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

Using the 14C carbonate method of McFarlane, the synthesis rates of albumin and fibrinogen were determined in four patients with protein-losing enteropathy, in one patient during the recovery phase after severe protein malabsorption and in nine control patients. The following results were obtained: (1) The synthesis rates of albumin and fibrinogen were significantly increased in all patients studied. (2) All patients had low serum albumin levels. The increase in albumin synthesis rate was remarkably uniform in all patients, the average being 645 mg/kg/day or 2.7 times the mean control value. (3) Plasma fibrinogen levels were normal in all patients. The fibrinogen synthesis rate varied over a wide range from 42.1 to 199.3 mg/kg/day, i.e. 2-8.5 times the control value.
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PMID:Synthesis rates of albumin and fibrinogen in patients with protein-losing enteropathy and in a patient recovering from protein malnutrition. 81 54

Diarrhea in streptozocin-induced chronically diabetic rats is caused by an impaired adrenergic regulation of intestinal fluid and electrolyte transport. Stimulation of alpha 2-adrenergic receptors on enterocytes normally promotes NaCl absorption and inhibits HCO3 secretion. The purpose of this study was to determine if adrenergic denervation of intestinal mucosa in chronically diabetic rats alters postsynaptic receptor response, and if the alpha 2-adrenergic agonist clonidine could correct observed fluid malabsorption. Mucosal norepinephrine stores, a measure of adrenergic tone, were markedly reduced in diabetic rats compared with nondiabetic littermates. In vitro, short-circuit current changes to exogenously added l-epinephrine were significantly greater in diabetics, suggesting that denervation hypersensitivity was due to increased numbers of postsynaptic alpha 2-adrenergic receptors. In vivo loop studies demonstrated net fluid secretion in the ileum and colon of diabetics. In diabetics, clonidine reversed the secretion to absorption, but it had no effect on fluid absorption in controls. We conclude that diabetic diarrhea in streptozocin-induced chronically diabetic rats is due to impaired adrenergic regulation of mucosal ion transport, accompanied by a postsynaptic denervation hypersensitivity that can be reversed by clonidine, and accompanied by net intestinal fluid secretion that can be effectively reversed with clonidine.
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PMID:Experimental diabetic diarrhea in rats. Intestinal mucosal denervation hypersensitivity and treatment with clonidine. 287 98

Studies in 24 recurrent oxalate stone-formers have shown that values for urinary calcium excretion for this group on at-home diets vary significantly (P less than 0.001) more than values for creatinine excretions. By placing stone-formers on controlled in-hospital diets and measuring their calcium excretions, we were able to predict probable outpatient hypercalciuria (greater than 7.5 mmol/day) with a sensitivity of 95% and a specificity of 95%. In this study, the renal loss of calcium during low-calcium diets was proportional to the absorptive hypercalciuria during high-calcium diets. Calcium loading experiments in fasted stone-formers and normal subjects indicated that citrate, at citrate:calcium molar ratios ranging from 0.12 to 1, stimulated urinary calcium excretion more than did calcium carbonate loading alone. In addition, citrate also significantly (P less than 0.05) increased the excretion of urinary oxalate by two normal subjects for a given load of calcium oxalate. Malabsorption of citrate and possibly other hydroxycarboxylic acids may thus predispose to oxalate nephrolithiasis by promoting calcium and oxalate absorption.
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PMID:Effect of citrate on the urinary excretion of calcium and oxalate: relevance to calcium oxalate nephrolithiasis. 291 May 76

Net electrolyte and water transport and unidirectional Na+ fluxes were examined in ligated colonic loops of clinically normal pigs and in pigs with swine dysentery (etiologic agent Treponema hyodysenteriae) in the presence or absence of theophylline. In normal pigs, theophylline abolished net Na+ absorption via a reduction in the lumen-to-blood flux, decreased Cl- absorption, and increased HCO3- accumulation in the lumen. In infected pigs, all net ion transport was abolished, with the addition of theophylline producing little effect. The absence of net Na+ absorption in infected pigs was also the result of a decreased lumen-to-blood flux. Seemingly, colonic malabsorption may be the primary transport alteration in swine dysentery. Concentrations of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) were measured in samples of colonic mucosa from normal and infected pigs after in vitro exposure to a Ringer's solution containing 0 or 20 mM theophylline. Basal values of cAMP or cGMP did not increase in infected colonic mucosa. There was a diminished capacity of the infected mucosa to respond to theophylline. Alterations in ion transport in conjunction with measurements of cAMP and cGMP indicated that the pathogenic mechanism(s) in swine dysentery were not similar to those of Salmonella, Shigella, Vibrio cholerae, or Escherichia coli diarrhea.
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PMID:Pathophysiologic features of swine dysentery: cyclic nucleotide-independent production of diarrhea. 630 41

