Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunosuppressive treatment with prednisolone and/or azathioprine has been assessed in three chronic liver diseases with immunological features, namely chronic active hepatitis, cryptogenic cirrhosis and primary biliary cirrhosis. In chronic active hepatitis, controlled prospective clinical trials have shown clinical, biochemical and hepatic histological improvement when prednisolone with or without azathioprine is employed. Azathioprine alone has no advantage over placebo tablets. Cirrhosis is probably not prevented. Selection of patients for treatment, the response and therapeutic regimes are discussed. Patients with hepatitis B surface antigen positive chronic active hepatitis have a worse therapeutic response than those patients with chronic active hepatitis who are HBsAg negative. In primary biliary cirrhosis, corticosteroid treatment is contra-indicated on account of bone thinning. Azathioprine has been used in controlled clinical trials and is of only marginal benefit.
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PMID:Immunosuppressive therapy in chronic liver disease. 71 60

Thirty-two autopsied cases of progressive neuronal degeneration of childhood with liver disease are reviewed. The typical clinical course is intractable seizures and liver failure following a period of developmental delay and failure to thrive in early infancy, but some children first present with seizures. Characteristic changes on the electroencephalogram, loss of visual-evoked potentials, occipital atrophy on computed tomographic scan, and particular changes on liver biopsy may assist diagnosis. Most patients succumb in less than 3 years, but some have a protracted survival into their teens, and very rarely they may present in early adulthood. Liver pathology comprises fatty change, hepatocyte loss, bile duct proliferation, fibrosis, and often cirrhosis. Gradual progression can be followed in sequential biopsies. Macroscopically, the cerebral cortex is variably involved, but usually there is patchy thinning and discoloration, with a striking predilection for the striate cortex. Microscopic changes include spongiosis, neuronal loss, and astrocytosis, which progresses down through the cortical layers. All areas may be affected but the calcarine cortex is usually most affected. Etiology is still obscure, though mitochondrial and slow viral disorders have been postulated.
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PMID:Progressive neuronal degeneration of childhood with liver disease (Alpers-Huttenlocher syndrome): a personal review. 224 81

Bone thinning causing both fractures and severe pain not associated with fractures has been recognized in patients with chronic liver diseases. The patients most commonly affected are those with primary or secondary biliary cirrhosis, but those with alcoholic liver disease and cirrhosis after active chronic hepatitis may also be involved. Chronic liver disease has also been recognized as an important cause of osteoporosis in both sexes, with the mechanism thought to be a combination of calcium and/or vitamin D. The 9.1% patients with chronic active hepatitis accompanied with osteodystrophy. But 50% cirrhotic patients accompanied with osteodystrophy. Bone densitometry was determined by Digital Image Processing Method (Osteodystrophy < mean-2SD: age- and sex-matched normal value). Serum levels of osteocalcin (BGP) and parathyroid hormone (PTH) in patients of hepatic cirrhosis without osteodystrophy were lower than those with osteodystrophy. These results were suggested that hepatic osteodystrophy was rapidly turnover osteodystrophy. To function physiologically, vitamin D must be hydroxylation in liver to 25-(OH)-D and subsequently by the kidney to 1 alfa, 25-(OH)2-D. Osteodystrophy associated with hepatic cirrhosis is due to a defect in the 1 alfa-hydroxylation by the kidney rather than a hepatic hydroxylation defect. 1 alfa OH-D3 is very useful for treatment for hepatic osteodystrophy.
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PMID:[Hepatic osteodystrophy]. 964 89

