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)

Intolerance of gluten, resposible for Coeliac disease, is essentially shown by an auto-immune enteropathy, even if the cutaneous manifestation (herpetiform dermatitis) and perhaps certain neurological signs (cerebral syndrome, peripheral neuropathy) may be independent as well as associated with the intestinal illness. This affection is of immunological nature, occuring in a genetic field that predisposes to the illness (familial form: concordance of 70% in homozygote twins; 90% of patients show an HLA molecule of type DQ2, DQ8 in almost all the other cases. The exogenous factor is the gluten content contained in wheat, rye and barley, more precisely by the intermediary "the prolamines" which are the "reactive" element that induces a the same time an inflammatory reaction of type TH11 locally (expressed by the histological aspect of a duodenal biopsy evolving as villous atrophy) and a humoral response with production of anti-gliadine and anti-transglutaminase antibodies (the role of the latter enzyme is intervention in the local transformation of antigens to make them antigenic). It is an illness of adults as well as children and this point must now be emphasized. Recent epidemiological studies insist on a high prevalence (1/300 in Europe). Clinical expression, at the start very polymorphic and so misleading, before the appearance of the more classical signs of malabsorption and development, always feared, towards a lymphoma. These signs are haematological (anemia of various types, hyper platelets by hyposplenism, haemorrhagic signs) cutaneous (herpetiform dermatitis, cutaneous vasculitis) mucosal (aphtose), hepatic (cytolysis), neurophysical (fatigue, troubles of behaviour, cerebral syndrome, neuropathy) and osteo-articulitis (osteopenia, arthralgias, diffuse pains). The association of certain auto-immune illnesses must be emphasized (diabetes, Hashimoto thyroiditis, Gougerot disease, primitive biliary cirrhosis). To think early of the possibility of intolerance to gluten, is to give the means of a very easy diagnosis (measurement of anti-gliadin, anti-endomysium and anti-transglutaminase, and secondarily duodenal biopsy if necessary), and it is early elimination of gluten food which will make the various clinical manifestations disappear and so prevent the risk of evolution to a tumoral pathology.
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PMID:[A great imitator for the allergologist: intolerance to gluten]. 1513 80

Fatigue is a symptom of liver disease. Indirect evidence suggests that this type of fatigue is centrally mediated. Non-alcoholic steatohepatitis (NASH), which may lead to cirrhosis, is associated with insulin resistance. An activated hypothalamic pituitary adrenal axis results in increased secretion of cortisol releasing hormone, cortisol and catecholamines. Prolonged exposure to high levels of cortisol is associated with insulin resistance, as exemplified by the metabolic syndrome. Accumulation in visceral fat is an independent factor associated with insulin resistance. Central (visceral) fat is less sensitive to insulin than the rest of body fat and the central nervous system and not peripheral insulin, appears to regulate lipolysis in visceral fat by, at least in part, adrenergic mechanisms. Aerobic training has documented beneficial effects on mental health and fatigue secondary to chronic illness. In addition, aerobic training increases insulin sensitivity. Thus, aerobic training may decrease fatigue in liver disease and improve NASH.
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PMID:Aerobic exercise: a potential therapeutic intervention for patients with liver disease. 1514 52

We report a case of fatal liver failure due to reactivation of lamivudine-resistant HBV. A 53-year-old man was followed since 1998 for HBV-related chronic hepatitis. Serum HBV-DNA was 150 MEq/mL (branched DNA signal amplification assay) and ALT levels fluctuated between 50-200 IU/L with no clinical signs of liver cirrhosis. Lamivudine (100 mg/d) was started in May 2001 and serum HBV-DNA subsequently decreased below undetectable levels. In May 2002, serum HBV-DNA had increased to 410 MEq/mL, along with ALT flare (226 IU/L). The YMDD motif in the DNA polymerase gene had been replaced by YIDD. Lamivudine was continued and ALT spontaneously decreased to the former levels. On Oct 3 the patient presenting with general fatigue, nausea and jaundice was admitted to our hospital. The laboratory data revealed HBV reactivation and liver failure (ALT: 1828 IU/L, total bilirubin: 10 mg/dL, and prothrombin INR: 3.24). For religious reasons, the patient and his family refused blood transfusion, plasma exchange and liver transplantation. The patient died 10 d after admission. The autopsy revealed remarkable liver atrophy.
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PMID:Fatal liver failure due to reactivation of lamivudine-resistant HBV mutant. 1516 53

