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)

During childhood, many people acquire primary infection with cytomegalovirus (CMV), one of the herpes viruses. If they later become immunosuppressed, such as occurs with human immunodeficiency virus (HIV) infection, CMV is likely to become reactivated. Severe disease caused by CMV is life-threatening in the HIV-infected population. CMV retinitis, gastritis, colitis, pneumonia, encephalitis and hepatitis have all been reported, but oral lesions due to infection with CMV are rarely reported. We report a case of oral CMV infection which at first was clinically indistinguishable from HIV-associated periodontal disease.
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PMID:Cytomegalovirus infection presenting as acute periodontal infection in a patient infected with the human immunodeficiency virus. 838 96

We describe three patients with advanced human immunodeficiency virus (HIV) infection, two with colitis and one with cholestatic hepatitis, for whom results of detailed endoscopic and histologic studies were suggestive of invasive spirochetosis. In the two patients with colitis, colonoscopic evaluation revealed either diffuse ulcerations or pustules; in both cases, there was histologic evidence of extensive superficial cell necrosis and infiltration of the mucosa and lamina propria with acute inflammatory cells. Spirochetes in the mucosa and crypts were visualized by Warthin-Starry silver staining. Morphologically similar spirochetes throughout the liver specimen from the patient with cholestatic hepatitis were demonstrated by Warthin-Starry silver staining. Analysis with electron microscopy revealed these organisms to be loosely coiled spirochetes. Despite extensive evaluation, no other pathogens were identified. Invasive spirochetal infection, as defined by the results of Warthin-Starry silver staining of involved tissues, should be considered in the differential diagnosis of patients with HIV infection who have otherwise unexplained colitis or cholestatic hepatitis.
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PMID:Invasive colitis and hepatitis due to previously uncharacterized spirochetes in patients with advanced human immunodeficiency virus infection. 858 36

Large bowel disease detected clinically by rectal prolapse was studied in 64 immunodeficient mice (37 athymic NCr-nu/nu, 12 BALB/c AnNCr-nu/nu, 9 C57BL/6NCr-nu/nu, and 6 C.B17/Icr-scid/NCr) naturally infected with Helicobacter hepaticus. Rectal prolapse was found in approximately 5% of immunodeficient mice maintained in a research facility over a period of 3.5 years. All mice had various degrees of chronic proliferative typhlitis, colitis, and proctitis, usually without concomitant hepatitis. Some mice had severe proliferative proctitis with cystic hyperplasia. Histologic study of the large bowel of 48 athymic NCr-nu/nu mice without H. hepaticus infection and housed in another clean facility revealed only 12% of the mice with minimal-to-mild large bowel inflammation. Helicobacter hepaticus infection is associated with large bowel disease in immunodeficient mice but is not seen in H. hepaticus-infected immunocompetent mice. This new pathogenic bacterial infection should be considered as another potential cause or co-factor for rectal prolapse and large bowel disease in mice.
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PMID:Inflammatory large bowel disease in immunodeficient mice naturally infected with Helicobacter hepaticus. 869 13

Tissues from a 9-year-old American Standardbred gelding with a history of anorexia, mild colic, and unexpected death were submitted to the Laboratories of Veterinary Diagnostic Medicine at the University of Illinois for histopathologic examination. Microscopic diagnoses were severe subacute, diffuse eosinophilic colitis with intralesional protozoa and a subacute to chronic eosinophilic portal hepatitis with granuloma formation. Two tissue-invading, ciliated protozoa were identified in large numbers within the colonic mucosa. The ciliates were Polymorphella ampulla and Cycloposthium sp., Phylum:Ciliophora. The eosinophilic colitis and portal hepatitis in association with the overpopulation and invasion by the ciliated protozoa suggests a causal etiology.
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PMID:Eosinophilic colitis and hepatitis in a horse with colonic intramucosal ciliated protozoa. 880 19

A 24-year-old male with Crohn's disease who developed three independent episodes of cholestatic liver disease over an eight-year period is described. The first episode was related to an idiosyncratic drug reaction while on sulfasalazine. The second episode, at the time of an exacerbation of his colitis, was characterized by moderate portal inflammation on liver biopsy and resolved quickly while he was on corticosteroid therapy. The most recent episode, occurring when the bowel disease was quiescent, was due to granulomatous hepatitis and resolved clinically with no specific therapy. Because numerous potentially serious hepatobiliary complications have been associated with inflammatory bowel disease, prompt and aggressive investigation in these instances is recommended.
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PMID:Cholestasis in Crohn's disease: a diagnostic challenge. 911 96

Cytomegalovirus(CMV) causes various inflammatory diseases such as encephalitis, interstitial pneumonitis (IP), retinitis, hepatitis, gastritis and colitis, and raises serious concern especially in immunocompromized patients such as AIDS patients and organ transplant recipients. In some instances such as retinitis, hepatitis, gastritis and colitis, the mechanism underlying the diseases in the direct viral replication. On the other hand, an immunopathological basis is implicated in CMV-associated IP (CMV-IP). The results of the experiments from the mouse model of CMV-IP suggested that the cytokines, such as IFN-gamma and TNF-alpha, and the cytokine-induced nitric oxide mediate CMV-IP. However, the reason how and why the CMV infection augments the production of the cytokines has been still unknown. In conclusion, it would be in mind that CMV-IP is not due to viral replication but due to the cytokines of the host's immune system. Therefore, the therapy against CMV-IP should target the cytokines, or the cytokine induced radicals.
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PMID:[The role of the host's immune system in the pathogenesis of cytomegalovirus-associated disease]. 946 72

