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)

A patient suffering from chronic hepatitis exhibited severe transfusion reactions after administration of fresh frozen plasma and a plasma fraction: PPSB (prothrombin complex concentrate). 1 month before these reactions, she received fresh frozen plasma during plasma exchange therapy. The patient's serum obtained 1 week and 6 months after the second reaction gave a precipitation arc against PPSB preparations when examined by double-diffusion technique in agarose gel. An antibody of IgG class present in these sera reacted with a purified preparation of the fourth complement component (C4). This was demonstrated by various experiments (protein A radioimmunoassay and passive hemagglutination) using purified C4 as antigen. The antibody had a limited specificity and reacted only with C4 of Rodgers specificity. Phenotype determination of the patient's C4 group showed that she was Chido positive and Rodgers negative. Her HLA group was A1, Aw30; B8,-; DR3,-. The patient had neither detectable anti-IgA nor other anti-immunoglobulin antibodies. She had not received blood or plasma transfusion before her hepatitis. The coexistence of a precipitating anti-C4 antibody and adverse transfusion reactions to plasma fractions containing large amounts of C4 indicates that in the absence of antibodies of other specificities, this antibody can be considered as the cause of the transfusion reaction.
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PMID:Adverse transfusion reactions associated with a precipitating anti-C4 antibody of anti-Rodgers specificity. 646 22

The different sensitivity of the male and the female liver is well established, but there is an obvious difference in male livers as well. One possible explanation for these differences might be the existence of genetic peculiarities among patients with alcoholic cirrhosis. In the early twentieth, Chvostek in Vienna was the first to draw attention to a constitutional element which he believed to be fundamental: Absent body hair, absent or extremely spare hair on the limbs, and pubic hair of the female type, i.e. with horizontal upper border (1) (Fig. 1). Chvostek laid special stress on the fact that these anomalies were of genetic origin and were not a secondary phenomenon do to alcoholism or cirrhosis. The feminine pattern of hair distribution, the so-called "Chvostek's habitus", is a frequently seen condition but the statistical proof of its association with alcoholic cirrhosis in man is still missing. The purpose of our study was to investigate if the feminine pattern of hair distribution in male patients with alcoholic cirrhosis is a genetic characteristic, this anomaly is more frequently encountered in the alcoholic type than in the post-hepatitis type of cirrhosis, the reported discrepancies of HLA frequencies are due to genetic differences.
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PMID:Constitutional factors in alcoholic cirrhosis. 653 37

Two cases of primary biliary cirrhosis (PBC) were observed in two brothers. Clinical, biochemical, immunological and genetic investigations (in particular by HLA typing) were systematically undertaken in nine subjects of this family (including the two above mentioned cases) in two generations. One case of granulomatous hepatitis associated with auto-immune thyroiditis was discovered in a sister. Immunological abnormalities were observed in six out of nine members of the family: anti-nuclear (four cases), anti-mitochondrial (two cases), anti-thyroid (two cases), auto-antibodies and rheumatoid factors (two cases). Six subjects (including the three with hepatic disease) had the same HLA haplotype (with in particular HLA DR4, which has been previously associated with sporadic PBC). However, the role of this haplotype in the transmission of PBC in a family could not be demonstrated. Biochemical and immunological survey might be of importance in the kindred of patients with PBC, thereby contributing to the screening of asymptomatic hepatic disease.
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PMID:[Familial autoimmune pathology comprising 2 cases of primary biliary cirrhosis]. 657 90

The progression of acute viral hepatitis non-A, non-B in a group of young female patients with well defined disease was evaluated retrospectively over a period of 21/2 years. The histologically proved chronification rate was 39 per cent. It was looked for a correlation between some parameters in the acute phase of the disease, the distribution of HLA antigens, and the progression to chronicity. There were no statistically ensured differences of HLA antigens between patients with chronic hepatitis non-A, non-B, patients with healed acute one, patients with chronic hepatitis type B, and the normal population. The level of transaminases within the acute phase of the illness did not allow to draw any conclusion for the further progression of the disease. But icteric patients seemed to develop chronic disease more seldom. In this time, the reason of the high chronification rate after infection by hepatitis virus(es) non-A, non-B is not yet clear.
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PMID:[Chronicity of non-A, non-B hepatitis. Evaluation of the clinical course with special reference to the types of distribution of HLA antigens and clinical criteria]. 681 4

A 19-year-old male, suffering from post-hepatitis aplastic anaemia, was transplanted with bone marrow cells from his HLA-identical, MLC non-reactive brother. Haematological recovery ensued, but the patient also developed grade IV graft-versus-host disease (GVHD). In addition to involvement of skin, liver and gut, the kidney seemed affected by GVHD since the patient has hypokalaemia and severe hyperkaluria. Other causes of urinary potassium loss were excluded. The amount of potassium loss correlated well with the severity of the GVH-reaction. Although coagulation disorders prohibited a kidney biopsy, the clinical course suggested GVHD to be the cause of the urinary potassium loss.
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PMID:Extreme potassium loss in a patient with severe graft versus host disease. 700 82

