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)

Diarrhea can result from damage to the intestinal lining caused by viruses or bacteria, malabsorption, inflammatory processes, bile salt and pancreatic enzyme deficiency, abnormal motility, or the presence of osmotically active solutes in the gut. While it is important to elicit information to determine the possible cause of diarrhea, be sure to check circulatory status first. Some patients may need rehydration therapy more urgently than they need a diagnosis. The main goals of treatment are to prevent dehydration and correct electrolyte imbalance, to provide supportive and symptomatic therapy, and to treat underlying disease. In most cases, a specific diagnosis is not necessary to guide initial treatment.
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PMID:Acute diarrhea. 984 23

Loss of bone is an almost universal accompaniment of aging that proceeds at an average rate of 0.5-1% per annum from midlife onwards. There are at least four nutrients involved in this process: calcium, salt, protein, and vitamin D, at least in women. The pathogenesis of osteoporosis in men is more obscure. Calcium is a positive risk factor because calcium requirement rises at the menopause due to an increase in obligatory calcium loss and a small reduction in calcium absorption that persist to the end of life. A metaanalysis of 20 calcium trials shows that this process can generally be arrested by calcium supplementation, although there is some doubt about its effectiveness in the first few years after menopause. Salt is a negative risk factor because it increases obligatory calcium loss; every 100 mmol of sodium takes 1 mmol of calcium out of the body. Restricting salt intake lowers the rate of bone resorption in postmenopausal women. Protein is another negative risk factor; increasing animal protein intake from 40 to 80 g daily increases urine calcium by about 1 mmol/day. Low protein intakes in third world countries may partially protect against osteoporosis. Vitamin D (sometimes called a nutrient and sometimes a hormone) is important because age-related vitamin D deficiency leads to malabsorption of calcium, accelerated bone loss, and increased risk of hip fracture. Vitamin D supplementation has been shown to retard bone loss and reduce hip fracture incidence in elderly women.
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PMID:Nutrition, osteoporosis, and aging. 992 42

Hereditary defects in the renal handling of filtered NaCl and water have important implications for understanding the physiological mechanisms that enable the kidney to optimize the match between glomerular filtration rate and tubular reabsorption. Null mutations in the water channel aquaporin 1 (AQP1) or the Na/H exchanger NHE3, two major fluid transporters in the proximal tubule, are states in which a reduction in proximal fluid absorption is accompanied by proportionate decrements in glomerular filtration rate. Compensation of the transport defect by a reduction in filtered load is so efficient that clinically symptomatic Na losses are not observed in either AQPI or NHE3 deficiency. On the other hand, severe syndromes of salt wasting are caused by transport deficiencies in the thick ascending limb or the collecting duct, indicating that the severity of Na dysregulation is unrelated to the basal absorption of NaCl in a given nephron segment. Loss of function of the Na,K,2Cl-cotransporter (NKCC2) or of the epithelial Na channel (ENaC) reduces Na absorption in thick ascending limbs or collecting ducts. In these states, the increased delivery of Na to downstream segments is not monitored by a sensor linked to the site of filtrate formation. In the absence of adaptations in the filtered load, intrarenal compensation of a circumscribed NaCl malabsorption by adjustment of NaCl transport in other nephron segments is remarkably insufficient, particularly in the immature kidney of the newborn.
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PMID:NaCl transport deficiencies--hemodynamics to the rescue. 1078 41

Protein energy malnutrition leading to growth failure is an inevitable consequence of chronic liver disease in childhood. Although the precise pathophysiology is not understood considerable progress has been made in understanding the mechanisms of fat malabsorption and protein turnover in liver disease. There are many difficulties with the correct assessment of nutritional parameters in children with liver disease related to their abnormal body composition and energy expenditure and care needs to be taken with the interpretation of results. The effects of malnutrition secondary to chronic liver disease are varied and include fat soluble vitamin deficiencies, generalised growth failure, impairment of gastrointestinal function, immunosuppression and hypotonia. It is now recognised that malnutrition is an important risk factor for liver transplantation and increases both mortality and morbidity. Strategies to prevent or reverse malnutrition are now established and include the use of specific infant formulas based on low salt protein and an increased concentration of medium train triglyceride (50-70%). Careful nutritional support in association with generous fat soluble vitamin supplementation may produce dramatic improvement in catch up weight gain but for those children in whom growth failure persists, the only management is liver transplantation.
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PMID:Nutrition and growth in patients with chronic liver disease. 1082 20

