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)

Necrolytic migratory erythema is characterized by waves of irregular erythema in which a central bulla develops, and subsequently erodes and becomes crusted. It usually occurs in patients with an alpha-islet cell tumor of the pancreas. However, necrolytic migratory erythema has also been observed in patients without an associated glucagonoma. We describe a woman with iatrogenic necrolytic migratory erythema. She received intravenous glucagon for hypoglycemia associated with an insulin-like growth factor II-secreting hemangiopericytoma. After chemotherapy, she developed necrolytic migratory erythema. The characteristics of the previously reported patients with nonglucagonoma-associated necrolytic migratory erythema are reviewed. In patients with nonglucagonoma-associated necrolytic migratory erythema, the dermatosis-related conditions most commonly observed were celiac disease or malabsorption, cirrhosis, malignancy, and pancreatitis; less common conditions included hepatitis, inflammatory bowel disease, heroin abuse, and odontogenic abscess. Although the pathogenesis of necrolytic migratory erythema remains unknown, hyperglucagonemia appears to have had a causative role in the development of this dermatosis in our patient. Patients who develop necrolytic migratory erythema should be evaluated for the presence of a glucagonoma; if a glucagonoma is ruled out, evaluation for other conditions known to occur with necrolytic migratory erythema, such as liver disease, malabsorptive disorders, and nonislet-cell tumors is warranted.
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PMID:Iatrogenic necrolytic migratory erythema: a case report and review of nonglucagonoma-associated necrolytic migratory erythema. 959 6

A 16-year-old girl is described with abetalipoproteinaemia who underwent liver transplantation for hepatic cirrhosis. After this procedure her serum lipoprotein profile was corrected; however, fat malabsorption and steatorrhea persisted because the primary defect, a mutant microsomal triglyceride-transfer protein, remains expressed in the intestine.
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PMID:Persistence of the intestinal defect in abetalipoproteinaemia after liver transplantation. 968 20

Chronic pancreatitis is characterized by progressive and irreversible loss of pancreatic exocrine and endocrine function. In the majority of cases, particularly in Western populations, the disease is associated with alcohol abuse. The major complications of chronic pancreatitis include abdominal pain, malabsorption, and diabetes. Of these, pain is the most difficult to treat and is therefore the most frustrating symptom for both the patient and the physician. While analgesics form the cornerstone of pain therapy, a number of other treatment modalities (inhibition of pancreatic secretion, antioxidants, and surgery) have also been described. Unfortunately, the efficacy of these modalities is difficult to assess, principally because of the lack of properly controlled clinical trials. Replacement of pancreatic enzymes (particularly lipase) in the gut is the mainstay of treatment for malabsorption; the recent discovery of a bacterial lipase (with high lipolytic activity and resistance to degradation in gastric and duodenal juice) represents an important advance that may significantly increase the efficacy of enzyme replacement therapy by replacing the easily degradable porcine lipase found in existing enzyme preparations. Diabetes secondary to chronic pancreatitis is difficult to control and its course is often complicated by hypoglycaemic attacks. Therefore, it is essential that caution is exercised when treating this condition with insulin. This paper reviews recent research and prevailing concepts regarding the three major complications of chronic pancreatitis noted above. A comprehensive discussion of current opinion on clinical issues relating to the other known complications of chronic pancreatitis such as pseudocysts, venous thromboses, biliary and duodenal obstruction, biliary cirrhosis, and pancreatic cancer is also presented.
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PMID:Chronic pancreatitis: complications and management. 1050 49

Malnutrition and micronutrient deficiencies are common in patients with liver diseases. The pathogenesis of protein-energy malnutrition in cirrhosis involves many factors, including poor oral intake, malabsorption, and metabolic abnormalities similar to stress. Encephalopathy may complicate cirrhosis but is usually not caused by diet. Protein restriction is only necessary in rare patients with refractory encephalopathy. The use of branched-chain amino-acid solutions is not supported by the literature. Chronic liver diseases without cirrhosis are not usually associated with protein-energy malnutrition, but vitamin and mineral deficiencies are common, especially with significant cholestasis. Fatty liver may result from excessive triglyceride uptake and production by the liver or by a secretory defect. Therapy for fatty liver depends on its cause. Chronic total parenteral nutrition may induce fatty liver and inflammation especially in patients with short-bowel syndrome. Deficiency of choline in parenteral nutrition has been proposed as the mechanism for liver disease. Acute liver diseases such as fulminant hepatic failure or alcoholic hepatitis are considered hypercatabolic diseases and thus require prompt nutritional intervention with a high-calorie enteral or parenteral formula. In fulminant hepatic failure, low-protein, fluid-restricted formulas are recommended.
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PMID:Nutrition and liver diseases. 1098 Sep 70

Nutritional support to patients in neonatal and pediatric intensive care units is critical not only to minimize negative nitrogen balance but also to promote growth and development. Continuous technological and logistical advances in the Western countries have improved the efficacy and reduced the complications of parenteral nutrition (PN) to the extent that despite the constraints of cost and infrastructure, PN is now fast growing in India. Although widespread availability is very much desired, it is important that the technique is developed with considerable expertise and used judiciously with full knowledge of its indications, limitations, dangers and benefits. Indications for PN include surgical conditions (short gut syndrome), very low birth weight infants (particularly with necrotizing enterocolitis and surgical anomalies), malabsorption syndromes, conditions requiring bowel rest (acute pancreatitis, severe ulcerative colitis and necrotizing enterocolitis) and several non-gastrointestinal indications (end stage liver disease, renal failure, multiple trauma and extensive burns). Provision of PN is associated with significant and sometimes life threatening complications. The possible complications are technical (thrombosis, perforation of vein, thrombophlebitis), infections, metabolic disturbances, hepatobiliary stenosis, cholestasis, fibrosis, cirrhosis or cholelithiasis and bone related complications like osteopenia and fractures. Meticulous monitoring is necessary not only to detect complications but also to document clinical benefit.
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PMID:Pediatric parenteral nutrition in India. 1113 60

