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)

The hypothesis that hepatitis B infection is etiologically related to hepatoma has been investigated by studying the interrelationships between hepatitis B surface antigen (HBsAg, Australia antigen) and the fast-moving 5'-nucleotide phosphodiesterase Band V isoenzyme (5'-NPDase-V). Sera from 58 patients with viral hepatitis were tested for 5'-NPDase-V and HBsAg. The isoenzyme was found in 34 of 37 patients who were also positive for HBsAg but in only 4 of 21 hepatitis patients who were HBsAg negative. Five patients convalescing from hepatitis were negative for both HBsAg and the isoenzyme. Preparative gel electrophoresis showed that these 2 markers were different proteins. Of 34 hepatoma patients, 29 were positive for 5'-NPDase-V. Only 1 isoenzyme-positive patient was positive for HBsAg by counterimmunoelectrophoresis. However, of 16 isoenzyme-positive hepatoma patients available for radioimmunoassay, 8 were NBsAg positive (50%). None of 21 hepatoma samples tested for antibody to NBsAg was positive. Of 21 "normal" carriers of HBsAg and 10 carriers with Down's syndrome, 4 persons were detected with the isoenzyme. The results suggest that HBsAg and 5'-NPDase-V in the presence of liver damage are associated and thus provide a new marker enzyme between hepatitis B infection and hepatoma.
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PMID:5'-nucleotide phosphodiesterase isoenzyme in patients with hepatitis B infection. 16 56

Whether a patient develops the HBsAg carrier state may depend on his genome. HBsAg subtypes may reflect the viral genome and may be of prognostic significance. Different subtypes predominate in different populations throughout the world. Altered immune response, as in patients with Down's syndrome, may increase the HBsAg carrier rate. Autoantibodies have been used to differentiate various types of hepatitis. There is an increased incidence of histocompatibility antigen HL-A1 and HL-A8 in patients who have chronic aggressive hepatitis. In primary hepatic carcinoma, the HBsAg carrier rate is increased. Because of the suggestion that neonatal hepatitis, biliary atresia and choledochal cyst may all result from infantile obstructive cholangiopathy, with the precise outcome depending on whether other conditions such as alpha 1-antitrypsin deficiency are also present, we have determined HBsAg in 166 children with a variety of diseases, among them Reye's syndrome, alpha 1-antitrypsin deficiency, and renal disorders. The HBsAg carrier rate in the sera of these patients was normal.
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PMID:Genetic factors and autoimmunity in viral hepatitis. 21 41

Medical histories of themselves and their first-degree relatives were obtained from parents of 82 leukaemic children (54 acute lymphoblastic (ALL), 28 acute myeloblastic (AML)) and from control couples matched for age. The possibility of a primary familial immunological abnormality as an aetiological factor in childhood leukaemia was suggested by binding some infections significantly more frequently reported in parents than in controls, but more strongly supported by the finding of a significantly (P less than 0.02) increased prevalence of disorders associated with autoimmunity (but not of other conditions such as peptic ulceration, infective hepatitis, tuberculosis or malignancy) amongst members of ALL families compared to those of controls. Analogy with Down's syndrome and the strain of NZB mice, in which diminished T-cell function is associated with autoimmune disease and lymphoid neoplasia, is discussed. Varicella and herpes zoster occurred respectively in 2 ALL mothers during their pregnancies involving the patients and in none of the other 388 pregnancies here reported. This supports previous evidence that antenatal varicella infections may be of aetiological importance in some cases of ALL.
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PMID:Family studies in acute leukaemia in childhood: a possible association with autoimmune disease. 28 5

