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)

Dietary regimens in gastrointestinal disease can be divided into two categories: First, those of proven value include: (a) Disaccharide elimination for disaccharidase deficiency and exclusion of monosaccharides for sugar malabsorption; (b) gluten-free diet for celiac/sprue; (c) elimination of certain allergens because of food allergies; (d) protein restriction for portal systemic encephalopathy; (e) low-carbohydrate diet for dumping syndrome; (f) low-fiber diet for diarrheal syndromes; and (g) low-fat diet for steatorrhea. Second, controversial diets include a bland diet for acid-peptic disorders, a high-fiber diet for colonic disorders, and a low-fat diet for gallbladder disease. It is important to separate facts from fancy in the dietary management of patients with gastrointestinal disease and base the recommendations for a particular diet on available objective evidence, not on traditional or fashionable trends.
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PMID:Diet therapy in gastrointestinal disease: a commentary. 47 89

Disturbances of the central and peripheral nervous system in Crohn's disease can be directly or indirectly caused by the disease itself or by the treatment. The first mentioned disturbances are very seldom. Cerebral arterial and venous thromboses can be attributed to hypercoagulation. Malabsorption of vitamin B 12 or folic acid can lead to a subacute combined degeneration of the spinal cord, sometimes in combination with a polyneuropathy and an encephalopathy. Spinal abscesses very seldom occur. An opticusneuropathy can be caused either by vasculitis or by a lack of vitamin A and/or vitamin B. Polyneuropathies in Crohn's disease which are not induced by drugs are manifested as mononeuritis multiplex or as symmetrical sensory neuropathy. An autoimmune process is being discussed as the probable cause of there diseases. In some cases large doses and prolonged administration of metronidazole can lead to cerebral dysfunctions with state of confusion, alterations of consciousness, cerebral convulsions and cerebellar syndrome. Most of these symptoms disappear rapidly after this drug is not longer administered. In long-term administration of metronidazole 10-50% of the patients develop a sensory polyneuropathy with a total dosis of at least 22.5 g, but mostly above 60 g. After the use of metronidazole is stopped, it takes a substantial period of time until there is a full recovery from the symptoms.
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PMID:[Neurologic concomitant diseases in Crohn disease]. 128 45

The normal gastrointestinal flora includes no more than 10(3) organisms/ml of gastric aspirate and no more than 10(5) organisms/ml of duodenal or jejunal juice. The organisms are primarily gram-positive and aerobic bacteria. In particular anatomical or functional predisposing conditions, an abnormal colonization takes place in the small bowel with microbial concentrations > or = 10(7)/ml of aspirate and with a predominance of anaerobes and coliforms. At times this small bowel bacterial overgrowth remains asymptomatic, but more often leads to a true malabsorption syndrome with symptoms, such as diarrhoea, weight loss and megaloblastic anemia. The most accurate procedure for confirming the presence of this condition is represented by the bacterological analysis of the jejunal aspirate. The routine use of this method is, however, notably hindered by the need for intubation of the patient and by the lack of laboratories suitably equipped for anaerobe culture. As an alternative to this complex procedure, numerous non-invasive tests have been perfected over the last few years, including the glucose- or lactulose- H2 breath test. The main aim of the treatment of the small bowel bacterial overgrowth is the suppression of the bacterial colonization using antimicrobial therapy. Among the local-action non-absorbable antibiotics, rifaximin, was shown to have bactericidal activity against aerobes and anaerobes bacteria, such as bacteroides, lactobacilli and clostrides. In controlled clinical trials the antibiotic has demonstrated therapeutic efficacy in bacterial origin diarrhoea, in porto-systemic encephalopathy, in diverticulosis and, finally, in small bowel bacterial overgrowth.
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PMID:Non-absorbable antibiotics and small bowel bacterial overgrowth. 148 97

