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

To assess whether malabsorption of specific sugars is easily detected in a pediatric population by interval measurement of breath hydrogen excretion, hydrogen concentration was determined following administration of oral sucrose to six sucrose-intolerant children with congenital sucrase-isomaltase deficiency and in 16 sucrose-tolerant control subjects. Breath samples were collected by means of a newly devised nasal prong technique not requiring active patient cooperation and suitable for use in all age groups. Breath hydrogen concentrations obtained by samples collected by this method correlated highly (r = 0.94) with the previously validated modified Haldane-Priestley tube method for sampling alveolar air. Identification of sucrose-intolerant individuals was achieved on the basis of hydrogen excretion: peak values, expressed as parts per million above baseline (deltappm), equalled 114 +/- 63 (mean +/- SD) versus 2.4 +/- 3.6 deltappm in control subjects (P = 0.007). Best discrimination between the groups occurred at 90 minutes postingestion. The findings validate this simple method for collection of expired air and demonstrate that breath hydrogen determination permits the noninvasive detection of sucrose malabsorption in children.
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PMID:Sucrose malabsorption in children: noninvasive diagnosis by interval breath hydrogen determination. 65 Mar 40

In 148 children, 4 months to 14 1/2 years old, 192 serum-xylose-tests (XT) and small bowel biopsies have been performed because of suspected intestinal malabsorption. The results of the XT and of the biopsies were compared to investigate the diagnostic value of the XT with respect to the morphology of the small bowel mucosa. Further we wanted to determine at which time after the oral intake of xylose the best correlation of XT and morphology can be expected. In children with normal mucosa the XT differed significantly from those with subtotal mucosal atrophy but not with partial villous atrophy. However, partial villous atrophy could be differentiated from subtotal villous atrophy with the same test. In children with subtotal villous atrophy a statistically significant age-dependency could be observed, comparing children being less or more than 2 years old and also a dependency from periods with gluten-free diet. Partial villous atrophy with or without coeliac disease cannot be differentiated by means of the XT. Best correlation of the XT and the morphology of the small bowel mucosa can be found 60 minutes after the oral xylose load; no additional information is obtained by more blood-xylose-determinations (e.g. 30, 90, 120, 180 minutes). Because of the rather high standard deviation of the individual blood xylose values no exact prediction can be made from the XT to the mucosal morphology. Therefore the XT is only of value for screening purposes and its results should not influence the indication for a small bowel biopsy, derived from clinical considerations.
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PMID:[Usefulness of the serum-xylose-test in comparison with small-intestine morphology in the malabsorption syndrome]. 90 47

Hip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The public health burden will increase as the increase in the numbers of elderly men in the community increases. In addition, the age-specific incidence of hip fractures may be increasing in some, but not all, countries. Vertebral fractures may be a public health problem as recent studies suggest that the prevalence in the community is 20-30%, similar to that reported in women. Forearm fractures should probably not be regarded as a public health problem. Peak bone mass is higher in men than women because men have bigger bones. Peak bone mineral density is the same. The amount of trabecular bone lost at the spine and iliac crest during ageing is similar in men and women. Cortical bone loss is less in men because endocortical resorption is less and periosteal formation is greater. Bone loss accelerates in elderly men because endocortical resorption and increasing cortical porosity increase the surface available for resorption. Bone fragility is less in men than women because: (a) the cross-sectional surface of the bone is larger; (b) trabecular bone loss is less as a percentage of the higher peak bone mass; (c) trabecular bone loss occurs by thinning rather than perforation; and (d) periosteal appositional growth compensates for endocortical resorption by maintaining the bending strength of bone. Reduced BMD in men with fractures may be due to reduced peak bone size and mass, and bone loss. Bone loss occurs by reduced bone formation. Whether men with fractures have increased bone fragility due to reduced periosteal appositional growth during ageing is unknown. The age-related decline in testosterone, adrenal androgens, growth hormone, and insulin-like growth factor 1 may contribute to reduced bone formation and bone loss. Men with vertebral fractures often have hypogonadism or illnesses with few clinical features that should be considered with a high index of suspicion (alcoholism, myeloma, malabsorption, primary hyperparathyroidism, haemochromatosis, Cushing's disease). Secondary hyperparathyroidism may contribute to bone loss by activating bone turnover and so increasing the number of bone remodelling units with impaired bone formation in each. There is no proven treatment for osteoporosis in men because there have been no trials using anti-fracture efficacy as an end point. Testosterone replacement should be considered in men with proven hypogonadism and vitamin D deficiency should be corrected if present. Calcium supplements and bisphosphonates are reasonable options given the lack of information.
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PMID:Osteoporosis in men. 936 40