Sera from 1283 patients and 73 staff members from Cherry Farm Psychiatric Hospital were screened for hepatitis B antigen over a five year period, following a single confirmed case of type B hepatitis in one villa. Apart from the presenting case, 10 asymptomatic carriers of hepatitis B antigen were detected, three of these being from the same villa and possessing the same antigen subtype as the presenting patient. Only two of 26 Down's syndrome patients and two of 44 Polynesian patients were positive. No staff members were positive. A case of frank hepatitis B occurred in a male nurse accidentally pricked with a needle contaminated with blood from one of the carriers. The low prevalence of hepatitis B antigen in this population for the mentally ill is possibly related to the reduced patient contact resulting from the isolated villa type of accommodation.
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PMID:Hepatitis B antigen in a psychiatric hospital population. 29 51

In the Tri-State Leukemia Survey, the history of diseases in 605 adult male leukemia cases 15 years and older and in 668 adult male population controls was examined. These diseases occurred at least 1 year before leukemia was diagnosed. The data were based on respondents' answers that the disease was diagnosed by a physician; the respondent was either the subject or his spouse. Of 30 diseases studied, 7 showed an excess among the patients with leukemia: infectious hepatitis, eczema, psoriasis, diabetes, arthritis and rheumatism, heart disease, and ankylosing spondylitis. Mumps had a lower reported occurrence among the cases, whereas pneumonia was less frequent in acute lymphatic cases than in population controls. Three diseases occurred significantly less in controls than in persons with specific histologic types of leukemia. Our data revealed a more frequent history of herpes zoster (shingles) in chronic lymphatic leukemia, more hives in acute chronic myeloid cases, and meningitis in acute myeloid leukemia. When we only considered the patients' responses, more of them admitted having had acne than did our controls. The remaining diseases--childhood viral diseases, infectious mononucleosis, smallpox, typhoid fever, dysentery, scarlet fever, tuberculosis, asthma, hay fever, and goiter did not occur more frequently in cases than in controls. The findings were consistent with evidence from previous laboratory and clinical studies. The increased occurrence of infectious hepatitis in our case series is consistent with the findings of other studies showing an increased frequency of Australia antigen in patients with hepatitis, leukemia, and Down's syndrome.
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PMID:Epidemiology of diseases in adult males with leukemia. 99 1

Pregnancy outcome was followed in 123 women showing maternal serum alpha-fetoprotein, less than or equal to 0.50 MOM. In 28 cases AFP was secondarily considered as normal either after ultrasonography and correction of gestation age or after a second sample normal result. In 95 cases AFP level was confirmed lowered; perinatal outcome was normal in 70 cases and abnormal in 25. Among these 25 cases, 3 autosomal trisomies occurred, 2 trisomies 18 and 1 trisomy 21; in the 22 other cases, we observed antepartum risk factors (10 cases with impending premature labor or premature labor, 9 cases with chronic hypertension, 2 cases with Ag HBs hepatitis and 1 case with diabetes).
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PMID:[Results of pregnancies characterized by a decrease in the level of alpha-fetoprotein in the maternal blood]. 246 77

Hepatitis serology was used to assess the nature and extent of hepatitis B virus (HBV) infection in the population of a residential centre for people with a mental handicap comprising 56 with Down's Syndrome (DS) and 193 with other mental handicaps (OMH). Markers of HBV were present in 170 cases (68%), of which 25 (10%) were HBsAg positive and potential carriers and 145 IgG anti-HBc positive (58%) indicating exposure to but not necessarily immunity from the virus. Of 25 who were HBsAg positive five were HBeAg positive, 17 were anti-HBe positive, two were HBsAg positive only and one was anti-HBe plus IgM anti-HBc positive. Age and length of residence were significantly associated with HBsAg, IgG anti-HBc and total markers of infection but the degree of mental handicap was not and the DS/OMH ratio only with HBsAg. The results indicated widespread HBV infection, no acute disease cases, relatively few infectious cases and a pre-disposition of DS residents to retain HBsAg in their sera. Vaccination of staff and at risk residents is recommended.
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PMID:Hepatitis B in a residential population with a mental handicap. 275 30

