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

Intestinal fat absorption was examined in rats with CCl4-induced liver cirrhosis. Marked lymphangiectasia of the small intestine was observed in rats after CCl4 was given subcutaneously biweekly for 10--12 weeks. Intestinal epithelial uptake of linoleic acid administered in the loop was not impaired, but accumulation of lipid droplets in the intestinal epithelial cells and disturbed lymphatic transport of absorbed fat were observed in these rats. These data suggest that lymphostasis of the intestine may play an important role in fat malabsorption in liver cirrhosis.
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PMID:Lymphatic role in the pathogenesis of fat malabsorption in liver cirrhosis in rats. 714 Apr 88

To evaluate possible effects of alcohol consumption on vitamin A and retinol-binding protein (RBP) status, baboons were pair-fed a nutritionally adequate liquid diet containing 50% of total calories either as ethanol or isocaloric carbohydrate. Fatty liver developed after 4 months of ethanol feeding with a 59% decrease (P less than 0.001) in hepatic vitamin A levels, and fibrosis or cirrhosis developed after 24-84 months with a 95% decrease (P less than 0.001). Similarly, hepatic vitamin A levels of rats fed ethanol (36% of total calories) were decreased after 3 weeks (42%, P less than 0.01) and continued to decrease up to 9 weeks. In contrast, vitamin A contents in the kidney and testis were increase 2-3 fold in ethanol-fed rats after 9 weeks. Serum vitamin A and RBP levels were not significantly changed in rats. When dietary vitamin A was increased 5-fold, hepatic vitamin A was again decreased in ethanol-fed rats. When dietary vitamin A was virtually eliminated, the depletion rate of vitamin A from endogenous hepatic storage was 2.5 times faster in ethanol-fed rats than in controls. It is concluded that chronic ethanol consumption decreases hepatic vitamin A, and that some mechanisms other than malnutrition and malabsorption may be involved in this process.
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PMID:Hepatic vitamin A depletion after chronic ethanol consumption in baboons and rats. 719 10

The mechanisms of vitamin D deficiency already described are triggered off by a variety of causes. Confinement indoors leads to defective photosynthesis and dietary restrictions to insufficient intake. Malabsorption results from digestive tract diseases: mainly adult coeliac disease, but also sequelae of gastrectomy, exocrine pancreatic insufficiency, chronic biliary obstruction and all other causes of steatorrhoea. Practically, osteomalacia of digestive origin usually results from multifactorial hypovitaminosis D. The same applies to primary or nutritional biliary cirrhosis, which frequently entails low vitamin D blood levels despite subnormal 25-hydroxylation. Osteomalacia is also found in renal osteodystrophy, where it is partly due to inhibition of 1,25-hydroxylase and subsequent deficiency of 1,25-dihydrocholecalciferol, though other, non vitaminic substances may also be involved. Two misleading forms of the disease must be borne in mind: one with renal tubular lsions, the other associated with functional pseudo-hypoparathyroidism. The aetiology of most cases of osteomalacia due to vitamin D deficiency can be elucidated by a few simple tests.
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PMID:[Osteomalacia due to vitamin D deficiency. Part two: Aetiology (author's transl)]. 742 86

This article reviews osteoporosis (OP) in adults with chronic liver disease. OP in this setting is characterized in general by low bone turnover. The pathogenesis is unclear but is probably not related to vitamin D abnormalities. Patients at high risk of OP include those with evidence of cirrhosis, hypogonadism, overt calcium malabsorption, steroid therapy and choleostatic liver disease (particularly primary biliary cirrhosis). OP is best managed by adequate calcium intake, regular weight bearing exercise, and the avoidance of alcohol and tobacco smoking. There is probably no reason for vitamin D supplementation. Hormonal replacement therapy when necessary is indicated in males and should be considered in females. Finally, liver transplantation has the potential to improve or stabilize OP in the median term, although it is associated with significant short-term deterioration.
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PMID:Osteoporosis in chronic liver disease: pathogenesis, risk factors, and management. 785 Oct 1