An extrahepatic portosystemic shunt that has neither liver cirrhosis nor portal hypertension is rare. A 60-year-old Japanese woman who had been suffering chronic liver disease and anemia with mild disorientation was admitted to investigate general fatigue with dizziness and disorientation. The laboratory data revealed mild pancytopenia and liver dysfunction including hyperammoniemia, an increased Indocyanine Green 15-min retention rate, and a decreased Fischer's ratio. Color Doppler ultrasonography, computed tomography, and arterial portography revealed an extrahepatic portosystemic shunt that extended tortuously from the superior mesenteric vein into the inferior vena cava, and decreased blood flow in the main portal vein. Judging from intraoperative measurement of portal pressure and intraoperative portography, shunt ligations were performed at both the efferent portion of shunt from the superior mesenteric vein and the afferent portion of the shunt into the inferior vena cava, and resection of the spleen was also performed. On the postoperative laboratory data, pancytopenia disappeared, and liver function improved. Postoperative abdominal imaging showed increased blood flow in the main portal vein and disappearance of the shunt vessel. Moreover, symptoms present before surgery also disappeared. In conclusion, surgical treatment of extrahepatic portosystemic shunts may result in better postoperative quality of life if it is performed in carefully selected patients.
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PMID:Surgical treatment for an extrahepatic portosystemic shunt: a case report. 1523 66

To test new treatment modalities, a pilot study with a novel noninvasive biophysical methodology (Delta-S DVD) that can artificially exert a "decrease of entropy" through the patented electromagnetic-driven delivery of "energy clusters" was designed. This process has been modulated and integrated by the body as a "self" source to support the energy-dependent functional stores, thus modifying reparative into regenerative mechanisms of liver parenchyma. Seven long-standing hepatitis C virus-positive (Child A-B) cirrhosis patients with overt symptoms and portal hypertension and failure or side effects of antiviral drug treatment underwent 40-min sessions of Delta-S DVD daily for six months and were followed up monthly. At the end of the first month, rapid improvement of symptoms and a decrease of portal hypertension were noted. At the end of treatment, all patients showed either a complete (80%) or a partial (20%) regression of fatigue (FISK score), peripheral edema, pruritus, and palmar erythema. As observed, despite having stopped beta-blockers, F1 esophageal varices disappeared (60%), whereas F2 decreased to F1. The Doppler ultrasound aspect of partial (40%) or total (20%) atrophy was either reduced (60%) or reverted to normal (20%), and the respiratory dynamics of the portal vein improved (80%) or normalized (20%), whereas gross scarring nodules disappeared in 40% of cases. These promising data pave the way for an innovative physiopathological approach with extensive clinical applications.
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PMID:Cirrhosis progression as a model of accelerated senescence: affecting the biological aging clock by a breakthrough biophysical methodology. 1524 89

While HCV was initially believed to uniformly cause liver inflammation with the consequence of liver cirrhosis in most of the infected patients, prospective studies have shown a much lower than expected rate of cirrhosis in patients infected for more than 20 years. However, a new problem associated with hepatitis C virus infection is emerging. This is the development of sometimes disabling fatigue. While many other viruses of the flaviviridae cause encephalitis, the most closely related virus to HCV in humans, the GB Virus C seems not to be associated with fatigue. Thus the mechanism for the development of fatigue in HCV infection seems specific for HCV. Delineating the mechanism will be a first step to develop treatment option for this currently untreatable impairment.
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PMID:Hepatitis C virus infection and the brain. 1555 27

