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)

Etanercept has recently been implicated in the induction of granulomatous reactions. We describe a patient with rheumatoid arthritis who developed granulomatous hepatitis after taking etanercept. Infectious and metabolic causes of liver disease had been excluded and the liver biopsy was not typical of sarcoidosis. Liver enzyme abnormalities improved after etanercept was discontinued. We suggest that etanercept was responsible for the development of granulomatous hepatitis. This has not been previously described and adds to the increasing reports of rare granulomatous reactions induced by etanercept therapy.
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PMID:Granulomatous hepatitis associated with etanercept therapy. 1900 62

109 patients with hemoblastosis (HB) were examined. Average age was 31.8 +/- 1.4 years in group of lymphogranulomatosis patients, and 44 +/- 5.3 years in group of acute leukemia patients. Group of 46 patients with clinical laboratory signs of hepatic lesion was marked out. Since features of portal blood flow (PBF) revealed at dopplerography did not depend on hepatitis aetiology, all patients with chronic hepatitis were analyzed in one group. These patients were examined clinicobiochemically: functional hepatic tests, markers of viral hepatitis B and C, ultrasonic abdominal scanning, PBF dopplerography, puncture biopsy of hepar. All patients had PBF disturbances such as decrease of portal vein blood flow, increase of venous drainage of hepar and spleen. The degree of disturbances intensity increased depending on degree of chronic hepatitis activity (the index of histological activity) and hepatic fibrosis stage. Thus, presence of chronic hepatitis in HB patients regardless of aetiology, is the factor aggravating patients' stage and corrupting PBF. PBF disturbances (decrease of arterial and venous inflow and increase of venous outflow) and development of fibrous changes apparently related with compression of vessels by connective tissue around central veins, inside of lobules and among of hepatic cells. Consequence of it is including anastomosises in blood flow which leads to redistribution of PBF and portal hypertension forming.
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PMID:[The stage of portal blood flow in patients with hemoblastosis combined with chronic hepatitis]. 1849 89

Anti-TNF agents are increasingly being used for a rapidly expanding number of rheumatic and systemic autoimmune diseases. As a result of this use, and of the longer follow-up periods of treatment, there are a growing number of reports of the development of autoimmune processes related to anti-TNF agents. The clinical characteristics, outcomes, and patterns of association with the different anti-TNF agents used in all reports of autoimmune diseases developing after TNF-targeted therapy, were analyzed through a baseline Medline search of articles published between January 1990 and May 2008 (www.biogeas.org). A total of 379 cases of autoimmune diseases secondary to TNF-targeted therapies were identified. The anti-TNF agents were administered for rheumatoid arthritis in more than 80% of cases. The use of anti-TNF agents has been associated with an increasing number of cases of autoimmune diseases, principally cutaneous vasculitis, lupus-like syndrome, systemic lupus erythematosus and interstitial lung disease. Other autoimmune diseases associated with TNF-targeted therapies have been recently described, e.g. sarcoidosis, antiphospholipid syndrome-related features, and autoimmune hepatitis or uveitis. Large, prospective, postmarketing studies are required to evaluate the risk of developing autoimmune diseases in patients receiving TNF-targeted therapies.
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PMID:Autoimmune diseases induced by TNF-targeted therapies. 1902 67

