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

Epidemiological studies have demonstrated a marked negative relationship between diarrhoea and physical growth and development of a child. Each day of illness due to diarrhoea produces a weight deficit of 20-40 gms. Poor nutrition is associated with more serious prolonged diarrhoea. 'Catch-up growth' often does not occur in malnourished children. Malnutrition, particularly wasting, is a strong predictor of diarrhoeal duration and the prolonged illness could exacerbate nutritional faltering, thereby increasing the subsequent risk of death. Poor appetite, vomiting, deliberate withholding of food resulting in poor intake; malabsorption of macro and micronutrients; hastening of intestinal transit time; disturbance of metabolic and endocrine functions; and direct loss of protein and other nutrients in gastrointestinal tract are some of the known mechanisms which have an impact on the nutrition during an episode of diarrhea. In addition diarrhoea of infectious origin causes cytokine induced malnutrition which results from the actions of proinflammatory cytokines like tumour necrosis factor and interleukin 1, 6 and 8. Preexisting malnutrition is associated with decreased turnover of epithelial cells resulting in delayed recovery which may prolong an episode of infectious diarrhoea by itself as well as by promoting tissue invasion by other enteropathogens. Malnutrition may also alter protective host factors and thereby favour intestinal colonization by the pathogenic microbes. Mucosal damage varying from moderately severe changes to flat lesions indistinguishable from those of celiac disease may occur in kwashiorkar. Diarrhoea malnutrition interaction represents a dangerous web which can be distangled by prevention of disease transmission by promoting exclusive breast feeding, hygienic weaning practices, safe drinking water and handwashing, improved host defences by breast feeding, improved nutrition, measles vaccine and other vaccines against enteropathogens in the offing; and promotion of standard case management with special emphasis on nutritional support and rehabilitation.
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PMID:Diarrhoea and malnutrition interaction. 1113 59