The hepatitis C virus (HCV) infection is a worldwide disease that is characterized by a preferential chronic evolution with mild to severe liver disease, including cirrhosis and, in lesser proportion, hepatocarcinoma. Out of these complications, HCV is frequently reported to complicate extrahepatic manifestations. Among those associated to HCV infection with a high degree of certainty, mixed cryoglobulinemia and its complications (skin, neurological, renal, rheumatological involvement) are the most prevalent (50%) in HCV-infected patients. The other diseases include noncryoglobulinemic systemic vasculitis, splenic lymphoma with villous lymphocytes, fatigue, porphyria cutanea tarda, sicca syndrome, and autoantibodies production. The extrahepatic manifestations that share mild-degree certainty of association with HCV infection include B-cell non-Hodgkin lymphoma, autoimmune thrombocytopenia, pruritus, and type II diabetes mellitus. The other diseases such as autoimmune thyroiditis, lichen planus are more questionable for their eventual association with HCV and others (pulmonary fibrosis with or without polymyositis, progressive encephalomyelitis, Mooren's corneal ulcers, erythema nodosum, chronic polyradiculonevritis) are mostly case reports. Howerver, even in cases of tight association, the mechanisms through which HCV may promote or induce extrahepatic manifestations remain unclear and merit further investigations.
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PMID:Hepatitis C virus-associated extrahepatic manifestations: a review. 1555 28

Since the discovery of hepatitis C virus (HCV) in 1989, significant advances have been made in our understanding of this important viral pathogen. Children at risk for HCV infection include recipients of potentially contaminated blood products and organ transplants, and infants born to HCV-infected mothers. Chronic HCV infection is usually asymptomatic in children but active hepatitis, cirrhosis and hepatocellular carcinoma can occur. The development of treatment strategies for chronic hepatitis C in children has directly evolved from clinical trials in adults. Sustained virologic response, defined by undetectable HCV RNA in serum 24 wk after completion of treatment, occurs in approximately 36% of children treated with conventional interferon alone and in about 50% of those given conventional interferon in combination with ribavirin. Pegylated interferon-based treatment regimens are better than those based on conventional interferon in adults but little is known about pegylated interferon in children. Factors associated with a favorable response to antiviral therapy in children are similar to those in adults and include infection with HCV genotype 2 or 3 and low pretreatment serum HCV RNA levels. Treatment related adverse events in children include 'flu-like' syndrome, fatigue, anorexia, weight loss, depression, anemia, leukopenia and thrombocytopenia.
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PMID:Treatment of chronic hepatitis C in children. 1559 40

Primary sclerosing cholangitis (PSC) happens mainly in middle-aged men and is seldom diagnosed in children. Childhood PSC undergoing liver transplantation is rarely reported. Here we present a 12-year-old girl who was admitted with a 6-day history of fever, abdominal pain, fatigue, jaundice, and splenomegaly. Liver histological examination revealed the destroyed bile ducts and bridging fibrosis. Endoscopic retrograde cholangiopancreatography (ERCP) showed beaded appearance of right intrahepatic ducts and absent left intrahepatic ducts. PSC was diagnosed. Because of decompensated liver function, she received a living-related orthotopic liver transplantation (OLT). The post-transplantation course was uneventful during the 12-month follow-up. She experienced neither additional episode of cholangitis nor recurrence of liver cirrhosis after OLT.
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PMID:A child with primary sclerosing cholangitis successfully treated by liver transplantation. 1562 73

The term 'non-alcoholic fatty liver disease' (NAFLD) includes cases with steatosis alone and those with non-alcoholic steatohepatitis (NASH). Usually there are no signs or symptoms, sometimes fatigue or pain, and apart from hepatomegaly the condition is revealed by abnormal liver biochemistry or by abdominal ultrasound. Most cases are associated with overweight or diabetes. Liver enzymes are usually elevated, especially GGT, ASAT and ALAT. Other conditions, including alcohol abuse and autoimmune hepatitis, have to be excluded. The diagnosis of steatosis can be made with ultrasound or CT scan. A liver biopsy is often needed to exclude other disease and to assess inflammation and fibrosis. Cirrhosis can develop. NAFLD is usually caused by two 'hits': the 'first hit' is peripheral insulin resistance, causing steatosis. The 'second hit' is caused by reactive oxygen species, inducing vicious cycles leading to inflammation. Weight loss, metformin or thiazolidinediones can improve NAFLD by increasing insulin sensitivity. Radical scavengers such as vitamin E, betaine and perhaps also urodeoxycholic acid may improve the hepatitis component. Further studies on treatment are needed.
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PMID:Non-alcoholic fatty liver disease: a brief review. 1569 51


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