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)

Juvenile rickets or osteopenia in rural black children is thought to be due to low calcium intake. Characteristic findings include mild calcium deficiency, normal serum phosphate levels, increased alkaline phosphatase concentrations and normal plasma vitamin D levels. The present series consisted of 62 black children (average age 6.82 years), 41 males and 21 females. Low levels of serum calcium and phosphate were present in 34 (54%) and 18 (29%) of the patients respectively. Alkaline phosphatase concentrations were raised (greater than 350 IU/l) in 38 (61%). Serum sodium, potassium, chloride, total bicarbonate, magnesium, ceruloplasmin and albumin levels were generally within normal limits. Urinary acidification was normal and barium studies were reported as normal in all but 4 children. Malabsorption was not an important feature. Serum vitamin D levels were not determined. All 18 patients with hypophosphataemia improved. Eleven children showed no clear response after at least 8 weeks in hospital--8 remained hypocalcaemic and 2 of the 3 patients with normal biochemical values showed no radiological improvement of osteopenia after 2 and 4 months in hospital, while the 3rd showed only very slight improvement after 7 months in hospital. It is not clear why these patients did not respond and whether even longer hospitalisation would have been effective.
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PMID:[Aspects of juvenile rickets/osteopenia in black children]. 360 15

This chapter reviews the pathogenesis of disordered divalent mineral and bone metabolism in alcoholism, emphasizing the role of impaired vitamin D physiology. Normally, vitamin D metabolites are derived principally from cholecalciferol, which is synthesized in the skin via the energy of sunlight. Most alcoholics have subnormal levels of 25-hydroxyvitamin D [25(OH)D]. Those with Laennec's cirrhosis also have low levels of vitamin D binding protein due to impaired hepatic protein synthesis and as a result, have low serum concentrations of total, but not free, 1,25-dihydroxyvitamin D. The causes of 25(OH)D deficiency in alcoholics include reduced hepatic 25-hydroxylase activity, lack of sun exposure, inadequate dietary intake, and malabsorption. Hypomagnesemia and hypophosphatemia, which are very common in hospitalized alcoholics, result from deficient intake, malabsorption, excessive renal losses, and cellular uptake of both ions. Hypocalcemia in alcoholics is caused primarily by hypoalbuminemia but can result also from deficient intake, malabsorption, hypomagnesemia, and renal calcium wastage. Low vitamin D activity may contribute significantly to the calcium and phosphate deficiencies. Osteoporosis is extremely common in alcoholics whereas osteomalacia is exceptional. However, both bone disorders respond well to vitamin D therapy. Thus, alcoholics should be screened periodically for vitamin D deficiency and osteopenia, and when either is detected they should receive vitamin D supplements.
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PMID:Disorders of divalent ions and vitamin D metabolism in chronic alcoholism. 375 48

We studied the effect of aluminum injections on bones of rats after intervals of 3, 6, and 9 weeks. To study reversibility, we allowed one group to recover for 3 weeks. Both weanling and adult rats were examined to determine the influence of age. The calcium, phosphate, creatinine, and parathyroid hormone levels were similar in aluminum-treated rats and controls. Aluminum could be seen by histochemical stain after 6 weeks, but at that time the bone was otherwise normal. By 9 weeks the bone formation (as measured by tetracycline labeling) in aluminum-treated rats was severely decreased on trabecular and endosteal surfaces. The periosteal surfaces showed normal formation. After 3 weeks of recovery, the bone formation rate in the young aluminum-treated rats was similar to that in the controls, although the serum and bone aluminum values had not significantly decreased. A higher percentage of aluminum was seen in the cement lines. In the adult rats, the bones had more stainable aluminum, and increased osteoid was noted along trabecular and periosteal surfaces. The doses of aluminum used in these rats greatly exceeded those that cause toxicity in humans; thus these findings may not directly apply to clinical practice. We conclude that aluminum administration can lead to decreased rates of bone formation in the rat, despite normal calcium level and renal function, and without decreased parathyroid hormone levels. The peritoneal route of administration could also have contributed to bone lesions by causing peritonitis, malabsorption, or both. Adult rats showed signs of early osteomalacia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Development and reversibility of aluminum-induced bone lesion in the rat. 379 13