The rumen and the mammalian large intestine are similar in many respects. Microbial protein appears to be synthesized and degraded in the digesta of both organs in a comparable manner. The VFA end-products of carbohydrate fermentation are produced in similar concentrations. Digesta pH is maintained with buffer added by the saliva or ileal fluid, HCO3 released into the lumen and rapid absorption of the organic acids. VFA are absorbed at equivalent rates by rumen epithelium and large intestinal mucosa. Over-production of VFA produces similar adverse effects. There is a considerable amount of species variation in the relative length and volume as well as the extent of sacculation of the large intestine. The caecum is the primary site for retention of digesta and microbial fermentation in the large intestine of rabbits, rodents and a few other species. However, the proximal colon is the major site of retention and fermentation in most mammals. Absorptions of Na and VFA appear to account for absorption of most of the water removed during passage of digesta through the large intestine. A relatively slow rate of Na absorption and release of HCO3 appears to provide the fluid and buffering capacity needed for efficient microbial digestion in the rumen and in the large intestine of some species. A more rapid absorption of Na by the large intestine of other species would aid in the conservation of Na and water. The many similarities between the large intestine and the rumen suggest that further comparison can provide additional information on both the function and diseases of these two organs. The rumen has proved to be accessible to a variety of procedures useful for the study of microbial digestive processes and its epithelium has provided a non-glandular tissue for studies of inorganic ion transport as well as the transport and metabolism of VFA. Comparative studies of the large intestine also can provide a better understanding of the functions and malfunctions of the human large intestine. The pig and some species of monkey would appear to be most suitable for examining the effects of diet and carbohydrate malabsorption. The equine large intestine provides a good system for studying events, such as those associated with the recycling of nitrogenous compounds. Furthermore, as demonstrated by comparative studies of the kidney and other organs, a great deal of information can be gained through examination of the various mechanisms that have been developed to serve similar functions.
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PMID:The large bowel--a supplementary rumen? 670 33

Oral rehydration therapy (ORT) has simplified treatment of diarrheal dehydration. Hospitals in India have diarrheal treatment and training units (DTUs) to help manage the many diarrheal cases. DTU staff keep children for 4-6 hours to correct the dehydration with ORT and feeding. Health personnel undergo training in diarrhea management at DTUs. ORT is the preferred treatment in almost all cases of acute diarrhea. It is not best for diarrheal cases which exhibit shock, profuse vomiting (3 times/hour), glucose malabsorption, abdominal distension or paralytic ileus, and high rate of purging (15 ml/kg body weight/hour). ORT successfully treats 95% cases of infantile diarrhea, even Rotavirus-caused diarrhea. Health workers should begin treating cases of severe dehydration with intravenous (IV) therapy and then administer ORT 3-4 hours later for infants and 1-2 hours later for adults. If IV therapy is not possible, the patient should receive oral rehydration solution (ORS) nasogastrically and then referred to a facility with IV therapy. WHO's ORS formula is safe for newborns and young infants. ORT is appropriate even when diarrheal cases are vomiting. ORT tends to stop vomiting 1-2 hours after initial ORS administration because it corrects acidosis. The glucose in WHO's ORS facilitates absorption of adequate sodium across the intestinal mucous membrane. ORS also restores the loss potassium ions and HCO3/citrate. If ORS is not available, sugar salt solution can be used. To achieve the optimum concentration, the amount of sucrose has to be twice that of glucose. ORS should be stored in a cool place, be covered, and used for no more than 24 hours. Antiemetics should not be given during ORT. Most diarrheas do not require any antibiotic. Sterile water is not necessary to prepare ORS. Rice gruel, coconut water, and pulse water are home available fluids which can treat dehydration. Breast feeding and regular feeding should continue during diarrheal episodes.
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PMID:Answers to questions in relation to oral rehydration therapy. 783 4

