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

Portal or/and mesenteric vein thrombosis is a rare condition with high mortality in an acute form. Therapy of thrombosis is not well defined, although there are some general guidelines that differ according to disease onset and clinical presentation. In acute thrombosis with bowel infarction, surgical resection with possible thrombolysis is advised. The best therapy for the subacute form is not known and the approach differs between centers. For chronic disease, prolonged anticoagulant therapy is recommended. Thrombolysis is well recognized in the treatment of acute ischemic coronary or cerebral diseases. Success of treatment is better if therapy is introduced within a few hours after symptoms have begun. We describe a 25-year-old patient with the subacute form of extensive portal, mesenteric and ileocolic vein thrombosis in the setting of underlying liver cirrhosis due to autoimmune disease. An aggressive therapeutic approach is advised, especially in patients who will eventually undergo liver transplantation, since portal and/or mesenteric vein thrombosis is relative contraindication for liver transplantation in the majority of transplant centers.
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PMID:Treatment of extensive subacute portal, mesenteric and ileocolic vein thrombosis with recombinant tissue plasminogen activator. 1776 37

Cryptococcus neoformans usually causes disease in patients with human immunodeficiency virus (HIV) infection. This descriptive study was based on a retrospective review of 33 HIV-uninfected patients with disseminated cryptococcosis from 1998 to 2005. An underlying condition associated with immunocompromise was documented in 30 patients (90.9%), including liver cirrhosis (36.4%), diabetes mellitus (33.3%) and autoimmune disease (27.3%). Disseminated cryptococcosis carried a high mortality rate in this series, reaching 63% overall, with a median survival of 21 days. All patients (12/12) with liver cirrhosis died within the first month after the diagnosis of cryptococcosis. Otherwise, high Acute Physiology and Chronic Health Evaluation II (APACHE II) score, female gender and smoking history were associated with worse one-month outcome.
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PMID:Disseminated cryptococcosis in HIV-uninfected patients. 1815 78

Angiogenesis, the development of new blood vessels from the existing vasculature, is essential in normal developmental processes. Uncontrolled angiogenesis is a major contributor to a number of disease states such as inflammatory disorders, obesity, asthma, diabetes, cirrhosis, multiple sclerosis, endometriosis, AIDS, bacterial infections and autoimmune disease. It is also considered a key step in tumour growth, invasion, and metastasis. Angiogenesis is required for proper nourishment and removal of metabolic wastes from tumour sites. Therefore, modulation of angiogenesis is considered as therapeutic strategies of great importance for human health. Numerous bioactive plant compounds are recently tested for their antiangiogenic potential. Among the most frequently studied are polyphenols present in fruits and vegetables. Plant polyphenols inhibit angiogenesis and metastasis through regulation of multiple signalling pathways. Specifically, flavonoids and chalcones regulate expression of VEGF, matrix metalloproteinases (MMPs), EGFR and inhibit NFkappaB, PI3-K/Akt, ERK1/2 signalling pathways, thereby causing strong antiangiogenic effects. This review focuses on the antiangiogenic properties of flavonoids and chalcones and examines underlying mechanisms.
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PMID:Antiangiogenic effects of flavonoids and chalcones. 1838 17

Giant cell hepatitis is a frequent reaction of the liver to different injuries in newborns and in childhood, but rare in adults. This form of hepatitis is often accompanied by cholestasis and shows fast progression to cirrhosis. In most cases autoimmune, metabolic, toxic or viral origin can be found, but sometimes the etiology remains hidden. This paper introduces two adult giant cell hepatitis cases. Hepatitis C virus infection was the possible origin in the first case and autoimmune disease in the other one.
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PMID:Giant cell hepatitis in adults. 1847 Jul 33