Abnormalities of humoral and cell-mediated immunity have been described in Down syndrome but reported findings have been inconsistent. Confounding factors have included age, institutional versus home life, hepatitis B antigenemia, and zinc deficiency. To clarify this problem, we studied 64 children with Down syndrome (DS) compared with an age-matched control group. All children had always lived at home. All the DS children were negative for hepatitis B surface antigen. Serum zinc concentration in the DS group was on average 12 micrograms/dl lower than age-matched control children. They also had significantly lower levels of immunoglobulin M, total lymphocyte count, T and B lymphocytes, and T helper and suppressor cells. In vitro lymphocyte response to phytohemagglutinin and concanavalin A was significantly reduced at all ages in the DS group. Lymphocyte response to pokeweed mitogen increased with age in control children but decreased in the DS children. By 18 yr, the mean response for DS was 60000 cpm lower than controls. The DS group had significantly higher concentrations of immunoglobulins A and G than controls and the difference increased with age. Complement fractions C3 and C4 were also higher in the DS group at all ages. The number of HNK-1 positive cells was higher in the DS group than controls at all ages. When hepatitis and institutionalization are excluded as confounding factors, DS children still differ in both humoral and cell-mediated immunity from an age-matched control group.
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PMID:Age-related changes in humoral and cell-mediated immunity in Down syndrome children living at home. 296 Sep 48

Structural chromosomal aberrations, in the form of breaks, were found in a significantly higher proportion of bone marrow cells in patients with infective hepatitis than in controls. These anomalies were observed during the first and third weeks after the onset of jaundice but had subsided by the sixth week. Chromosomal aberrations did not appear to be related to the severity of infective hepatitis or to the sex or age of the patients.The distribution of chromosomal abnormalities did not appear to be random; they were observed predominantly in the A(2) and B(4-5) series. Since no abnormalities were detected in the G-group chromosomes, no evidence in support of a relationship between infective hepatitis and Down's syndrome was obtained. Numerical chromosomal aberrations were not observed, nor was any evidence obtained that mitotic activity of bone marrow cells is suppressed in patients with infective hepatitis.
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PMID:Chromosomal aberrations in infective hepatitis. 424 40

A great deal of interest and speculation has arisen from the discovery of a specific antigen, Australia antigen, in the serum of a high proportion of patients with viral hepatitis. This antigen has been found also in the serum of some patients with other conditions, including Down's syndrome, leukemia, leprosy, chronic renal disorders, and chronic active liver disease. It is not found in the serum of normal persons. Australia antigen has been postulated as the causative agent of viral hepatitis. In most patients the antigen can be detected for less than two weeks during the acute phase of the disease. Its persistence in other conditions may be due to an impairment of the immune response. The course of acute viral hepatitis is usually uncomplicated, full recovery of liver function taking place within four to six weeks, with restoration of normal liver histology within three to four months. Follow-up studies of patients in whom hepatitis has developed during epidemics have failed to reveal evidence of subsequent chronic progressive liver disease. This suggests that most cases of chronic active hepatitis are not the result of preceding acute viral hepatitis. However, the recent finding of Australia antigen in the serum of a small number of patients raises the possibility that sporadic viral hepatitis may be one of the causes of the chronic active hepatitis. Alternatively, the presence of the antigen may be interpreted as being due to an altered immune response. The treatment of acute hepatic coma remains unsatisfactory. Several new forms of therapy have been tried in recent years in an uncontrolled way. These include multiple exchange blood transfusions, isolated pig liver perfusion, human cross-circulation, and cross-circulation with baboons. Transient improvement may follow any of these procedures, but evidence that they influence the final outcome of the disease is lacking. The rapid fluctuations in the neurological status of individual patients makes it difficult to interpret the effects of therapy. Also, until satisfactory objective criteria of degrees of coma are universally accepted it will be impossible to compare one mode of therapy with another.
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PMID:Current concepts in viral hepatitis. 552 Jul 27


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