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)

A distinction is drawn between coeliac-mesenteric occlusion in intestinal infarct, vascular insufficiency, and fully compensated occlusion. The clinical picture of the first is that of acute abdomen with serious circulatory shock syndrome, whereas chronic insufficiency is marked by episodic pain triggered by eating, effort, drugs, etc., canalisation disturbances, meteorism, constipation or diarrhoea, intestinal stenosis, wasting and malabsorption. Their medical management and its principles, possibilities and limits are discussed.
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PMID:[Clinical aspects and medical therapy of celiac-mesenteric vascular insufficiency]. 62 74

The pathology of primary familia amyloidosis with polyneuropathy is described on the basis of post-mortem examination of six cases from Northern Sweden. Clinically the disease is characterized by progressive sensory and motor disturbances with loss of sensation, muscular wasting and flaccid paralysis. Impotence, urinary bladder dysfunction, motility disturbances of the gastro-intestinal tract and postural hypotension indicate affection of the autonomic nervous system as well. Malabsorption, cardiac insufficiency and vitreous opacites also occur. As regards the distribution of amyloid, the following findings seemed to be characteristic. Usually there were no gross lesions indicating the amyloid disease. Histopathologically, amyloid deposits were observed in great extent in the peripheral nervous system and in various parts of the peripheral autonomic nervous system as well. It occurred extensively in the walls of blood vessels of various calibres, in the perivascular collagenous connective tissue and adjacent to the smooth musculature. Amyloid deposition was also found more or less abundantly in various other organs and tissues. No deposits, however, or only insignificant amounts, were found in the central nervous system, either in the parenchyma of the liver, in the islets of Langerhans, or in the bone marrow. Clinical manifestations seemed to be related to the local deposition of the amyloid substance. Our clinical and pathological findings in this particular type of familial amyloidosis conformed mostly to those previously described.
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PMID:Postmortem findings in primary familial amyloidosis with polyneuropathy. 115 99

The AIDS wasting syndrome (AWS) is characterized by > 10% loss of baseline body weight during 6 months and may occur in patients with or without associated chronic diarrhea. To determine whether the presence of small-intestinal malabsorption is associated with the development of AWS in human immunodeficiency virus (HIV)-infected patients with chronic diarrhea, we retrospectively reviewed the results of D-xylose testing performed in the clinical evaluation of 21 consecutive HIV-infected patients with chronic diarrhea. A thorough search for small-intestinal pathogens was performed including upper endoscopy, duodenal biopsy, and aspirate for culture and ova and parasite examination. These studies were negative in all patients except two who were excluded from the study. In the 19 patients with no identifiable pathogens, the 1-h serum D-xylose concentration was significantly lower in patients with AWS than in those without, 8.3 +/- 0.8 versus 23.7 +/- 3.4 mg/dl, respectively, p < 0.001. Urine D-xylose excretion during 5 h was also significantly lower in the group with AWS, although creatinine clearance was similar in the two groups. Patients with AWS were more often refractory to standard antidiarrheal therapy with loperamide or diphenoxylate and carried a poor prognosis (90% mortality at 1 year versus 22% mortality in the group without AWS). These data indicate that small intestinal malabsorption is a major component in the severe wasting seen in some HIV-infected patients with chronic diarrhea. Patients with markedly abnormal D-xylose tests may require more potent antidiarrheal therapy and are expected to have a high mortality as a possible consequence of intestinal dysfunction.
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PMID:D-xylose malabsorption: characteristic finding in patients with the AIDS wasting syndrome and chronic diarrhea. 145 20

Involuntary weight loss or wasting indicative of severe protein energy malnutrition is a frequent complication of acquired immune deficiency syndrome (AIDS). Malnutrition, with its associated adverse effects on immunocompetence, may contribute to the progression of AIDS itself. Since death from wasting is ultimately related to the magnitude of tissue depletion, restoration of body cell mass may enhance survival. The mechanism of weight loss in AIDS has not been clearly elucidated. The etiology is likely to be multifactorial, the result of interactions between decreased caloric intake, malabsorption, and alterations in energy expenditure secondary to hormonal and/or metabolic abnormalities. Although weight loss is occasionally reversible with treatment of underlying infections and/or easily identifiable and reversible causes, the majority of patients are not this fortunate. Enteral and parenteral nutrition, which are expensive, cumbersome, and potentially morbid, have been suggested by some as therapeutic options. Megestrol acetate, a synthetic, orally active progestational agent, has been reported to stimulate appetite and weight gain. Data regarding the use of megestrol acetate for the treatment of cachexia related to human immunodeficiency virus (HIV) infection demonstrate convincingly its effectiveness in treating many patients with HIV-related anorexia and cachexia.
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PMID:HIV-related cachexia: potential mechanisms and treatment. 146 29