While the rate of malnutrition is relatively modest in alcoholic patients without alcoholic liver disease, the rate of malnutrition is virtually 100% in patients with alcoholic hepatitis and/or alcoholic cirrhosis. The reasons for malnutrition in the alcoholic hepatitis patient include various factors such as anorexia, poor diet, malabsorption, and altered metabolic state. When the patient is hospitalized, the malnutrition frequently worsens because of fasting for tests, continued anorexia, and complications such as gastrointestinal bleeding. Patients with severe acute hepatitis appear to be both hypermetabolic and hypercatabolic, whereas data are much more conflicting concerning patients with more stable liver disease. Most studies suggest that patients with alcoholic liver disease require at least 60 g of protein per day to maintain positive nitrogen balance. Consistent alterations in plasma amino acid profiles occur in alcoholic liver disease, and specialized nutritional formulations have been devised to correct this amino acid profile with the intent of improving overall nutritional status, hepatic encephalopathy, and mortality. The effects of nutritional support (including use of specialized products) on outcome, on acute hepatic encephalopathy, and on chronic or latent portal systemic encephalopathy are reviewed.
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PMID:Nutrition and alcoholic liver disease. 190 86

D-lactate accumulates in some patients with malabsorption who continue oral intake of carbohydrate leading to a clinical syndrome of acidosis and encephalopathy. To assess the possibility that D-lactate contributes to acidosis and/or metabolic bone disease in patients with malabsorption receiving long-term parenteral nutrition yet maintaining oral intake, D-lactate levels in serum and urine were measured in 14 long-term parenteral nutrition subjects (average duration of support 74 months) and 27 control subjects. Significant elevations in both serum and urine D-lactate were found in only two parenteral nutrition subjects. Both subjects with elevated D-lactate levels had bone pain, x-ray evidence of fractures, and biopsy evidence of osteomalacia. These studies suggest that D-lactate accumulation may be a heretofore unappreciated metabolic abnormality associated with metabolic bone disease and acidosis in patients with malabsorption who are supported by long-term parenteral nutrition.
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PMID:D-lactate and metabolic bone disease in patients receiving long-term parenteral nutrition. 249 43

With a normal and varied food intake, the vitamin supply is often sufficient to avoid vitamin deficiency. Since synthetic vitamins have become available, it has become possible to take with one dose the amount of vitamins normally taken up from food in one year. In these pharmacological doses vitamins must therefore be considered as drugs. And in pharmacological doses, their actions are often different and not directly linked to their physiological activity. Two types of pathologic state are unquestionably the concern of vitaminotherapy: More or less specific and intense vitamin deficiencies: Rickets, scurvy, beri beri, pellagra, vitamin deficiency related to alcohol consumption, polyneuritis, encephalopathy, malabsorption, mucoviscidosis, etc. Genetic defects of vitamin metabolism: Prescriptions for these cases represent only a tiny part of the vitamin pharmaceutic market. The prescription of vitamins as adjuvants in other pathologic states without vitamin deficiency, such as neurological pains, psychosis, prevention of common cold, alopecia, anemia, asthenia, carpal tunnel defect, etc., is frequent. The results may be good; however, in some cases, the efficacy is due to chance or placebo effect, and there is no scientific or experimental evidence of beneficial activity. At the moment, the pharmacological vitamin research is very active. New products with vitamin-like structures are being synthesized for specialized therapeutic applications. They will in the near future probably replace elevated and mega-doses for clinical prescription, except, of course, for the treatment of vitamin deficiency. On the other hand, the use of multivitamin preparations in nutritional dosage will greatly increase.
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PMID:Clinical conditions requiring elevated dosages of vitamins. 250 93

D-Lactate-associated encephalopathy is a rare clinical syndrome characterized by dizziness, ataxia, confusion, headaches, memory loss, lethargy, and aggressiveness which may progress to frank but reversible coma. It occurs in patients with profound dysfunction of the short-bowel syndrome and is believed to result from massive carbohydrate malabsorption with resultant over-production of D-lactate and other organic anions by the colonic flora. Extremely elevated serum levels of D-lactate (but not L-lactate) confirm the diagnosis, but currently D-lactate is not clearly established as the putative neurotoxin. We describe a patient who repeatedly developed D-lactate encephalopathy after surgical removal of nearly the entire jejunum and ileum. Markedly elevated D-lactate serum levels were documented during an encephalopathic episode. Potential pathophysiologic mechanisms and the treatment rationale are discussed.
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PMID:D-lactate-associated encephalopathy after massive small-bowel resection. 276 Apr 34