In eight patients with clinical sure Vogt-Koyanagi Harada-syndrome (VKHS) immunological examinations were performed. We tested whether there were signs of former or present infections (measles HHT and complement fixation test (C.F.T.), rubella HHT, hepatitis HBs-antigen, adenovirus AG, varicella-zoster C.F.T., herpes simplex C.F.T., cytomegaly IgM and IgG, toxoplasmosis immunofluorescence, tuberculosis Middlebr. Dubois). In none of all cases we could find HLA B12. The rheumatic tests, LDH, albumin an electrophoresis, coeruloplasmin and haptoglobin were negative. The uveal pigment failed to stimulate the leucocyte cultures from VKHS-patients in leucocyte-migration-inhibition-test and in leucocyte-adherence-inhibition-test.
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PMID:[Immunological examinations in Vogt-Koyanagi-Harada disease (author's transl)]. 703 82

HLA antigens were studied among 94 chronic alcoholics. Concerning A and B-loci, there was no significant change of phenotype frequency (PF) in the HLA typing between the patients and controls (80 healthy subjects). However, there was a significant difference in the PF of CW3 between chronic alcoholics and controls (58.5% in alcoholics vs 30.0% in controls). The corrected p value was less than 0.05 with relative risk value being 3.29 HLA-DR loci were also detected in 26 patients, but there was no significant difference between the patients and controls. All alcoholics were subdivided according to the hepatic morphology, and the PF of HLA was examined. A significant high frequency of HLA CW3 was found in patients with hepatitis (64%) compared to controls (30%). There was also an increased PF of CW3 in the liver cirrhosis group (59% in cirrhosis group vs 30% in controls). In conclusion, chronic alcoholics have a significantly higher PF of HLA-CW3 as compared to controls. This characteristic feature becomes even more distinct in alcoholics with severe hepatic lesions.
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PMID:HLA antigens as immunogenetic markers of alcoholism and alcoholic liver disease. 724 36

An immunogenetic study of autoimmune chronic active hepatitis (CAH) showed the relative risk (RR) for this disease was 11.6 for patients who were HLA-B8, 11.7 for patients who were DR3 and 2.3 for patients who were Gma+x+. Moreover, the Gm haplotype Gma+x+ was present in 18 of 40 (45%) patients with HLA-B8, but in none of 10 patients negative for HLA-B8, whereas in 180 healthy controls Gma+x+ was evenly distributed among those positive (24%) and negative (18%) for HLA-B8. The RR was lowest in patients lacking HLA-B8 but positive for Gma+x+. Relative to this low-risk group, the risk was increased 39 times in subjects with both HLA-B8 and Gma+x+, 15 times in subjects with HLA-B8 who were not Gma+x+ and twice in subjects who were neither HLA-B8 nor Gma+x+. Statistical analysis indicated that the three-factor effect (disease risk affected by non-additive effects of HLA-B8 and Gma+x+) was significant (P less than 0.01), as were the main effects of HLA-B8 (P less than 0.001) and Gma+x+ (P less than 0.02). Thus in the presence of HLA-B8, genes linked to Gma+x+, an immunoglobulin CH allotype, may contribute to the development of autoimmune chronic active hepatitis; in the absence of HLA-B8 these same genes appear to be inactive. This may indicate interactions between MHC gene products and VH gene products in the presentation and recognition of autoantigen(s) in autoimmune hepatitis.
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PMID:Interaction of HLA and Gm in autoimmune chronic active hepatitis. 724 97

HLA A and B locus antigens were determined in 17 patients who had recovered from unexplained hepatitis following halothane anaesthesia. The greatest deviations from expected frequencies were observed with A1, A11 and BW22, but these differences were not statistically significant when the P values were corrected for the number of antigens tested. Although a larger series might show such deviations to be significantly different, HLA typing is of no predictive value in determining those at risk to hepatitis following repeated halothane exposure.
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PMID:HLA A and B locus antigens in patients with unexplained hepatitis following halothane anaesthesia. 733 Aug 46

Murine F9 and PCC4 teratoma cells do not express H-2 major transplantation antigens according to virus-specific T-lymphocyte cytotoxic or serological assays. However, such cells can be infected with and readily replicate many types of viruses (coxsackie B 3, mouse hepatitis, Sindbis, Semliki Forest [SFV], lymphocytic choriomeningitis, Pichinde, vesicular stomatitis, herpes simplex type 1) to the same extent as do murine F12 teratoma cells and mouse embryo fibroblasts, all of which express the H-2 determinants. In contrast, F9 and PCC4 cells are not productively infected with murine cytomegalovirus, whereas F12 and mouse embryo fibroblast cells are. In addition to replicating in H-2-negative murine teratoma cells, SFV replicates in H-2-negative murine lymphoblastoid cells. The ability of SFV to infect cells without H-2 antigens and then to effect viral antigenic expression in the cells' cytoplasm and on their surface with similar kinetics and in equivalent amounts as cells with H-2 antigens indicates that the H-2 receptor is not needed for SFV infection. Daudi cells, which lack HLA antigens, block the replication of SFV. This occurs at some point after receptor binding, as demonstrated by diminished viral mRNA. In addition, a possible membrane defect precludes viral exit in Daudi cells transfected with SFV infectious RNA. These results indicate that a cell's possession of H-2 antigens is not a requirement for SFV infection and that major histocompatibility complex antigens are not specific receptors for this virus.
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PMID:Does the major histocompatibility complex serve as a specific receptor for Semliki Forest virus? 737 8


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