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)

Recurrent amyloidosis is an uncommon but well-documented event in up to 26% of renal allograft recipients transplanted for amyloid renal disease. Both primary and secondary amyloidoses recur. De novo primary and secondary amyloid have not been previously reported. We report the first occurrence of de novo secondary amyloid in a renal allograft recipient. The cause of the secondary amyloidosis is unproven, but possible etiologies include inflammation secondary to occult hepatitis, rheumatoid arthritis, or chronic rejection. Colchicine therapy has not resulted in decreased proteinuria or improved renal function.
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PMID:De novo amyloidosis in a renal allograft: a case report and review of the literature. 837 47

Visceral involvement was investigated in 168 patients with general peritonitis. Toxic hepatitis, toxic nephropathy, myocardia dystrophy, pulmonary impairment were determined in 85.7%, 83.3%, 69.6% and 19% of them, respectively. 44 (26.2%) patients with terminal peritonitis developed polyorganic insufficiency. Principal approaches to management of visceral pathology in peritonitis are analyzed.
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PMID:[Visceral pathology in peritonitis]. 857 3

Hepatitis C virus (HCV) is the predominant cause of posttransplant non-A, non-B hepatitis among renal allograft recipients. Prior studies evaluating the impact of HCV in kidney transplantation have been retrospective in design and based largely on changes in serum transaminases. We studied a group of HCV-infected end-stage renal disease patients prospectively with pretransplant liver biopsies and close virologic and biochemical follow-up posttransplant. Fourteen patients have been followed a mean of 11.6 +/- 5.6 months posttransplant (range, 5-21 months). Six had changes of chronic hepatitis on pretransplant liver biopsy while 8 showed only mild histologic abnormalities. Circulating viral titers increased several-fold over baseline levels during posttransplant follow-up. Viral replication was particularly enhanced immediately following a course of antilymphocyte therapy. Although all patients showed a 2-3 fold increase in alanine aminotransferase (ALT) following transplantation, there were no association noted between pretransplant liver histology, the use of FK506 and/or cyclosporine-based immunosuppression, and the magnitude of ALT change posttransplant. The only clinical outcome found to differ significantly was a higher incidence of cytomegalovirus infection among patients with chronic hepatitis. All patients are alive with functioning grafts. There have been no episodes of fulmiinant or subfulminant liver failure. We conclude that HCV-infected patients can be safely transplanted with excellent short-term follow-up. Continued monitoring with sequential liver biopsies will be needed to define the long-term course of HCV infection in an immuno-suppressed population.
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PMID:A prospective study of hepatitis C virus infection in renal allograft recipients. 862 54

Hepatitis, A is usually a mild and self-limiting infection of the liver. Whereas the clinical course is usually benign in children, complications such as prolonged cholestasis and fulminant liver failure have been reported in adults. Acute functional renal failure is an uncommon event in the absence of fulminating liver disease. So far, only cases of acute hepatitis A with biopsy-proven interstitial renal disease or tubular necrosis have been reported [Geltner et al. 1992. Kramer et al. 1986]. We present the case of a 35-year-old, previously healthy male with non-fulminant cholestatic viral hepatitis A, who developed progressive oliguric renal failure requiring dialysis therapy. Kidney biopsy ruled out glomerular disease and tubular necrosis. In the absence of bleeding and other causes of fluid depletion this case may be another variant of hepatorenal syndrome whose etiopathogenesis is only poorly understood.
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PMID:Acute renal failure complicating non-fulminant hepatitis A. 879 33

In hepatitis C, both susceptibility to infection and the course of disease may depend on differences in the immune response. As the major histocompatibility complex (MHC) plays a crucial role in antigen presentation, we investigated a possible relationship between susceptibility to hepatitis C virus (HCV) infection and human leucocyte antigen (HLA) alleles. Therefore, phenotype frequencies of HLA were compared in 186 anti-HCV positive patients with end-stage renal disease (ESRD) to 328 anti-HCV negative patients with ESRD. HLA class I alleles were determined serologically and HLA class II alleles (DRB1, DQA1, DQB1) by the polymerase chain reaction sequence-specific oligonucleotide (PCR-SSO) technique. Additionally, in anti-HCV positive patients we looked for a relationship between the activity of hepatitis C (indicated by elevation of transaminases or the presence of viremia) and HLA determinants. For the three criteria (antibody status, elevation of transaminases and viremia) a significant association to HLA alleles was not found in patients with ESRD. This suggests that neither susceptibility to HCV infection nor the biochemical activity of hepatitis and HCV-RNA positivity seem to be strongly related to HLA status in Caucasian patients with end-stage renal disease.
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PMID:No significant influence of HLA determinants on susceptibility to hepatitis C virus infection in Caucasian patients with end-stage renal disease. 902 18