Metabolic bone disease occurring in renal or intestinal disorders has been reviewed with particular reference to etiological factors. Hyperparathyroidism is seen as a recurring cycle of renal damage-hyperphosphatemia-hypocalcemia-parathyroid stimulation-mobilization of bone calcium and phosphate-renal tubular phosphate rejection. In intestinal cases, the initial stimulus is presumably hypocalcemia. Osteomalacia is seen as resulting from phosphate depletion for the following reasons:1. Experimentally, rickets results from dietary phosphate restriction in rats.2. Such rickets is not prevented by the presence of normally adequate amounts of dietary vitamin D, and may therefore be termed "resistant" in the clinical sense.3. Osteomalacia or rickets in intestinal malabsorption and renal tubular disorders is associated with hypophosphatemia due to excessive fecal or urinary loss.4. Renal tubular rickets has been healed by oral phosphate loading in some studies.5. Acidosis may induce osteomalacic changes, experimentally and clinically (for example, in uretero-sigmoidostomy). Reversal of systemic acidosis with oral bicarbonate has resulted in phosphate retention and a rising serum phosphate in one such case.6. Preliminary data from analysis of full-thickness bone biopsy in two osteomalacic patients shows a significant reduction in calcium and phosphate content.7. Despite the hyperphosphatemia of azotemic renal failure, over-all phosphate depletion may be present in this situation also due to: * Diminished dietary phosphate in low protein diets * Nausea and vomiting * Occasional diarrhea * The use of oral phosphatebinding antacids * Perpetuation of urinary phosphate losses by reduction in proportion of tubular reabsorbed phosphate (secondary hyperparathyroidism) and possibly high filtered load per nephron * Repeated losses of phosphate to bath fluid during dialysis.
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PMID:Metabolic bone disease secondary to renal and intestinal disorders. 489 May 32

Adults with intestinal malabsorption due to celiac disease show reduced central serotonin metabolism, probably induced by a lack of essential dietary factors. Investigating a role proposed for vitamin B6 deficiency, a regular finding in untreated celiacs, the present study yields no support for the hypothesis that direct inhibition at the decarboxylation step by vitamin B6 deficiency accounts for low central serotonin turnover in adult celiacs: 11 untreated patients showing reduced 5-HIAA in the cerebrospinal fluid (71+/- 26.8 pmol/ml) had a significantly higher concentration of the metabolically active B6 vitamer pyridoxal 5'-phosphate in lumbar cerebrospinal fluid (0.06 +/- 0.34 ng/ml) than controls (0.24 +/- 0.07 ng/ml) (p less than 0.01). Cerebrospinal fluid tryptophan, precursor of serotonin, was normal (2035 %/- 649 pmol/ml). Raised pyridoxal 5'-phosphate in the cerebrospinal fluid in untreated celiac disease is an unexpected finding. Possibly it is secondary to the diminished central monamine metabolism in these patients, but further studies are needed bearing in mind that mental depression is a major cause for disability in adult celiac disease.
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PMID:High level of pyridoxal 5'-phosphate in the cerebrospinal fluid of adult celiac patients. 618 88

Proximal muscular weakness is a feature of many metabolic bone diseases but is not well recognized in spinal osteoporosis. Thirty-six post-menopausal women presenting with back pain, with or without osteoporosis, were therefore studied in order to define the relationship between abnormal electromyographic findings and disturbed vitamin D metabolism, as both low plasma 1,25 dihydroxy vitamin D concentrations and malabsorption of calcium have been reported in osteoporosis. Patients with abnormal electromyograms had lower concentrations of plasma 1,25 dihydroxy vitamin D (mean 78.3 pmol/l, SD 20.5, n = 15) than normal subjects of similar age (mean 110.4 pmol/l, SD 39.4, n = 21; P less than 0.01), but electromyographic abnormality was not associated with changes in radiocalcium absorption, plasma 25 hydroxy vitamin D, plasma calcium or phosphate or urinary calcium or hydroxy-proline excretion or impaired renal function. There was no relationship between abnormal electromyography and osteoporosis assessed by spinal radiographs and iliac crest biopsy. These findings are consistent with our previous suggestion that muscle weakness in many unrelated bone disorders is related to low plasma 1,25 dihydroxy vitamin D concentrations, but suggest that there is no relationship between proximal myopathy and spinal osteoporosis in post-menopausal women.
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PMID:Vitamin D metabolites in post-menopausal women and their relationship to the myopathic electromyogram. 622 23

