Liver fatty syndrome

Fatty liver of pregnancy Placental abruption Preeclampsia/eclampsia Retained fetus syndrome Pulmonary syndrome syndrome Empyema Hyaline membrane disease... 

Athyros VG, Mikhailidis DP, Didangelos TP, Giouleme OI, Liberopoulos EN, Karagiannis A et al. Effect of multifactorial treatment on non-alcoholic fatty liver disease in metabolic syndrome a randomised study. Cur Med Res Opin 2006 22(5) 873-83. 

Artificial liver support systems aim at the extracorporeal removal of water soluble and protein-bound toxins (albumin being the preferential binding protein) associated with hepatic failure. Albumin contains reversible binding sites for substances such as fatty acids, hormones, enzymes, dyes, trace metals and drugs [26] and therefore helps elimination by kidneys of substances that are toxic in the unbound state. It should be noticed that the range of substances to be removed is broad and not completely identified. Clinical studies showed that the critical issue of the clinical syndrome in liver failure is the accumulation of toxins not cleared by the failing liver. Based on this hypothesis, the removal of lipophilic, albumin-bound substances, such as bilirubin, bile adds, metabolites of aromatic amino acids, medium-chain fatty acids, and cytokines, should be benefidal to the dinical course of a patient in liver failure. 

Methionine is intimately related to lipid metabolism in the liver. Methionine deficiency is one of the causes of the fatty liver syndrome. Lack of methionine prevents the methylation of phosphatidylethanolamine to phosphatidylcholine, resulting in an ability by the liver to build and export very low density lipoprotein. The syndrome can be treated by the administration of choline, and for this reason, choline has often been referred to as the lipotropic factor. 

Excess adiposity, particularly the abdominal obesity associated with increased waist circumference, is associated with insulin resistance, hypertension, and proinflammatory states. The prevalence of this complex of comorbidities associated with obesity, now referred to as the metabolic syndrome, is reaching epidemic proportions in the United States (Grundy et al., 2004 Roth et al., 2002). Indeed, increased abdominal adiposity is one of a cluster of factors that are used in the diagnosis of metabolic syndrome. Abdominal tissue in the trunk occurs in several compartments, including subcutaneous and intraperitoneal or visceral fat. Visceral fat in particular appears to contribute to perturbed fuel metabolism by at least two mechanisms. First, hormones and free fatty acids released from visceral fat are released into the portal circulation and impact directly on metabolism of the liver. Second, the visceral adipose depot produces a different spectrum of adipocytokines than that produced by subcutaneous fat (Kershaw and Flier, 2004). 

Brunt EM. Nonalcoholic steatohepatitis. Semin Liver Dis 2004 24 3-20. Marchesini G, Bugianesi E, Forlani G, et al. Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome. Hepatology 2003 37 917-923. Wanless IR, Lentz JS. Eatty liver hepatitis (steatohepatitis) and obesity an autopsy study with analysis of risk factors. Hepatology 1990 12 1106-1110. Zimmerman HJ. Hepatotoxicity. The adverse effects of drugs and other chemicals in the liver, 2nd edn. Philadelphia Lippincott Williams Wilkins, 1999. Mason P. Cystic fibrosis - the disease. Hosptal Pharmacist 2005 12 201-207. Tolman KG, Eonseca V, Tan MH, et al. Narrative review hepatobiliary disease in type 2 diabetes mellitus. Ann Intern Med 2004 141 946-956. 

Fatty Liver and Kidney Syndrome in Biotin-Deficient Chicks... 

Cot Death Cot death, or Sudden Infant Death Syndrome, when an apparently healthy child dies suddenly, and from no apparent cause, has some similarities with the fatty liver and kidney syndrome in birds. It has been suggested that it may result from marginal biotin deficiency, together with a precipitating metabolic stress. 

There is circumstantial evidence to support this suggestion, because the liver content of biotin is lower in infants who have died from cot death than in infants who have died from known causes. By parallel with the fatty liver and kidney syndrome, it has been suggested that a modest metabolic stress, such as a mild fever, causes a higher requirement for gluconeogenesis than can be met, resulting in acute hypoglycemia. There are rapid postmortem changes in... 

Bannister DW (1976a) The biochemistry of fatty liver and kidney syndrome. Biotin-mediated restoration of hepatic gluconeogenesis in vitro and its relationship to pyruvate carboxylase activity. Biochemical Journal 156, 167-73. 

Bannister DW (1976b) Hepatic gluconeogenesis in chicks effect of biotin on gluconeogenesis in biotin-deficiency and fatty liver and kidney syndrome. Comparative Biochemistry and Physiology B 53, 575-9. 

Whitehead CC, Bannister DW, Evans A], Siller WG, and Wight PA (1976) Biotin deficiency and fatty liver and kidney syndrome in chicks given purified diets containing different fat and protein levels. British Journal of Nutrition 35,115-25. 

Elevation of y-GT is found in cholestasis, liver cirrhosis, viral hepatitis, fatty liver, porphyria, toxic liver damage, pancreatitis and pancreatic cancer, myocardial infarction, nephrotic syndrome, diabetes mellitus, right heart failure, obesity, nicotine abuse, and brain tumours. There is a good correlation of y-GT with CEA in colon cancer, involving a metastatic spread to the liver - an increase in y-GT in neoplastic disease is likewise supportive of the diagnosis of hepatic metastases. 

Elevation of cholesterol is found in fatty liver, particularly under diabetic metabolic conditions. A rather marked increase in cholesterol can be observed in all forms of cholestasis differentiation between intra- or extrahepatic cholestasis, however, is not possible. This elevation of cholesterol in obstruction is due to an enhanced synthesis of cholesterol in hepatocytes and intestinal walls as well as to the retention of bile lipids. Marked elevations of cholesterol are detectable in primary biliary cirrhosis and in cholesterol storage disease. A pronounced increase in cholesterol is also found in Zieve s syndrome (L. Zieve, 1958). 

An elevation of ChE activity can be detected in fatty liver, obesity, diabetes mellitus, exudative enteropathy, nephrotic syndrome, hyperthyroidism, Meulengracht s icterus, chronic obstructive jaundice, etc. Specificity in liver diseases is 61%, and sensitivity is 49%. In cirrhosis, however, sensitivity is 88% normal ChE therefore widely excludes cirrhosis. In connection with other hepatobiliary enzymes, ChE can be useful in the diagnosis and assessment of the course of liver disease. There is a very good correlation of ChE activity with coagulation factors in liver diseases however, the correlation is less significant with albumin synthesis. 

Amyloidosis, fatty liver, glycogenoses, Wolman s syndrome, hyperchylomicronaemia, Wilson s disease, Zellweger s cerebrohepato renal syndrome, Niemann-Pick disease, mucopolysaccharidoses, etc. 

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