Patients with symptomatic collagenous-lymphocytic colitis should eliminate dietary secretagogues such as caffeine- or lactose-containing food from their diet. When possible, use of nonsteroidal anti-inflammatory drugs should be discontinued. If steatorrhea is documented, a low-fat diet may be helpful. In the presence of bile salt malabsorption, binding resins such as cholestyramine might be useful. Nonspecific diarrheal agents such as loperamide hydrochloride, diphenoxylate hydrochloride and atropine, deodorized tincture of opium, or codeine might prove effective in some patients. Antibacterial agents such as bismuth subsalicylate (8 chewable 262-mg tablets daily) have been effective in symptom control. Metronidazole and erythromycin achieve response rates of 60%. Sulfasalazine, at the usual dose of 2 to 4 g daily, used in collagenous-lymphocytic colitis, demonstrated cessation of diarrhea in 1 to 2 weeks for 50% of patients. Other 5-aminosalicylic (5-ASA) compounds are preferred for patients with a history of sulfa allergy, and those who experience adverse reactions to sulfasalazine. Adrenocorticoid medication is reserved for patients whose conventional treatment with sulfasalazine or 5-ASA has failed. Resolution of diarrhea has been documented in 80% to 90% of patients within 1 week of treatment, however, in most patients, long-term therapy is required. Surgical management is reserved for those patients with disease refractory to medical therapy. Colectomy with ileostomy resulted in clinical and histologic resolution in small case series. If there is no abatement of symptoms, rule out other etiologies of diarrhea such as thyroid dysfunction, celiac disease, or bacterial overgrowth.
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PMID:Lymphocytic and Collagenous Colitis. 1109 41

We investigated the gastrointestinal handling and post-absorptive metabolic handling of [1,1,1-13C]tripalmitin and [1-13C]glycocholate during recovery from severe childhood malnutrition. Eight children were studied on three occasions: at admission (phase 1), during rapid catch-up growth (phase 2) and when weight-for-height had reached 90 % of the reference (phase 3). Breath samples were obtained over a 24 h period and stools were collected over 3 d following the administration of each tracer. At admission, the lipid content of stool expressed as a percentage of ingested lipid was 6 (range 0.7-28.9) but less variation was shown between children at phase 2 (3.3 (range 0.9-4.1)) and phase 3 (1.4 (range 0.4-2.5)). The excretion of 13C in stool varied markedly between children at admission (11.1 (sd 5.4) % administered dose) and during rehabilitation (phase 2, 15.4 (sd 16.5) % administered dose; phase 3, 6.2 (sd 10.2) % administered dose). About 5 % of the absorbed label was recovered on breath at each stage (% absorbed dose; phase 1, 5.1 (sd 6.0); phase 2, 5.2 (sd 3.1); phase 3, 6.4 (sd 6.6)). None of the children exhibited significant bile salt malabsorption as a consequence of small intestinal overgrowth. Of the 13C measured in stool, more label was recovered in fatty acids than triacylglycerols during each of the three phases and this was interpreted to reflect a failure to absorb the products of digestion. The results show that not all the children had problems associated with the digestion and absorption of 13C-labelled tripalmitin in severe malnutrition and during recovery, which was not reflected in gross lipid balance across the gastrointestinal tract. Absorbed lipid was more likely to be deposited as adipose tissue than to satisfy the immediate needs for energy.
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PMID:Gastrointestinal handling and metabolic disposal of 13C-labelled tripalmitin during rehabilitation from childhood malnutrition. 1143 Jul 75

Animals with induced or natural null mutations in renal NaCl and water transporter genes provide a powerful tool to study the physiological mechanisms that enable the kidney to optimize the match between glomerular filtration rate and tubular reabsorption. Deficiencies in the Na/H exchanger NHE3 and in the water channel aquaporin 1 (AQP1) cause reductions in proximal fluid absorption which are accompanied by proportionate decrements in glomerular filtration rate (GFR). Compensation of the transport defect by a reduction in filtered load is so efficient that clinically symptomatic Na losses are not observed in either NHE3 or AQP1 deficient animals. On the other hand, severe syndromes of salt wasting are caused by loss of function of the Na,K,2Cl-cotransporter (NKCC2) in the thick ascending limb, or of the epithelial Na channel (ENaC) the collecting duct indicating that the severity of Na dysregulation is unrelated to the basal absorption of NaCl in a given nephron segment. In these states, the increased delivery of Na to downstream segments is not monitored by a sensor linked to the site of filtrate formation. In the absence of adaptations in the filtered load intrarenal compensation of a circumscribed NaCl malabsorption by adjustment of NaCl transport in other nephron segments is sometimes insufficient, particularly in the immature kidney of the newborn.
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PMID:Sodium transport deficiency and sodium balance in gene-targeted mice. 1167 27