The most frequently suggested causes of malnutrition are as follows: poverty, low parental education, lack of sanitation, low food intake, malabsorption, diarrhea and other infections, poor feeding practices, family size, short birth intervals, maternal time availability, child rearing practices, and seasonality. The purpose of this study of 1178 children 0-59 months of age from 30 villages in Arua District, Uganda, was to assess the nutritional status of this population and to identify sensitive predictors of mortality and major causes of malnutrition. Anthropometric and socioeconomic and health-related data were obtained between February and March, 1987, on the randomly selected population. Follow-up after a year provided mortality data on the sampled population. The results showed that nutritional status before the first 5 months of life was satisfactory; deterioration followed. Wasting or low weight-for-height existed predominantly among those aged 6-24 months. Stunting was high after 5 months. The proportion of underweight children was greater in the 2nd year of life; improvement occurred thereafter. Mortality rates were around 10% during the first year and declined thereafter to .5% in the 4th year. Mortality was higher among those with low weight-for-age or weight-for-height. The relative risk for mortality was 3 at less than -3 standard deviation (SD) weight-for-age. For less than -2 weight-for-height the relative risk was 4.6. Mortality was higher for children 12 months of age. Weight-for-age was the most sensitive indicator of mortality for the percentage of survivors correctly identified over 88%; for lower specificity weight-for-height was a more sensitive indicator. Paternal occupation was the only household indicator related to child mortality; i.e., high mortality was related to a father's occupation as alcohol distributor, and low mortality, to his occupation as tobacco grower or businessman. In the stepwise multiple regression, a father's education was positively correlated with weight-for-age, and a mother's education, with height-for-age. Negative influences were age, breast feeding, use of unprotected water supplies in the dry season, skin infections, and diarrhea within 2 weeks before the survey. Paternal education was positively associated, and skin infections negatively association, with weight-for-height. Unrelated factors are identified; justification of significant factors is discussed.
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PMID:Determinants of child nutrition and mortality in north-west Uganda. 146 51

Two appetite stimulants, megestrol acetate and cyproheptadine were administered in a randomized trial to 14 patients who had no evidence of opportunistic infection or malabsorption but were wasted (had lost more than 5 kg body weight) as a result of human immunodeficiency virus (HIV) infection. Energy intakes were calculated from a 7 day weighed dietary record. Mean energy intakes per kilogramme body weight were similar in both treatment groups (greater than 34 kcal/kg) and were higher than that in well British males. Energy intakes increased by just over 500 kcal during both treatments, but fell to pretreatment levels after therapy. Patients in both treatment groups gained a moderate amount of weight. Megestrol acetate was associated with impotence in 4 patients. Insufficient calorie intake alone is not a common cause of wasting associated with HIV and the role of appetite stimulants is likely to be limited.
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PMID:Megestrol acetate vs cyproheptadine in the treatment of weight loss associated with HIV infection. 150 60

Studies of body composition in acquired immunodeficiency syndrome (AIDS) patients demonstrated body cell mass depletion out of proportion to losses of body weight or fat. The timing of death from wasting was related to the extent rather than the specific cause. However, some patients remain stable for indefinite periods, indicating that wasting is not a constant phenomenon. The development of malnutrition is multifactorial and includes disorders of food intake, nutrient absorption and intermediary metabolism. Nutritional repletion has been demonstrated in several studies. The effect of treating infections that promote wasting was shown in a study of ganciclovir therapy for cytomegalovirus colitis, in which untreated patients underwent progressive wasting whereas treated patients repleted body mass. Total parenteral nutrition had a variable effect upon body composition, with repletion occurring in patients with eating disorders or malabsorption syndromes and progressive depletion occurring in patients with serious systemic infections. Enteral nutrition also can replete body mass in AIDS patients without severe malabsorption. Pharmacologic stimulation of appetite also may lead to weight gain. The results of these studies indicate that nutritional support can improve nutritional status in properly selected AIDS patients.
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PMID:Nutritional effects and support in the patient with acquired immunodeficiency syndrome. 154 39