Bleeding from gastroesophageal varices is a frequent and often deadly complication of cirrhosis. The key factor in the natural history of esophageal varices is increased portal pressure, which in cirrhosis is due to the combination of increased hepatic vascular resistance and increased portal collateral blood flow. The maintenance and aggravation of this situation leads to the progressive dilation of the varices and thinning of the variceal wall, until the tension exerted by the variceal wall exceeds the elastic limit of the vessel, leading to variceal hemorrhage. Mortality from a variceal bleeding episode has decreased in the last two decades from 40% to 20% due to the implementation of effective treatments and improvement in the general medical care. Initial treatment should include adequate fluid resuscitation and transfusion to maintain the hematocrit at 25% to 30%, and prophylactic antibiotics (norfloxacin or amoxicillin-clavulanic acid). It is currently recommended that a vasoactive drug be started at the time of admission. Drug therapy may be started during transferal to hospital by medical or paramedical personnel and maintained for up to five days to prevent early rebleeding. Terlipressin, a vasopressin derivative, is the preferred agent because of its safety profile and proven efficacy in improving survival. Somatostatin is as effective as terlipressin, but may require higher than the usually recommended dosage. Octreotide is effective in conjunction with endoscopic therapy, but is the second choice because it has not been shown to reduce mortality. Vasopressin may be used where terlipressin is not available, but should be given in combination with transdermal nitroglycerin. Endoscopic elastic band ligation is the recommended endoscopic treatment, but injection sclerotherapy is still employed in many centres for active variceal bleeding. Failures of medical therapy (drugs plus endoscopic therapy) should undergo a second course of endoscopic therapy before proceeding to transjugular intrahepatic portosystemic shunt or, in rare occasions, to portosystemic shunt surgery. Administration of recombinant activated factor VII may decrease the number of treatment failures among patients with advanced liver failure (Child-Pugh class B and C).
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PMID:Medical management of variceal bleeding in patients with cirrhosis. 1499 22

Regression of hepatic cirrhosis is a controversial issue. Recently, a list of histopathological features, observed in human material, was suggested as a hallmark of cirrhosis in the process of regression. An investigation for the presence of these morphologic features was performed at monthly intervals in rats with proved carbon tetrachloride (CCl4)-induced cirrhosis over a period of 9 months following discontinuation of treatment, using sequential liver biopsies. Within the first 4 months, features of the "hepatic repair complex" were identified, together with the enlargement of the hepatic nodules and thinning of the fibrous septa. Subsequent to the 4 months, the histological picture, composed of large and inconspicuous nodules and delimited by thin and frequently incomplete fibrous septa "incomplete septal cirrhosis", appeared to be stabilized. These fibrous septa, when injected with India ink from the portal trunk, presented blood vessels that were seen to drain directly into the sinusoids. These findings suggested that when the cause of cirrhosis is removed, the liver may adapt itself to a new and permanent structure, probably compatible with normal or near-normal function, which may render hepatic cirrhosis clinically, although not morphologically, reversible.
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PMID:Morphological signs of cirrhosis regression. Experimental observations on carbon tetrachloride-induced liver cirrhosis of rats. 1613 51

Atherosclerosis is a complex inflammatory disease comprising multiple plaque phenotypes. The development of advanced atheromatous plaques with necrotic core represents the result of the invasion of lipid pools by macrophages. The release of activated proteolytic enzymes degrades the surrounding tissue and contributes to the formation of vulnerable plaque. Thinning of the fibrous cap and necrotic core expansion are considered to be critical for the progression toward plaque rupture and acute thrombosis. The pathogenic mechanisms leading the progression of atherosclerotic lesions are various and involve endothelial cells, inflammatory cells, and platelets. Nonalcoholic fatty liver disease (NAFLD) includes a spectrum of diseases ranging from simple fatty liver to nonalcoholic steatohepatitis (NASH) and may progress to cirrhosis and hepatocellular carcinoma. The prevalence of this pathology is quite high in the general population and is one of the most important causes of liver-related morbidity and mortality in children. NAFLD is considered the hepatic feature of the metabolic syndrome and this has stimulated interest in its possible role in the atherosclerosis development. Clinical observations indicated that NAFLD might be an independent risk factor for coronary artery disease. Moreover, NASH may increase atherosclerotic and cardiovascular risks by local overexpression of inflammatory mediators, endothelial damage, and regulators of blood pressure. NASH development is correlated with hepatic progenitor cell activation and the release of proatherogenic adipokines. These aspects suggest the necessity for an early therapeutic intervention in NASH patients, not only for ameliorating the liver injury, but also for improving the systemic proatherogenic state.
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PMID:Nonalcoholic fatty liver disease and atherosclerosis. 2307 71