We present here three paediatric patients with primary sclerosing cholangitis. In case 1, the serum gamma-glutamyl transpeptidase was decreased only temporarily by ursodeoxycholic acid (UDCA) treatment and 34 months later, sulphasalazine was added because of microscopic colitis. The enzyme level decreased with dual therapy. Similarly, in case 3, first diagnosed as autoimmune hepatitis, the transpeptidase levels remained elevated for 18 months during treatment with UDCA, prednisolone and mizoribin. The enzyme decreased only after a diagnosis of primary sclerosing cholangitis complicated with ulcerative colitis was established and sulphasalazine was introduced. Case 2 also had Crohn's colitis and was put on UDCA and sulphasalazine from the start. The enzyme level was normalized within 1 month and has remained normal for the following 5 years. Liver biopsies were analysed repeatedly in these three patients. In case 1, periductal fibrosis remained unchanged while being treated by UDCA. There appeared to be no progression in liver cirrhosis in case 3 while being treated by UDCA, prednisolone, and mizoribin. In case 2, who has been treated with both UDCA and sulphasalazine from the start, periductal fibrosis and portal fibrosis were remarkably improved 45 months later. We suggest that sulphasalazine in addition to UDCA might be a viable treatment for children with primary sclerosing cholangitis.
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PMID:Three paediatric cases of primary sclerosing cholangitis treated with ursodeoxycholic acid and sulphasalazine. 973 77

Hepatitis, proliferative typhlitis, and colitis were characterized in young adult and older SCID/NCr mice naturally infected with Helicobacter hepaticus. Liver lesions consisted of Kupffer, Ito, and oval cell hyperplasia along with multifocal to coalescing coagulative hepatocyte necrosis. Numerous Warthin-Starry-positive bacteria were observed in the parenchyma, and there were minimal to mild accumulations of monocytic cells and neutrophils. Proliferative typhlitis was characterized by moderate to marked mucosal epithelial cell hyperplasia with mild monocytic and neutrophilic infiltration. Minimal to mild colitis with mucosal epithelial cell hyperplasia of the colon was most marked in older mice. Comparable gastrointestinal lesions were not observed in uninfected control SCID/NCr mice. H. hepaticus was cultured from fetal viscera of 2 of 11 pups sampled late in gestation from infected SCID/NCr females, suggesting transplacental infection of H. hepaticus. As expected, most of the naturally infected SCID/NCr mice had no serum immunoglobulin G response against H. hepaticus. These findings contrast with those in infected immunocompetent A/JCr mice, which develop a significant immune response to H. hepaticus associated with prominent multifocal mononuclear cell infiltrates in the liver, with only rare bacteria observable at the periphery of inflammatory foci or in the biliary canaliculi. The results demonstrate that chronic inflammatory and proliferative lesions simultaneously affecting the liver, cecum, and colon are associated with natural infection of SCID/NCr mice with H. hepaticus and that lesions are progressive with age. Concurrent infection with H. hepaticus may confound studies that have been attributed to similar lesions due to other experimental manipulations of SCID/NCr mice.
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PMID:SCID/NCr mice naturally infected with Helicobacter hepaticus develop progressive hepatitis, proliferative typhlitis, and colitis. 978 60

Primary sclerosing cholangitis (PSC), a chronic inflammatory process affecting the extrahepatic and/or medium to large bile ducts, is not rare in children. It has features suggesting an autoimmune pathogenesis, although the mechanism of tissue damage remains unknown. The clinical presentation of childhood primary sclerosing cholangitis is highly variable and frequently without obvious features of cholestasis. Clinical similarity to autoimmune hepatitis is common. Association with chronic colitis is less common than in adults. Cholangiography is essential for the diagnosis and examination of the medium to large intrahepatic ducts is mandatory, as 40% of children lack extrahepatic duct involvement. Histological findings may help to distinguish childhood PSC from autoimmune hepatitis. In children, sclerosing cholangitis may also develop secondary to other disease processes, notably Langerhans histiocytosis, congenital immunodeficiencies and cystic fibrosis. Neonatal sclerosing cholangitis is chronic inflammatory disease of bile ducts which presents initially with neonatal cholestasis; its pathogenesis remains uncertain and may not be the same as for primary sclerosing cholangitis. Effective treatment modalities for childhood PSC remain undetermined. Liver transplantation is required for children who progress to biliary cirrhosis and hepatic decompensation.
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PMID:Primary sclerosing cholangitis in children. 1038 70

Two patients (a 48-year-old woman and a 62-year-old man) developed clinical and laboratory signs of hepatotoxicity due to troglitazone (Rezulin), a thiazolidinedione used in treatment of diabetes mellitus. There was no clear clinical evidence of drug allergy, although the woman experienced colitis before the onset of recognized hepatotoxicity. Liver biopsies showed bridging necrosis and fibrosis in the woman and hepatitis with granuloma formation in the man. The abnormalities in liver chemistries resolved promptly upon cessation of the drug. Cases involving 46 patients reported to the United States Food and Drug Administration are also reviewed. Troglitazone is a useful new oral antihyperglycemic agent, but in about 1.9% of patients hepatotoxicity has occurred, which may be severe and even fatal. Frequent monitoring of serum liver chemistries in patients taking the drug is essential.
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PMID:Hepatotoxicity due to troglitazone: report of two cases and review of adverse events reported to the United States Food and Drug Administration. 1063 96


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