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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Relationships between nutrition and infection are generally complex, bidirectional, and not perfectly worked out. Healthy people can adapt to simple decreases in intake or increases in expenditure. However, the imposition of infection with associated cytokines may impair such adaptations, resulting in wasting of lean tissue. In human immunodeficiency virus (HIV) infection, nutritional abnormalities are common. Lean body mass depletion is associated temporally with death in a subset of acquired immune deficiency syndrome (AIDS) patients. Weakness, fatigue, and anorexia are important symptomatic complaints affecting quality of life. Pathophysiologic mechanisms remain speculative, although there is reason to suspect four theoretic factors: decreased intake, malabsorption, hypermetabolism, and altered metabolism. More than one disturbance may be necessary for clinical wasting to develop; ie, a primary abnormality plus a failure of homeostatic adaptation. Excess cytokine production also may be involved, but this is uncertain. Therapeutics remain empiric in the absence of known mechanisms. Current options are restricted to diet adjustments or supplements, treatment of underlying diseases (where possible), and rarely, parenteral alimentation. Promising investigational possibilities include an appetite stimulant (megestrol acetate) and therapies to oppose cytokine production or actions, but definitive beneficial effects on nutritional status, subjective performance, disease activity, or survival have not yet been demonstrated. Advances in clinical therapeutics await an improved understanding of pathophysiologic mechanisms and carefully designed clinical trials testing proposed interventions.
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PMID:Current approach to the treatment of human immunodeficiency virus-associated weight loss: pathophysiologic considerations and emerging management strategies. 225 24

Enterocytozoon was 1st described in 1985, in an AIDS patient with intestinal malabsorption and diarrhea. Since then, additional cases of infection with this organism have been observed, but only in individuals with AIDS and malabsorption. Intestinal tissue biopsies were obtained from a 45-year-old man prior to AIDS diagnosis, again nine months later and then at autopsy two months later. When the biopsies were examined electron microscopically, both sets contained the microsporidian parasite. However, the 2nd intestinal biopsy, when wasting was much more severe, contained infection in almost every small intestinal enterocyte examined. The parasite was actively developing, allowing us to detail its life cycle. The parasite is apansporoblastic, polysporous and has characteristics not previously reported in the Microsporida: (1) an electron lucent inclusion not usually seen in Microsporida is prominent and always present; (2) extremely elongated sausage-shaped nuclei occur in the proliferative phase of parasite development; (3) the polar tube development uniquely involves the production of electron dense discs, yet results in the formation of a typical spore; and (4) polar tube development occurs prior to the final division of the multi-nucleate sporont. On the basis of these characteristics, we are placing this genus in a new family, Enterocytozoonidae, n. fam.
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PMID:Intracellular development of Enterocytozoon, a unique microsporidian found in the intestine of AIDS patients. 231 90

The association of coeliac disease and partial lipodystrophy is described. The patient also had deficiencies of serum IgA and C3 complement (the latter associated with partial lipodystrophy). In addition, there was subclinical dermatitis herpetiformis confirmed by skin biopsy. The facial wasting of fully developed partial lipodystrophy may be misinterpreted as a sign of malabsorption but the facial, upper limb, and truncal lipodystrophy contrasts with normal pelvic and lower limb appearances.
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PMID:Partial lipodystrophy in coeliac disease. 237 78

Earlier studies have revealed hypomagnesemia with cyclosporine treatment in renal and bone marrow transplant recipients. The present study was designed to investigate the possible effect of cyclosporine on Mg metabolism in normal rats. Sprague-Dawley rats were randomized into the cyclosporine group, which was given 15 mg/kg/day cyclosporine by gastric gavage, and the control group, which received the vehicle alone. Food intake, body weight, serum concentration, urinary excretion, fecal excretion, and tissue content of Mg were determined weekly for 3 weeks. In addition, intestinal absorption of Mg was determined by using in vivo perfusion. Serum Mg concentration fell significantly after 1 week of cyclosporine treatment and remained low throughout the observation period. This was associated with reduced food intake and renal Mg conservation during the first week but normal food intake and severe renal Mg wasting thereafter. In vivo perfusion studies performed at 1 and 3 weeks showed no significant difference in intestinal absorption of Mg between the two groups, thereby excluding intestinal malabsorption as a possible culprit. Likewise, fecal Mg excretion showed no significant difference in the two groups. It was surprising that tissue Mg content (in muscle, liver, and kidney) was increased in the cyclosporine-treated group at 3 weeks. We conclude that cyclosporine administration in rats leads to a fall in serum Mg concentration primarily as a result of renal Mg wasting and possibly as a result of a shift of Mg to the tissue compartments with no discernible effect on gastrointestinal handling of Mg.
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PMID:Effects of cyclosporine on magnesium metabolism in rats. 267 Dec 13

