Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 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

Protein energy malnutrition leading to growth failure is an inevitable consequence of chronic liver disease in 60% of children. Malnutrition should be anticipated by serial anthropometric assessment and prevented by early intervention with nutritional support. Both morbidity and mortality postliver transplantation have been related to the degree of pretransplant malnutrition, and thus nutritional status is an important risk factor for survival postliver transplantation. As survival following pediatric liver transplantation improves, with most centers reporting 1 y survival rates of 90-95% and 5 y survival rates of 80-85%, attention has focused on achieving nutritional rehabilitation, normal psychosocial development, and normal quality of life. An understanding of the etiology of protein malnutrition in liver disease is essential when planning therapeutic strategies. Considerable research progress has been made exploring the pathophysiology of malnutrition, including long-chain fat malabsorption with essential fatty acid deficiency, abnormal energy metabolism, substrate utilization, and nitrogen metabolism in liver disease. Effective strategies are emerging and future advances include docosahexaenioc acid, branched chain amino acids, and structured lipids. The key to success is a multidisciplinary approach to nutritional intervention, including pediatric dietitian, liaison nurse, feeding psychologist, and clinician.
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PMID:Feeding the child with chronic liver disease. 978 65

In the rapidly increasing elderly population, diarrhoea as a result of drug therapy is an important consideration. The elderly consume a disproportionately large number of drugs for multiple acute and chronic diseases. Drugs can compromise both immune and nonimmune responses. Aging decreases the quality and proportion of T cells which in turn reduces the production of secretory IgA, the primary immune response of the gut. Acid production in the stomach decreases with increasing age and this compromise its vital 'self-sterilising' function, thus increasing the risk of diarrhoea due to viral, bacterial and protozoal pathogens. Other nonimmune defence mechanisms include the motility of the small intestine and the host-protective commensal bacteria of the colon. Drug induced hypomotility may result in bacterial overgrowth, deconjugation of bile salts and diarrhoea. Less commonly, diarrhoea may occur due to hypermotility because of a cholinergic-like syndrome. In the colon the host-protective commensal bacteria provide a powerful defence against pathogens. Disruption of this commensal population by antibiotic therapy may result in Clostridium difficile supra-infection which causes diarrhoea through toxin production. This is especially important in the elderly patient on chemotherapy for malignancy and those with multiple diseases. The organism responds to vancomycin, metronidazole and bacitracin. Metronidazole is the suggested drug of choice, with vancomycin reserved for relapses. Drugs also cause diarrhoea by interfering with normal physiological processes. Drugs impair fluid absorption by activating adenylate cyclase within the small intestinal enterocyte which increases the level of cyclic AMP. This causes active secretion of Cl- and HCO3-, passive efflux of Na+, K+ and water and inhibition of Na+ and Cl- into the enterocyte. Examples of these drugs (secretagogues) are bisacodyl, misoprostol and chenodeoxycholic acid (used to dissolve cholesterol gallstones). Drugs may also affect a second mechanism that regulates water and electrolyte transport, the Na+, K+ exchange pump. The energy for this pump is provided by the ATPase mediated breakdown of ATP. ATPase may be inhibited by digoxin, auranofin, colchicine and olsalazine. A number of drugs cause osmotic diarrhoea including antacids containing magnesium trisilicate or hydroxide. Lactulose is being used increasingly in compensated liver disease to increase protein tolerance and prevent hepatic encephalopathy. Sorbitol, an osmotic laxative agent also used in some liquid pharmaceutical preparations, induces diarrhoea by virtue of its osmotic potential. Another mechanism by which drugs cause diarrhoea is by mucosal damage of the small and large bowel. In the small intestine mucosal damage causes diarrhoea and fat malabsorption, as may occur with neomycin and colchicine. In the colon, for example, gold salts and penicillamine cause colitis of varying severity. Though the causes of diarrhoea are diverse, a drug-associated aetiology should always be considered and actively sought and addressed to prevent the complications of dehydration, electrolyte imbalance and undernutrition.
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PMID:Mechanisms of drug-induced diarrhoea in the elderly. 978 28

A case of macroamylasemia was seen in a 40-year-old HIV-positive bisexual male treated at the Fort Worth-Tarrant County Health Department (Ryan White Clinic). Macroamylasemia is a rare condition encountered sometimes in persons with HIV infection. Apart from the setting of HIV infection and acquired immunodeficiency syndrome, macroamylasemia is seen also in various conditions including liver disease, diabetes, cancer, malabsorption, and autoimmune disorders. Although this biochemical phenomenon requires no therapy, it should be considered in the differential diagnosis of patients who have persistently high levels of serum amylase and yet do not exhibit any clinical symptoms of pancreatitis or salivary gland inflammation.
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PMID:Macroamylasemia in HIV infection. 985 22

Protein-energy malnutrition is an inevitable consequence of chronic liver disease, particularly in the developing infant. Severe malnutrition with loss of fat stores and muscle wasting affects between 60% and 80% of infants with liver disease (Beath, 1993a; Holt et al, 1997). Reduced energy intake secondary to anorexia, vomiting and fat malabsorption, in association with a disordered metabolism of carbohydrate and protein, increased energy requirements and vitamin and mineral deficiencies, contributes towards growth failure. Reversal of malnutrition is one of the key aims of liver transplantation and is achieved in the majority of long-term survivors. The aetiology of persistent growth failure post-transplantation is multifactorial and is related to pre-operative malnutrition, glucocorticoid administration, feeding problems and post-operative complications. Strategies to prevent pre- and post-transplant growth failure include early referral for liver transplantation and a multidisciplinary approach to nutritional support, which may increase survival and improve the quality of life and outcome of liver transplantation.
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PMID:Cholestasis and end-stage liver disease. 1007 9