On September 21-22, 1995, an international meeting entitled "Targeting of Novel Therapeutics to the Liver and GI Tract" was held at the Natcher Conference Center on the campus of the National Institutes of Health. The conference was sponsored by the National Institute of Diabetes and Digestive and Kidney Diseases through the Division of Digestive Diseases and Nutrition and Digestive Diseases Interagency Coordinating Committee (DDICC). Section 440A of Public Law 94-562 in 1976 created the DDICC for the purpose of coordinating the digestive disease-related research activities of relevant federal health agencies into a coordinated program aimed at combating digestive diseases. As part of this federal effort, an assessment of the "state of the art" for targeted drug therapeutics to the liver and gene therapy was undertaken through the conference, cochaired by Dr. Mark Zern (Thomas Jefferson Medical College) and Dr. Flossie Wong-Staal (University of California, San Diego, CA). The conference was divided into four sessions: Session I was Vectors and Techniques; Session II was Liver and Metabolic Diseases; Session III was Hepatitis and GI Disease; and Session IV was Approaches for HIV Infection. This summary focuses on the new technologies and the studies directly pertaining to liver disease. Table 1 lists the techniques and their applications. Table 2 describes viral vectors that have been employed for the purpose of hepatic gene therapy. Table 3 summarizes the studies presented as posters at the conference.
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PMID:Hepatic drug delivery and gene therapy. 902 68

We report 81 of 107 cases of hemolytic uremic syndrome (HUS), admitted between July 1994 and February 1996, following an outbreak of Shigella dysenteriae type 1 dysentery in Kwazulu/Natal. All patients, excluding 1, were black with a mean age of 38 months (range 1-121); 50 (61.7%) were males. The mean duration of dysentery was 11.3 days (range 1-41) and HUS 15 days (range 1-91). Most patients had acute oliguric renal failure (90.1%), 42 (51.6%) required peritoneal dialysis. Complications included encephalopathy 30 (37.0%), convulsions 12 (14.8%) and hemiplegia 2 (2.3%), gastrointestinal perforation 8 (9.9%), protein losing enteropathy 26 (32.1%), toxic megacolon 4 (4.9%), rectal prolapse 5 (6.2%), hepatitis 11 (13.6%), myocarditis 5 (6.2%), congestive cardiac failure 3 (3.7%), cardiomyopathy 3 (3.7%), infective endocarditis 1 (1.2%), septicemia 15 (18.5%), disseminated intravascular coagulation 17 (21%). Leukemoid reactions were found in 74 (91.3%) patients, hyponatremia in 56 (69.1%), and hypoalbuminemia in 67 (82.7%). Stool culture for Shigella dysenteriae type I was positive in only 7 (8.6%) patients; Shiga toxin assays were not performed. Outcome was as follows: recovery 32 (39.5%), impaired renal function 8 (9.9%), chronic renal failure 26 (32.1%), end-stage renal disease 1 (1.2%), and death 14 (17.3%) patients.
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PMID:Post-dysenteric hemolytic uremic syndrome in children during an epidemic of Shigella dysentery in Kwazulu/Natal. 932 80

The hepatitis G virus is a newly discovered flavivirus that has been linked to acute and chronic hepatitis of unknown cause. We determined the prevalence of hepatitis G virus infection in 179 selected patients undergoing liver transplantation at three centers participating in the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Liver Transplantation Database. Pretransplantation and posttransplantation specimens were tested for hepatitis G virus RNA by polymerase chain reaction. Before transplantation, 9 of 38 (24%) patients with fulminant hepatic failure, 9 of 62 (15%) with cryptogenic cirrhosis, 3 of 35 (9%) with cholestatic liver disease, and 5 of 44 (11%) with chronic hepatitis C were positive for hepatitis G virus RNA (P = .27). Patients with and without viral RNA were similar in clinical features, liver test abnormalities, and survival after transplantation. Posttransplantation serum specimens were tested from 73 patients; 9 of 11 (82%) who were positive for viral RNA before transplantation remained positive, but 35 of 62 (56%) patients who were initially negative became positive after transplantation, a rate consistent with that predicted from the number of blood products administered. Only 5% of de novo HGV infections could be attributed to preexisting hepatitis G virus RNA in the donor. Comparison of patients with and without hepatitis G virus infection showed no difference in incidence of hepatitis after transplantation. Thus, hepatitis G virus infection was present in 15% of patients before and appeared de novo in half of patients after liver transplantation. Although hepatitis G virus infection was not associated with poor outcome, the frequency of this infection after transplantation calls for further long-term evaluation.
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PMID:Hepatitis G virus infection before and after liver transplantation. Liver Transplantation Database. 940 76

