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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite regular long-term parenteral vitamin D2 treatment, four patients with biliary cirrhosis had multiple symptoms of bone disease and bone biopsy specimens showed osteomalacia without osteoporosis. Three patients also had a proximal myopathy. Plasma calcium values (after correction for albumin), phosphorus, magnesium, and serum 25-hydroxy-vitamin D were within normal limits. Treatment with 1,25-dihydroxy-cholecalciferol (1,25-(OH)2D3) relieved symptoms in three of the four patients and improved those in the fourth. Histological examination of bone showed improvement in all four patients, but serum and urinary biochemical changes were not pronounced. We conclude that 1,25-(0H)2D3 treatment has a beneficial effect on bone and muscle in hepatic osteomalacia, either because vitamin D 1-hydroxylation fails in biliary cirrhosis or because hepatic osteomalacia is resistant to vitamin D2 metabolites.
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PMID:Parenteral 1,25-dihydroxycholecalciferol in hepatic osteomalacia. 62 Feb 4

The antioxidant status of alcoholic patients was assessed by direct measurement of the plasma antioxidants alpha-tocopherol and beta-carotene and of selenium as a marker of glutathione peroxidase. Overall, the alcoholic group showed significant decreases in the mean plasma values of beta-carotene, zinc and selenium when compared to the control subjects. When the patients were subdivided according to their liver histology, beta-carotene showed a progressive decrease in plasma concentration with increasing liver damage, whereas alpha-tocopherol levels were only depleted in the patients with cirrhosis. There were significant decreases in the plasma concentrations of both alpha-tocopherol and selenium in all patients with alcoholic skeletal muscle myopathy, whereas patients with normal muscle biopsies showed adequate antioxidant status. Such results support a role for free radical-mediated damage in end organ injury, particularly myopathy, in alcohol misusers.
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PMID:The antioxidant status of patients with either alcohol-induced liver damage or myopathy. 141 10

One hundred and fifty-one inpatients with a history of chronic heavy alcohol intake were examined for evidence of muscle disease. Ninety-two patients (60 per cent) had histologically abnormal biopsies of the quadriceps muscle. The most common abnormality, which was often severe, was type II muscle fibre atrophy. Seven patients (5 per cent) had histological evidence of acute myopathy, one of whom presented with the full clinical picture of acute rhabdomyolysis. Twenty-three patients had cirrhosis, 36 were significantly malnourished and 98 had evidence of a peripheral neuropathy. None of these features, however, were sufficient to account for the muscle abnormalities. There was no clear relationship between musculo-skeletal symptoms and muscle biopsy histology. Serum creatine kinase activity was elevated in only 23 subjects and was an insensitive indicator of subclinical acute myopathy and of chronic alcoholic myopathy. Follow-up studies after abstinence from alcohol invariably showed both objective and subjective improvement of muscle function - often in the absence of any clinical recovery from the peripheral neuropathy. Continued alcohol consumption was accompanied by persistence and often deterioration of muscle fibre atrophy. It is concluded that chronic skeletal myopathy is a frequent consequence of alcohol abuse and may result from a direct toxic effect of ethanol on muscle fibres.
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PMID:Alcoholic skeletal myopathy, a clinical and pathological study. 299 70

In the last years, considerable advances have been made in the study of the proteins and polypeptides of the cytoskeleton, and its three main components: microfilaments (MF), intermediate filaments (IMF) and microtubules (MT). The principal properties of these elements and those of many associated proteins are recalled. The actin MF are mainly involved in cell contractility, the IMF in cell shape, while the MT and their associated proteins are involved in intracellular transport. Some pathological modifications of the cytoskeleton will be considered. In the liver, accumulations of keratin result in the formation of Mallory's hyalin, found in several types of cirrhosis and hepatomas. In muscle, accumulations of desmin are observed in various myopathies. An accumulation of alpha-actinin at the Z bands characterizes nemalin myopathy. In several forms of hemolytic anemias, alterations of the membranous cytoskeletal components of the red blood cells--spectrin, ankyrin, actin--may explain their abnormal shape and excessive fragility. In the nervous system, many pathological conditions are related to abnormal cytoskeletal components. In Parkinson's disease, Lewy bodies are an accumulation of neurofilaments (IMF). In Alzheimer's disease, and some related conditions, the intraneuronal tangles are associated with modifications of MT and neurofilaments. The role of MT and in particular of the MT-associated protein tau, as demonstrated recently, confirms the involvement of the MT. The observed disturbances of MT-related axonal flow may explain some of the known functional changes in these forms of dementia.
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PMID:[Pathology of the cytoskeleton]. 329 78