Breath tests are a simple and safe alternative to more invasive investigation strategies for many gastroenterological conditions. Both the hydrogen breath tests and the new 13C stable radioisotope breath tests are nonradioactive and safe in children and pregnancy. The range of diseases that can be identified include Helicobacter pylori infection, lactose and fructose intolerance, bacterial overgrowth, bile salt wastage, pancreatic insufficiency, liver dysfunction, and abnormal small bowel transit. In this review, the physiology supporting these tests and the principles of normal gas dynamics in the gut are briefly reviewed and then related to the test preparation and interpretation in two parts: 1) detection of H. pylori and 2) small bowel, pancreatic, and hepatobiliary disorders. A MEDLINE search reviewing all English language abstracts from 1966 to March, 2001 was performed, with an additional review of abstracts from major national meetings from 1997 to 2001. Using the information from this review, the performance characteristics of the various tests were detailed, and an attempt is made to provide some literature-based guidance regarding their indications and limitations. The interpretation of "flat" breath tests and the selective use of methane collection and colonic alkalinization are discussed. Breath tests are valuable tools that are, in general, underutilized in evaluating dyspepsia and functional bloating and diarrhea, as well as suspected malabsorption, including lactose intolerance.
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PMID:Using breath tests wisely in a gastroenterology practice: an evidence-based review of indications and pitfalls in interpretation. 1201 15

Fecal bile salt excretion was studied in healthy volunteers, patients with regional ileitis, and patients with ileal resection. 10 muc of carboxyl-(14)C-cholic acid was given orally. Stools and urine were collected daily for 5-10 days, the bile salts extracted, and the radioactivity assayed. Urinary excretion was negligible. All patients with ileal resection excreted bile salts in the feces significantly faster than controls, and five of the six excreted 50% of the radioactivity within 24 hr. Their mean intestinal transit time was 5.6 hr compared to 26 hr for the controls. Two of the three patients with regional ileitis excreted bile salts almost as rapidly as patients with ileal resection. Vitamin B(12) absorption was also defective in those patients, but the intestinal transit time was not decreased. To study the effect of rapid intestinal transit on bile salt excretion, four of the control subjects were given orally 1200 ml of 10% mannitol for 7 days, and the labeled cholic acid excretion rate was again studied. The mean intestinal transit time was markedly shortened, mild steatorrhea developed, and the fecal bile salt excretion rate increased slightly. It is concluded that ileal resection and ileal disease are major factors and rapid intestinal transit is a minor factor in causing excessive fecal bile salt loss. The relevance of bile salt wastage to lipid malabsorption is unknown because of insufficient information about compensatory jejunal absorption, maximum rate of hepatic bile salt synthesis, and the minimum necessary intraluminal concentration of conjugated bile salt.
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PMID:Bile salt malabsorption in regional ileitis, ileal resection and mannitol-induced diarrhea. 1206 74

A small but significant subgroup of patients with irritable bowel syndrome (IBS) report a sudden onset of their IBS symptoms after a bout of gastroenteritis. Population-based surveys show that although a history of neurotic and psychologic disorders, pain-related diseases, and gastroenteritis are all risk factors for developing IBS, gastroenteritis is the most potent. More toxigenic organisms increase the risk 11-fold, as does an initial illness lasting more than 3 weeks. Hypochondriasis and adverse life events double the risk for postinfective (PI)-IBS and may account for the increased proportion of women who develop this syndrome. PI-IBS is associated with modest increases in mucosal T lymphocytes and serotonin-containing enteroendocrine cells. Animal models and some preliminary human data suggest this leads to excessive serotonin release from the mucosa. Both the histologic changes and symptoms in humans may last for many years with only 40% recovering over a 6-year follow-up. Celiac disease, microscopic colitis, lactose intolerance, early stage Crohn's disease, and bile salt malabsorption should be excluded, as should colon cancer in those over the age of 45 years or in those with a positive family history. Treatment with Loperamide, low-fiber diets, and bile salt- binding therapy may help some patients. Serotonin antagonists are logical treatments but have yet to be evaluated.
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PMID:Postinfectious irritable bowel syndrome. 1276 24


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