Common variable immunodeficiency is an important form of primary immunodeficiency disease. The most recognized histologic manifestation of common variable immunodeficiency is a paucity of plasma cells in gut biopsies. However, chronic inflammation can affect other organs including the liver. This study was designed to characterize the histologic findings in liver biopsies of individuals with common variable immunodeficiency. Thirteen liver biopsies from 10 patients were identified. The most common indication for biopsy was elevated liver enzymes, hepatomegaly, and/or splenomegaly. The biopsies typically showed mild portal and mild-to-moderate lobular chronic inflammation with minimal or absent interface activity. Plasma cells were absent in all cases. The biopsy specimens showed no fibrosis (n = 5) or mild portal fibrosis (n = 5). In 2 patients with follow-up biopsies, no fibrosis progression was identified. Four individuals showed small numbers of scattered portal and/or lobular granulomas, 3 of whom had diagnoses of coexistent sarcoidosis. Overall, the inflammatory changes in the biopsies were reminiscent of those seen in individuals with chronic inflammation of the gut, which can lead to translocation of intestinal luminal antigens to the liver and a mild hepatitis. Subsequent review of concurrent intestinal biopsies available in 7 individuals showed intestinal inflammation in 5 of 7 cases. In conclusion, liver biopsies in individuals with common variable immunodeficiency show mild portal and lobular inflammation with no or mild portal fibrosis. The etiology of the common variable immunodeficiency hepatitis remains unclear but, in some cases, may be secondary to mucosal inflammation in the gastrointestinal tract.
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PMID:Hepatitis in common variable immunodeficiency. 1908 66

Biological agents are increasingly used for a rapidly-expanding number of rheumatic and systemic autoimmune diseases, with a growing number of reports of the paradoxical induction of autoimmune processes, overwhelmingly associated with anti-TNF agents. In this review, we analyze the clinical characteristics and outcomes of autoimmune diseases developing after biological therapies through a baseline Medline search as one of the objectives of the BIOGEAS project, created by the Spanish Society of Internal Medicine. The latest update of our registry (15 July 2009) included more than 800 cases of autoimmune diseases secondary to biological therapies, including a wide variety of both systemic (lupus, vasculitis, sarcoidosis and antiphospholipid syndrome) and organ-specific (interstitial lung disease, uveitis, optic neuritis, peripheral neuropathies, multiple sclerosis and autoimmune hepatitis) autoimmune processes. The majority of cases appeared between one month and one year after initiation of the biological agent and complete resolution was observed in nearly 75% of cases after cessation of therapy. The induced autoimmune diseases with the poorest outcomes were interstitial lung disease, inflammatory ocular disease and central nervous system demyelinating diseases.
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PMID:Autoimmune diseases induced by biological agents: a double-edged sword? 1985 1

Many systemic diseases present with articular manifestations. An understanding of the clinical, laboratory and radiological features of these diseases can lead to early diagnosis and appropriate therapy. This article describes the articular presentation and management of four generalized disorders: idiopathic hemachromatosis; sarcoidosis; hepatitis-B virus-induced arthritis, and polymyositis-dermatomyositis induced arthritis.
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PMID:Articular manifestations of systemic diseases. 2128 70

Descriptive reports of liver histologic features in celiac disease (CD) are sparse, and the effect of a gluten-free diet (GFD) on the course of liver injury is poorly understood. We reviewed liver biopsy specimens in 30 patients with CD and performed immunostains for IgG, IgG4, IgM, and IgA. Subsequent liver biochemical tests and compliance with the GFD were recorded. Of the patients, 19 had autoimmune-mediated liver disease (AILD; autoimmune hepatitis, 9; primary sclerosing cholangitis, 7; and primary biliary cirrhosis, 3). The remaining 11 patients had cryptogenic hepatitis (5), hepatitis C (2), steatohepatitis (2), sarcoidosis (1), and T-cell lymphoma (1). The liver disease diagnosis preceded the CD diagnosis in all groups except steatohepatitis. Although 82% of patients without AILD had symptomatic CD, only 26% of patients with AILD had such symptoms. The pathology of the specific liver disease was not atypical in histologic features or IgG/IgM ratios. While GFD improved cryptogenic hepatitis, it did not seem to affect AILD. We propose that AILD and cryptogenic hepatitis in patients with CD represent distinct clinical, histologic, and immunohistochemical entities rather than 2 ends of a spectrum of liver injury.
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PMID:The liver in celiac disease: clinical manifestations, histologic features, and response to gluten-free diet in 30 patients. 2168 40

