Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in situ distribution patterns of intercellular adhesion molecule-1 and human leukocyte antigen-DR antigens were studied in serial sections of 61 liver biopsy specimens from patients with hepatitis B virus infection using immunohistochemical techniques. In addition, the topographical relationship between the display of HBcAg on one hand and the expression of intercellular adhesion molecule-1 by hepatocytes on the other was analyzed with a double-staining immunohistochemical procedure in 14 selected liver biopsy samples showing chronic persistent or chronic active hepatitis and signs of active hepatitis B virus replication as reflected by the presence of variable amounts of HBcAg in a nuclear or cytoplasmic pattern of immunoreactivity. Coexpression of intercellular adhesion molecule-1 and human leukocyte antigen-DR antigens by hepatocytes correlated positively with the site and extent of the inflammatory infiltrate, which was composed of lymphocytes expressing lymphocyte function-associated antigen-1. In healthy HBsAg-positive carriers without inflammatory liver disease, no intercellular adhesion molecule-1 or human leukocyte antigen-DR expression was found on hepatocytes; in acute hepatitis, intercellular adhesion molecule-1 and human leukocyte antigen-DR were strongly expressed throughout the liver parenchyma on liver cell membranes and on sinusoidal lining cells. In chronic persistent and chronic active hepatitis and in active cirrhosis, intercellular adhesion molecule-1 and human leukocyte antigen-DR showed membranous positivity on focal clusters of hepatocytes in areas of periportal or intraacinar inflammation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hepatic expression of intercellular adhesion molecule-1 (ICAM-1) in viral hepatitis B. 197 79

To assess the clinical and prognostic implications of human leukocyte antigen B8 in corticosteroid-treated severe autoimmune chronic active hepatitis, 81 consecutive patients were tested for histocompatibility antigens on the A and B loci, treated with corticosteroids, and followed prospectively for 111 +/- 8 mo. The 47 patients with HLA-B8 were younger (38 +/- 2 yr vs. 48 +/- 2 yr; p less than 0.01), had higher serum levels of aspartate aminotransferase (658 +/- 60 U/L vs. 465 +/- 49 U/L; p = 0.02) and bilirubin (7 +/- 1 mg/dl vs. 2.8 +/- 0.4 mg/dl; p = 0.003), and more commonly had histologic features of bridging necrosis, multilobular necrosis, and cirrhosis (85% vs. 56%; p less than 0.01) at presentation than the 34 patients without HLA-B8. Remission (79% vs. 71%), relapse after drug withdrawal (76% vs. 71%), treatment failure (13% vs. 6%), progression to cirrhosis (46% vs. 32%), and death from liver failure (6% vs. 3%) occurred as frequently in patients with and without HLA-B8. Importantly, HLA-B8-negative patients with HLA-A1 relapsed less frequently than HLA-B8-positive patients with and without HLA-A1- and HLA-B8-negative counterparts without HLA-A1. It is concluded that HLA-B8-positive patients are younger and have more severe disease at presentation than HLA-B8-negative patients. The HLA-B8 phenotype does not influence the response to corticosteroid therapy. HLA-B8-negative patients with HLA-A1 relapse less frequently than other phenotypes.
 ...
PMID:Clinical and prognostic implications of HLA B8 in corticosteroid-treated severe autoimmune chronic active hepatitis. 233 97

Both cryptogenic liver cirrhosis and idiopathic portal hypertension without pathological findings of liver cirrhosis (IPH) are relatively common in Japan. To find differrence between IPH and cryptogenic liver cirrhosis of Japanese, we investigated human leukocyte antigen (HLA), familial clustering of liver diseases as well as prevalence of HBs antigen in 31 patients with IPH. The age of patients with IPH ranged between 6 and 67 years old (mean, 40 years). The ratio of female to male in patients with IPH was 3.1. The incidence of chronic liver diseases in the relatives of patients with cryptogenic liver cirrhosis was significantly high (29.1%), whereas that in the relatives of patients with IPH was not high (12.9%) as compared with hospitalized controls (8.9%). The phenotype frequencies of the specificities of HLA A and B loci in patients with IPH did not differ from those in healthy controls. And the incidence of HBs antigen and antibody in patient with IPH (3.2% and 20.7%, respectively) was similar to those in normal subjects in Japan. These findings suggest that IPH in Japan is a different clinical entity from cryptogenic liver cirrhosis and that HB virus may not be one of the main causes of IPH.
 ...
PMID:Human leukocyte antigen (HLA) in patients with idiopathic portal hypertension (IPH). 746 6

