Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The inflammatory bowel diseases are considered an abnormal host immune response to an environmental stimulus. Evidence suggests a role for intestinal bacteria in initiating and/or providing an ongoing stimulus for inflammation in inflammatory bowel disease. Helicobacter pylori is the major cause of active chronic gastritis and peptic ulcers in humans and has been linked to gastric carcinoma and lymphoma. Studies in various animal models, particularly mice, have identified enterohepatic Helicobacter species that are capable of causing hepatitis and enterocolitis. We hypothesize that Helicobacter species may have a role in maintaining inflammation in humans with inflammatory bowel disease. In order to investigate this, biopsy specimens were obtained from patients with and without inflammatory bowel disease. DNA was extracted from the tissues and subjected to PCR with primers designed to detect the ribosomal DNA of members of the Helicobacter species. DNA from six biopsy samples from 60 inflammatory bowel disease patients tested positive. This included 5 of 33 ulcerative colitis patients that were positive compared to 0 of 29 age-matched controls (P < 0.04). Sequencing of the bands produced by PCR amplification revealed >or=99% homology with H. pylori. These results indicate that a member of the Helicobacter species may be involved in some cases of ulcerative colitis.
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PMID:Detection of species-specific helicobacter ribosomal DNA in intestinal biopsy samples from a population-based cohort of patients with ulcerative colitis. 1476 33

We report the case of a 49-Year-old-man with primary sclerosis cholangitis (PSC) and ulcerative colitis who developed two acute episodes of pseudo-angiocholitis. Both episodes were triggered by septic hepatitis translocated from ulcerative colonic adenocarcinoma. The biliary MRI did not show any signs of lithiasis or cholangiocarcinoma. cholangiocarcinoma, intra-hepatic lithiasis and colonic cancer are potential diagnoses in patients with PSC who develop angiocholitis.
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PMID:[Acute "pseudo-angiocholitis" due to colonic adenocarcinoma in a man with primary sclerosis cholangitis and ulcerative colitis]. 1503 32

Background and aim: Alternative splicing of human glucocorticoid receptor (hGR) premessenger RNA (mRNA) generates two highly homogenous isoforms, termed hGRalpha and hGRbeta. hGRalpha is a ligand-activated transcription factor, which, in the hormone-bound state, modulates the expression of glucocorticoid-responsive genes by binding to specific glucocorticoid response element DNA sequences. In contrast, hGRbeta may be an endogenous inhibitor of glucocorticoid action and transcriptionally inactive. hGRbeta protein has been known to correlate with the development of glucocorticoid resistance. Glucocorticoids can effectively relieve autoimmune hepatitis (AIH), but some patients with this disease are refractory even when glucocorticoids are administered. The aim of this study was to determine the incidence of hGRbeta mRNA in patients with AIH by reverse transcription polymerase chain reaction (RT-PCR), and to compare the clinical characteristics of hGRbeta-positive and -negative patients with AIH. Materials and methods: RNA was obtained from peripheral blood mononuclear cells (PBMCs) of 62 patients, consisting of 26 with AIH, 10 with primary biliary cirrhosis (PBC), seven with chronic viral hepatitis (CVH), 10 with ulcerative colitis (UC), six with pemphigus, and three with systemic lupus erythematosus (SLE), and 10 healthy volunteers. The total RNA obtained was reverse transcribed, the resulting complementary DNA amplified using specific primers for hGRalpha and hGRbeta. Results: The hGRalpha mRNA was detected in RNA from PBMCs of all patients and healthy volunteers. The hGRbeta mRNA was detected in 15 (57.6%) patients with AIH. This incidence was significantly higher than that for patients with PBC (0%) or CVH (28.6%) or for healthy volunteers (20.0%) ( [Formula: see text] ). Of the hGRbeta-positive and -negative groups, serum ALT and total bilirubin (TB) levels were significantly higher in the positive group ( [Formula: see text] ). The total dose of glucocorticoid was higher in the positive group, but the difference was not statistically significant. However, the average monthly dose was significantly higher in the positive group ( [Formula: see text] ). The rate of relapse of AIH was significantly higher in the positive group (60.0%) than in the negative (10.0%) ( [Formula: see text] ). The rate of usage of immunosuppressive drugs was higher in the positive group (33.3%) than in the negative (18.2%), but the difference was not statistically significant. Conclusions: These data show that hGRbeta expression in PBMCs of patients with AIH assessed by RT-PCR is closely associated with resistance to glucocorticoids which affects the outcome of therapy with this drug.
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PMID:Expression of human glucocorticoid receptor in lymphocytes of patients with autoimmune hepatitis. 1520 78

