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)

The loss of bone which starts at the menopause is self-limiting (exponential) and possibly mainly trabecular. It merges into an age-related linear loss of bone which is probably mainly cortical. The menopause is associated with a rise in obligatory urinary calcium loss resulting from an increase in the filtered load of calcium which may be due to the complexed fraction. The dependence of the urinary hydroxyproline on the urinary calcium and sodium suggests that the bone resorption is a response to calcium losses rather than a primary event. In osteoporotic women, there is a further increase in filtered load of calcium and obligatory calcium loss, frequently coupled with malabsorption of calcium. Urinary hydroxyproline can be suppressed by calcium administration in those with normal absorption and by calcitriol in those with calcium malabsorption. It is known that calcium deficiency causes osteoporosis in experimental animals, but there is controversy about the role of calcium deficiency in the pathogenesis of human osteoporosis. Calcium supplementation inhibits cortical bone loss in postmenopausal women but there is some doubt as to whether it can inhibit trabecular bone loss in women close to the menopause. This may be partly a matter of dose, formulation and time of administration.
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PMID:Calcium and osteoporosis. 307 47

Hypoalbuminemia is considered one of the hallmarks of protein-calorie malnutrition and chronic liver disease. Recently, serum albumin has also been proposed as a critical predictor of the response to nutritional support and tolerance to enteral feeding in critically ill patients. Albumin is essential for maintenance of plasma colloidal osmotic pressure, prevention of edema, and transport of certain drugs and nutrients. Experimental studies have shown that rapid plasma expansion and reduced plasma protein concentration and osmotic pressure induce a net secretion of sodium and water into the small intestinal lumen. However, the effects of chronic hypoalbuminemia per se on intestinal absorption, independent of malnutrition, have not been fully studied. It is documented that both chronic illness and malnutrition may profoundly affect intestinal anatomical structure and function, inducing some degree of malabsorption. In the last few years, some have advocated albumin infusion to improve clinical response to patients with hypoalbuminemia receiving parenteral nutritional support or to reduce intestinal intolerance and diarrhea in patients receiving enteral tube feeding. A review of the literature shows that both clinical and experimental data to support these suggestions are scarce and further investigations are needed. Hypoalbuminemia is one of many parameters of malnutrition, and it is unlikely that correction of a single parameter for a short time would lead to major clinical benefits.
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PMID:The role of albumin in nutritional support. 314 98

The impact of acute Yersinia enterocolitica infection on jejunal and ileal solute and water transport was examined. New Zealand White rabbits (500-600 g) were infected with Y. enterocolitica and compared with unmanipulated controls and pair-fed controls. Transport studies were performed 6 days after infection on jejunum and ileum by an in vivo single-pass perfusion technique and in vitro under short-circuited conditions in Ussing chambers. When studied in vivo, Y. enterocolitica infection resulted in decreased water and electrolyte absorption in the jejunum under basal conditions and in both jejunum and ileum in the presence of glucose. Glucose absorption was also decreased in jejunum and ileum. When studied in vitro, net basal Na+ and Cl- transport was not altered in jejunal or ileal epithelium from infected animals. Glucose-stimulated Na+ absorption was decreased in ileal epithelium, and absorption of 3-O-methyl-D-glucose was decreased in both jejunum and ileum. Secretory capacity of Cl-, as assessed by isobutylmethyl xanthine stimulation, was unimpaired in both jejunum and ileum. Decreased food intake alone, in the pair-fed animals, had little effect on intestinal transport. The results indicate that malabsorption, rather than active intestinal secretion, is the major small intestinal transport defect in acute Y. enterocolitica infection. Furthermore, the abnormalities can be directly attributed to injury induced by the organism itself, rather than malnutrition.
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PMID:Effect of acute Yersinia enterocolitica infection on in vivo and in vitro small intestinal solute and fluid absorption in the rabbit. 333 34

