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)

A group of 245 well nourished infants with acute diarrhea were screened for carbohydrate malabsorption by evaluating stool pH and reducing substances in the stools. Carbohydrate malabsorption was diagnosed in 28 cases (11%). Clinical features of carbohydrate intolerance were present in only one case. The duration of diarrhea after admission ranged from 1 to 13 days (mean 3.9 days). An oral lactose tolerance test was consistent with lactase deficiency in 32% of all cases. Thin layer chromatography showed many carbohydrates including monosaccharides in the stools, indicating that the defect in intestinal absorption was not specific for lactose.
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PMID:Carbohydrate malabsorption in acute diarrhea. 788 63

The clinical efficacy of a diluted oral rehydration salts (ORS) solution was compared in a pilot study with that of intravenous (i.v.) therapy and of standard World Health Organization (WHO)/United Nations Childrens Fund (UNICEF) ORS solution in children with acute diarrhea. Sixty-one boys aged 3 to 24 months, admitted to hospital with acute diarrhea and signs of dehydration, were randomly assigned to groups receiving standard ORS solution, diluted ORS solution, or i.v. therapy. In children treated with standard ORS solution and small amounts of plain water, the total fluid intake was 25-39% greater, the stool output was 58-77% greater (p < 0.01), and the duration of diarrhea was 30-55% greater than in the other treatment groups. Intake of plain water, taken separately or added to the ORS solution, was greater in children given diluted ORS solution (73 +/- 23 ml/kg) than in those given standard ORS solution (21 +/- 32 ml/kg) (p < 0.001). The mean serum sodium concentration increased by 2.2 mEq/L in children given standard ORS solution, whereas it decreased by 2.9 mEq/L in those given diluted ORS solution. This study shows that some children develop worsening diarrhea and increasing serum sodium concentrations when treated with standard ORS solution and given only small amounts of plain water. This is probably caused by the slight hypertonicity of standard ORS solution combined with transient partial glucose malabsorption. This can be avoided if water, breast milk, or another low-solute drink is given liberally during maintenance therapy with ORS solution, as recommended by the WHO.
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PMID:Is a low-osmolarity ORS solution more efficacious than standard WHO ORS solution? 796 83

Interest in imported tropical diseases has increased with the rising number of travellers to the tropics. This is especially true in the case of tropical gastroenterologic disorders. The causative organisms of chronic diarrhoea are different from those causing acute diarrhoea. Bacteria are relatively unusual; parasites, e.g. Entamoeba histolytica or Giardia lamblia or an opportunistic parasitic infestation associated with an HIV infection are more likely. Furthermore, non-infectious causes, such as postinfective tropical malabsorption, lactase deficiency or coeliac disease have to be considered. Today, elderly people often undertake a journey to the tropics; in these cases the diarrhoea may be associated not only with an increased susceptibility to tropical bowel infections but also with causes previously present, such as diverticulosis, carcinoma or inflammatory bowel disease. The classification of chronic diarrhoea following a visit to the tropics is essentially the same as that for acute diarrhoea: diarrhoea with and without fever and with and without blood. In addition, malabsorption is an important feature of chronic diarrhoea.
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PMID:'The tropics in our bathroom': chronic diarrhoea after return from the tropics. 857 32

In this review the Author expose the most common gastroenterological problems in pediatric practice. The following illnesses are examined: infantile colics, recurrent abdominal pain, gastroesophageal reflux, vomiting, alimentary intolerances, coeliac disease, malabsorption syndromes, hepatic pathologies, acute diarrhoea, persistent postenteric diarrhoea, chronic constipation. For all problems are provided the actual indications of diagnosis and therapy on the basis of modern literature suggestions.
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PMID:[The most common gastrointestinal problems in pediatric practice]. 876 74

Piglet cryptosporidiosis is characterized by intestinal villous damage and malabsorption and by reduced NaCl absorption in response to prostaglandin (PG) release from inflamed tissue. We hypothesized that the PG effect is mediated by the enteric nervous system. Piglets were infected with cryptosporidium and ileal mucosa was studied in Ussing chambers. Studies with tetrodotoxin and indomethacin showed that 75% of the PG-induced alteration in NaCl transport was mediated by the enteric nervous system. Prostacyclin was elevated in infected tissue, and its analog, carbacyclin, mimicked the altered transport response in indomethacin-treated tissue. This carbacyclin response was abolished by tetrodotoxin. The vasoactive intestinal peptide (VIP) receptor antagonist, VIP-10-28, and the muscarinic antagonist, atropine, individually reduced and together abolished the response to carbacyclin, whereas the nicotinic blocker, hexamethonium, reduced the carbacyclin response by 75%. The somatostatin analog, octreotide, and the a-2 adrenergic agonist, clonidine, each abolished the carbacyclin response and partially or completely rectified the altered NaCl transport of the infection. These results indicate that PGs alter NaCl transport in this infection primarily by stimulating cholinergic interneurons that innervate VIPergic and cholinergic motor nerves. The enteric nervous system may be a potential target for pharmacological control of the acute diarrhea in this infection.
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PMID:Role of the enteric nervous system in piglet cryptosporidiosis. 896 31