Short-bowel syndrome is functionally defined as a state of malabsorption following loss of small bowel. Most cases occur in the neonatal period after extensive resection for necrotizing enterocolitis, or due to congenital anomalies of the gastrointestinal tract. A smaller percentage originate later in life from surgical treatment of Crohn's disease, neoplastic disorders, or vascular events. The physiological, morphological and functional intestinal gradient determines the clinical picture leading to better tolerance of jejunal than ileal resections. The subsequent adaptation process requires enteral feeding with a different impact of specific nutrients, and is also influenced by a number of humoral mediators such as enteroglucagon, gastrin, growth factors, prostaglandins and polyamines. Nutritional management starts parenterally via a central venous line covering basic demands, substituting current losses and restoring pre-existing deficiencies. Continuous enteral tube feeding is added as soon as postoperative ileus resolves, beginning with an elemental diet, which is gradually increased first in concentration, then in quantity, and supplemented by small oral meals. Cycling of parenteral nutrition is the next step. As soon as sufficient stability is reached, the child should be discharged home under continued outpatient care. Main long-term problems comprise bacterial overgrowth, fluid and electrolyte disequilibration, nutritional deficiencies, parenteral nutrition-related liver disease, and central venous line complications such as sepsis and thrombosis.
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PMID:Enteral and parenteral nutrition in patients with short-bowel syndrome. 1053 60

Bile acids, the water-soluble, amphipathic end products of cholesterol metabolism, are involved in liver, biliary, and intestinal disease. Formed in the liver, bile acids are absorbed actively from the small intestine, with each molecule undergoing multiple enterohepatic circulations before being excreted. After their synthesis from cholesterol, bile acids are conjugated with glycine or taurine, a process that makes them impermeable to cell membranes and permits high concentrations to persist in bile and intestinal content. The relation between the chemical structure and the multiple physiological functions of bile acids is reviewed. Bile acids induce biliary lipid secretion and solubilize cholesterol in bile, promoting its elimination. In the small intestine, bile acids solubilize dietary lipids promoting their absorption. Bile acids are cytotoxic when present in abnormally high concentrations. This may occur intracellularly, as occurs in the hepatocyte in cholestasis, or extracellularly, as occurs in the colon in patients with bile acid malabsorption. Disturbances in bile acid metabolism can be caused by (1) defective biosynthesis from cholesterol or defective conjugation, (2) defective membrane transport in the hepatocyte or ileal enterocyte, (3) defective transport between organs or biliary diversion, and (4) increased bacterial degradation during enterohepatic cycling. Bile acid therapy involves bile acid replacement in deficiency states or bile acid displacement by ursodeoxycholic acid, a noncytotoxic bile acid. In cholestatic liver disease, administration of ursodeoxycholic acid decreases hepatocyte injury by retained bile acids, improving liver tests, and slowing disease progression. Bile acid malabsorption may lead to high concentrations of bile acids in the colon and impaired colonic mucosal function; bile acid sequestrants provide symptomatic benefit for diarrhea. A knowledge of bile acid physiology and the perturbations of bile acid metabolism in liver and digestive disease should be useful for the internist.
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PMID:The continuing importance of bile acids in liver and intestinal disease. 1059 55

Protein energy malnutrition leading to growth failure is an inevitable consequence of chronic liver disease in childhood. Although the precise pathophysiology is not understood considerable progress has been made in understanding the mechanisms of fat malabsorption and protein turnover in liver disease. There are many difficulties with the correct assessment of nutritional parameters in children with liver disease related to their abnormal body composition and energy expenditure and care needs to be taken with the interpretation of results. The effects of malnutrition secondary to chronic liver disease are varied and include fat soluble vitamin deficiencies, generalised growth failure, impairment of gastrointestinal function, immunosuppression and hypotonia. It is now recognised that malnutrition is an important risk factor for liver transplantation and increases both mortality and morbidity. Strategies to prevent or reverse malnutrition are now established and include the use of specific infant formulas based on low salt protein and an increased concentration of medium train triglyceride (50-70%). Careful nutritional support in association with generous fat soluble vitamin supplementation may produce dramatic improvement in catch up weight gain but for those children in whom growth failure persists, the only management is liver transplantation.
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PMID:Nutrition and growth in patients with chronic liver disease. 1082 20

Alagille syndrome (AGS) is frequently associated with growth failure, which has been attributed to concurrent congenital anomalies, cholestasis, and malabsorption and/or malnutrition. However, the underlying cause of the growth failure is not well understood. Our objective is to analyze the growth pattern in 26 patients with AGS and the possible effect that orthotopic liver transplantation (OLT) may have on this pattern. The standardized height, weight, and growth velocity of 26 pair-matched patients with AGS were compared. Thirteen patients underwent OLT. Repeated-measure ANOVA methods were used for the statistical analysis. The overall mean standardized height (z score) was -2.92 in the OLT group versus -1.88 in the non-OLT group (P =.03). The overall mean standardized weight was -1. 21 in the non-OLT group and -1.67 in the OLT group (P =.23). In 15 patients, birth weight was 2.82 +/- 0.4 kg, for a mean standardized weight of -0.95, and weight at diagnosis was 4.53 +/- 2.12 kg, for a mean standardized weight of -1.56. Bone age was delayed in the 9 patients who underwent bone-age analysis. Growth hormone therapy administered to 2 patients did not improve growth. Patients with AGS had growth failure secondary to other factors in addition to liver disease. Growth failure beginning in the prenatal period supports a genetic basis for this feature. Growth improvement up to normal levels should not be expected as a benefit of OLT in these patients. Growth failure as a primary indication for OLT should be cautiously examined in patients with AGS.
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PMID:Does liver transplantation affect growth pattern in Alagille syndrome? 1098 57

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


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