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)

Increased fecal bile acid loss and defective in vitro ileal bile acid uptake were demonstrated in an 8-year-old boy with diarrhea starting in the neonatal period. His continuously normal physical development and good nutritional status are in keeping with a well-preserved cholic acid pool and normal duodenal bile acid concentration. Isolated bile acid malabsorption can remain well compensated and present as the chronic nonspecific diarrhea syndrome of childhood.
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PMID:Well-compensated primary bile acid malabsorption presenting as chronic nonspecific diarrhea. 394 38

A rapid breath hydrogen analyzer to detect lactose malabsorption is described. After ingestion of a lactose solution the patient expires into a mouthpiece attached to a hydrogen sensor at 30-min intervals for 3 1/2 h. The hydrogen of the expired air causes a voltage change that can be transformed into ppm from a calibration curve. A tolerance test with a load of 100 g lactose was performed in 43 consecutive patients with various gastrointestinal disturbances, referred to the laboratory for the commonly used lactose tolerance test based on plasma glucose measurements. Eleven patients developed symptoms of lactose intolerance during the test. Biopsy specimens from the distal duodenum or proximal jejunum showed partial villous atrophy in one, in whom celiac disease with lactose intolerance was diagnosed; the other 10 had normal specimens. In nine of them lactose intolerance was diagnosed and confirmed by observation for months on a lactose-poor diet. The 10th patient (H.P.L.) did not improve on such a diet. He also showed pronounced symptoms of intolerance during a test with monosaccharides (glucose + galactose). His intestinal disease remained undiagnosed. The 11 patients with symptoms of intolerance and 3 patients without symptoms during the lactose load showed a flat plasma glucose curve after drinking the lactose solution--that is, a maximum rise of the glucose concentration of 1.5 mmol/l. One of the symptom-free patients dropped out and could not be observed, another did not improve on a lactose-poor diet, and the third noticed a favorable effect of the diet on stool consistency but not on other abdominal symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hydrogen concentration in expired air analyzed with a new hydrogen sensor, plasma glucose rise, and symptoms of lactose intolerance after oral administration of 100 gram lactose. 404 33

A severely affected case of Hartnup disease is reported, where the patient responded rapidly to nicotinamide. This supports the view that all the clinical features, except reduced stature from general nutritional defect, are secondary to tryptophan and nicotinamide deficiency rather than to an unknown toxic factor. Severe malabsorption of both tryptophan and phenylalanine was demonstrated. The dipeptide carnosine was absorbed normally whereas when the two constituent amino acids, beta-alanine and L-histidine, were ingested, absorption of the former was normal but that of the latter was grossly defective. The suggestion is advanced that in cases of Hartnup disease protein nutrition is maintained by intestinal uptake of amino acids as oligopeptides rather than as free amino acids. By contrast, both modes of absorption are probably important in normal subjects. Radiology of the small intestine is abnormal in Hartnup disease when a large amount of protein is admixed with the barium meal.
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PMID:Studies on intestinal absorption of amino acids and a dipeptide in a case of Hartnup disease. 424 31

A 68-year-old man presenting with chronic intermittent diarrhea and progressive ataxia was found to have idiopathic hypoparathyroidism. Intrinsic factor-resistant vitamin B(12) malabsorption was demonstrated. Both the diarrhea and vitamin malabsorption were reversed by correction of hypocalcemia.His neurological profile was a combination of peripheral nerve, posterior column and cerebellar deficits. He had calcifications in the dentate nuclei of the cerebellum. Possible etiological factors such as vitamin B(12) deficiency, folic acid deficiency and steatorrhea have been excluded. Posterior column and cerebellar abnormalities improved with treatment. It is postulated that hypocalcemia causes functional, reversible spinal cord and cerebellar dysfunction.
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PMID:Idiopathic hypoparathyroidism with impaired vitamin B 12 absorption and neuropathy. 433 89

Several authors have recently reported a neurological disorder associated with chronic vitamin E deficiency in man. Except in one patient, this deficiency has always been secondary to an underlying disease resulting in lipid malabsorption. We report a second case of such a neurological syndrome in a patient in whom vitamin E deficiency was an isolated finding. The clinical picture in our patient was characterized by a diffuse muscle weakness most prominent distally and in the lower limbs, generalized areflexia, a decrease in proprioception and vibration sense and slight limb and gait ataxia. His condition improved on alpha tocopherol therapy so that it is very likely that vitamin E deficiency is responsible for his neurological deficit. Since in our patient as well as in several other reported cases this condition has been treatable, it is important that this syndrome be recognized in children presenting a suggestive clinical picture even if they do not have lipid malabsorption.
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PMID:A progressive neurological syndrome associated with an isolated vitamin E deficiency. 650 2

