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 frequency of occurrence of alpha-1-antitrypsin (A1AT) deficiency among total of 3228 Polish children with chronic liver diseases and chronic disease of respiratory tract was determined. It was observed that among children with chronic liver diseases which disclosed more frequent defect (concentration of A1AT below 150 mg/dl was found in 10.3% of children), the highest occurrence of deficiency was in children with neonatal hepatitis (23.1%). The deficiency was connected with the presence of ZZ and MZ phenotypes of A1AT.
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PMID:Inherited defect of alpha-1-antitrypsin associated with chronic liver and respiratory tract diseases in children. 248 74

We measured antibody (anti-HCV) to hepatitis C virus, which causes non-A, non-B hepatitis, by radioimmunoassay in prospectively followed transfusion recipients and their donors. Of 15 patients with chronic non-A, non-B hepatitis documented by liver biopsy, all seroconverted for the antibody; of 5 with acute resolving non-A, non-B hepatitis, 3 (60 percent) seroconverted. The development of anti-HCV was delayed (mean delay, 21.9 weeks after transfusion, or 15 weeks after the onset of clinical hepatitis) and took approximately one year in one patient. Antibody has persisted in 14 of the 15 patients with chronic disease (mean follow-up, greater than or equal to 6.9 years; maximum, greater than or equal to 12), but has disappeared in the 3 with acute resolving disease after a mean of 4.1 years. Anti-HCV was detected in samples of donor serum given to 14 (88 percent) of the 16 anti-HCV-positive patients for whom all donor samples were available. Only 33 percent of the anti-HCV-positive donors tested had an elevated serum concentration of alanine aminotransferase; 54 percent were positive for antibody to the hepatitis B core antigen (anti-HBc). We conclude that hepatitis C virus is the predominant agent of transfusion-associated non-A, non-B hepatitis and that screening of donors for anti-HCV could prevent the majority of cases of the disease. "Surrogate" assays for anti-HBc and alanine aminotransferase would have detected approximately half the anti-HCV-positive donors involved in the transmission of hepatitis that we identified.
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PMID:Detection of antibody to hepatitis C virus in prospectively followed transfusion recipients with acute and chronic non-A, non-B hepatitis. 250 15

The presence of serum markers of hepatitis B virus (HBV) infection in different stage of illness has a specific pathogenic and diagnostic significance. Based on the frequency of the appearance of HBV markers in patients' sera at different stages of the illness, we attempted a grouping possibly helpful for differentiation, epidemiologic and prognostic evaluation of hepatitis. The significance for chronic disease development of the dynamics of HBV marker levels in the serum is discussed.
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PMID:Dynamics of serum markers in the different course of hepatitis B virus (HBV) infection. 288 87

The acute and chronic effects of mouse hepatitis virus type 3 on the microcirculation of the liver in both semisusceptible C3HeB/FeJ and fully resistant A/J mice were studied. In the C3HeB/FeJ mice, abnormalities of microcirculatory flow were noted as early as 12 hr after infection and by 24 hr, localized avascular foci appeared. Disturbances were characterized by granular blood flow, sinusoidal microthrombi, distortion of sinusoids by edematous hepatocytes and necrotic lesions. Following the acute infection, Day 10, two patterns of chronic disease were observed. Eighty percent of the mice developed chronic granulomatous hepatitis whereas in the remaining 20% a more severe chronic aggressive hepatitis was observed which was characterized by ongoing hepatocellular necrosis and a marked mononuclear cell infiltrate. In both cases, in vivo microcirculatory abnormalities were found predominantly around visible lesions. Onset of the microcirculatory abnormalities was found to be concomitant with a rise in monocyte related procoagulant activity. Procoagulant activity rose acutely and remained elevated throughout the chronic phase but was higher in animals with severe disease. In contrast to the above, normal blood flow and histology were seen in the resistant A/J mice at all times following infection, and procoagulant activity remained at basal levels despite active viral replication as demonstrated by immunofluorescence studies and recovery of infectious virus. These observations suggest a role for monocyte procoagulant activity in the development of microcirculatory abnormalities following mouse hepatitis virus type 3 infection which may be important in the pathogenesis of the disease.
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PMID:Acute and chronic changes in the microcirculation of the liver in inbred strains of mice following infection with mouse hepatitis virus type 3. 299 Nov 7

Until 20 years ago the only chronic viral diseases known were those considered to be confined to the nervous system. As a result of recent advances in epidemiology, molecular biology and immunology, new viral diseases have been recognized and their clinical features and pathogenesis elucidated. Chronic disease may result from infection with the hepatitis B and D viruses and whatever agent or agents cause hepatitis non-A, non-B, the herpesviruses, Epstein-Barr virus, cytomegalovirus and human T-lymphotropic virus type III. These diseases have common features, including long-term or even lifetime asymptomatic carriage, viremia, with virus free in the plasma or attached to circulating mononuclear cells, presence of virus in body secretions, irreversible tissue injury in target organs and oncogenic potential. New information on these diseases is reviewed. Other chronic diseases for which the cause is currently unknown may eventually prove to be due to viral infection. In addition, vaccines may be developed for prophylaxis of some chronic viral diseases and associated malignant diseases.
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PMID:Chronic viral diseases. 302 3

The hepatitis B virus or Dane particle has been linked to hepatocellular carcinoma and is a major cause of chronic liver disease. Hepatitis B virus is found in blood and many body fluids including human tears. A 31-year-old White male was inadvertently discovered to have chronic active hepatitis secondary to a hepatitis B infection, during an autoimmune disorder work-up for recurrent episcleritis. It was also discovered that two of the patient's family members had developed chronic disease from the virus. Optometrists should be aware of the serious implications of this disease and take the proper precautions when examining hepatitis patients so that the possible risk of contracting infection through contaminated tears will be reduced.
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PMID:Hepatitis B virus in human tears: ocular examination of an asymptomatic carrier. 334 82