Hepatitis B and hepatitis C are two common pathogens causing chronic hepatitis in patients with end-stage renal disease (ESRD). With the acceptance of hepatitis B s antigen (HBsAg) screening, infected patients have been identified and isolated over the past 20 years. Consequently, hepatitis B is now being seen less frequently in dialysis units. Even though hepatitis B has become less of a problem, non-A, non-B hepatitis has been recognized as a significant problem since 1979. With the availability of serological testing for hepatitis C virus (HCV), more specific information is now available in regard to HCV infection in dialysis patients. The prevalence of anti-HCV in haemodialysis (HD) patients is quite variable, ranging from 5 to over 50%. Anti-HCV positivity is associated with previous blood transfusions, mode of therapy and duration of haemodialysis. In Spain and Italy, the annual seroconversion rates of HCV antibodies in dialysis patients are 2-9%; this rate was much higher in Taiwan (15%). Whether patients with HCV infection should be identified and isolated during HD treatment is an issue of controversy. Transplantation is associated with increases in hepatitis B virus (HBV) replicative markers. The survival disadvantage in HBsAg-positive recipients usually did not become apparent until 8 years after transplantation. Hepatitis C virus-infected renal transplant recipients are presumably in a similar situation to patients with hepatitis B, although confirmatory data are currently lacking. Coinfection of HBV and HCV may lead to aggressive liver disease and cirrhosis. A hepatitis B vaccine is recommended for all susceptible dialysis patients. Dialysis patients have lower response rates to hepatitis B vaccines than do other people. Currently, no vaccine is available for hepatitis C. To date, there are no effective treatments available for hepatitis B and hepatitis C. Combination therapy with interferon/lamivudine for hepatitis B and interferon/ribavirin for hepatitis C may offer a promise of effective control of viral replication in the future.
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PMID:Hepatitis in patients with end-stage renal disease. 940 43

The etiology of liver disease remains unknown in about 4 to 23% of dialysis patients and 10 to 16% of renal transplant recipients. A search for other causative agents of liver disease led to the discovery of the GB group of viruses. We studied the association between the presence of GB virus C (GBV-C) infection, known risk factors for parenterally-transmitted infections and history or laboratory evidence of liver disease among end-stage renal disease (ESRD) patients referred for renal transplantation to the New England Organ Bank, MA. Stored sera from patients on the renal transplantation waiting list between November 1986 and June 1990 were tested for antibody to hepatitis C virus (HCV). Sera were available in 1544 of 3243 (48%) patients, and anti-HCV was detected by ELISA3 in 287 (19%). All 287 anti-HCV positive patients formed the anti-HCV positive cohort and 286 randomly selected anti-HCV negative patients formed the anti-HCV negative cohort (573 patients overall). Additional sera were available for GBV-C RNA testing in 465 of 573 (81%) patients, and GBV-C RNA was detected by RT-PCR in 146. The overall extrapolated prevalence of serum GBV-C RNA was 29%. The prevalence of serum GBV-C RNa among anti-HCV positive patients (35%) was not significantly different from that among anti-HCV negative patients (29%; P = 0.22). In a univariate analysis, compared to patients without GBV-C RNA, patients with serum GBV-C RNA were younger [odds ratio (OR) 0.98 per year of age, P = 0.01], had a lower proportion of males (OR 0.64, P = 0.03), lower proportion of patients with diabetes mellitus (OR 0.44, P = 0.01), higher proportion of patients with a previous transplantation (OR 1.53, P = 0.04), longer duration of dialysis at the time of enrollment (OR 1.004 per month on dialysis, P = 0.03), and a higher proportion of patients with history of transfusions (OR 4.58, P = 0.01). Serum GBV-C RNA was not associated with a significantly increased OR for history of liver disease or non-A, non-B hepatitis, or elevated serum alanine aminotransferase levels. In a step-wise multivariate regression analysis, a younger age (OR 0.98 per year of age, P = 0.03), and history of blood transfusions (OR 3.89, P = 0.03) were associated with an increased OR for serum GBV-C RNA, while diabetes mellitus was associated with a decreased OR for GBV-C RNA (OR 0.47, P = 0.01). Anti-HCV was not a predictor of serum GBV-C RNA (OR 1.07, P = 0.77). The results of this study support the fact that GBV-C is a parenterally transmitted virus and shed light on the modes of transmission of GBV-C among ESRD patients. However, the association with liver disease remains to be established.
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PMID:Predictors of GBV-C infection among patients referred for renal transplantation. 960 18


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