results suggest that blood donors who incubate hepatitis B (HBsAg not yet detectable) are an important source of transfusion hepatitis.
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PMID:Subtypes of HBsAg among hepatitis patients. 7 35

Evidence for a new hepatitis-specific antigen has been obtained from double immunodiffusion assays between acute and convalescent sera obtained from patients with non-A, non-B post-transfusion hepatitis. The designation hepatitis C (HC) antigen is proposed. HC was found in the acute-phase sera of all 13 non-A, non-B post-transfusion hepatitis patients with longer incubation and duration periods (type 2) tested, but only transiently in 4 out of 10 acutephase sera obtained from patients with type 1 non-A, non-B hepatitis, with shorter incubation and duration periods. The antigen was also detected in 2 out of 16 single specimens obtained during the acute phase from acute hepatitis patients who had not received a blood-transfusion. This suggests presence of a carrier state. No patients with alcoholic hepatitis and no healthy blood-donor carried HC antigen. The antigen seems distinct from those of hepatitis A and B (surface and core). It migrated in the serum beta-globulin region and had a buoyant density of 1.30 and a molecular weight between 100 000 and 300 000. Antibodies against HC antigen were found in only 30% of the type-2 non-A, non-B post-transfusion hepatitis patients and did not persist for long. However, these antibodies were directed specifically against HC antigen and moved in a manner similar to 7S globulin on rate-zonal centrifugation.
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PMID:Hepatitis "C" antigen in non-A, non-B post-transfusion hepatitis. 8 9

Serial determinations of HBeAg and anti-HBe were made in sera of 155 selected patients with acute hepatitis B who were followed up for one to four years. In the early phase of hepatitis, HBeAg was present in 43 cases (27.7%) and anti-HBe in 12 cases (7.7%). Evaluation of the outcome of hepatitis showed that development of chronic hepatitis occurred in 11 out of 43 HBeAg positive patients, in 10 out of 100 HBeAg negative patients (P = less than 0.05) and in 2 out of 12 patients carrying anti-HBe. Nine out of 11 HBeAg positive chronic subjects showed persistent HBe antigenemia over two months, while the remaining 32 patients, who recovered completely, lost HBeAg within two to three weeks from the onset of the disease. These data suggest that the prognostic value of HBeAg in acute hepatitis patients may be taken into account when HBeAg persists in the serum and that anti-HBe does not invariably protect from the development of chronic hepatitis.
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PMID:Persistence of e antigen as prognostic marker in acute hepatitis B. 8 94

6 cases of non-A non-B hepatitis which followed administration of four different batches of concentrates of coagulation factor IX from commercial and non-commercial sources are described. Of 17 patients who received the concentrate on account of chronic liver disease, 4 developed hepatitis, and in 3 of these the illness proved fatal. The incubation periods ranged from 42 to 103 days (mean 65 days). 3 chimpanzees were inoculated with concentrate from the same batch used on the above patients, a further commercial batch upon which no adverse reactions had been reported, and plasma from a known non-A non-B carrier. All developed hepatitis after 10 weeks' incubation. Liver biopsy when serum-aminotransferase was at its highest level showed features consistent with acute hepatitis. As in the patients, viral markers for hepatitis A and B, cytomegalovirus, and Epstein-Barr virus were unchanged.
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PMID:Transmission of non-A non-B hepatitis to chimpanzees by factor-IX concentrates after fatal complications in patients with chronic liver disease. 8 7

Cellular and humoral immunity combine to determine the outcome following exposure to hepatitis virus and are implicated in the proposed pathogenetic mechanism for acute and chronic hepatitis. Although antibody to HBsAg is found in virtually all following recovery from hepatitis B, a cell-mediated response to HBsAg can be detected in most patients during the acute phase, and it has been suggested that this may cause the acute hepatic damage by an attack on virus-infected cells. Patients who have chronic active hepatitis also frequently have cell-mediated immunity to HBsAg, regardless of whether the antigen can be detected in their sera; thus, previous exposure to hepatitis B may be important in initiating the disease even in antigen-negative cases. Cell-mediated responses to liver-specific lipoprotein, a membrane antigen, occur transiently in many patients who have acute hepatitis and are persistent in virtually all with untreated chronic active hepatitis. The relative importances and precise mechanisms of these immune responses in the pathogenesis of acute and chronic hepatitis remain to be determined.
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PMID:Cellular and humoral immunity in viral hepatitis. 8 10

Twelve infants, born to mothers with hepatitis B virus infection, were inoculated within 7 days of birth with immune serum globulin containing antibody to hepatitis B surface antigen (HBsAg) titers of 1:32 to 1:64 as measured by passive hemagglutination. Six of nine infants (66.7%) born to HBsAg-positive carrier mothers became HBsAg-positive within 3 mo of age. In addition, two of three treated infants born to mothers with acute hepatitis B during the delivery period also developed HBsAg. The hepatitis e antigen was detected in four of five carrier mothers and in two mothers with acute hepatitis, whose infants subsequently became HBsAg positive. In addition, hepatitis B-specific DNA polymerase activity was detected in the seven HBsAg-positive mothers who transmitted the virus to their infants. All eight infants have remained persistently HBsAg positive. Thus, the immune serum globulin containing low-titer antibody to HBsAg is not protective when given to infants born to HBsAg carrier mothers or to mothers with acute hepatitis B during the delivery period.
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PMID:Failure of immune serum globulin to prevent hepatitis B virus infection in infants born to HBsAg-positive mothers. 8 62

An epidemic of acute hepatitis B followed the administration of human immunoglobulin to members of the staff of a mission hospital in India and their families. Jaundice developed in 123 (38%) of 325 persons inoculated. Hepatitis-B surface antigen was detected in three of the batches of immunoglobulin which were available for testing.
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PMID:Epidemic hepatitis B caused by commercial human immunoglobulin. 8 88


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