Previous studies have provided evidence that an anaerobic bacterium, which degrades dietary oxalate to CO2 and formate, is present in colonic contents of a number of herbivorous species, laboratory rodents and humans. The present study examines the possibility that these bacteria degrade significant amounts of oxalate and can influence colonic oxalate absorption. Guinea pigs adapted to a diet containing 2% sodium oxalate or fed a normal diet were challenged with 67, 135, 170 or 200 mg of sodium oxalate containing 0.5 microCi of [14C]oxalate, which was injected into the cecum. Adapted animals excreted approximately 2% of the 14C in the urine, regardless of the dose, whereas unadapted animals excreted significantly higher amounts in the urine at the two lower doses and died at the two higher doses. Conversely, antibiotic treatment of adapted guinea pigs reduced the ability of their cecal flora to degrade oxalate, and a correspondingly greater percentage of an injected oxalate load was excreted in the urine. Oxalate degradation rates in cecal fluid were depressed by the secondary bile salt deoxycholate, and in vitro studies with pure isolates of guinea pig and human strains of oxalate degraders confirmed that these bacteria were highly sensitive to low concentrations of deoxycholate. Results indicate that these bacteria may be important in preventing excess absorption of oxalate and raise the possibility that the hyperoxaluria associated with bile salt malabsorption of ileal disease in part may be due to suppression of these bacteria by the bile salts.
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PMID:Intestinal oxalate-degrading bacteria reduce oxalate absorption and toxicity in guinea pigs. 337 43

Two patients with the syndrome of Ramsay Hunt (dyssynergia cerebellaris myoclonica, DCM), associated with malabsorption due to adult coeliac disease, are reported. Both presented with progressive cerebellar ataxia, action myoclonus, and epilepsy. One had gastrointestinal symptoms (recurrent diarrhea and weight loss which responded satisfactorily to a gluten-free diet), but the other did not. In both patients, jejunal biopsy revealed subtotal villous atrophy; serum folate and vitamin E level were also reduced. Neither a gluten-free diet nor vitamin supplements improved the neurological picture. However, some symptomatic relief was afforded by treatment with clonazepam, sodium valproate, carbamazepine, and piracetam. It could be argued that the association between these two disorders is coincidental. However, since we have found this combination in 2 of 14 consecutive cases with DCM, a causal relationship seems likely, although the underlying mechanism remains unknown. Patients with the Ramsay Hunt syndrome should be investigated for malabsorption, and also undergo small intestinal biopsy.
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PMID:Ramsay Hunt syndrome and coeliac disease: a new association? 847 11

Juvenile rickets or osteopenia in rural black children is thought to be due to low calcium intake. Characteristic findings include mild calcium deficiency, normal serum phosphate levels, increased alkaline phosphatase concentrations and normal plasma vitamin D levels. The present series consisted of 62 black children (average age 6.82 years), 41 males and 21 females. Low levels of serum calcium and phosphate were present in 34 (54%) and 18 (29%) of the patients respectively. Alkaline phosphatase concentrations were raised (greater than 350 IU/l) in 38 (61%). Serum sodium, potassium, chloride, total bicarbonate, magnesium, ceruloplasmin and albumin levels were generally within normal limits. Urinary acidification was normal and barium studies were reported as normal in all but 4 children. Malabsorption was not an important feature. Serum vitamin D levels were not determined. All 18 patients with hypophosphataemia improved. Eleven children showed no clear response after at least 8 weeks in hospital--8 remained hypocalcaemic and 2 of the 3 patients with normal biochemical values showed no radiological improvement of osteopenia after 2 and 4 months in hospital, while the 3rd showed only very slight improvement after 7 months in hospital. It is not clear why these patients did not respond and whether even longer hospitalisation would have been effective.
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PMID:[Aspects of juvenile rickets/osteopenia in black children]. 360 15