Hepatic encephalopathy is one of the major complications in decompensated liver cirrhosis. The current study was conducted to clarify the mechanisms of zinc deficiency in liver cirrhosis and its involvement in hepatic encephalopathy via ammonia metabolism. Ten patients each with compensated or decompensated liver cirrhosis and 11 healthy volunteers were enrolled in the study. Serum zinc levels and its daily urinary excretion were measured, an oral zinc-tolerance test was performed to examine zinc malabsorption, and the effects of diuretics on zinc excretion and of zinc supplementation on ammonia metabolism in the skeletal muscle were studied. The mean serum zinc levels in patients with decompensated liver cirrhosis were found to be significantly lower than the levels in controls and patients with compensated liver cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.
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PMID:Effects of zinc deficiency/zinc supplementation on ammonia metabolism in patients with decompensated liver cirrhosis. 1177 97

Anorexia nervosa is a syndrome with multifactorial etiology in which several genetic, biologic, psychological and social factors are involved. Patients affected by anorexia nervosa (AN) may develop multiple endocrine abnormalities, e.g. amenorrhea, hypothalamus-pituitary-adrenal axis hyperactivity, low T3 syndrome and peculiar changes of somatotroph axis function. These endocrine abnormalities are also found after prolonged starvation and may represent an adaptive response developed in order to save energy and proteins. It is still a matter of debate whether these endocrine changes are etiologic or secondary. In fact, several evidences suggest the existence in AN of hypothalamus functional alterations, which may be involved in the development and maintenance of the food intake disorder; on the other hand, the increased CRH secretion seems to be secondary to malnutrition as well as GH hypersecretion coupled to low IGF-I levels; the latter is a common finding in AN, as well as in other undernutrition and malabsorption conditions, type 1 diabetes mellitus, liver cirrhosis and catabolic states. Hypothalamic amenorrhea, which is one of the diagnostic criteria for AN, is not linked only to the reduction of body weight but reflects also deep alterations of gonadotropin secretory pattern. Low T3 syndrome is frequently found in AN; on the other hand, an iodide-induced hypothyroidism is quite uncommon. T3 reduction in AN seems to be an adaptive response to prolonged starvation; however the presence of a simultaneous central dysregulation cannot be excluded. Finally, AN patients frequently show defects in urinary concentration or dilution with inappropriate secretion of antidiuretic hormone, which may be due to intrinsic defects in the neurohypophysis or to abnormalities of its regulatory afferent neurons.
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PMID:[Endocrine abnormalities in anorexia nervosa]. 1271 47

The gastrointestinal (GI) manifestations of cystic fibrosis (CF) are varied and include pancreatic insufficiency, meconium ileus, distal intestinal obstruction syndrome (DIOS), liver disease, and other less common manifestations. Treatment of pancreatic insufficiency consists of providing appropriate pancreatic enzyme replacement therapy and may include raising duodenal pH to allow for optimal action of these enzymes. Despite a number of pancreatic enzyme replacement products, malabsorption cannot be normalized. Management of DIOS depends on the severity of the symptoms; adequate hydration is very important. Polyethylene glycol solutions are being increasingly used. The precipitating cause of the episode of DIOS should be looked for so future episodes can be prevented. Liver disease is relatively silent and annual monitoring of liver function and status is recommended. Treatment is mainly supportive and the role of ursodeoxycholic acid in the prevention of cirrhosis needs to be better defined. Nutritional status is an important part of management of all GI and liver manifestations of CF. A team approach and the assistance of a registered dietitian are extremely valuable in managing the GI and liver manifestations of CF.
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PMID:Treatment of Gastrointestinal Problems in Cystic Fibrosis. 1295 49

Cholestasis is a condition, where the bile flow into the intestine is defective. The causes may be extrahepatic (in large biliary ducts) or intrahepatic (at the level of hepatocytes or minor biliary ducts). The lack of bile in the intestine results in serious consequences, mainly malabsorption, malnutrition and skeletal changes. The compounds, which are normally excreted in the bile, accumulate and liver biliary cirrhosis ensues. Cholestatis is characterized by a typical laboratory picture, outlined in publications, which serves for differentiation of individual forms of cholestasis. There are various causes of cholestasis, listed in the survey. Extrahepatic cholestasis must be treated as early as possible (by endoscopy or surgery). The highest attention is devoted mainly to chronic intrahepatic cholestatis: primary biliary cirrhosis. It affects mainly women at middle age and is most frequently considered as an autoimmune disease. A survey of present therapeutic possibilities for cholestasis is given. Ursodeoxycholic acid became the main therapeutic drug. It must be administered as early as possible and for long period of time in all cases.
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PMID:[Cholestasis]. 1451 97

A wide range of cholestatic liver diseases result from various primary defects in bile formation. Clinical features include jaundice, pruritus, failure to thrive, fat malabsorption, cholelithiasis, and variably progressive cirrhosis. Accurate diagnosis of these disorders is essential for determination of prognosis and selection of the most appropriate therapies. Severe genetic defects in canalicular bile acid and phospholipid excretion lead to progressive liver disease that often requires liver transplantation. Defects in bile acid biosynthesis and aminophospholipid transport may be responsive to medical or non-transplant surgical approaches.
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PMID:Disorders of bile formation and biliary transport. 1456 77


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