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)

Glucocorticoid induced osteoporosis (GC-OP) is the most important form of all secondary osteoporoses. Mainly from in vitro and animal studies a lot of information exists concerning the underlying pathogenetic mechanisms. Some findings are still controversial but it is generally accepted that the three most important mechanisms are inhibition of osteoblastic matrix formation, stimulation of osteoclastic bone resorption and deterioration of intestinal calcium resorption with consecutive mild secondary hyperparathyroidism. In the individual patients the time between the beginning of corticoid therapy and clinical manifestation of osteoporosis varies considerably. If there is really a threshold dosage of corticoids is still debated. Besides dosage and duration of steroids age, sex, other risk factors of osteoporosis and underlying disease may be important factors. In contrast to the clinical prominence of GC-OP only little experience exists in counteracting the detrimental effects of corticoids on bone tissue. For pure prevention it seems reasonable to overcome intestinal calcium malabsorption by calcium or vitamin D. Concerning treatment of manifest GC-OP we studied the effect of salmon calcitonin (sCT) in patients with chronic obstructive lung disease. 18 patients injected themselves 100 U sCT every second day subcutaneously while 18 randomized patients served as untreated controls. There was a significant pain reduction in the sCT group and after six months the mineral content of the distal radius had increased by 2.7% despite a daily mean intake of 16.2 mgs prednisone during that time. In the control group (mean daily prednisone dose 16.8 mgs) the mineral content decreased with 3.5% on the average (p less than 0.001).
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PMID:Glucocorticoid-induced osteoporosis. 266 65

The level of serum 25-hydroxyvitamin D (25-OH-D3) was determined in 94 cases of healthy volunteers and 98 patients with various diseases. The mean level of the controls was 16.2 +/- 4.6 ng/ml (x /- S). The patients were divided into 5 groups, 1) Osteomalacia and rickets 42 cases, showing typical changes of bone in X-ray films. In 12 of them the disease was caused by vitamin D deficiency. The mean value of 25-OH-D3 was 3.3 +/- 2.0 ng/ml, being much lower than that of controls (P less than 0.001). In 14 cases of hypophosphatemia, 8 cases of renal tubular acidosis and 8 cases of renal insufficiency all complicated with osteomalacia the mean value of 25-OH-D3 was 17.9 +/- 11.4, 18.2 +/- 9.6 and 19.2 +/- 5.6 ng/ml (P greater than 0.05) respectively. 2) Intestinal malabsorption 18 cases. The mean level of 25-OH-D3 was 4.5 +/- 3.2 ng/ml (P less than 0.001). Some of them had hypocalcemia and/or secondary hyperparathyroidism. 2 showed osteoporosis and 1 osteomalacia. 3) Chronic liver disease 24 cases, the mean value of 25-OH-D3 was 6.2 +/- 5.6 ng/ml, being much lower than that of the controls (P less than 0.001). 4) 10 cases after taking anti-epileptic drugs had a mean level of 25-OH-C3 6.9 +/- 5.8 ng/ml (P less than 0.001). 1 had X-ray evidence of osteomalacia. 5) 4 cases of overdosage of vitamin D had a mean value of 110.3 +/- 22.5 ng/ml, being much higher than that of the controls (P less than 0.001). Competitive protein binding assay for measuring 25-OH-D3 is a simple and economic method. It is sensitive and specific as it provides distinct discrimination between healthy controls and patients with vitamin D deficiency or overdosage.
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PMID:[Clinical significance of competitive protein binding assay of 25-hydroxyvitamin D concentration]. 273 43

The formation of a neobladder by the transformation of sections of the terminal ileum has become an important alternative to supravesical urinary diversion. The discussion about the optimal urosurgical technique however has, so far ignored the problems of consecutive enteric defunctionalization and deficiency symptoms resulting from the anatomical shortening of the ileum. The analysis of experimental investigations and functionally comparable syndromes, such as Crohn's disease, permits an insight into the pathophysiological consequences. These relate to disorders in the bile acid and vitamin B12 metabolism and to the potential induction of a secondary hyperoxaluria, with a subsequent oxalate calculus diathesis. Further more, the reduction of the absorption area in the ileum can lead to calcium and vitamin D malabsorption with the development of intestinal osteopathy. These pathophysiological relationships must be taken into account in the long-term medical care of patients with ileal neobladder. The preventive and therapeutic measures are described.
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PMID:[Ileocystoplasty and enteropathies]. 276 94