Primary biliary cirrhosis (PBC) is an autoimmune disease of the liver characterized by progressive bile duct destruction eventually leading to cirrhosis and liver failure. The serological hallmark of the disease is the presence of circulating antimitochondrial antibodies (AMA). These reflect the presence of autoreactive T and B cells to the culprit antigens, the E2 subunits of mitochondrial 2-oxo-acid dehydrogenase enzymes, chiefly pyruvate dehydrogenase (PDC-E2). The disease results from a combination of genetic and environmental risk factors. Genetic predisposition is indicated by the higher familial incidence of the disease particularly among siblings and the high concordance rate among monozygotic twins. Environmental triggering events appear crucial to disrupt a pre-existing unstable immune tolerance of genetic origin allowing, after a long latency, the emergence of clinical disease. Initiating mimetopes of the vulnerable epitope of the PDC-E2 autoantigen can be derived from microbes that utilize the PDC enzyme or, alternatively, environmental xenobiotics/chemical compounds that modify the structure of native proteins to make them immunogenic. A further alternative as a source of antigen is PDC-E2 derived from apoptotic cells. In the effector phase the biliary ductular cell, by reason of its proclivity to express the antigen PDC-E2 in the course of apoptosis, undergoes a multilineage immune attack comprised of CD4(+) and CD8(+) T cells and antibody. In this article, we critically review the available evidence on etiopathogenesis of PBC and present interpretations of complex data, new developments and theories, and nominate directions for future research.
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PMID:Etiopathogenesis of primary biliary cirrhosis. 1852 30

Chronic hepatitis C virus (HCV) infection is a worldwide public health problem with a global prevalence of 2-3%. It is believed that about 170 million people are currently infected (about 3% of the world's population), and a further 3-4 million are infected each year. HCV is the main reason for liver transplantation in the developed world, and the main cause of liver-related morbidity and mortality in a number of countries, including Italy. It is not only a frequent cause of chronic liver diseases such as hepatitis, cirrhosis and hepatocellular carcinoma, but is also involved in the pathogenesis of various autoimmune and rheumatic disorders (arthritis, vasculitis, sicca syndrome, porphyria cutanea tarda, lichen planus, nephropathies, thyroid diseases, and lung fibrosis), as well as in the development of B-cell lymphoproliferative diseases. Furthermore, patients suffering from C hepatitis tend to produce rheumatoid factor, cryoglobulins and a large series of autoantibodies (ANA, anti-SSA/SSB, SAM, ATG, aCL). The use of glucocorticoids or immuno-suppressant agents in HCV infected individuals, which are needed to treat autoimmune and rheumatic disorders, leads to a risk of worsening the clinical outcome of HCV. Under these conditions, the viral infection often needs to be treated with antiviral agents, mainly pegylated interferon combined with ribavirin. However, cyclosporine A seems to be safe and effective in patients with autoimmune disease (AD) and concomitant chronic HCV infection as is documented by the reduction in viremia and transaminases, particularly in patients with high baseline levels. Finally, HCV is the main trigger of mixed cryoglobulinemia. An attempt at viral eradication is therefore indicated in most patients, and is particularly effective in the case of mild or moderate manifestations. In severe cases, rituximab is an apparently safe and effective alternative to conventional immunosuppression and, specifically, it controls B-cell proliferation.
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PMID:HCV infection: pathogenesis, clinical manifestations and therapy. 1857 Jul 53

The liver plays an important role in the disposition of copper. Most dietary copper passes through the liver where it can be used for protein and energy production or excreted through the biliary route. Because copper is a prooxidant, its intracellular handling is tightly managed. In Wilson disease, in which synthesis of ceruloplasmin and biliary excretion of copper are defective, copper accumulates in the liver and leads to progressive liver damage. The features of hepatic Wilson disease are highly variable. The spectrum of liver disease includes mild inflammation, fatty liver, an autoimmune disorder, and cirrhosis. Wilson disease thus resembles drug hepatotoxicity, and indeed it can be regarded as a prototypic example of endogenous hepatotoxicity. Biomarkers developed for detecting drug hepatotoxicity may be relevant to Wilson disease. Biomarkers developed through metalloproteomics, which for copper seeks to define a set of proteins that have copper-binding capacity, or through genomic studies may also be relevant to Wilson disease and other disorders of copper handling, whether copper is deficient or overloaded.
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PMID:Liver as a key organ in the supply, storage, and excretion of copper. 1877 7

