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)

The aim of the present study was to evaluate the influence of severe protein-energy malnutrition on the antioxidant defense system in the small and large intestine in rats at weaning. Chronic diarrhea and the subsequent malnutrition were induced by oral intake of a lactose-enriched diet. Twenty rats were weaned at 21 days of age, and the control group was fed a semipurified synthetic diet for two weeks. The malnourished group was fed the same diet but carbohydrates were replaced by lactose, and they developed diarrhea one day after. Rats were killed, and macroscopic and histological features were analyzed, DNA content was measured, and alkaline phosphatase, myeloperoxidase, and gamma-glutamyltranspeptidase activities were determined to assess the degree of intestinal injury. Glutathione levels as well as the activities of intestinal glutathione transferase, glutathione reductase, total glutathione peroxidase, selenium-dependent glutathione peroxidase, superoxide dismutase, and catalase were measured to study the antioxidant defense system. Malnourished rats showed loss of body weight and an increase in length and weight in jejunum and ileum, while no significant changes were observed in colon. Epithelial cells showed fewer and shorter microvilli, larger mitochondria with low inner density and loss of cristae, dilated endoplasmic reticulum, and Golgi apparatus. The protein-to-DNA ratio was higher in the jejunum, ileum, and colon of malnourished rats. Glutathione levels decreased 40% in jejunum and 50% in colon of malnourished rats. A 40-50% decrease in the activity of all the enzymes of the antioxidant defense system was observed in the jejunum and ileum of malnourished rats, while only catalase and glutathione transferase activities decreased 50% in colon. These results suggest that early chronic diarrhea and severe protein-energy malnutrition impair the antioxidant defense system in both the small and large intestine, which may have a role in the pathogenesis and maintenance of the vicious circle of malabsorption-diarrhea-malnutrition in infancy.
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PMID:Chronic diarrhea impairs intestinal antioxidant defense system in rats at weaning. 1111 81

In the present study. we explored the nutritional consequences of cryptosporidiosis. In order to ascertain the direct responsibility of C. parvum for impairment of staturoponderal development observed during the infection in neonatal animals, we investigated the absorption of two major components of the total amino acids in dam's milk (leucine and glutamate) across the ileal mucosa. The infection resulted in significant (47% and 34%, respectively) reductions in leucine and glutamate fluxes (P<0.01). Moreover, the leucine aminopeptidase and alkaline phosphatase activities were reduced in the infected ileal mucosa. Interestingly, the reduction in weight gain, which began at day 6 post-infection (PI), persisted until day 20 PI, although no cryptosporidia were detected in the ileal mucosa after day 12 PI. We thus provide evidence that the malabsorption of amino acids during cryptosporidiosis contributes to impairing the development of neonatal animals, with consequences that persist beyond eradication of the parasite.
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PMID:Impairment of amino-acid absorption in suckling rats infected with Cryptosporidium parvum. 1172 11

Weight loss after biliopancreatic diversion or duodenal switch is due to decreased calorie absorption secondary to fat malabsorption. Fat malabsorption may also cause essential fat-soluble vitamin deficiencies, which may have severe clinical consequences and alter calcium metabolism. Serum vitamins A, D, E, and K, zinc, parathyroid hormone, corrected calcium, and alkaline phosphatase levels were measured in a cohort of patients who had previously undergone biliopancreatic diversion. Two bariatric surgery units were involved in the study: New York University School of Medicine (New York, NY), and the Wesley Medical Center (Brisbane, Australia). A total of 170 patients completed the study. The incidence of vitamin A deficiency was 69%, vitamin K deficiency 68%, and vitamin D deficiency 63% by the fourth year after surgery. The incidence of vitamin E and zinc deficiency did not increase with time after surgery. The incidence of hypocalcemia increased from 15% to 48% over the study period with a corresponding increase in serum parathyroid hormone values in 69% of patients in the fourth postoperative year. There is a progressive increase in the incidence and severity of hypovitaminemia A, D, and K with time after biliopancreatic diversion and duodenal switch. Calcium metabolism is affected with an increasing incidence of secondary hyperparathyrodisim and evidence of increased bone resorption in 3% of patients. Long-term nutritional monitoring is necessary after malabsorptive operations for morbid obesity.
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PMID:Serum fat-soluble vitamin deficiency and abnormal calcium metabolism after malabsorptive bariatric surgery. 1474 35