Fenamates are a class of nonsteroidal anti-inflammatory drugs that frequently have gastrointestinal side effects. Diarrhea is seen fairly commonly. Malabsorption has been reported only 3 times with mefenamic acid, one of the family of fenamates. A case of steatorrhea due to meclofenamate sodium is presented here. Fenamates block net fluid absorption and also lead to histological abnormalities of the small intestine. The cause of the malabsorption seen in fenamate therapy is not known.
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PMID:Steatorrhea associated with meclofenamate sodium therapy. 368 10

The regulatory functions of anions in colonic absorption of sodium are unknown. Absorption of sodium ions was assessed with chloride, butyrate, nitrite, sulphate and oxalate anions in segments of proximal/distal colon and in defunctioned colon. Efficiency of sodium absorption was related to availability of CO2 in mucosal cells: CO2 availability was enhanced (P less than 0.01) by sodium nitrite or diminished (P less than 0.01) in defunctioned colon. Sodium nitrite stimulated absorption of sodium in the distal colon where bicarbonate secretion predominated and n-butyrate stimulated absorption of sodium in the proximal colon where hydrogen ion secretion predominated. Sodium absorption was very significantly diminished (P less than 0.01) in defunctioned colon. Results indicate that sodium absorption in the colon is both a double anion exchange system as well as cation/anion co-transport. Anions act differently on sodium absorption along the length of the colon and prolonged lack of anions plays a part in sodium malabsorption of the defunctioned colon.
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PMID:Anion control of sodium absorption in the colon. 371 59

An investigation of variables important to calcium stone formation in urine indicated significantly increased daily excretion of calcium and oxalate and decreased excretion of ascorbate and citrate by recurrent calcium stone formers. In addition, urine volume, sodium, mucopolysaccharide, and protein were also significantly increased. We compared the uptake of citrate and ascorbate from the gut into the blood in normal controls and stone formers. These studies indicated significantly depressed absorption of both these hydroxycarboxylic acids in recurrent calcium stone formers. We also found that concurrent administration of citrate inhibited ascorbate absorption and increased urinary oxalate excretion after an ascorbate load in normal subjects and stone formers. These findings suggest a mechanism that explains hyperoxaluria in stone patients on the basis of a malabsorption of citrate, ascorbate, and possibly other hydroxycarboxylic acids.
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PMID:Chemical factors important to calcium nephrolithiasis: evidence for impaired hydroxycarboxylic acid absorption causing hyperoxaluria. 380 7

A better understanding of the physiologic response to and nutritional consequences of acute diarrhea can facilitate an improved outcome for this and other infectious diseases. Acute diarrhea causes the host to undergo a sequence of hormonal, metabolic, and immunologic responses, all of which have nutritional consequences. Its most profound effect is on the malabsorption of water and electrolytes by the intestinal epithelial cell, the electrolyte, leading to dehydration. Diarrhea is defined as any alteration of fluid and electrolyte movement that results in increased fecal water due to an excessive amount of solute in the stool. Infectious agents that damage the enteric mucosa cause villous atrophy, which is accompanied by increased proliferation, migration, and extrusion of epithelial cells; this results in alterations of fluid and electrolyte movement and is the final common pathway to the development of diarrhea. During the acute stages of diarrhea, there are increased losses of fecal weight and volume as well as sodium and chloride and the level of disaccharidase enzymes is depressed. Different bacteria affect different parts of the gastrointestinal tract. After bacterial adherence and surface colonization of the intestinal epithelium, diarrhea can result from any of 3 major mechanisms: 1) production and release of enterotoxins, 2) direct invasion of the mucosa or submucosa, and 3) adhesion and cytotoxic disruption of the microvilli of the enterocyte. There is evidence of diarrhea-associated changes in the plasma concentration of certain gastrointestinal hormones and indications that calcium plays a key role in the intracellular regulation of electrolyte transport. The impact of diarrhea will be more significant in the debilitated or marginally nourished child. To improve the host response to infection, nutrients that are essential for optimal immune function and are rapidly being metabolized should be selectively replaced, while nutrients needed by the offending organism can be withheld.
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PMID:Nutritional implications and physiologic response to pediatric diarrhea. 394 85


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