In a family in which the father was the mother's uncle, 3 of the 7 children were affected by a syndrome of malabsorption with various clinical symptoms. Diarrhea appeared in 2 of the children at birth, and in the third child at six months. The diarrhea led to failure-to-thrive, muscular wasting and abdominal swelling. However, the children improved spontaneously over the years. During childhood all 3 had manifest steatorrhea. Serum cholesterol was between 39 and 100 mg/dl, while triglycerides were normal to high. Reevaluation during the past year revealed areflexia, deficiency of vitamins A and E and of apoproteins A and B, and prolonged PT time in 2 of the children. Electron and light microscopy of small intestinal biopsies revealed vacuoles in the enterocytes. Electrophysiological tests revealed major disturbances in sensory conduction and brain-stem function. These cases differ from those described in the literature. Although in hypobetalipoproteinemia, 1 of the parents would be expected to be heterozygous and have low serum levels of APO B, in this family the parents had normal levels. Their children had low levels of serum APO A, while in patients with hypobetalipoproteinemia the levels are normal. There is a report of a case of deficiencies of both apolipoproteins, but the patient was asymptomatic, had chylomicronemia after a prolonged fast, and lower cholesterol levels than our patients. 8 other cases of apolipoprotein deficiency have been reported with biochemical characteristics similar to those of our patients, but with retention of chylomicrons in the small intestine.
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PMID:[Familial hypobetalipoproteinemia with steatorrhea and malabsorption]. 180 Feb 74

Magnesium, the second most abundant intracellular cation, is essential for life. The consequences of deficiency are severest in the smallest and youngest members of each species and may include sudden unexpected death. Magnesium deficiency, usually diagnosed by hypomagnesemia, may be congenital, as in premature infants, infants of magnesium-deficient mothers and infants with intrauterine growth retardation. It may be acquired or caused by low magnesium intake, the use of magnesium-wasting drugs, illness provoking gastrointestinal or renal losses of the mineral, or high metabolic demands imposed by catch-up growth or postsurgical healing. Finally, the deficiency may be conditioned, caused by excessive dietary calcium, phosphorus or protein in relation to dietary magnesium, especially during a period of rapid growth or tissue repair. Magnesium therapy is safe when a low dosage is given with monitoring of plasma or serum magnesium levels, with occasional checking of calcium and potassium levels. A parenteral dose of 0.1 ml/kg/day of 50% magnesium sulfate USP (approx. 0.2 mmol/kg/day or 0.4 mEq/kg/day) may be given for 5 dose days. An oral dose of 1.0 ml of 10% magnesium chloride solution providing 0.5 mmol/kg/day magnesium or 1.0 ml/kg/day of 10% magnesium chloride USP (0.5 mmol/kg/day) or magnesium magonate (Magonate) 1.0 ml/kg/day (0.45 mmol/kg/day) may be given for extended periods; higher doses may be required for malabsorption syndromes. Hypermagnesemia, which usually results from magnesium overdosage or inadequate renal function, is a potential threat to neonates born to magnesium-treated eclamptic mothers. Most show marked improvement after 36 h of conservative management that includes calcium salts and intravenous infusions of glucose and saline, but obtunded neonates may require dialysis.
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PMID:Magnesium in perinatal care and infant health. 184 56

Malnutrition is a frequent problem in persons infected with the human immunodeficiency virus. The origin of malnutrition in patients with AIDS may be multifactorial. The primary mechanisms include disorders of food intake, alterations in intermediary metabolism, and nutrient malabsorption. Attention to the problems of malnutrition in patients with AIDS is of paramount importance because the timing of death in these patients may be more closely related to degree of body cell mass depletion than to any specific underlying infection. Nutritional support can improve nutritional status in selected patients, and repletion of body cell mass may be associated with functional improvement. Early assessment, attention to nutritional requirements, and prompt intervention can minimize wasting and replete body cell mass. This article examines the evidence for malnutrition in patients with AIDS, reviews the studies of nutritional support, and presents an approach to the management of malnutrition in AIDS.
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PMID:Malnutrition in patients with AIDS. 212 39


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