The zinc, an important enzymatic cofactor, is involved in many metabolic processes. Its deficiency might be due either to malabsorption or to excessive utilization. In the medical literature of the latest 10 years, zinc was considered to play a part in the immune processes. The authors of the present paper intend to study the zinc and immunoglobulin levels in various diseases, i.e., chronic progressive hepatitis, liver cirrhosis (LC), dermatitis, bronchial asthma. This preliminary investigation was carried out in 30 patients with LC in whom serum zinc values were assayed by atomic absorption spectrophotometry and the immunoglobulin levels were determined using the Mancini type simple radial immunodiffusion technique. All these patients presented considerable decrease of serum zinc concentration, the values ranging between 3.06 and 7.65 mumol/l as compared with 19.8 +/- 1.5 mumol/l in the controls, alongside with the increase of immunoglobulins G and M. In the patients treated with Zincum metallicum CH5 it was observed after about 30 days of treatment that the clinical state was considerably improved and IgG and IgM as well as serum zinc had resumed their normal values. This treatment should not be interrupted since in LC, without permanent additional supply, the serum zinc returns rapidly to the initial deficit or even lower.
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PMID:Treatment with zincum metallicum CH5 in patients with liver cirrhosis. Preliminary study. 786 38

Alcohol causes primary malnutrition by displacing nutrients in the diet and secondary malnutrition via malabsorption and cellular injury through direct cytotoxicity. Hepatotoxicity results from metabolic disturbances associated with the oxidation of ethanol via liver alcohol dehydrogenase (ADH) and the redox changes produced by the generated NADH (the reduced form of nicotinamide adenine dinucleotide), which in turn affects the metabolism of lipids, carbohydrates, proteins, and purines. Ethanol is also oxidized in liver microsomes by an ethanol-inducible cytochrome P450, which contributes to the alcoholic's tolerance and his increased vulnerability to the toxicity of industrial solvents, anesthetics, commonly prescribed drugs, over-the-counter analgesics, chemical carcinogens, and retinoids. Increased acetaldehyde generation, with formation of protein adducts, results in antibody production, enzyme inactivation, decreased DNA repair, impaired utilization of oxygen, glutathione depletion, free radical-mediated toxicity, lipid peroxidation, and increased collagen synthesis. Therapy may eventually improve with the use of supernutrients such as S-adenosyl-L-methionine, which replenishes glutathione, restores methylation, and attenuates liver injury, as well as dilinoleoylphosphatidylcholine, which prevents cirrhosis.
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PMID:Herman Award Lecture, 1993: a personal perspective on alcohol, nutrition, and the liver. 823 56

Liver disease is accompanied by major qualitative and quantitative disturbances in plasma lipoprotein metabolism, the extent and intensity of which depend on the degree of parenchymal damage, cholestasis, or both. The main objective of this study was to determine the cholesteryl ester transfer CETP activity and its association with the lipoprotein neutral lipid composition in patients with either liver cirrhosis or cholestasis, as compared to normal controls. Lipoproteins were isolated by ultracentrifugation, lipids and apolipoproteins were measured by conventional methods, and the fatty acid composition was established by gas chromatography; CETP activity in lipoprotein-deficient plasma was measured by determining the transfer of [3H]cholesteryl esters from HDL to VLDL. Lipoprotein lipase and hepatic lipase activities were measured in post-heparin plasma by radiochemical methods. In patients with liver cirrhosis, low levels of VLDL, HDL, apo B, and Lp(a) were observed, as well as a change in the composition of HDL particles, with increases in the relative proportion of triglyceride and free cholesterol. Respectively, the last two changes could be attributed in part to the low hepatic lipase activity observed in this study, and to the low lecithin:cholesterol acyltransferase activity previously observed by others. In patients with cholestasis, a moderate hyperlipidemia due to the elevation of LDL was found. In contrast, HDL and apo A-I levels were very low reflecting a low number of HDL particles, which also had altered compositions with increases in the triglyceride and free cholesterol contents relative to apo A-I and esterified cholesterol, respectively. As regards the fatty acid composition of lipoprotein lipids, the two groups of patients showed, in general, a lower proportion of linoleic acid and a compensating higher proportion of oleic acid as compared to the controls, changes that were observed in both cholesteryl esters and triglycerides. In contrast, the proportions of oleic and palmitoleic acids in phospholipids were increased, whereas that of stearic acid was decreased in patients as compared to controls. In patients with liver cirrhosis, as well as in controls, no changes were observed in the fatty acid compositions of cholesteryl ester, triglycerides, or phospholipids among the different lipoproteins, which probably reflects the equilibration reached by the action of CETP. In patients with cholestasis, no differences were observed in fatty acid composition among the lipoprotein phospholipids but, interestingly, cholesteryl esters from VLDL had a significantly lower linoleic acid content than those from HDL, whereas triglycerides from VLDL had significantly higher oleic acid and lower linoleic acid contents than those from HDL. This distinct fatty acid composition of the neutral lipids between lipoproteins was associated with a significant decrease (25%) in the cholesteryl ester transfer activity in patients with cholestasis. We suggest that fat malabsorption due to the biliary defect may induce a decrease in cholesteryl ester transfer protein synthesis or section, which in turn would slow the equilibration of the neutral lipids among plasma lipoproteins.
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PMID:Cholesteryl ester transfer activity in liver disease and cholestasis, and its relation with fatty acid composition of lipoprotein lipids. 874 May 80