To determine if malabsorption of zinc contributes to the zinc deficiency found in cirrhosis, the absorption of an oral dose of ZnCl2, labeled with 65Zn and a nonabsorbed marker 51CrCl3, was determined from the ratio of these isotopes in a stool specimen. Average 65Zn absorption in 25 alcoholic cirrhotics, 37 +/- 17% (SD), was low compared to 55 +/- 16% in 31 healthy volunteer controls (P less than 0.01). In contrast, mean 65Zn absorption, 47 +/- 11%, in 11 nonalcoholic cirrhotics was not significantly different from the average result in healthy controls. Low 65Zn absorption was accompanied by low leukocyte zinc in a subgroup of alcoholic cirrhotics with ascites and/or ascites and encephalopathy, but not in the subgroup in which these clinical features were absent. Thus, low zinc absorption contributes to zinc deficiency in decompensated alcoholic cirrhosis. The failure to find similar abnormalities in nonalcoholic cirrhosis suggests that the long-standing consumption of alcoholic beverages contributes to the malabsorption of zinc.
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PMID:Zinc absorption and leukocyte zinc in alcoholic and nonalcoholic cirrhosis. 397 39

This report describes a case of d-lactic acidosis observed by the authors and then reviews all case reports of d-lactic acidosis in the literature in order to define its clinical and biochemical features and pathogenetic mechanisms. The report also reviews the literature on metabolism of d-lactic acid in humans. The clinical presentation of d-lactic acidosis is characterized by episodes of encephalopathy and metabolic acidosis. The diagnosis should be considered in a patient who presents with metabolic acidosis and high serum anion gap, normal lactate level, negative Acetest, short bowel syndrome or other forms of malabsorption, and characteristic neurologic findings. Development of the syndrome requires the following conditions 1) carbohydrate malabsorption with increased delivery of nutrients to the colon, 2) colonic bacterial flora of a type that produces d-lactic acid, 3) ingestion of large amounts of carbohydrate, 4) diminished colonic motility, allowing time for nutrients in the colon to undergo bacterial fermentation, and 5) impaired d-lactate metabolism. In contrast to the initial assumption that d-lactic acid is not metabolized by humans, analysis of published data shows a substantial rate of metabolism of d-lactate by normal humans. Estimates based on these data suggest that impaired metabolism of d-lactate is almost a prerequisite for the development of the syndrome.
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PMID:D-lactic acidosis. A review of clinical presentation, biochemical features, and pathophysiologic mechanisms. 955

Previous investigations showed that Schistosoma mansoni infection aggravates protein malabsorption in undernourished mice and this can be reverted by administration of casein hydrolysate. The present study was undertaken to evaluate the effects of ingestion of casein hydrolysate for long periods. Albino Swiss mice were divided into eight groups. Diets contained 5% (undernourished) or 20% (controls) casein levels. For each group there were sub-groups ingesting whole or hydrolysed casein for 12 weeks. Infection with S. mansoni developed in half of the animals under each diet. All undernourished mice developed malabsorption. Low albuminemia was detected in infected animals independently of the protein level in the diet. However, albuminemia was lower in infected controls than in undernourished non-infected mice, suggesting a deficient liver protein synthesis. Infected mice fed on a 20% protein hydrolysed diet exhibited low weight gain and high mortality rates. On the other hand, non-infected mice ingesting the same diet had the highest body weights. We are investigating the hypothesis that infected mice, even when fed normal diets, are unable to metabolise large amounts of amino acids due to the liver lesions related to schistosomiasis and as a result die of hepatic coma. In some of them, the excessive accumulation of ammonia in the blood enhances the outcome of an encephalopathy.
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PMID:A long-term intake of a protein hydrolysate seems to increase the risk of encephalopathy in mice infected with Schistosoma mansoni. 992 50


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