We surveyed histochemically detectable copper in various liver diseases with emphasis on chronic biliary disease (CBD) and venous outflow impairment. Using rhodanine, we graded copper accumulation in 298 liver specimens: venous outflow impairment (n = 64), CBD (n = 123), Wilson disease (WD) (n = 12), chronic hepatitis C (n = 32), steatohepatitis (n = 28), sarcoidosis (n = 15), cholestatic hepatitis (n = 12), and acute large bile duct obstruction (n = 12). Copper was detected in 39% of specimens; all had chronic liver disease. Copper increased with increasing fibrosis. CBD accumulated copper more frequently than other chronic diseases (except WD), both in early (61% vs 3%) and late (94% vs 59%) stages and in larger amounts. Rhodanine was positive in 73% of livers with CBD, 20% with sarcoidosis, 9% with chronic hepatitis C, and 7% with steatohepatitis. Copper was detected in 14% of chronic venous outflow impairment specimens; with 1 exception, stainable copper was absent in early stages but detected in 38% of cirrhotic livers. In conclusion, rhodanine helps differentiate CBD from other conditions, including venous outflow impairment; in the absence of advanced fibrosis, rhodanine positivity strongly favors CBD. In contrast, rhodanine positivity is nonspecific in cirrhosis, but the absence of copper in that setting excludes CBD.
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PMID:Revisiting the topic of histochemically detectable copper in various liver diseases with special focus on venous outflow impairment. 2327 Sep 2

Hepatic sarcoidosis is usually asymptomatic but rarely leads to adverse liver-related outcome. Co-existence of viral hepatitis and hepatic sarcoidosis is a rare, but recognised phenomenon. Obtaining a balance between immune suppression and anti-viral therapy may be problematic. Immunosuppression in the presence of viral hepatitis can lead to rapid deterioration of liver disease. Similarly, anti-viral therapy may exacerbate granulomatous hepatitis. Here we present two cases of viral hepatitis co-existing with sarcoidosis that illustrate successful management strategies. In one, hepatitis B replication was suppressed with oral anti-viral therapy before commencing prednisolone. In the second, remission of hepatic sarcoidosis was achieved with prednisolone, before treating hepatitis C and obtaining a sustained virological response with pegylated interferon and ribavirin therapy.
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PMID:Hepatic sarcoidosis complicating treatment-naive viral hepatitis. 2335 20

The paper is devoted to differential diagnostics of portal hypertension (PH) in view of frequent diagnostic mistakes (10-15%) associated with this pathology. PH syndrome is usually interpreted by practitioners as a clinical manifestation of liver cirrhosis even if it is not necessarily related to the involvement of this organ. In patients with hepatic pathology, PH is likely to develop not only in case of fibrotic transformation and false lobule formation but also in case of disturbed blood flow in the portal vein, e.g. when granulomatous lesion of parenchyma takes place. Pathophysiological mechanisms and clinical peculiarities of intra-, sub-, suprahepatic and mixed forms of this condition are discussed. Etiological factors leading to the development of PH syndrome are considered. An original observation is presented of a patient with generalized sarcoidosis and histologically confirmed thoracic lymph nodes, spleen, lungs, liver; moderate granulomatous hepatitis, septal fibrosis (Knodel histology activity index 1-1-3-3- (8 scores)), PH, grade 1 oesophageal varicosis, splenomegaly, splenorenal anastomoses. The involvement of liver in the pathological process did not exceed 20%. Clinical, laboratory and instrumental studies rarely reveal manifestations of these changes. The diagnosis is verified histologically (discovery of granulomas formed by epithelial and giant multinuclear cells without signs of caseous necrosis. The reported case is distinctive for the development of PH in association of multiple giant heatic granulomas preventing the normal blood flow.
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PMID:[Portal hypertension as a clinical manifestation of hepatic lesions in sarcoidosis]. 2351 59


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