Small intestine bacterial overgrowth is a malabsorption syndrome and, therefore, it may contribute to the occurrence of metabolic bone disease. However, studies that evaluate the magnitude of this problem and the potential underlying mechanisms are still needed. Fourteen patients with bacterial overgrowth and 22 comparable healthy volunteers took part in this study. All patients were affected by conditions known to predispose to bacterial overgrowth. Diagnosis was based on the following criteria: increased breath hydrogen levels in the fasting state and/or increased breath hydrogen excretion after the ingestion of 50 g of glucose solution, improvement after a 10-day course of antibiotic therapy of severity of symptoms and of H2 excretion parameters. Measurement of bone mineral density by dual-energy x-ray absorptiometry at lumbar spine and femoral level and evaluation of nutritional status were performed. Physical activity, sunlight exposure, and cigarette smoking were also evaluated. Patients showed lumbar and femoral bone mineral density values significantly lower than control group; also the prevalence of bone loss at both lumbar and femoral levels was higher in patient group than in healthy volunteers. Body mass index was significantly lower in patients than in healthy volunteers. Lumbar and femoral bone mineral density were significantly correlated and both correlated with body mass index and with duration of symptoms. No correlation between BMD values and physical activity, sunlight exposure, and cigarette smoking was evident. Our results show that small intestine bacterial overgrowth is an important cofactor in the development of metabolic bone disease. The severity of bone loss is related to poor nutritional status and duration of malabsorption symptoms.
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PMID:Small intestine bacterial overgrowth and metabolic bone disease. 1134 52

Adding either H(2)-receptor antagonists (cimetidine or ranitidine) or proton pump inhibitors to an adequate amount of lipolytic activity improves fat malabsorption in most cases and abolishes steatorrhoea in up to 40% of children and adults with cystic fibrosis and in adults with chronic pancreatitis. Acid suppression improves fat absorption because the resultant increase in pH within the upper gastrointestinal tract improves the survival of lipolytic activity, reduces duodenal volume flow and prevents the precipitation of bile acids. These effects increase the concentration of intraduodenal lipolytic activity and promote the aggregation of bile acids and the micellar solubilization of lipid. The amount of lipase that should be recommended is controversial, but we interpret our studies as indicating that at least 90 000 United States Pharmacopeia (USP) units should be ingested with meals. This amount of lipolytic activity taken with an agent that suppresses gastric acid secretion improves fat absorption in most patients and may even abolish steatorrhoea.
Best Pract Res Clin Gastroenterol 2001 Jun
PMID:Gastric acid suppression and treatment of severe exocrine pancreatic insufficiency. 1140 40

There are now a wide variety of drugs available that are able profoundly to reduce the production of gastric acid. These drugs are currently widely prescribed for the treatment of peptic ulceration and gastro-oesophageal reflux disease. One of the main functions of gastric acid is to kill ingested bacteria. Colonization of the gastric lumen occurs in patients on anti-secretory medication, the degree of bacterial overgrowth depending upon the degree of elevation of the pH. There have been concerns that these bacteria may produce carcinogenic nitrosamines and increase the risk of gastric cancer, but there is at present no definitive evidence in support of this. A profound suppression of gastric acid may also facilitate the colonization of the upper small intestine, leading to deconjugation of the bile salts and malabsorption. There is some evidence that profound gastric acid suppression may decrease the number of ingested pathogens required to produce enteric disease. This chapter discusses these potential bacterial complications of therapeutic acid suppression and the evidence for them.
Best Pract Res Clin Gastroenterol 2001 Jun
PMID:Occurrence and significance of gastric colonization during acid-inhibitory therapy. 1140 43

Gastric acid suppression therapy has for many years been the cornerstone of the treatment of peptic disease. The availability of more potent inhibitors of gastric acid secretion and the increasing demand for maintenance therapy has renewed interest in the potential side-effects of profound and/or long-lasting therapy. This chapter focuses on the potential interference of gastric acid suppression therapy with the process of the digestion and absorption of nutrients. The theoretical mechanisms by which hypochlorhydria resulting from gastric acid suppression therapy may hamper digestion and absorption are multiple and well documented. Clinical studies evaluating the effect of gastric acid suppression therapy on the assimilation of nutrients are, on the other hand, scarce and have, moreover, yielded conflicting results. The reason for the latter may be related, at least in part, to elements of study design. Data indicating overt malabsorption or clear deficiencies in patients on long-term gastric acid suppression therapy are currently lacking. Nevertheless, it seems prudent, while awaiting the results of additional long-term studies, regularly to monitor these patients, especially those with increased nutrient demand, poor intake or suboptimal stores.
Best Pract Res Clin Gastroenterol 2001 Jun
PMID:Alteration in digestion and absorption of nutrients during profound acid suppression. 1140 45