CD96, previously named T cell activation increased late expression (Tactile), is a transmembrane molecule that functions as an activated receptor on natural killer cells. It is well known that many transmembrane molecules have soluble forms, which were either shed from the cell surface or spliced at mRNA level. In many cases, the levels of soluble forms in the circulation could be used as biomarkers of lymphocyte activation in bacterial or virus infection, tumour, transplantation and autoimmune disease. To investigate whether CD96 could be released into the sera and the possible biological function of soluble hCD96 (sCD96), we generated and characterized five clones of anti-hCD96 mouse monoclonal antibodies (mAb) and developed a sandwich enzyme-linked immunosorbent assay (ELISA) system based on two anti-hCD96 mAbs with different epitope specificities. Using this ELISA system, sCD96 in serum samples from 99 healthy individuals could be detected. Furthermore, we found that the level of sCD96 in serum samples from patients with chronic viral hepatitis B or classes B and C of hepatic cirrhosis classified using the Child-Pugh score was much higher (P < 0.001 versus healthy individuals; P = 0.006 versus healthy individuals respectively) than that from healthy individuals (0.98 ng/ml). Our study demonstrates for the first time that sCD96 existed in sera, and suggests that sCD96 may be used as a serous marker for some diseases such as chronic viral hepatitis B infection or hepatic cirrhosis in classes B and C. The level of sCD96 in patients' serum may have some relationship with a chronic inflammatory reaction.
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PMID:Establishment of an enzyme-linked immunosorbent assay system for determining soluble CD96 and its application in the measurement of sCD96 in patients with viral hepatitis B and hepatic cirrhosis. 1904 Jun 4

A 66-year-old female presented with acute illness of severe hepatic dysfunction. She had a past history of chronic hepatitis of low disease activity. After admission and clinical investigation including liver biopsy, it showed an underlying chronic liver disease suggestive of autoimmune hepatitis (AIH) with early liver cirrhosis. Together with other clinical features, this patient was diagnosed as definite AIH type 1 by using the IAIHG (International Autoimmune Hepatitis Group) criteria. During this episode, superinfection by Epstein-Barr virus (EBV) was evidenced by positive PCR (polymerase chain reaction) test, and serial changes of EBV VCA IgM and IgG tests. Severe hepatic impairment was evidenced by markedly elevated AST level 3090 IU/L, high bilirubin level 26.4 mg/dL, and presence of ascites. The patient gradually recovered and liver function improved in agreement with the decline of EBV VCA titers. Immunosuppressive therapy resulted in further improvement of the aminotransferases levels. This is an unusual case of EBV superinfection on pre-existing AIH with early cirrhosis, which caused enhancement of the autoimmune disease process and resulted in severe hepatic decompensation and jaundice. We herein describe the case and briefly review the literature.
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PMID:Chronic autoimmune hepatitis with Epstein-Barr virus superinfection: a case report and review of literature. 1910 93

Reactivation of hepatitis B refers to the abrupt increase in hepatitis B virus (HBV) replication in a patient with inactive or resolved hepatitis B. Reactivation can occur spontaneously, but more typically is triggered by immunosuppressive therapy of cancer, autoimmune disease, or organ transplantation. Reactivation can be transient and clinically silent, but often causes a flare of disease that can be severe resulting in acute hepatic failure. Most instances of reactivation resolve spontaneously, but if immune suppression is continued, re-establishment of chronic hepatitis occurs which can lead to progressive liver injury and cirrhosis. The best-described instances of reactivation occur in hepatitis B surface antigen (HBsAg) carriers with inactive or minimally active disease who are given cancer chemotherapy for lymphoma or leukemia. Typically, serum HBV DNA rises during chemotherapy, followed by a disease flare and HBV DNA clearance with immune reconstitution after chemotherapy is stopped. Special forms of reactivation occur after solid organ and bone marrow transplantation in which chronic infection often results. Several randomized, placebo-controlled trials have shown that reactivation can be prevented by antiviral prophylaxis. Routine prophylaxis is therefore recommended for persons with HBsAg undergoing cancer chemotherapy or transplantation, but major questions remain. Which patients should be screened for HBsAg and should all be treated? Which antiviral should be used and for how long? Should persons with resolved hepatitis B without HBsAg receive prophylaxis? Future research should address the underlying molecular mechanisms of reactivation as well as its optimal means of diagnosis, treatment, and prevention in different patient populations.
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PMID:Reactivation of hepatitis B. 1939 3


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