To determine the nature and prognostic implications of autoimmune hepatitis with an acute presentation, 12 patients with a disease duration of 3 months or less (mean duration, 2.3 +/- 0.2 months) were compared to 14 patients with a disease duration of 12 months or more (mean duration, 15.1 +/- 0.9 months). Liver tissue specimens were graded under code for lobular, portal and architectural changes. Patients with acute and chronic presentations were indistinguishable by age, sex, human leukocyte antigen phenotype, immunoserologic markers, and biochemical indices of liver inflammation. Moderate to severe lobular hepatitis was present more frequently in patients with acute presentations (75% versus 29%, p = 0.2), but differences were not statistically significant. Bridging fibrosis and cirrhosis were seen with equal frequency in both groups (79% versus 73%). Remission, relapse, treatment failure, progression to cirrhosis, and death from hepatic failure occurred with similar frequencies in patients with acute and chronic presentations. We conclude that autoimmune hepatitis with an acute presentation is indistinguishable by clinical and laboratory features from that with a chronic presentation and it is probably a pre-existent subclinical disease that is unmasked by disease progression or an abrupt exacerbation. Lobular hepatitis is an important histologic feature regardless of disease duration. The response to corticosteroid therapy is unaffected by the perceived duration of disease prior to treatment.
 ...
PMID:The nature and prognostic implications of autoimmune hepatitis with an acute presentation. 789 Sep 4

The immunogenicity of hepatitis B vaccine is unknown for patients with chronic hepatitis C, although hepatitis B vaccination is highly recommended in these patients. We therefore studied in a prospective open trial of 59 patients with chronic hepatitis C (mean age 42 years, hepatitis C for >10 years, Child-Pugh score < or = 5) and 58 healthy hospital staff persons the rate of nonresponse (anti-HBs <10 mIU/mL at 9 months) to recombinant hepatitis B vaccine (Gen H-B-Vax(R),10 microg intradeltoidal at month 0, 1, and 6). Nonresponse was observed in 18/59 (31%) patients with chronic hepatitis C and 5/58 (9%) healthy staff persons (P <.005) (vs. 7% in historical controls; P <.005), low response (anti-HBs 10-99 mIU/mL) in 19% of patients with chronic hepatitis C and 17% of staff persons. High-dose booster vaccination led to seroconversion in 12/15 (80%) of primary nonresponders. Primary nonresponse to HB vaccine was related neither to presence of early-stage liver cirrhosis nor magnitude of serum hepatitis C virus (HCV) RNA concentration, nor explained by the presence of human leukocyte antigen (HLA) types (B8 DR3, B44, DR7, DQ2) predisposing to low antibody response to hepatitis B surface antigen. The rate of primary nonresponse to the standard regimen of recombinant hepatitis B vaccine is surprisingly high in patients with longstanding chronic hepatitis C. Therefore, the antibody to HBV surface antigen (anti-HBs) titer response should be determined in these patients. Depending on the response titer, higher booster doses may be required to achieve and maintain seroprotection in these patients.
 ...
PMID:Decreased immunogenicity of recombinant hepatitis B vaccine in chronic hepatitis C. 1096 Feb 83

In immunocompetent patients, specific human leukocyte antigen (HLA) class II alleles have been associated with the severity of hepatitis C virus (HCV)-related disease, in particular, HLA-DRB1*11 has been found to exert a protective effect. The authors have analyzed the role of HLA class I and II alleles in determining the frequency, timing, and progression of histologically proven recurrent hepatitis C in 89 patients who underwent a liver transplant for HCV-related cirrhosis. In addition, the influence of HLA mismatch between donor and recipient, HCV genotype, and use of steroid pulses was also evaluated. Median patient follow up was 35 months (range 4-119). HLA-DRB1 typing was performed by genomic analysis in all cases. Liver biopsies were obtained routinely and at least at yearly intervals. Histologically proven recurrent hepatitis was observed in 46 patients (52%), 10 patients progressing to stage 5-6 fibrosis in most cases within 2 years after transplant. By univariate analysis, 3 variables, HLA-B14, HLA-DRB1*04, and HLA-DRB1 donor/recipient mismatch, showed a significant effect on time to recurrent hepatitis C disease. These parameters were included in a multivariate regression model along with HCV genotype, treatment with steroid pulses and DRB1*11. HLA-B14, HLA-DRB1*04, and HLA-DRB1 donor/recipient mismatch were confirmed to provide a significant and independent contribution to the risk of hepatitic disease recurrence. As for the severity of the disease, none of the 10 patients with stage 5-6 hepatitis carried the HLA-DRB1*11 allele, in line with what was observed in nontransplant subjects. Our results suggest that in posttransplant recurrent hepatitis C, immunogenetic factors are relevant in determining HCV infection outcome.
 ...
PMID:Influence of immunogenetic background on the outcome of recurrent hepatitis C after liver transplantation. 1082 62