The consequences of vitamin D deficiency upon the skeleton are well known and management in the absence of renal failure is relatively straightforward. Vitamin D, either by mouth or parenterally will correct the deficiency and heal the osteomalacia. The mechanisms underlying the causation of vitamin D deficiency are now better understood and indicate the importance of underlying calcium malabsorption and secondary hyperparathyroidism leading to 1,25(OH)2D-induced catabolism of 25(OH)D and possibly also of vitamin D itself. In such situations, e.g., gastrointestinal and pancreaticobiliary disease, calcium supplementation in addition to vitamin D is indicated. The reasons behind nutritional vitamin D deficiency and the possible role of meat in protecting from osteomalacia await further elucidation, but from epidemiological studies, calcium deficiency, per se, is not implicated in the etiopathogenesis. The concept of vitamin D insufficiency is poorly understood, and difficult to define since a single value or close range of serum 25(OH)D values is unlikely to predict the needs of all subjects. Oral calcium intake and renal function are also likely to be relevant to the level of 25(OH)D which is found to be sufficient or insufficient for any given individual to maintain a normal serum calcium level without secondary hyperparathyroidism. There is increasing evidence that vitamin D insufficiency, by leading to sustained hyperparathyroidism, is prejudicial to the skeleton, particularly cortical bone. Since it is without symptoms until fractures occur, it should be actively sought in those clinical situations now recognized as contributing to risk. It can only be identified by the periodic measurement of serum 25(OH)D and the calcitropic hormones PTH and 1,25(OH)2D. In addition, BMD should be measured in a predominantly cortical site such as the proximal forearm, as well as the more conventional sites of spine and hip. The implications of these recommendations are an increase in the use of assays for PTH and vitamin D metabolites in the groups of subjects discussed in this review. Patients with chronic malabsorption states might reasonably be expected to have measurements performed twice-yearly. When vitamin D insufficiency is found, treatment with either vitamin D, calcium or both will be necessary, depending on the etiology of the insufficiency state in the inividual. In some malabsorptive states, calcium malabsorption is the cause of hyperparathyroidism and oral calcium alone can be used to reverse excess PTH activity in those with an adequate state of vitamin D nutrition. However, even in those vitamin D replete individuals, vitamin D catabolism will be enhanced and a small additional oral dose of vitamin D can do no harm. Regular monitoring of PTH and vitamin D metabolites will remain a necessity to ensure continued efficacy of treatment. Current recommendations for dietary supplements of vitamin D are clearly inadequate [61]. There is compelling evidence for supplements of 800 IU per day in the elderly and other high risk populations. Such a dose is safe and without side effects. The available evidence suggests that this should be combined with calcium supplements of 1200 mg/day [19] and that the current UK recommendations for a daily calcium intake of 700 mg contrast with those from the USA at 1,200 mg for people over 50 years old. Physicians need to be aware of both the small but important problem of vitamin D depletion and osteomalacia with its sometimes ambiguous presentation, and the more common but covert vitamin D (and calcium) insufficiency with its widespread and varied clinical associations.
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PMID:Vitamin D nutrition and bone disease in adults. 1170 21

Malnutrition is more common in elderly persons than in younger adults. Ageing itself, however, neither leads to malabsorption nor to malnutrition with the exception of a higher frequency of atrophic gastritis in older persons. Malnutrition in elderly people is therefore a consequence of somatic, psychic or social problems. Typical causes are chewing or swallowing disorders, cardiac insufficiency, depression, social deprivation and loneliness. Undernutrition is associated with a worse prognosis and is an independent risk factor for morbidity and mortality. Awareness of this problem is therefore important. For the evaluation of nutritional status, it must be remembered that most normal values are derived from younger adults and may not necessarily be suitable for elderly persons. Suitable tools for evaluating the nutritional status of elderly persons are e.g. the body mass index, weight loss within the last 6 months, the Mini Nutritional Assessment (MNA) or the Subjective Global Assessment (SGA). An improvement in the nutritional status can be achieved by simple methods such as the preparation of an adequate diet, hand feeding, additional sip feeding or enteral nutrition.
Best Pract Res Clin Gastroenterol 2001 Dec
PMID:Nutrition in the elderly. 1186 82

Malabsorption of carbohydrates, lipids, amino acids, minerals and vitamins has been described in the elderly. The ability of the intestine to adapt may be impaired in the elderly and this may lead to further malnutrition. Dietary manipulation may prove to be useful to enhance the needed intestinal absorption with ageing. There is an age-associated increase in the prevalence of dyslipidaemia as well as diabetes. These conditions may benefit from nutritional intervention targeted at reducing the absorption of some nutrients. With the continued characterization of the proteins involved in sterol and fatty acid absorption, therapeutic interventions to modify absorption may become available in the future.
Best Pract Res Clin Gastroenterol 2002 Feb
PMID:Nutrient absorption and intestinal adaptation with ageing. 1197 25


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