"Overlap syndromes" have been reported among various autoimmune liver diseases, particularly between primary biliary cirrhosis and autoimmune hepatitis (AIH) in adults and between AIH and autoimmune cholangitis in children. The overlap syndrome of AIH and primary sclerosing cholangitis (PSC), however, has been scarcely reported. Furthermore, in most of the reported cases of AIH/PSC overlap syndrome, PSC and AIH were believed to occur simultaneously. We report a case of a 34-year-old woman who has ulcerative colitis and PSC (diagnosed by colonoscopy, histology, and cholangiogram) and 7 years later develops rapidly progressive liver failure and hemolytic anemia from AIH. Liver biopsy showed dense portal lymphoplasmacytic infiltrate with interface hepatitis and acidophil bodies confirming AIH. She responded well to immunosuppressive therapy with steroids, both with respect to her liver disease and her autoimmune hemolytic anemia. Additionally, her clinical symptoms of fatigue, jaundice, and pruritus improved markedly and quickly. Overlap or "crossover" syndrome should be considered in all patients with PSC when they present with sudden deterioration of the liver function and changes in liver enzymes. By making the diagnosis of AIH in a patient with well-established PSC, appropriate treatment can be initiated, resulting in the patient's prompt recovery.
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PMID:Rapid progression of autoimmune hepatitis in the background of primary sclerosing cholangitis. 1549 11

HMGB1 and HMGB2 are abundant nonhistone chromosomal proteins in eukaryotic organisms. Their respective primary sequences are highly conserved. Our previous studies showed that these proteins are novel autoantigens of anti-neutrophil cytoplasmic antibodies in sera from patients with ulcerative colitis (UC), rheumatic disease and autoimmune hepatitis (AIH). In the present paper, we showed that anti-HMGB1 and HMGB2 antibodies in sera of patients with UC do not recognize HMGB1 in neutrophils while they recognize the protein in lymphocytes. Anti-HMGB2 monoclonal antibody FBH7, recognizing HMGB1 in lymphocytes, showed a similar profile to the antibodies in the patients' sera. In order to elucidate the difference in immunoreactivity to HMGB1 between neutrophils and lymphocytes, we mapped the epitope for FBH7 by means of several methods. The results showed that FBH7 recognizes the intact conformation composed of 52-56 residues of HMGB1 in lymphocytes. This suggested that HMGB1 in neutrophils is conformationally changed in the epitope or the peripheral structure of the epitope from the protein in lymphocytes. The apparent conformational change of HMGB1 between neutrophils and lymphocytes will be important for understanding the functional difference of HMGB1 in these cells.
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PMID:Conformational difference in HMGB1 proteins of human neutrophils and lymphocytes revealed by epitope mapping of a monoclonal antibody. 1549 85

Chronic inflammatory processes produce an excess of ROS and DNA-reactive aldehydes from lipid peroxidation (LPO), such as trans-4-hydroxy-2-nonenal (HNE) and malondialdehyde (MDA), which can modify cellular macromolecules and drive to malignancy. Etheno-modified DNA bases are generated inter alia by reaction of DNA with the major LPO product, HNE. We are investigating steady-state levels of etheno-DNA adducts in organs with diseases related to persistent inflammatory processes that can lead to malignancies. We have developed ultrasensitive and specific methods for the detection of etheno-DNA base adducts in human tissues and in urine. Etheno-DNA adduct levels were found to be significantly elevated in the affected organs of subjects with chronic pancreatitis, ulcerative colitis and Crohn's disease. When patients with alcohol abuse-related hepatitis, fatty liver, fibrosis and cirrhosis were compared with asymptomatic livers, excess hepatic DNA damage was seen in the three latter patient groups. Etheno-deoxyadenosine excreted in urine was measured in HBV-infected patients diagnosed with chronic hepatitis, cirrhosis and hepatocellular carcinoma. As compared to controls, these patients had up to 90-fold increased urinary levels. Impaired or imbalanced DNA-repair pathways may influence the steady-state levels of etheno-DNA adducts in inflamed tissues. In conclusion, etheno-DNA adducts may serve as potential lead markers for assessing progression of inflammatory cancer-prone diseases. If so, the efficacy of human chemopreventive interventions for malignant disease prevention could be verified.
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PMID:Accumulation of lipid peroxidation-derived DNA lesions: potential lead markers for chemoprevention of inflammation-driven malignancies. 1609 77