Acquired hemosiderosis resulting from massive iron deposits in various organs, including heart, liver, and pancreas, may lead to architectural and functional disturbances of these organs. Even though iron overload can occur in nonuremic as well as in uremic individuals, the dialysis patient is at particular risk for developing hemosiderosis. Many dialysis patients receive exogenous iron from either oral iron therapy or blood transfusions. In addition, these patients seem to be at high risk for retaining iron. A diagnosis of excess iron deposition should be considered if the patient has unexplained cardiomyopathy, hepatic cirrhosis, proximal myopathy, diabetes mellitus, arthropathy, or immune dysfunction such as listeriosis. Several techniques are available for determining iron overload. Diagnostic tests include measuring serum ferritin levels, staining bone marrow preparations for excess iron, measuring tissue hemosiderin concentrations, magnetic resonance imaging, and the deferoxamine (DFO; Desferal) "challenge test." The simplest treatment for iron overload in nonuremic patients is removal of iron by venesection. However, in patients in whom venesection is not feasible, the chelating agent DFO can effectively remove excess iron. In the dialysis patient, DFO therapy can be combined with either dialysis or hemoperfusion to remove the iron-DFO complex that would otherwise be removed by the kidney. DFO therapy in the nondialyzed individual has proven to be successful, but before treatment, the benefits of the treatment must be weighed against possible adverse side effects such as cataracts, changes in color vision, and anaphylaxis. In the dialysis patient, indications for iron removal are less clearly defined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Management of iron overload in dialysis patients. 329 89

Acute renal failure developed in a patient accompanied by systemic manifestations such as myopathy and skin rash. The patient, a middle aged house wife, had been taking 600 mg of germanium (Ge) preparation daily for 18 months as an elixir. The main component of the preparation was GeO2 and some organic compound was also present. Histological study of the kidney post mortem showed foamy cell transformation of glomerular epithelia, degeneration of tubular epithelia with red blood cell casts and urate crystals, and a mild proliferation of mesangial matrix. Analysis of the tissue content of Ge, prompted by her history, revealed an increased accumulation of the metal. As compared to a non-user died of liver cirrhosis, the concentration of the metal was higher particularly in the spleen (183X), thyroid gland (175X), psoas muscle (93X), jejunum (76X), and renal cortex (69X). So far, neither accumulation of Ge in humal tissue nor systemic toxicity of the Ge in human has been reported. The relevance of massive accumulation of Ge to the renal failure as well as to other systemic manifestations the patient presented remains to be clarified.
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PMID:Accumulation of germanium in the tissues of a long-term user of germanium preparation died of acute renal failure. 383 68

Alcohol has acute and chronic cardiovascular effects. Acutely, alcohol depresses cardiac function and alters regional blood flow. Even when withdrawn from alcohol for several days, alcoholics may still manifest evidence of left ventricular dysfunction. In some alcoholics a severe muscle disorder may ensue with the clinical features of a dilated cardiomyopathy. The concomitant presence of a thiamine deficiency or cirrhosis may produce hemodynamic changes that can obscure the clinical features of alcohol-induced heart muscle disease. Alcoholics may also develop acute myocardial infarction with patent coronary arteries; some may have cardiac arrhythmias even without other evidence of heart disease. Although epidemiological studies suggest that moderate users of alcohol have fewer coronary events than teetotalers, such studies also demonstrate a relation between alcohol abuse and hypertension and an increased occurrence of coronary disease. Thus, the injurious cardiovascular effects of alcohol must be considered when establishing recommendations for its use.
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PMID:Cardiovascular effects of alcohol with particular reference to the heart. 639 13