Osteoporosis is more common in chronic alcoholics than in age-matched controls. Possible aetiological factors are: malabsorption of calcium and vitamin D; liver disease and abnormal parathyroid function. The possibility that alcohol may directly affect osteoblastic function has, however, received little attention. We measured plasma osteocalcin, a protein synthesised specifically by osteoblasts, in chronic alcoholics. Our data show that these have low plasma osteocalcin but normal calcium, magnesium and parathormone, which suggest that alcohol may be directly toxic to osteoblasts.
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PMID:Bone disease in chronic alcoholism: the value of plasma osteocalcin measurement. 278 3

This article presents two cases of osteomalacia related to vitamin D deficiency after radiation therapy. Both patients had typical signs of serious small bowel affection with malabsorption and diarrhea, and fractures, osteoporosis, histological osteomalacia and serological vitamin D deficiency. Both patients responded to combined treatment with vitamin D, calcium, magnesium and vitamin B12. We discuss pathogenetic mechanisms, symptomatology and therapy, and review the literature. It is suggested that examination of serum 1.25 dihydroxy- and 25 hydroxy vitamin D levels be added to the diagnostic tests whenever small bowel damage after radiation is suspected.
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PMID:[Radiation injury of the intestine]. 281 76

Using a commercial kit method we obtained a vitamin D metabolite level within the normal range in a patient with biopsy-proven osteomalacia. This suggested that the ethanol extraction method employed had not removed serum factors known to falsely elevate the measurement of vitamin D metabolites. We therefore compared the levels measured after ethanol extraction and after purification by chromatography on Sep-pak C18 or Sephadex LH-20. Vitamin D metabolite levels after ethanol extraction of sera correlated with, but were higher than, those after chromatography on Sep-pak C18 cartridges (r = 0.84; 134 +/- 76 vs 76 +/- 46 nmol/l: mean +/- SD; p less than 0.01). Results were similar after chromatography on Sep-pak C18 and Sephadex LH-20 (r = 0.95; 79 +/- 46 vs 68 +/- 41 nmol/l). Sera from 5 patients (4 with osteomalacia, 1 with chronic pancreatitis/malabsorption) had vitamin D metabolite levels in the normal range after ethanol extraction but had low levels after Sep-pak C18 chromatography; four of these sera also had low levels after chromatography on Sephadex LH-20. These findings indicate that chromatography of serum on Sep-pak C18 cartridges corrects falsely elevated vitamin D metabolite levels measured by protein binding assay.
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PMID:Chromatography of serum on Sep-pak C18 corrects falsely elevated vitamin D metabolite levels measured by protein binding assay. 284 7

The interaction between malabsorption syndrome (MAS) and dietary vitamins A and D was studied in broiler chicks reared in floor pens for 4 weeks. The chicks were naturally infected with MAS, whereas hatchmates fed the same diets but in a separate facility (battery brooder) did not exhibit signs of MAS and, therefore, were considered controls. MAS significantly reduced body weights, bone ash, serum calcium and phosphorus concentrations, and liver lipids and increased the incidence of skeletal abnormalities (tibial dyschondroplasia and rickets). Rather than ameliorating the effects of MAS, vitamin A caused a further reduction in body weight and bone ash. A possible nutrient interaction between vitamin A and vitamin D or vitamin E in birds with MAS may account for the exacerbative effect of vitamin A.
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PMID:Exacerbative effect of vitamin A on malabsorption syndrome in chicks. 299 37

In juvenile X-linked hypophosphatemic (Hyp) mice, whole body calcium balances are significantly lower than in genetically normal mice. This is associated with low duodenal vitamin D-dependent calcium-binding protein and a failure of skeletal mineralization. To seek more specific evidence of an intestinal defect in these mice, absorption of 45Ca was measured in isolated duodenal segments in vivo in mice from 2-13 weeks of age. The duodenum was isolated by sutures and 45Ca was injected into the lumen in 150 mM NaCl and 2 mM CaCl2 at pH = 7.2. Absorption was measured by the amount of isotope remaining in the lumen and by the plasma isotope level. Hemizygous Hyp male and heterozygous Hyp female mice absorbed significantly less 45Ca at 4 and 7 weeks of age than genetically normal mice while Hyp mice at 2, 10, and 13 weeks of age were not significantly affected. At 4 and 7 weeks of age, the Hyp mice also had significantly reduced plasma radioactivity midway through the collection period as well as at the end of the period. To explore a possible mechanism for this malabsorption, 1,25(OH)2-vitamin D receptors were measured in cytosol prepared from 4-week-old normal and Hyp duodenum. There were non-significant differences between the normal and Hyp mice in both binding affinity, Kd, and the number of receptors, nmax. In conclusion, juvenile Hyp mice at 4 and 7 weeks of ages malabsorbed calcium from their duodenum. Hyp mice younger than this period were not affected nor were adult Hyp mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduced absorption of 45calcium from isolated duodenal segments in vivo in juvenile but not adult X-linked hypophosphatemic mice. 300 89

