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)

Deterioration in nutritional status occurs late in the progress of cancers at certain sites, but at all stages in patients with gastrointestinal cancer. Weight loss with decrease in body fat and muscle wastage, occurs to a varying degree. Superficially, the clinical condition resembles simple food deprivation. However, the derangements in metabolism are often and some patients show an elevated resting energy expenditure, disturbances of carbohydrate, fat and protein metabolism and generally, a failure to adapt to reduced food intake, which is characteristic of cachexia. Cancer cachexia then becomes characterized by signs of marked negative energy and protein balance, including hypoalbuminemia, weight loss, and anemia. On the other hand, toxohormone extracted from tumor tissues was considered as the main cause to produce cancer cachexia. However, it has become clearer that cytokines, e.g. cachectin/TNF, IL-1, LT and IFN gamma play an important role to produce cachexia. Patients who are malnourished have an incidence of postoperative complications double that seen in adequately nourished patients. The effectiveness of cancer-chemotherapy is also different in nutritional status of patients. Although in patients requiring hyperalimentation, enteral nutritional support may feasible and enteral feeding has a distinct metabolic advantage compared with parenteral feeding, there is a definite role for total parenteral nutrition in patients who have severe chronic radiation enteritis, side effect of chemotherapy, weight loss and malabsorption. Tentative weight gain and correction of hypoalbuminemia without improving patient survival may be expected by this intravenous hyperalimentation.
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PMID:[Palliative therapy in cancer 2. Nutrition control]. 169 91

The endocrine abnormalities associated with acquired immunodeficiency syndrome (AIDS) are reviewed. These include adrenal insufficiency, hyporeninemic hypoaldosteronism, panhypopituitarism, hypogonadism, and alterations in thyroid function tests. AIDS-related infections or neoplasms may lead to hypercalcemia, whereas malabsorption may cause hypocalcemia. The possibility that AIDS-associated cachexia and hypertriglyceridemia may be caused by cachectin (tumor necrosis factor) is discussed, along with possible therapy for cachexia with megestrol acetate. Ketoconazole, sulfonamides, and pentamidine have specific, potentially deleterious metabolic effects when used in AIDS patients. Because treatment of endocrinological abnormalities of AIDS is often effective, improved diagnosis and appropriate therapy of these abnormalities will result in improved quality of life and, possibly, longer survival of patients with AIDS.
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PMID:Endocrinologic and metabolic manifestations of the acquired immunodeficiency syndrome. 224 1

The small intestine is a major target in HIV infection. Chronic diarrhoeal disease associated with malabsorption is the principal clinical manifestation of such infection. Reduced intestinal immunity and opportunistic enteric infections play a major role in clinical disease, but an enteropathy induced by HIV per se has also been implicated. The immunopathology of reduced intestinal immunity and its progression during HIV infection is poorly understood. HIV genome and proteins have been detected reproducibly in cells of the lamina propria resembling macrophages, but direct epithelial infection with HIV is controversial. Another factor which may contribute to diarrhoea is autonomic neuropathy within the jejunum. Small intestinal disease causes malabsorption of fat and disaccharides and may contribute to the weight loss seen in advancing HIV infection. However, malnutrition seen in HIV infection is multifactorial and may occur as a constitutional sign of infection in the absence of overt intestinal disease. Reduced food intake does not appear to be a causative factor in the weight loss in constitutionally well stage IV patients and there is some evidence that release of cytokines (TNF alpha/cachectin) into plasma or locally into tissue may mediate such events. The response of HIV-infected individuals to nutritional support is variable, but it is becoming increasingly apparent that the response is limited by the presence of severe systemic infection. However, aggressive nutrition is an important therapeutic mode which should be offered to all HIV-infected patients.
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PMID:Malabsorption, malnutrition and HIV disease. 228 81