To investigate the pathogenesis of hepatic osteodystrophy (HOD) in parenchymal liver disease, we developed a laboratory model in animals using carbon tetrachloride (CCl4) and thioacetamide. Biochemical and histological parameters in the model were measured. In rats with both chronic non-cirrhotic liver injury and CCl4-induced cirrhosis, tibial bone volume was significantly lower than in controls. In CCl4-treated cirrhotic rats, the osteoid volume decreased while the urinary calcium/creatinine ratio increased. In all CCl4-treated rats, bone volume was significantly correlated with both the serum albumin concentration and the number of goblet cells reflecting intestinal villous atrophy. The serum concentration of vitamin D metabolites was not correlated with bone volume. Whole body retention of 47Ca was significantly lower in CCl4-treated cirrhotic rats than in controls. Furthermore, the bone volume in thioacetamide-treated cirrhotic rats was significantly lower than in controls. These data demonstrate that chronic parenchymal liver injury itself causes osteoporosis (i.e. HOD) due to a combination of low bone formation rates and high resorption rates, that HOD begins at the stage of chronic non-cirrhotic liver injury, that bone volume in HOD parallels liver damage and that the principal pathogenesis of HOD seems to be intestinal Ca malabsorption due to lower serum albumin and villous atrophy, while serum levels of vitamin D metabolites have little influence on the pathogenesis of HOD.
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PMID:Bone changes and mineral metabolism disorders in rats with experimental liver cirrhosis. 903 34

During the past six years, we have treated eight patients with cystic fibrosis (CF) for nephrolithiasis. In seven patients, the stones were comprised of calcium oxalate. Another six patients had calcium oxalate crystalluria. In our CF population of 140 patients, this represents a cumulative incidence of calcium oxalate nephrolithiasis of 5.7 percent and an additional 4.2 percent incidence of crystalluria. Experience with these patients is reviewed. Pancreatic insufficiency was universally associated with nephrolithiasis or crystalluria. Diabetes and cirrhosis were also common. Predisposing factors and potential mechanisms of stone disease in pancreatic insufficient CF patients are discussed, focusing on the relationship between fat malabsorption in CF to oxalate metabolism.
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PMID:Cystic fibrosis and calcium oxalate nephrolithiasis. 927 85

A continuously increasing production level in poultry breeding has resulted in changes in metabolism. Selection procedures in breeding programmes are focused on an increase in growth rate and on a decrease in feed conversion ratio (less feed intake per unit of deposited tissue). These procedures do not pay attention to the maintenance requirements of birds. Imbalances between production (protein and fat deposition) and supply of energy for maintenance requirements lead to homeostatic dysregulation and to diseases of organs which supply the energy for production and maintenance. The alarming increase in metabolic diseases, such as heart failure syndrome, ascites, and oedema in the lungs and heart, can be directly related to an insufficient oxygen supply. A low oxygen consumption and heat production is one of the mechanisms by which a low feed conversion ratio can be achieved, as is induced hypothyroidism by which physical activity and thus heat production is reduced. Other diseases, such as liver cirrhosis, malabsorption syndrome, sudden death syndrome in broilers, and fatty liver-hemorrhage syndrome, which is nowadays the most important disease in laying hens in the Netherlands, can be related to an imbalance between the production rate and maintenance requirements. A continued selection on the basis of retained energy (in protein and fat) without paying attention to the maintenance requirements of birds will be detrimental for the health and welfare of poultry. These undesirable developments in poultry husbandry should be a challenge for sciences focused on welfare and stress in animals. Such a scientific approach to animals suffering from dysgenic changes in metabolism is needed to solve serious problems in poultry breeding.
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PMID:Pathological changes in metabolism of poultry related to increasing production levels. 932 54


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