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 primary bile acid, chenodeoxycholic acid, and the secondary bile acid, deoxycholic acid, when present at a concentration of greater than 3 mM, induce salt and water secretion from the human colon and cause a marked increase in the permeability of the human colon to molecules of a molecular weight of 200-500 daltons. Scanning electron microscopy indicates that this action may be associated with tissue damage in some species. In the healthy individual, the primary bile acids, cholic and chenodeoxycholic acid, are dehydroxylated in the colon and are simultaneously precipitated from solution; at pH less than 7, deoxycholic and lithocholic acid are insoluble. In patients with bile acid diarrhea resulting from bile acid malabsorption, dehydroxylation is decreased, and the concentration of bile acids in the colon is markedly elevated. The major secretory bile acid in solution is chenodeoxycholic acid. Administration of cholestyramine, a resin that binds bile acid, reduces the elevated concentration of chenodeoxycholic acid and abolishes the diarrhea. These facts can be used to develop a unifying hypothesis which proposes that elevated concentrations of primary bile acids in the colon play a role in diarrhea and pseudomembranous colitis induced by clindamycin.
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PMID:Bile acids, diarrhea, and antibiotics: data, speculation, and a unifying hypothesis. 32 6

A steady-state perfusion technique has been used in vivo in normal subjects to show that at concentrations occurring during therapeutic use (500 mg/1, 1.1 mmol/l) the antibiotic clindamycin reversibly inhibits bicarbonate-stimulated water and electrolyte absorption from the human jejunum. Lactose-stimulated water and electrolyte absorption was not affected by the addition of clindamycin at the same concentration. Clindamycin-induced malabsorption of water and electrolytes may contribute significantly to the diarrhoea that occurs during clindamycin therapy in the absence of pseudomembranous colitis.
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PMID:Inhibition of jejunal water and electrolyte absorption by therapeutic doses of clindamycin in man. 642 96

Based on experimental evidence in animals showing that the oral administration of Saccharomyces boulardii is effective in reducing morbidity and mortality due to Clostridium difficile-induced pseudomembranous colitis, we conducted an open trial to examine the effects of the living yeast, given as primary therapy, in a selected group of infants and children with persistent intestinal symptoms related to toxinogenic C. difficile overgrowth. Over a period of 10 consecutive months, we studied 19 eligible patients (median age 8 months) who presented with enteral symptoms lasting for > 15 days and who had solely C. difficile in stools with positive cytotoxin B assay. Serotyping of the strains and determination in vitro of production of toxins A and B were performed subsequently. The patients presented with persistent or protracted diarrhea, malabsorption, and failure to grow (n = 8), or with repeated attacks of colics, emesis, and hypermeteorism without diarrhea (n = 4), or with both entities (n = 7). Patients with chronic protracted diarrhea (n = 3) had depressed jejunal disaccharidase activities and ultrastructural changes of enterocytes, including sparce and shortened microvilli. None had evidence of colitis. All the strains of C. difficile tested (n = 17) belonged to pathogenic serotypes (A1, A8, C, F, G, H, and K) and produced in vitro high levels of toxins A (n = 16) and B (n = 17). S. boulardii was given orally in a lyophilized form over 15 days (250 mg two to four times per day according to age).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Saccharomyces boulardii for Clostridium difficile-associated enteropathies in infants. 831 51

Diarrhoea is a relatively frequent adverse event, accounting for about 7% of all drug adverse effects. More than 700 drugs have been implicated in causing diarrhoea; those most frequently involved are antimicrobials, laxatives, magnesium-containing antacids, lactose- or sorbitol-containing products, nonsteroidal anti-inflammatory drugs, prostaglandins, colchicine, antineoplastics, antiarrhythmic drugs and cholinergic agents. Certain new drugs are likely to induce diarrhoea because of their pharmacodynamic properties; examples include anthraquinone-related agents, alpha-glucosidase inhibitors, lipase inhibitors and cholinesterase inhibitors. Antimicrobials are responsible for 25% of drug-induced diarrhoea. The disease spectrum of antimicrobial-associated diarrhoea ranges from benign diarrhoea to pseudomembranous colitis. Several pathophysiological mechanisms are involved in drug-induced diarrhoea: osmotic diarrhoea, secretory diarrhoea, shortened transit time, exudative diarrhoea and protein-losing enteropathy, and malabsorption or maldigestion of fat and carbohydrates. Often 2 or more mechanisms are present simultaneously. In clinical practice, 2 major types of diarrhoea are seen: acute diarrhoea, which usually appears during the first few days of treatment, and chronic diarrhoea, lasting more than 3 or 4 weeks and which can appear a long time after the start of drug therapy. Both can be severe and poorly tolerated. In a patient presenting with diarrhoea, the medical history is very important, especially the drug history, as it can suggest a diagnosis of drug-induced diarrhoea and thereby avoid multiple diagnostic tests. The clinical examination should cover severity criteria such as fever, rectal emission of blood and mucus, dehydration and bodyweight loss. Establishing a relationship between drug consumption and diarrhoea or colitis can be difficult when the time elapsed between the start of the drug and the onset of symptoms is long, sometimes up to several months or years.
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PMID:Drug-induced diarrhoea. 1064 76

This article presents commonly encountered and clinically significant entities affecting the gastrointestinal (GI) system with emphasis on assisting the clinician in developing management strategies to reduce the associated risks. Xerostomia, osteoradionecrosis, gastroesophageal reflux disease, and ulcerative diseases occurring in the proximal portion of the GI system and antibiotic-associated diarrhea, pseudomembranous colitis, adynamic ileus, and malabsorption problems occurring in the distal portion are presented. Lastly, suggestions for managing patients who have splenomegaly and splenectomy are addressed.
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PMID:Gastrointestinal diseases and considerations in the perioperative management of oral surgical patients. 1808 27