The interposition of a bowel segment as a bladder substitute into the urinary tract may result in impaired calcium metabolism. We studied 25 male patients (aged 45 to 77 yr) who had undergone a Vescica Ileale Padovana (VIP) reconstruction following cystectomy 29 to 75 mo before. Bone mineral density of the spine and femur was measured by dual x-ray absorptiometry. Blood and 24-h urine samples were analyzed for the main parameters of bone metabolism. Sixteen healthy men were enrolled as a control group. Although blood pH did not differ between patients and control subjects, VIP subjects showed lower levels of plasma HCO3- (P < 0.005) and higher serum chloride (P < 0.001). Bone alkaline phosphatase was higher (P < 0.001), and urine calcium, phosphate, and creatinine levels were lower in VIP patients (P < 0.01, P < 0.01, and P < 0.05, respectively). Bone mineral density at the femoral neck (P < 0.03) and Ward's triangle (P < 0.05) was decreased in VIP patients. When subdivided according to time since operation, patients who had the ileal neobladder implanted for a shorter period of time showed lower blood pH (P < 0.03) and urine calcium (P < 0.05) levels and higher urinary hydroxyproline (P < 0.02). Duration of the ileal neobladder was positively correlated with PTH (r = 0.46, P < 0.03) and blood pH (r = 0.47, P < 0.02). Furthermore, pH values were positively correlated with urine calcium (r = 0.48, P < 0.02). In conclusion, in patients with ileal neobladder, a mild metabolic acidosis is responsible for an increased bone turnover and lower bone mass. Moreover, a decrease over time in the absorption capacity of the ileal pouch might result in calcium malabsorption, which represents an additional risk factor for reduced bone mass in these patients.
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PMID:Bone density and skeletal metabolism in patients with orthotopic ileal neobladder. 933 83

In the rapidly increasing elderly population, diarrhoea as a result of drug therapy is an important consideration. The elderly consume a disproportionately large number of drugs for multiple acute and chronic diseases. Drugs can compromise both immune and nonimmune responses. Aging decreases the quality and proportion of T cells which in turn reduces the production of secretory IgA, the primary immune response of the gut. Acid production in the stomach decreases with increasing age and this compromise its vital 'self-sterilising' function, thus increasing the risk of diarrhoea due to viral, bacterial and protozoal pathogens. Other nonimmune defence mechanisms include the motility of the small intestine and the host-protective commensal bacteria of the colon. Drug induced hypomotility may result in bacterial overgrowth, deconjugation of bile salts and diarrhoea. Less commonly, diarrhoea may occur due to hypermotility because of a cholinergic-like syndrome. In the colon the host-protective commensal bacteria provide a powerful defence against pathogens. Disruption of this commensal population by antibiotic therapy may result in Clostridium difficile supra-infection which causes diarrhoea through toxin production. This is especially important in the elderly patient on chemotherapy for malignancy and those with multiple diseases. The organism responds to vancomycin, metronidazole and bacitracin. Metronidazole is the suggested drug of choice, with vancomycin reserved for relapses. Drugs also cause diarrhoea by interfering with normal physiological processes. Drugs impair fluid absorption by activating adenylate cyclase within the small intestinal enterocyte which increases the level of cyclic AMP. This causes active secretion of Cl- and HCO3-, passive efflux of Na+, K+ and water and inhibition of Na+ and Cl- into the enterocyte. Examples of these drugs (secretagogues) are bisacodyl, misoprostol and chenodeoxycholic acid (used to dissolve cholesterol gallstones). Drugs may also affect a second mechanism that regulates water and electrolyte transport, the Na+, K+ exchange pump. The energy for this pump is provided by the ATPase mediated breakdown of ATP. ATPase may be inhibited by digoxin, auranofin, colchicine and olsalazine. A number of drugs cause osmotic diarrhoea including antacids containing magnesium trisilicate or hydroxide. Lactulose is being used increasingly in compensated liver disease to increase protein tolerance and prevent hepatic encephalopathy. Sorbitol, an osmotic laxative agent also used in some liquid pharmaceutical preparations, induces diarrhoea by virtue of its osmotic potential. Another mechanism by which drugs cause diarrhoea is by mucosal damage of the small and large bowel. In the small intestine mucosal damage causes diarrhoea and fat malabsorption, as may occur with neomycin and colchicine. In the colon, for example, gold salts and penicillamine cause colitis of varying severity. Though the causes of diarrhoea are diverse, a drug-associated aetiology should always be considered and actively sought and addressed to prevent the complications of dehydration, electrolyte imbalance and undernutrition.
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PMID:Mechanisms of drug-induced diarrhoea in the elderly. 978 28

