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

The authors relate the results of 10 years of observations of 113 patients suffering from gluten enteropathy (GE) of the adults. In all the patients, the diagnosis was supported by the presence of hyper-regenerative atrophy of the small intestinal mucosa (total in 70% and subtotal in 30%). Metabolic disorders and cellular immunity were investigated. At the onset of the observations 70.7% of the patients demonstrated malabsorption, stage III gravity, and 29.3% stage II. It has been proved that permanent and strict adherence to the agluten diet and administration of corticosteroids in the most severe cases in combination with pathogenetic therapy of diarrhea and metabolic disorders permit attaining a steady clinical remission, improvement of normalization of the biochemical and immunological characteristics, a tendency toward normalization of the small intestinal mucosa, and even the recovery of its normal structure in part of the cases.
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PMID:[Gluten enteropathy]. 150 90

Two siblings had olivopontocerebellar degeneration, failure to thrive, hepatic fatty change and cirrhosis, and a dyslipoproteinemia characterized by low cholesterol and elevated triglycerides. This condition was distinct from other cerebellar atrophies and ataxias and was not due to malabsorption or malnutrition. Cerebellar degeneration progressed rapidly during the first year of life, and both children died from intercurrent infections and surgical complications at 11 and 17 months. Stereotyped clinical and pathologic findings in the two patients suggest a previously unreported genetic metabolic disorder affecting the liver and the CNS.
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PMID:Lipoprotein disorder, cirrhosis, and olivopontocerebellar degeneration in two siblings. 370 66

Patients are often referred to diabetologists on account of a flat curve of oral glucose tolerance test. This abnormality, however, is virtually never associated with a serious metabolic disorder and in any case, it never points to a disease that cannot be diagnosed by questioning or by straightforward clinical examination, nor confirmed by a more specific laboratory test. The curve may be flat for technical reasons (e.g. rejection of the glucose administered, timing of blood withdrawals and assays), for physiological reasons (differences between venous and arteriolo-capillary blood), or for pathological reasons (interaction with drugs, pituitary, thyroid or adrenal insufficiency, digestive malabsorption) but it never implies organic hypoglycaemia nor diabetes mellitus.
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PMID:[Flat curves of oral glucose tolerance tests (author's transl)]. 738 51

The aim of this study was to evaluate the prevalence of lactose malabsorption in a population of 75 (43 males, 32 females) apparently healthy school-children using the H2 breath test with cow's milk. The children, ranging in age from 8 years and 6 months to 15 years and 2 months (mean: 11 years, 7 months) were divided into 2 age groups: Group I (no. = 26): age < 11 years and Group II (no. = 49): age > 11 years. After on overnight fasting, lasting at least 8 hours, samples of expired air were collected at 0 time and at 30-min intervals following the administration of 250 ml cow's milk for a total time of 3 hours. The H2 breath concentration was then measured by gas chromatography (Micro-Lyzer Quintron Instruments Company mod. 12). A net rise of more than 20 ppm H2 was considered as lactose malabsorption. Subjects with symptoms such as excessive flatulence, abdominal pain, or diarrhoea, were considered as lactose intolerant. Two-hundred and 50 ml of cow's milk (12 g of lactose) was considered a more physiological vehicle than the traditional lactose aqueous solution. The examined children, all on free diet, showed a fasting alveolar from 0 to 43 ppm (mean +/- SD = 7.9 +/- 7.6). Sixty-six children out of 70 (93.3%), who completed the test had a total absorption of lactose. Two out of 4 children with lactose malabsorption originated from areas (East Africa and Central America), where a high incidence of this metabolic disorder is a characteristic findings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prevalence of lactose malabsorption in Roman school children. A H2 breath test study using a cow's milk]. 830 22

Weight loss, anorexia, metabolic disorder and malabsorption are leading symptoms of HIV infection. Recent data help us to understand wasting as being intrinsically linked to immunodysregulation and enteropathy. In therapy, the role played by anabolic steroids and growth hormone has been newly defined. The new antiviral drugs may efficiently prevent clinical progression, including wasting. New metabolic side effects have, however, been encountered.
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PMID:HIV infection and malnutrition. 1056 77

A 51-year-old woman who had been treated with levothyroxine sodium because of hypothyroidism after total thyroidectomy for thyroidal cancer was admitted to our hospital for persistent hypothyroidism despite large dose administration of levothyroxine (600 microg/day). The patient complained of severe general fatigue and body weight gain. Free thyroxine, free triiodothyronine and thyrotropin levels were 0.97 ng/dl, 1.55 pg/ml and 24.51 microU/ml, respectively, under oral administration of levothyroxine. Levothyroxine loading test performed by liquid form, pulverized tablets via nasogastric tube and intravenous administration revealed no evidence of malabsorption or metabolic disorder of levothyroxine, although oral intake of tablets was ineffective due to her factitiousness. We report here a possible case of "pseudomalabsorption of levothyroxine" to emphasize the clinical recognition of this disorder in patients with resistant hypothyroidism.
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PMID:Pseudomalabsorption of levothyroxine: a case report. 1081 Dec 92