Phosphorus is the sixth most abundant element in the body after oxygen, hydrogen, carbon, nitrogen, and calcium. It comprises about 1% of the total body weight of humans. Eighty-five percent of it is stored in the bone in the form of hydroxyapatite crystal; 14% is in the soft tissues in the form of energy-storing bonds with nucleotides (ATP, GTP), nucleic acids in chromosomes and ribosomes, 2,3-DPG in the red blood cells, and phospholipids in the cells' membranes. Less than 1% is in the extracellular fluids. Phosphate balance is maintained by multiple systems. The gut is responsible for the absorption of two thirds of the 4-30 mg/kg/day of phosphate intake. Absorption sites are all along the gut; in humans the most active site is the jejunum. The kidney filters 90% of the plasma phosphate and reabsorbs it in the tubuli. In states of hypophosphatemia the kidney can reabsorb the filtered phosphates very efficiently, reducing the amount excreted in the urine virtually to zero. The healthy kidney can excrete high loads of phosphate and rid the body of phosphate overload. Through the vitamin D-PTH axis the endocrine system regulates the phosphate balance by influencing the kidney, gut, and bone. Other hormones, including thyroid, insulin, glucagon, glucocorticosteroid, and thyrocalcitonin, play a lesser role in regulation of phosphate metabolism. Because of the complex control of phosphate homeostasis, various clinical conditions may lead to hypophosphatemia. These include nutritional repletion, gastrointestinal malabsorption, use of phosphate binders, starvation, diabetes mellitus, and increased urinary losses due to tubular dysfunction. The clinical picture of phosphate depletion is manifested in different organs and is due mainly to the fall in intracellular levels of ATP and decreased availability of oxygen to the tissues, secondary to 2,3-DPG depletion. The various manifestations of phosphate depletion are listed in Table 2. The treatment of hypophosphatemia consists of administering enteral or parenteral phosphate salts. An important aspect of dealing with the potentially serious effects of phosphate depletion is to prevent the depletion from happening in the first place. Hyperphosphatemia can occur in renal failure, hemolysis, tumor lysis syndrome, and rhabdomyolysis. The treatment of hyperphosphatemia usually consists of fluid administration (in the absence of kidney failure). In chronic hyperphosphatemia, phosphate binders such as aluminum and magnesium salts can reduce the phosphate load. The use of these phosphate binders is limited by their potential side effects.
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PMID:Consequences of phosphate imbalance. 306 Jan 61

The role of the liver as a contributory factor in the vitamin D deficiency of cholestatic liver disease has been studied in vivo in dogs with chronic bile duct ligation, whereas controls underwent diversion of the bile flow through the urinary bladder via a choledococystostomy anastomosis. The hepatic extraction of vitamin D3 was evaluated by the multiple indicator dilution technique, and the formation of 25-hydroxyvitamin D3 was assessed by directly sampling the hepatic effluent for up to 150 min after vitamin D3 administration. The serum and hemodynamic data indicate that dogs with chronic bile duct ligation had severe cholestasis and hepatocellular injury; histologically, macronodular cirrhosis was present. Dogs with choledococystostomy anastomosis had normal livers and normal liver function. The data indicate that the absence of normal bile flow into the intestinal lumen led to a progressive depletion of vitamin D reserve in both animals with choledococystostomy anastomosis and those with chronic bile duct ligation. However, neither the hepatic fractional extraction of vitamin D3, its hepatic clearance nor its transformation into 25-hydroxyvitamin D3 was significantly changed by chronic bile duct ligation. The results of the present studies indicate that the hepatic handling of vitamin D3 including its C-25 hydroxylation, is well preserved in the presence of severe cholestasis. They also suggest that the state of vitamin D depletion which often accompanies chronic cholestatic liver disease can largely be accounted for by factors such as secondary malabsorption of the vitamin due to the absence of adequate amounts of bile salts in the intestinal lumen, or by other factors which seem independent of the hepatic metabolism of vitamin D.
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PMID:Severe cholestasis leads to vitamin D depletion without perturbing its C-25 hydroxylation in the dog. 319 71


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