In a 64-year-old man who had been treated with prednisolone (PSL) and 6-mercaptopurine (6MP) for a long period, for ulcerative colitis (UC), hepatocellular carcinoma (HCC) was detected incidentally. The UC was in remission with these medications. After he had been taking these medications for about 8 years, HCC was detected by computed tomography (CT), done for the evaluation of an other disease. Blood chemistry examination results were normal, except that the protein induced by vitamin K antagonist (PIVKA)-II level was 7940 AU/ml. We performed resection of liver segment V. With comparative genomic hybridization, chromosomal aberrations were recognized; these were gains of 1q, 3ptel-21, 8p12, and 22q11.23-22q13.1. Generally, HCC is associated with hepatitis virus infection in most cases, but in this patient, the HCC was not related to hepatitis C virus (HCV) or HBV. It is presumed that this case was related to the immunosuppressive therapy for UC and was associated with the gains of 1q, 3p, and 8p.
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PMID:Development of hepatocellular carcinoma following treatment with 6-mercaptopurine for ulcerative colitis: investigation of chromosomal aberration by comparative genomic hybridization. 1613 76

Immunosuppression is currently the treatment of choice for severe inflammatory bowel disease (IBD). Thus, it was anticipated that the course of preexisting IBD should improve after orthotopic liver transplantation (OLT). Despite sufficient allograft immunosuppressive therapy, however, exacerbation of IBD or the development of de novo IBD after OLT were described in some cases, primarily in patients transplanted for end-stage primary sclerosing cholangitis (PSC). In addition, the development of de novo IBD in patients undergoing OLT for indications other than PSC was described. Evaluating our collective of 314 liver transplanted patients we found five patients transplanted for various indications other than PSC (autoimmune hepatitis [AIH], acute-on-chronic hepatitis B, Wilson's disease, and cryptogenic cirrhosis) who developed de novo IBD after OLT despite sufficient immunosuppressive therapy with tacrolimus or cyclosporine. PSC was widely excluded in these patients by clinical and histological examinations and there was no sign of an enteric infection. It was remarkable that all patients were suspected to have an autoimmune background. Four of our patients were women and almost all patients showed histologically typical signs of an ulcerative colitis (UC). To prevent allograft rejection, three of five patients were treated with cyclosporine and the other two with tacrolimus. After diagnosis, treatment with aminosalicylates and corticosteroids led to complete clinical and histological remission. However, relapses occurred frequently after termination of specific therapy. In combination with previous reports, our cases indicate an immune dysregulation leading to the development of de novo IBD after OLT under immunosuppressive therapy. Reviewing the literature, it should be considered that apart from the autoimmune background, immunosuppressive therapy may itself play a major role in the development of de novo IBD. From the clinical point of view, it is of critical importance to detect this phenomenon, since diarrhea is an important cause of morbidity and mortality in transplanted patients and therapy for this disorder completely differs from the treatment for other causes of diarrhea. Aminosalicylates and courses of corticosteroids offer an effective treatment.
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PMID:Five cases of de novo inflammatory bowel disease after orthotopic liver transplantation. 1679 37

Postinfantile giant cell hepatitis (PGCH) is rare. It is characterized by the presence of multinucleated giant cells in liver biopsy, and although it has been associated with several etiological agents, in many cases its etiology remains unclear. The case is presented herein of an adult woman with PGCH in the setting of ulcerative colitis and autoimmune hepatitis. The presence of autoimmune hepatitis in the patient is consistent and supports the autoimmune pathogenesis of PGCH in a subgroup of patients. Furthermore, this finding, along with others, suggests that PGCH may be included in the list of hepatic complications of inflammatory bowel disease.
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PMID:Postinfantile giant-cell hepatitis associated with ulcerative colitis and autoimmune hepatitis. 1707 32

We aimed to investigate the frequency of rheumatic diseases in patients suffering from autoimmune thyroid diseases (ATD). Sixty-five patients (56 F, 9 M), who were followed by diagnosis of ATD, were questioned and examined for the presence of rheumatic disease. Basic laboratory tests and antithyroid antibodies, antinuclear antibody and rheumatoid factor (RF) levels were also measured by appropriate methods. Various rheumatic diseases were detected in 40 (62%) of patients with ATD. The most frequent rheumatic conditions were fibromyalgia, recurrent aphthous stomatitis, osteoarthritis, keratoconjunctivitis sicca and xerostomia and carpal tunnel syndrome which were detected in 20 (31%), 13 (20%), 10 (15%), 9 (14%) and 8 (12%) of patients, respectively. Autoimmune diseases, except Sjogren's syndrome, which were detected in ten patients with ATD, are as follows-vitiligo: two; autoimmune hepatitis: two; oral lichen planus: one, ulcerative colitis: one, inflammatory arthritis in four patients (two of them had rheumatoid arthritis, one had psoriasis and psoriatic arthritis and one had mixed collagen tissue disease). RF was positive in two patients, one of them had rheumatoid arthritis and FANA was positive in six (9%) patients; all of them had hypothyroidism. The frequency of rheumatic diseases seems to be higher in patients suffering from ATD. Initial evaluation and a regular checking for rheumatic diseases in patients suffering from ATD were recommended.
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PMID:Frequency of rheumatic diseases in patients with autoimmune thyroid disease. 1710 43


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