The intestinal absorption of calcium (Ca) has been shown to depend on vitamin D3, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], and dietary phosphorus (P) concentration. This study was designed to evaluate the role of dietary P independent of vitamin D3 or 1,25(OH)2D3. Vitamin D-deficient rats were studied during dietary P restriction and were compared with control groups raised on a normal-phosphorus diet (NP). Balance studies were sued. Net intestinal Ca absorption was significantly lower with dietary P restriction compared with the NP group. This malabsorption of Ca was corrected by the administration of either D3 for 1,25(OH)2D3, despite hypophosphatemia. Everted gut sacs showed a marked reduction in the uptake of 45Ca in the duodenum, jejunum, and ileum during dietary P restriction. We concluded that dietary P concentration plays a major role in intestinal Ca absorption in the vitamin D-deficient rats. These findings suggest an effect of the low-phosphate diet on the vitamin D-dependent, Ca-transport mechanism.
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PMID:Intestinal absorption of calcium: role of dietary phosphate and vitamin D. 626 9

Five patients with primary biliary cirrhosis and vitamin D deficiency (serum 25-hydroxyvitamin D less than 6 ng/ml) are presented. All patients had low serum 24,25-dihydroxyvitamin D3 concentrations. Three patients had histological osteomalacia, negative calcium balance, and subnormal serum 1,25-dihydroxyvitamin D3. Malabsorption of a standard dose of [3H]vitamin D3 was found in three of four patients with steatorrhea, enabling the effective dose of vitamin D3 given to be calculated. Oral vitamin D3 400-4000 IU/day (effectively 400-1860 IU/day) resulted in a return to normal of the serum vitamin D metabolites, correction of the impaired intestinal calcium absorption and healing of the osteomalacia. Increases in serum calcium, phosphate, and the renal tubular reabsorption of phosphate occurred with a concomitant decrease in serum parathyroid hormone. It is suggested that osteomalacia in primary biliary cirrhosis is the end result of vitamin D deficiency; the hepatic and renal hydroxylations of vitamin D are normal and target tissues are responsive to endogenously produced metabolites of vitamin D.
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PMID:Vitamin D deficiency, osteomalacia, and primary biliary cirrhosis. Response to orally administered vitamin D3. 629 63

X-linked hypophosphatemia is a human and mouse disease characterized by reduced renal tubular reabsorption of phosphate, hypophosphatemia, and dwarfism. The gene is X-linked and dominant. There have been conflicting reports in the literature regarding possible malabsorption of minerals by the intestine as well. In this study we examined the mineral status in adult X-linked hypophosphatemic (Hyp) mice by measuring trace minerals in blood, bone, muscle, liver and hair and by performing a balance study for Ca, P, Mg, Na and K. The results indicate that Hyp mice have higher than normal levels of plasma iron, bone manganese and zinc, liver iron, and muscle zinc. The trace minerals in hair were not significantly affected. The balance study showed that the content of Ca, P, Mg, Na and K of the urine and feces of normal and Hyp mice were nonsignificantly different. Hyp mice did consume more diet per gram body weight. We conclude that there is no deficiency in intestinal mineral absorption in adult Hyp mice. No tissues studied were found to have reduced trace mineral levels. In fact, where differences occurred, Hyp mice had elevated trace mineral levels in various tissues and blood. This was probably the result of the increased dietary intake per gram body weight in the Hyp mice.
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PMID:Abnormal trace mineral metabolism in adult X-linked hypophosphatemic mice: a possible role of increased food intake. 673 60

Rickets, hypocalcemia, hypophosphatemia, and hyperparathyroidism were found in a low-birth-weight premature infant. The concentration of plasma calcitriol (1,25-dihydroxyvitamin D) was 145 pg/mL. With additional exogenous calcitriol (37.5 ng/kg/24 hr) given for eight weeks, the biochemical abnormalities were corrected and healing of rickets was evident. Three months later, while receiving only 400 IU of ergocalciferal daily, the patient had normal levels of serum calcium, phosphate, and alkaline phosphatase with a serum calcitriol concentration of 36 pg/mL. These observations suggest that rickets of prematurity may involve a malabsorption of calcium and phosphorus with an elevated calcitriol level needed to overcome this inadequate absorption. Additional doses of calcitriol may be of benefit in these infants, although it must be given carefully. Furthermore, the role of phosphate supplementation in these infants requires consideration.
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PMID:Rickets of prematurity. Supranormal levels of serum 1,25-dihydroxyvitamin D. 696 86


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