The spectrum of drug-induced cholestasis ranges from 'bland' reversible cholestasis to chronic forms due to the vanishing bile duct syndrome. Agents known for many years to cause cholestasis include estrogens and anabolic steroids, chlorpromazine, erythromycin, and the oxypenicillins; structurally similar congeners of these drugs (tamoxifen, newer macrolides) may also cause cholestasis. Contemporary drugs linked to cholestastic liver injury include ticlopidine, terfenadine, terbinafine, nimesulide, irbesartan, fluoroquinolones, cholesterol-lowering 'statins,' and some herbal remedies (greater celandine, glycyrrhizin, chaparral). Amoxillin-clavulanate, ibuprofen, and pediatric cases of the vanishing bile duct syndrome are recent additions to a long list of drugs associated with the vanishing bile duct syndrome. Particular human leukocyte antigen profiles have recently been identified among those who have developed cholestasis with specific drugs (tiopronin and amoxicillin-clavulanate), and the mechanistic relevance of these genetic associations is being explored. The treatment of drug-induced cholestasis is largely supportive. The offending drug should be withdrawn immediately. Cholestyramine or ursodeoxycholic acid are used to alleviate pruritus, with rifampicin and opioid antagonists being reserved for those who fail first line therapy. Nutritional support is essential for those with prolonged cholestasis, a subgroup who are at risk of developing biliary cirrhosis and liver failure. Timely referral for liver transplant assessment is crucial in these patients.
 ...
PMID:Drug-induced cholestasis. 1135 18

Chronic hepatitis C virus (HCV) infection develops in 85% of exposed individuals and 20% develop cirrhosis. However, the pathogenesis of this process is not well-understood. The objective of this study was to determine whether HCV-reactive T cells play a role in the process of development of cirrhosis during chronic HCV infection. We analyzed 21 human leukocyte antigen (HLA)-A2 patients with chronic HCV infection (9 with histology of inflammation and 12 with histology of fibrosis/cirrhosis). The frequency of CD8(+) T cells reactive to 12 HCV-derived epitopes was determined by an interferon-gamma enzyme-linked immunospot (ELISPOT) assay. The frequency of CD4(+) Th1 and Th2 cells reactive to the HCV core antigen was determined by interferon-gamma and interleukin-5 ELISPOT assays, respectively. Patients with histology of inflammation showed a significantly higher CD8(+) T-cell response to five HCV-derived epitopes (YLLPRRGPRL [core], CINGVCWTV [NS3], LLCPAGHAV [NS3], ILAGYGAGV [NS4B], and GLQDCTMLV [NS5B]) as compared with patients with histology of fibrosis/cirrhosis. Also, patients with histology of inflammation showed a significantly higher CD4(+) Th1 response to the HCV core antigen as compared to patients with histology of fibrosis/cirrhosis. These results indicate that a lack of an optimal T-cell response to HCV is associated with the development of cirrhosis during chronic HCV infection.
 ...
PMID:Lack of optimal T-cell reactivity against the hepatitis C virus is associated with the development of fibrosis/cirrhosis during chronic hepatitis. 1255 24

To investigate the influence of immunogenetics on response to interferon (IFN)-alpha treatment, human leukocyte antigen alleles were characterized in 100 unrelated Taiwanese patients with chronic hepatitis C virus (HCV) infection. A11, B51, Cw15, and DRB1*15 were positively correlated with sustained response, whereas A24 was inversely associated with response to IFN-alpha, after adjustment for cirrhosis, pretreatment virus load, and viral genotype. Homozygote-genotype analysis showed that A24 and DQB1*05 probably had gene-dosage effect on sustained response. DRB1*15 was in strong linkage disequilibrium with DQB1*05 and DQB1*06, but only haplotype DRB1*15-DQB1*05 was associated with response to IFN-alpha. Haplotype A11-DRB1*15 was strongly associated with sustained response. This suggests a role for a complex host-immunogenetics interplay in the response to IFN-alpha, in patients with chronic HCV infection.
 ...
PMID:Human leukocyte antigen class I and II alleles and response to interferon-alpha treatment, in Taiwanese patients with chronic hepatitis C virus infection. 1282 72

Refractoriness to platelet transfusion indicates a condition in which an expected increase in platelet count is not attained after platelet transfusion. We report herein two cases of refractoriness to platelet transfusion that were caused by the presence of antibodies against the human leukocyte antigen following partial hepatectomy for hepatocellular carcinoma. Due to low postoperative platelet counts in the first case, the patient was transfused with 75 units of platelet concentrate for 3 days after surgery, but was unable to gain a significant increase in the platelet count because of platelet transfusion refractoriness due to anti-human leukocyte antigen antibodies. This case was not complicated and had a favorable clinical course. Despite being transfused with 60 units of platelet concentrate during the 2 days after surgery, the patient's platelet count in the second case did not increase because of the presence of anti-human leukocyte antigen antibodies. Bleeding from the cut surface of the liver into the intraperitoneal cavity was found on the second postoperative day because of a decrease in platelet count. On postoperative day 5, disseminated intravascular coagulation occurred. Perioperative refractoriness to platelet transfusion is an intractable complication since no efficient treatment is available. Preoperative examinations for anti-platelet antibodies should be performed in patients undergoing hepatectomy for hepatocellular carcinoma. This is especially true in cases of decreased platelet counts due to preceding liver cirrhosis and when the prediction for postoperative platelet transfusions is necessary.
 ...
PMID:Refractoriness to platelet transfusion following partial hepatectomy for hepatocellular carcinoma: report of two cases. 1282 97


1 2 3 4 5 6 Next >>