Despite recommendations from several bodies such as the World Health Organization and others that feeding should be continued during diarrhea, the practice of withholding food during the early stages of diarrhea is still widespread. This contributes to a deterioration in patients' nutritional state. The principal controversy in the nutritional therapy of acute gastroenteritis centers on the relative risks of cows'-milk feeds. The two things that need to be considered in determining the optimum approach to feeding the child with acute diarrhea are the optimum timing for feeding children in relation to the onset of and recovery from symptoms and, secondly, the effects of specific food ingredients in the diet. Recent studies have demonstrated that the vast majority of young children with acute diarrhea can be successfully managed with continued feeding of undiluted non-human milk. Routine dilution of milk and routine use of lactose-free formula are not necessary, especially when oral rehydration therapy and early feeding (in addition to milk) form the basic approach to the clinical management of diarrhea in children. Confounding factors are the severity of the diarrhea, coexistent malnutrition, and young age (< 1 y); such infants are much more likely to have complications from early feeding with undiluted milk and some would advocate use of specifically designed lactose-free formula in such children. Children who are fed exclusively with human milk and those who receive solid foods with or without human milk may safely continue to receive their usual diets during diarrhea. Those who are fed exclusively with non-human milk--especially when very young and with severe diarrhea or malnutrition--should be closely observed if they continue to consume milk or they should receive a special formulation (e.g., a cereal-milk mixture or fermented milk product). The use of nutrient-dense mixtures of common foods may be advisable to promote compensatory growth in those who lose weight during illness or because of anorexia or malabsorption.
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PMID:Nutritional management of acute diarrhea. 978 56

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

Increased concentrations of reactive oxygen species (ROS) and depleted antioxidant defences have been implicated in a cycle of infection, malabsorption and malnutrition, leading to persistent diarrhea. In order to determine whether in non-malnourished children oxidative stress predisposes to the development of persistent diarrhea, infants with acute diarrhea (< 7 days) (n = 39) were compared to infants with persistent diarrhea (> 14 days) (n = 38). Lipid peroxidation was assessed by the TBARs assay and expressed as malondialdehyde equivalent content (nmol MDA/ml plasma), and levels of plasma antioxidants vitamin A and vitamin E were determined. In infants with acute and persistent diarrhea nutritional status, as assessed by weight/height and height-for-age, hemoglobin levels, serum albumin and immunoglobulin levels, did not differ between groups. Serum vitamin A and vitamin E levels did not differ in infants with acute or persistent diarrhea. TBARs, expressed as nmol MDA/ml plasma did not differ between infants with acute or persistent diarrhea and furthermore did not differ from levels in a healthy, similar age, control group. Non-malnourished infants with persistent diarrhea do not exhibit plasma antioxidant depletion or enhanced lipid peroxidation. In these infants, oxidative stress, as reflected in plasma, does not play a role in the pathogenesis of persistent diarrhea.
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PMID:Oxidative stress is not enhanced in non-malnourished infants with persistent diarrhea. 1169 27

Zinc has been recognized as an antioxidant with potential for chronic and acute effects. Oxidative damage produced by free radicals, including nitric oxide (NO), is responsible for certain types of intestinal malabsorption syndromes and diarrhea. Under physiologic or mildly stimulatory conditions for NO synthesis, the small intestine characteristically is in a proabsorptive state; however, an excessive production of NO triggers formation of cyclic nucleotides, which cause secretion and malabsorption. In this study, we hypothesized that low-molecular-weight, soluble zinc chelates could modulate the effects of induced NO excess on the small intestine. In vitro experiments demonstrated that zinc-citrate or zinc-histidine at > or =0.66 mM, as well as a known NO scavenger, 2-[carboxyphenyl]-4,4,4,4-tetramethylimidazoline-1-oxyl-3-oxide, at 2 microM, were effective at removing chemically generated NO. In vivo jejunal perfusions, conducted in healthy rats under anesthesia, showed that c-PTIO reduced the proabsorptive effects produced by 1 mM L-arginine, the precursor of NO. In a standard oral rehydration solution, 1 mM zinc-citrate partially reversed the antiabsorptive effects on potassium caused by an excess of NO generated from 20 mM L-arginine but did not alter sodium or water absorption. The data are consistent with the view that soluble zinc compounds incorporated into an oral rehydration solution may deserve further attention as a means to scavenge NO with fluids used for the treatment of chronic or acute diarrhea, especially in malnourished children who are often zinc deficient.
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PMID:Zinc as a potential enteroprotector in oral rehydration solutions: its role in nitric oxide metabolism. 1259 91

Bacterial proliferation in the small intestine can induce the protraction of diarrhea due to malabsorption of the nutrients. We performed the culture of the small intestine juice for the aerobic and anaerobic flora in 40 infants with persistent and acute diarrhea. Bacterial proliferation was observed in 32 (80%) patients, being 30 (75%) due to the aerobic microflora and 17 (43%) due to the anaerobic microflora. There was no statistical difference in the bacterial growth between acute and persistent diarrhea. The aerobic bacteria most frequently isolated was E. coli in 23 patients, and Bacteroides sp was the most prevalent anaerobic bacteria, isolated in 9 cases. The transitory flora was significantly more abundant in patients with persistent diarrhea.
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PMID:[Proliferation of anaerobic flora in the small intestine of infants with acute and protracted diarrhea]. 1468 14


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