Serum levels of procollagen type III peptide were measured by radioimmunoassay in 76 consecutive patients with acute viral hepatitis, in order to see if this index of hepatic fibrogenesis is also predictive for the development of chronic active hepatitis in high-risk patients. Serum procollagen levels were high (from 14.2 to 109.2 ng/ml, median 33.7 ng/ml) in 74 (97%) patients and normal (from 4 to 14 ng/ml, median 9.1 ng/ml) in 2 (3%) patients. The baseline serum procollagen levels were similar in all the subgroups of patients independently of the type of hepatitis. In the 59 patients with resolving hepatitis, serum procollagen levels returned to normal values from 2 to 48 weeks (mean 15). In the 17 patients with unresolved hepatitis, procollagen levels remained within the normal limits in 6 of 7 patients with non-progressive chronic disease, while were elevated (from 17.4 to 22.2 ng/ml) in 4 of 5 patients with chronic active hepatitis. Unlike transaminase activity, which could not discriminate between benign and progressive liver disease, serum levels of procollagen helped in identifying patients with unresolved hepatitis, who were developing chronic active disease.
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PMID:Serum procollagen type III peptide levels in patients with acute viral hepatitis. 337 38

Of 228 consecutive hepatitis B surface antigen (HBsAg)-positive patients who had simultaneous hepatitis B surface antibody (anti-HBs) determinations, HBsAg and anti-HBs were found concurrently in 73 (32%). Concurrence was found with greater frequency in patients with chronic active hepatitis than in those with acute hepatitis (36/57 vs 13/38, p less than 0.02). Patients with chronic active hepatitis had concurrent markers more commonly than those with chronic persistent hepatitis or asymptomatic carrier state (36/57 vs. 24/133, p less than 0.001). No major risk factors were identified. Hepatitis B e antigen was detected more frequently in patients with concurrence (68% vs. 42%, p less than 0.01). Subtyping was possible in 30 patients with chronic infection, including 18 with chronic active hepatitis, 7 with chronic persistent hepatitis, and 5 with a carrier state. In 25 patients, HBsAg subtype ad was found with antibody to subdeterminant y and in four instances, HBsAg subtype ay was found with antibody to subdeterminant d. Only 1 patient had homotypic HBsAg and anti-HBs. Of 38 patients who had successive determinations, concurrence was constant in 29. In 9 others, anti-HBs was detected intermittently and the heterotypia of the recurrent antibody remained constant. Antibody to hepatitis delta-virus was not detected. We conclude that concurrent HBsAg and anti-HBs are found frequently in acute and chronic hepatitis B. The markers are commonly heterotypic in chronic disease. The presence of heterotypic markers is not associated with specific risk factors or delta-infection. Concurrence is associated with evidence of viral replication and features of active inflammation.
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PMID:Frequency and significance of concurrent hepatitis B surface antigen and antibody in acute and chronic hepatitis B. 362 15

The clinical, radiographic and microbiological data of 47 patients with Mycoplasma pneumoniae infection admitted to three Norfolk hospitals during a 20-month period between 1982 and 1983 have been reviewed. Thirty-nine presented with pneumonia and eight with non-pulmonary infection. The M. pneumoniae specific IgM test was positive in 42 of 45 patients tested (89 per cent); in 39 the levels were diagnostic on admission. Cold agglutinins were detected in 27 (57 per cent) and a fourfold rise in complement fixation titre was demonstrated in 13 (29 per cent). Sputum culture was positive in 12 (26 per cent). The extrapulmonary manifestations observed were haemolytic anaemia (17 per cent), Stevens Johnson syndrome (4.1 per cent), neurological abnormalities (4.1 per cent), arthritis (2.1 per cent), hepatitis (2.1 per cent) and pericarditis (2.1 per cent). One patient with multilobe pneumonia, pericardial effusion and haemolytic anaemia died. Six patients presented with a history of illness longer than a month; in three the clinical and radiographic picture suggested chronic disease (pulmonary tuberculosis, lymphoma and unresolving pneumonia). There were no distinctive clinical or radiographic features of M. pneumoniae infection. Diagnosis, therefore, relies on serological tests of which the most useful is the rapid, specific IgM test, positive in 86 per cent of the admission sera.
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PMID:The clinical spectrum and diagnosis of Mycoplasma pneumoniae infection. 373 68

The histopathology of hepatitis delta virus disease was studied in carriers of HBsAg with chronic hepatitis delta antigen-positive hepatitis and in serial biopsies of patients with acute hepatitis delta virus hepatitis that progressed to chronicity. There was no histologic feature distinctive of hepatitis delta virus from other types of viral hepatitis. Biopsy specimens of patients with chronic disease exhibited portal and periportal inflammation with piecemeal necrosis, conforming to a picture of aggressive hepatitis often accompanied by cirrhosis. Characteristic was a marked intralobular infiltration by mononuclear cells and a degenerative eosinophilic change of the hepatocytic cytoplasms conducive to the formation of acidophilic bodies. Liver specimens from patients with hepatitis delta virus hepatitis exhibited aspects of focal, confluent and bridging necrosis. The disease progressed to chronicity irrespective of the original histological features. The expression of intrahepatic hepatitis delta antigen was reduced in the phase of the acute hepatitis but increased in parallel with the development of chronic active liver disease. In late-stage cirrhosis, expression of hepatitis delta antigen was usually low.
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PMID:A histological study of hepatitis delta virus liver disease. 379 8


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