Thirty-eight infants and young children with gastroenteritis were investigated for lactose malabsorption. Each of them was given an oral lactose load of either 0.5 g/kg or 2 g/kg after which breath hydrogen excretion was measured, and each was observed to see if he had clinical symptoms of lactose intolerance. Only one patient, given 2 g/kg lactose, had clinical intolerance. His breath hydrogen excretion however was negative. Three of 18 patients given 0.5 g/kg lactose had positive breath hydrogen tests. None of these was symptomatic. Lactose intolerance in gastroenteritis was rare in our study, and the hydrogen breath test was not an appropriate technique for detecting it.
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PMID:Lactose malabsorption during gastroenteritis, assessed by the hydrogen breath test. 725 57

A 5-mo-old male had disabling diarrhea and malabsorption following massive small bowel resection. His transit time was 10 min. After 9 mo of conservative treatment, a 24-cm isoperistaltic segment of colon was interposed 6.5 cm from the ligament of Treitz. Transit time was increased to 105 min, and he was eventually able to be maintained on an enteric diet without significant diarrhea. Colon interposition requires little manipulation of the remaining small intestine and does not rely on active intestinal obstruction to effect an increased transit time.
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PMID:Colon interposition for the short bowel syndrome. 733 85

Macromolecular absorption of food and microbial antigens being enhanced in the intestine under pathological conditions may well be the cause of such diseases as food allergy, coeliac disease, Crohn's disease, atopic eczema, etc. The polyethyleneglycol-4000 (PEG-4000) and food antigens absorption was found to be similar in the animal intestine. The PEG-4000 gastrointestinal permeability is considerably increased in the rats with anaphylaxis, experimental biliary malabsorption and experimental colitis. Fatty acids of the omega-3 and omega-6 series as well as histidine were found to change the permeability for the PEG-4000.
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PMID:[Disordered permeability of the gastrointestinal tract barrier for macromolecules and the possibilities for its experimental dietetic correction]. 840 45

Digestion is a process which takes place in resting conditions. Exercise is characterised by a shift in blood flow away from the gastrointestinal (GI) tract towards the active muscle and the lungs. Changes in nervous activity, in circulating hormones, peptides and metabolic end products lead to changes in GI motility, blood flow, absorption and secretion. In exhausting endurance events, 30 to 50% of participants may suffer from 1 or more GI symptoms, which have often been interpreted as being a result of maldigestion, malabsorption, changes in small intestinal transit, and improper food and fluid intake. Results of field and laboratory studies show that pre-exercise ingestion of foods rich in dietary fibre, fat and protein, as well as strongly hypertonic drinks, may cause upper GI symptoms such as stomach ache, vomiting and reflux or heartburn. There is no evidence that the ingestion of nonhypertonic drinks during exercise induces GI distress and diarrhoea. In contrast, dehydration because of insufficient fluid replacement has been shown to increase the frequency of GI symptoms. Lower GI symptoms, such as intestinal cramps, diarrhoea--sometimes bloody--and urge to defecate seem to be more related to changes in gut motility and tone, as well as a secretion. These symptoms are to a large extent induced by the degree of decrease in GI blood flow and the secretion of secretory substances such as vasoactive intestinal peptide, secretin and peptide-histidine-methionine. Intensive exercise causes considerable reflux, delays small intestinal transit, reduces absorption and tends to increase colonic transit. The latter may reduce whole gut transit time. The gut is not an athletic organ in the sense that it adapts to increased exercise-induced physiological stress. However, adequate training leads to a less dramatic decrease of GI blood flow at submaximal exercise intensities and is important in the prevention of GI symptoms.
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PMID:Is the gut an athletic organ? Digestion, absorption and exercise. 846 Feb 88

Giardia lamblia undergoes surface antigenic variation. The variant-specific surface proteins (VSPs) are a distinct family of cysteine-rich proteins. Characteristically, cysteine residues occur mostly as CXXC tetrapeptides. Four of the reported five VSPs contain a putative metal-binding domain that resembles other metal-binding motifs; the fifth is closely related but lacks an essential histidine. Three different native VSPs bound Zn2+. Co2+, Cu2+, and Cd2+ inhibited Zn2+ binding. Analysis of recombinant VSP fusion proteins showed that the putative binding motif bound Zn2+. Surprisingly, peptide fragments from other regions of the VSP contain numerous CXXCXnCXXC motifs that also bound Zn2+. Analysis of deduced amino acid sequences showed well-conserved CXXC spacing in three out of five VSPs, suggesting conservation of structure despite amino acid sequence divergence. The function of VSPs is unknown, but by binding Zn2+ or other metals in the intestine, VSPs may contribute to Zn2+ malnutrition or inhibition of metal-dependent intestinal enzymes, which would lead to malabsorption, a well-known consequence of giardiasis.
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PMID:Variant-specific surface proteins of Giardia lamblia are zinc-binding proteins. 851 91


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