Reduced gastrointestinal HCO3- secretion contributes to malabsorption and obstructive syndromes in cystic fibrosis. The apical HCO3- transport pathways in these organs have not been defined. We therefore assessed the involvement of apical Cl-/HCO3- exchangers and anion conductances in basal and cAMP-stimulated duodenal HCO3- secretion. Muscle-stripped rat and rabbit proximal duodena were mounted in Ussing chambers, and electrical parameters, HCO3- secretion rates, and 36Cl-, 22Na+, and 3H+ mannitol fluxes were assessed. mRNA expression levels were measured by a quantitative PCR technique. Removal of Cl- from or addition of 1 mM DIDS to the luminal perfusate markedly decreased basal HCO3- secretion but did not influence the HCO3- secretory response to 8-bromo-cAMP, which was inhibited by luminal 5-nitro-2-(3-phenylpropylamino)-benzoate. Bidirectional 22Na+ and 36Cl- flux measurements demonstrated an inhibition rather than a stimulation of apical anion exchange during cAMP-stimulated HCO3- secretion. The ratio of Cl- to HCO3- in the anion secretory response was compatible with both Cl- and HCO3- being secreted via the CFTR anion channel. CFTR expression was very high in the duodenal mucosa of both species. We conclude that in rat and rabbit duodena, an apical Cl-/HCO3- exchanger mediates a significant part of basal HCO3- secretion but is not involved in the HCO3- secretory response to cAMP analogs. The inhibitor profile, the strong predominance of Cl- over HCO3- in the anion secretory response, and the high duodenal CFTR expression levels suggest that a major portion of cAMP-stimulated duodenal HCO3- secretion is directly mediated by CFTR.
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PMID:Independence of apical Cl-/HCO3- exchange and anion conductance in duodenal HCO3- secretion. 1284 23

Intestinal malabsorption is severe and of early onset in virtually all people who have cystic fibrosis. The main cause is deficiency of pancreatic enzymes. Bicarbonate deficiency, abnormal bile salts, mucosal transport problems, motility differences, and anatomical structural changes are other contributory factors. Effective treatment should allow a normal to high-fat diet to be taken, control symptoms, correct malabsorption, and achieve a normal nutritional state and growth. Appropriate pancreatic enzyme replacement therapy will achieve normal or near-normal absorption in most people with cystic fibrosis. Early identification and treatment of intestinal malabsorption is critical to achieving optimal nutritional status. The occurrence of fibrosing colonopathy in a few patients on very high doses of those enzymes which have the copolymer Eudragit L30 D55 in their covering resulted in guidelines in the UK to avoid doses equivalent to more than 10,000 IU lipase per kg per day, and also to avoid preparations containing this copolymer in children and adolescents. For patients not responding to 10,000 IU lipase per kg per day review of adherence to treatment, change of enzyme preparation, variation in time of administration, and reduction in gastric acid may improve absorption. The importance of early investigation to exclude other gastrointestinal disorders as a cause of the patient's symptoms, rather than merely increasing the dose of enzymes, is stressed. With modern pancreatic enzymes in doses up to or only slightly in excess of 10,000 IU lipase per kg per day, adequate control of gastrointestinal symptoms and absorption can be achieved, and a normal nutritional state and growth rate maintained in most people with cystic fibrosis.
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PMID:Diagnosis and treatment of intestinal malabsorption in cystic fibrosis. 1628 83


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