Calcium malabsorption, hypocalcemia and skeletal demineralization are well-recognized features of untreated celiac disease. This study investigates calcium absorption and bone mineral density (BMD) after a prolonged, over 4 years, treatment with a gluten-free diet. Twenty-four adult females with treated celiac disease and twenty age- and sex-matched control subjects were studied. Mean body mass index (MBI), energy intake, serum calcium, and serum 25(OH)D concentrations in treated celiacs did not differ from controls. However, while both dietary calcium and protein intake were significantly higher in celiacs (P<0.012), fractional calcium absorption was lower (mean percentage+/-SD; treated 39.8+/-12 versus controls 52.3+/-10, P<0.001). Thus, after adjusting for calcium intake, the estimated amount of calcium absorbed daily was similar in both groups. Whole body, spine and trochanter BMD were significantly lower in treated celiac patients compared with controls (P<0.05). There were significant inverse correlations between: serum parathyroid hormone (PTH) and femoral neck or total body BMD (P<0.01), PTH and duration of gluten-free diet (P=0.05), and fractional calcium absorption and alkaline phosphatase (P=0.022). Increased calcium intake could potentially compensate for the reduced fractional calcium absorption in treated adult celiac patients, but may not normalize the BMD. In addition, the inverse correlation between PTH and time following treatment is suggestive of a continuing long-term benefit of gluten withdrawal on bone metabolism in celiac patients.
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PMID:Calcium absorption and bone mineral density in celiacs after long term treatment with gluten-free diet and adequate calcium intake. 1522 Dec 5

The somatostatin analogue lanreotide is effective in reducing growth hormone levels in patients with acromegaly. Acromegaly is characterized by calcium homeostasis alterations. The aim of our study was to evaluate the effects of lanreotide on bone turnover markers in a group of acromegalic patients and to verify a possible increase of intact parathormone (iPTH) levels in a transient or persistent way. Serum GH, IGF-I and serum and urinary markers of bone metabolism were measured before treatment and on months 3 and 24. In short-term treatment (3 months), lanreotide significantly decreased GH, IGF-I, serum calcium, osteocalcin and alkaline phosphatase levels, but increased iPTH level (49 +/- 16.7 vs pre-treatment 28.3 +/- 7.6 ng/L, p<0.001). During long-term study (24 months) GH and IGF-I were significantly still low; serum calcium and alkaline phosphatase levels returned to pre-treatment levels. iPTH level was significantly still higher compared with pre-treatment (46.4 +/- 9.2 vs 28.3 +/- 7.6 ng/L, p<0.05). No changes were seen in serum albumin, creatinine and vitamin D during short and long term treatment. The changes of most bone markers during lanreotide treatment can be explained by the decrease of GH and IGF-I. The increase of iPTH concentration suggests that lanreotide has ulterior and long-standing actions on calcium homeostasis: intestinal malabsorption of calcium due to the lanreotide could contribute to this "secondary" hyperparathyroidism. The clinical relevance of these long-standing effects needs to be further investigated.
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PMID:Long-term treatment of acromegaly with lanreotide: evidence of increased serum parathormone concentration. 1564 68

In order to examine the etiology of refractory rickets, we evaluated the case records of patients presenting between 1990 and 2002. Subjects with impaired renal functions were excluded. Of 131 patients, 25.9 % each had hypophosphatemic rickets and distal renal tubular acidosis (RTA), 19.6 %vitamin D dependent rickets (VDDR), 11.3 % proximal RTA, 9.1 % liver disease and 6.1 % malabsorption. A significant proportion of patients with VDDR and proximal RTA showed deformities in the first year of life, whereas those with distal RTA and hypophosphatemic rickets presented later. Patients with hypophosphatemic rickets had predominant involvement of lower limbs; hypercalciuria was found in 4. Distal RTA was associated with marked rickets and normal levels of alkaline phosphatase. Hypophosphatemia and low tubular reabsorption of phosphate, though characteristic of hypophosphatemic rickets, was also seen in patients with VDDR (19.2%) and distal RTA (17.6 %). Our findings suggest that application and interpretation of appropriate investigations are useful in determining the cause of non-azotemic refractory rickets allowing initiation of specific therapy.
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PMID:Non-azotemic refractory rickets in Indian children. 1569 54

A 78 year old woman had suffered ten spontaneous bone fractures, the first occurring when she was 57 years old. She is now wheel-chair bound. After 21 years, the underlying osteomalacia due to oligosymptomatic celiac disease with malabsorption was diagnosed. The treatment consists of a gluten free diet and substitution of calcium and vitamin D until there is a normalisation of calcium, vitamin D and alkaline phosphatase. Any spontaneous fracture deserves a careful search for metabolic bone disease. An elevation of alkaline phosphatase indicates osteomalacia rather than osteoporosis.
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PMID:[Ten fractures in 21 years]. 1592 67