A six-month-old beagle was presented with a three-month history of failure to gain weight, lethargy, intermittent vomiting and seizures. Hypoglycaemia, portosystemic shunt, lead intoxication, gastrointestinal diseases and hereditary metabolic disorders were considered. Laboratory test results of low serum cobalamin (Cbl) concentrations, anaemia, leucopenia and methylmalonic aciduria while the dog was receiving a balanced commercial canine diet were suggestive of a congenital selective Cbl malabsorption. Treatment with repeated injections of parenteral cyanocobalamin (CN-Cbl) at 50 microg/kg every two weeks corrected the Cbl-deficient state and reversed all the clinical abnormalities. Selective Cbl malabsorption has previously been described in giant schnauzers and border collies and represents a unique readily treatable hereditary metabolic disorder.
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PMID:Persistent cobalamin deficiency causing failure to thrive in a juvenile beagle. 1102 27

Convinced that morbid obesity was not due to food excess but rather to a metabolic disorder, we searched in the literature for data in favor of a metabolic disorder. We have found evidence in support of the thesis that the cause of morbid obesity is the inability to burn excessive caloric intake normally. It would involve the difficulty to increase heat with the amount of calories taken, which would be faulty and force fat deposition. This mechanism called dietinduced thermogenesis (DIT) allows the dispersion by heat of excessive calories to obtain energy balance. Results from bariatric surgery and particularly biliopancreatic diversion (BPD) give further support to this thesis. BPD would improve heat production to a meal (DIT) by one of these mechanisms: increased insulin sensitivity, change in intestinal hormone secretion, or chronic lipid malabsorption. Available results show that surgery, to be efficient, must change the physiology and not solely decrease food intake.
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PMID:Contribution of bariatric surgery to the comprehension of morbid obesity. 1576 Apr 94

H (2)- and (13)C-breath tests are valuable non-invasive diagnostic tools for gastroenterological diseases. H (2)-breath tests are clinically established for the diagnosis of carbohydrate intolerance resulting from malabsorption (H (2)-breath tests with lactose, fructose, saccharose, sorbitol), of bacterial overgrowth (glucose H (2)-breath test) and for measurement of orcoceal transit time (lactulose H (2)-breath test). The (13)C-urea breath test is regarded as the "gold standard" procedure for the diagnosis of Helicobacter pylori infection. Moreover, (13)C-breath tests for measurement of gastric emptying can be considered as clinically established, meanwhile. (13)C-breath tests for the evaluation of pancreatic exocrine function or liver function can also be used clinically; however, they currently offer no substantial advantage over other diagnostic procedures. A major disadvantage of all breath tests is that they lack standardization although modifications of the test meal or solution, of the test performance and of the evaluation of data may markedly influence the results. Thus, this article presents the recommendations of the German Society of Neurogastroenterology and Motility and of the German Society of Digestive and Metabolic Diseases for clinically relevant H (2)- and (13)C-breath tests. Indications for the examinations, the procedures to be followed, the analysis of the obtained data and the conclusions to be drawn are delineated. The literature on which the recommendations are based is reviewed. However, personal experience of the authors is also taken into account since numerous questions regarding optimal test performance are not clarified by adequate studies.
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PMID:[Clinically relevant breath tests in gastroenterological diagnostics--recommendations of the German Society for Neurogastroenterology and Motility as well as the German Society for Digestive and Metabolic Diseases]. 1614 16

Disaccharide intolerance presents a pathogenic heterogeneous and most complex clinical entity. It usually occurs due to primary or secondary deficit of disaccharide activity, and rarely because of disorders of absorption or monomer metabolism. Symptomatology of disaccharide maldigestion and/or malabsorption depends on the severity of the basic disorder, the level of its overload and the patient's age. In the youngest children, due to a rapid gastrointestinal transit and a low compensatory capacity of the colon, osmotic-fermentative diarrhoea forms the basis of clinical features. Diarrhoeal disorder can be occasionally so intensive that it disturbs not only water and electrolytic balance, but also the nutritive status of the child. In older children and adults, as well as in milder forms of the disorder, the symptomatology, most often without diarrhoea, is dominated by abdominal colic, loud peristaltic sounds, meteorism and increased flatulence. Metabolic disorders followed by conversion disorders of galactose and fructose into glucose are characterized by a hypoglycaemic crisis, as well as by various multisystemic damages due to the deposit of toxic metabolic products. The diagnosis of gastrointestinal forms of disaccharide intolerance is based on the pathologic clinical and laboratory response during the overload test, while that of the metabolic form is based on the confirmed presence of specific enzyme and/or genetic defect. Treatment of disaccharide intolerance is based on the elimination diet. Besides, in the secondary forms of the disorder, it is also necessary to apply the treatment of the basic disease.
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PMID:[Disaccharide intolerance]. 2136 93


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