To determine the significance of type II fiber atrophy in alcoholic myopathy and its relationship with ethanol-related diseases a prospective study was carried out in 100 chronic alcoholics who showed clinical suspicion of skeletal myopathy. Measurement of muscle strength, laboratory analysis, nutritional assessment and open biopsy of deltoid muscle were performed in each case, as well as electrophysiological testing for peripheral neuropathy. Hepatic ultrasonography and liver biopsy, echocardiography and radionuclide cardiac scanning were carried out in selected subjects. According to histomorphometric analysis, type II fiber atrophy was found in 33 cases (33%), being selective for type II B fiber in 23 (70%). Skeletal myopathy was diagnosed in 61 cases, alcoholic cardiomyopathy in 26, peripheral neuropathy in 23 and cirrhosis in 12. Patients with type II fiber atrophy had a significantly higher total lifetime dose of ethanol, presented a greater incidence of skeletal myopathy and peripheral neuropathy, and exhibited significantly lower values of percentage of ideal body weight and lean body mass than their counterparts. However, the only independent factors for developing type II fiber atrophy were the coexistence of caloric malnutrition (p = 0.004) and the presence of skeletal myopathy (p = 0.043). Selective type II fiber atrophy is a non-specific finding in alcohol-induced muscle damage appearing, overall, in the patients with caloric malnutrition as well as in those with histologic evidence of myopathy.
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PMID:Significance of type II fiber atrophy in chronic alcoholic myopathy. 765 May 33

This study was carried out in an attempt to differentiate between the contribution of liver impairment and direct actions of alcohol in myopathy of alcoholic liver disease. Using an animal model of cirrhosis we have previously shown that protein synthetic potential in muscle was not significantly altered. We therefore investigated the possibility that muscle degradation is increased. Cirrhosis was induced by carbon tetrachloride gavage in male rats receiving phenobarbitone in their drinking water. Controls were given phenobarbitone alone. After 135 days the free, latent and total activities of the lysosomal enzymes cathepsin B and cathepsin D in gastrocnemius muscle were unaffected by the induction of experimental cirrhosis when expressed relative to tissue wet weight, protein or DNA. The non-lysosomal enzyme neutral protease was also measured in gastrocnemius muscle from control and cirrhotic rats. There was no difference between the two groups in the free, latent or total activities. Addition of ethanol and acetaldehyde to the assay mixtures in some cases significantly altered the relative activities of the proteases in latent and free compartments of the cirrhotic tissues. In control tissues a different pattern of response emerged. It is concluded that in cirrhosis, at least in the carbon tetrachloride-induced rat model, there is no change of the activity of cathepsin B and D and the neutral protease activity in gastrocnemius. Small but significant effects of ethanol and its metabolite acetaldehyde on latent and free muscle protease activity were demonstrated.
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PMID:Skeletal muscle protease activities are unaltered in cirrhotic rats but altered in response to ethanol and acetaldehyde in vitro. 766 39

Two-hundred and fifty chronically alcoholic men (mean age, 41 +/- 11 years) entering an alcoholism treatment program were studied. Detailed clinical history, nutritional assessment and measurement of muscle strength by electronic myometer were performed in each case. In addition, hepatic ultrasonography and liver biopsy, echocardiography and radionuclide cardiac scanning, and electrophysiologica testing of peripheral nerves were performed when there was clinical evidence of liver disease, cardiomyopathy or neuropathy, respectively. Alcoholic cirrhosis was diagnosed in 20 cases, skeletal myopathy in 117, dilated cardiomyopathy in 20 and peripheral neuropathy in 41 cases. No patients with chronic myopathy or cardiomyopathy showed either clinical or laboratory evidence of malnutrition. Patients with cirrhosis showed a significantly lower lean body mass than controls (P = 0.03) and significantly lower nutritional protein levels than those alcoholics without cirrhosis. Alcoholics with peripheral neuropathy had significantly lower anthropometric parameters and nutrition protein levels than their counterparts (P < 0.001). However, in the multivariate analysis, the only independent factor for developing these complications of alcoholism was the total lifetime dose of ethanol (P < 0.001). We conclude that alcohol-related diseases are common in asymptomatic alcoholic men and these diseases appear to be due to an accumulative toxic effect of ethanol. Age and nutritional status do not seem to play a part in the development of such diseases.
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PMID:Relationship between ethanol-related diseases and nutritional status in chronically alcoholic men. 827 78


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