A 41-yr-old woman with primary biliary cirrhosis developed weakness and wasting in proximal muscles, areflexia, and decreased proprioceptive and vibratory sensation. Investigations revealed law serum levels of vitamin E and electromyographic and muscle biopsy changes consistent with a neuropathy. Sural nerve histology demonstrated axonal dystrophy with patchy demyelination. These features closely resemble a neurologic syndrome associated with chronic cholestatic liver disease and vitamin E deficiency in children. Adults with chronic cholestasis may also be susceptible to neurologic damage from prolonged malabsorption of vitamin E.
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PMID:Neurologic syndrome associated with low levels of vitamin E in primary biliary cirrhosis. 301 81

A high energy intake, compensating for malabsorption, and the energy cost of lung disease, lung infections, and the underlying metabolic abnormality, is required to ensure normal growth in patients with cystic fibrosis. This goal can be readily achieved by adherence to a high quantity, normally balanced diet (with 40% of the energy as triglycerides of long-chain fatty acids). In contrast, this goal cannot be reached in the majority of patients adhering to low-fat and thus low-energy-containing diets, which almost inevitably lead to malnutrition with wasting and stunting. The prevention of malnutrition may well have considerably enhanced the prognosis of patients at one clinic. Further work is needed to define the interrelationship of nutrition and lung disease, and to define the appropriate nutrient requirements induced by the lung disease per se, recurrent infections, and the underlying disease process.
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PMID:The impact of nutrition in cystic fibrosis: a review. 304 37

We evaluated nutritional status, pulmonary impairment, nutritional intake, and fat absorption in 73 cystic fibrosis (CF) patients to identify the primary factor(s) influencing growth. In general, the growth pattern in our patients was satisfactory since 60/73 were not underweight. When caloric intake is greater than or equal to 95% of RDA, wasting does not occur regardless of the degree of malabsorption, dietary fat content, or lung involvement. In the group of patients who consume less than the RDA, underweight is related to the severity of pulmonary disease; indeed, 11/13 underweight patients have a chest x-ray score over 15. Steatorrhea is well controlled in most patients; only 11 of 73 show a fat excretion greater than 25% of fat intake. The daily number of capsules of Pancrease varies from 4 to 57. The amount of Pancrease to be given was individualized to meet each patient's requirements using fat balance studies to determine the necessary daily Pancrease dose, then distributing the total dose in proportion to the fat content of each meal.
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PMID:The management of enzymatic therapy in cystic fibrosis patients by an individualized approach. 340 60

Diabetic diarrhea and steatorrhea occur predominantly in young adult males who have juvenile-onset diabetes mellitus complicated by neuropathy. The presentation is often severe, with nocturnal or postprandial watery diarrhea and tenesmus. Massive malabsorption of fat may occur; however, malabsorption of other nutrients and generalized wasting are quite rare. Because the symptoms are relatively refractory to treatment, it is important to rule out other, more easily treatable causes of this presentation. Bacterial overgrowth, exocrine pancreatic insufficiency, and celiac disease are also associated with diabetes mellitus and can mimic this process. Although the mechanism of diabetic diarrhea and steatorrhea remains unclear, neuropathy, gastrointestinal motor abnormalities, bacterial overgrowth, and bile acid abnormalities have been implicated in the pathogenesis.
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PMID:Small intestinal manifestations of diabetes mellitus. 665 61

A case of malabsorption syndrome (organic wasting, hypokaliaemia, metabolic acidosis, diarrhoea, hypochromic anaemia) following removal of 4 m of ileus for thrombophlebitis of the mesentery is described. In the first seven months, the patient was hospitalised five times to correct these imbalances by means of PA, with repeated venous incannulation. PA was continued at home each evening, together with heparin therapy (25,000 U calcic heparin/day). The patient later died following the appearance of serious venous thrombosis. The question of this complication and its prevention is discussed.
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PMID:[Clinical aspects of long-term parenteral alimentation in the "short intestine syndrome". Clinical case]. 678 Sep 32

Impairment of active intestinal absorption of glucose and leucine was observed in rats 2-3 wk after oral treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (5 and 100 mg/kg). At the higher dose level used this response was complicated by the effects of severely reduced food consumption. Malabsorption of specific nutrients may help occasion the body wasting seen in many animals after acute exposure to TCDD.
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PMID:Intestinal absorption of nutrients in rats treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). 733 35


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