Many studies demonstrated that 5-fluorouracil (5-FU) treatment of rodents caused the damage of small intestine, resulting in the malabsorption, while we recently found that repeated administration of 5-FU to rats increased Na(+)-dependent glucose absorption in the small intestine. This study investigated the cause of enhanced glucose absorption. 3-O-methyl-d-glucose (3-OMG) absorption was examined using the everted intestine technique. d-Glucose uptake, phlorizin binding, Western blot analysis and membrane fluidity were examined using small intestinal brush-border membrane vesicles (BBMV). Repeated oral administration of 5-FU to rats increased Na(+)-dependent 3-OMG absorption in the small intestine, while alkaline phosphatase activity in the small intestine decreased. Na(+)/K(+)-ATPase activity of 5-FU-treated rats was about three-fold higher than that of control rats. Although the amount of Na(+)-dependent glucose co-transporter (SGLT1) in 5-FU-treated rats decreased, the overshoot magnitude of d-glucose uptake in BBMV was not altered. Maximum binding of phlorizin in 5-FU-treated rats was 1.5-fold larger than that of control rats, but not altered the maximal rate of d-glucose absorption, Michaelis constant of d-glucose and dissociation constant of phlorizin. The membrane fluidity of 5-FU-treated rats increased. The enhanced d-glucose absorption in 5-FU-treated rats seems to occur secondarily due to the activation of Na(+)/K(+)-ATPase activity in basolateral membranes (BLM). Because the amounts of SGLT1 in 5-FU-treated rats decreased, the increase of turnover rate of SGLT1 and/or an expression of unknown Na(+)-dependent glucose co-transporter with high affinity for d-glucose and phlorizin sensitivity would contribute to the enhancement of d-glucose transport in 5-FU-treated rats.
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PMID:Enhanced glucose absorption in the rat small intestine following repeated doses of 5-fluorouracil. 1599 45

A nearly 5 year-old boy presented with proximal muscle weakness, reduced muscle bulk, a positive Gower sign and Trendelenburg gait. He was known to have cholestatic liver disease. Investigations revealed markedly low serum total calcium, elevated alkaline phosphatase, very low serum 25-hydroxyvitamin D, and radiographs consistent with active rickets despite the ongoing administration of a water-soluble preparation of vitamin D. Only i.v. calcitriol acutely corrected the hypocalcemia, despite trying several oral preparations, suggesting that malabsorption secondary to chronic liver disease was the cause of his rickets. Intramuscular calciferol quickly corrected his muscle weakness and X-ray findings. Myopathy secondary to vitamin D deficiency is an uncommon diagnosis in children. Intermittent calciferol is an inexpensive and practical treatment for vitamin D deficiency, especially if associated with malabsorption.
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PMID:Treatment of malabsorption vitamin D deficiency myopathy with intramuscular vitamin D. 1612 49

Osteomalacia is characterized by defective mineralization and low bone mineral density (BMD). Clinical and biochemical improvements typically occur within a few weeks of starting treatment, though the bone mineral deficits may take longer to correct. We report a case series of 26 patients with frank osteomalacia (pseudo fractures on X-rays, elevated serum total alkaline phosphatase and parathyroid hormone, normal/low serum calcium and phosphorus, and low serum 25-hydroxy vitamin D) who were followed-up for changes in BMD during treatment using dual- energy X-ray absorptiometry (DXA). There were 23 patients with nutritional vitamin D deficiency, 2 with malabsorption syndrome, and 1 with renal tubular acidosis. All patients were treated with vitamin D and calcium; the 3 patients with associated disorders were treated accordingly. At baseline, there was low BMD at all sites tested. The rate of increase in vertebral and hip BMD was rapid in the initial few months, which subsequently slowed down. In contrast to the large increases in BMD at the femoral neck and lumbar spine, the radial BMD did not recover. At the time when most patients had marked clinical and biochemical improvement (2.8+/-1.4 mo), the vertebral and hip BMD, although improved from baseline, had not completely recovered. Bone loss at the forearm (cortical site) appears to be largely irreversible. Although the clinical correlates of these changes are presently unclear, BMD measurements are useful in assessing the initial severity of bone loss as well as the response to therapy.
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PMID:Changes in bone mineral density following treatment of osteomalacia. 1673 41


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