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 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

For years, brown tumors have been considered to be a characteristic of primary hyperparathyroidism. However, since 1963 several reports indicate the incidence of brown tumors in patients with renal secondary hyperparathyroidism to be 1.5%-1.7%. The appearance of multiple brown tumor lesions is rather uncommon in secondary hyperparathyroidism which is also true for malabsorption as its cause. We report on a 56-year-old man presenting with pain in the bones and multiple osteolyses. A bone biopsy specimen and the laboratory examinations were indicative of secondary hyperparathyroidism caused by malabsorption most likely due to Billroth's II/I gastric resection. Thus, the patient's osteolyses represent brown tumors which have been induced by nutritional secondary hyperparathyroidism.
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PMID:Multiple brown tumors in a patient with nutritional secondary hyperparathyroidism. 292 41

Clinical, pathologic, and biochemical data are reported in two male infants who had rapidly progressive renal failure, enlarged kidneys, hepatosplenomegaly, and fat malabsorption. One infant, studied prior to the onset of significant renal insufficiency, manifested renal Fanconi syndrome, hyperparathyroidism, and marked hypocalcemia. After a brief period of dialysis, both received renal transplants. Neither has clinical evidence of reoccurrence of the renal disorder in the transplant, but both still have hepatic abnormalities. Morphologic features present in both patients include a renal lesion characterized by tubulointerstitial injury with a tubulocystic component and hepatic abnormalities with bile duct proliferation, portal fibrosis, and inflammation. These cases do not readily conform to any single published diagnostic category, including nephronophthisis-congenital hepatic fibrosis or infantile polycystic kidney disease, and appear to be unique.
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PMID:Progressive tubulointerstitial renal disease in infancy with associated hepatic abnormalities. 352 22

We performed iliac bone histomorphometry after in vivo double tetracycline labeling 3-14 years after intestinal bypass surgery for obesity in 21 patients, selected because of clinical suspicion of metabolic bone disease, and compared the results with those of 40 age-matched normal control subjects. Osteomalacia defined by rigorous kinetic criteria was found in six cases, histologic features of secondary hyperparathyroidism without significantly impaired mineralization in one case, and possible osteomalacia masked by impaired matrix synthesis in one case. In the patients with definite osteomalacia, nonfracture bone pain was more frequent, corrected plasma calcium lower, plasma alkaline phosphatase and magnesium higher, and secondary hyperparathyroidism more severe than in the other patients. In the patients without osteomalacia there was a 24.5% reduction in trabecular bone volume compared to the controls; in contrast to age-related bone loss and post-menopausal osteoporosis, this was due mainly to reduction in the thickness rather than the density of trabecular plates. About two-thirds of the reduction in trabecular thickness was due to reduction in interstitial bone thickness, representing the cumulative effect of increased depth of osteoclastic resorption cavities, probably due in part to secondary hyperparathyroidism. About one-third of the reduction in trabecular thickness was the result of reduced mean wall thickness, representing insufficient osteoblastic matrix synthesis, probably due in part to malabsorption of an unidentified nutrient necessary for normal bone health. Resorption indices were not increased at the time of the biopsy, but there were persistent defects in the recruitment and activity of osteoblasts. Clinically significant bone loss after intestinal shunt surgery, as in several other clinical situations, results from the combined effects of an unsustained increase in bone resorption and a sustained decrease in bone formation.
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PMID:Metabolic bone disease with and without osteomalacia after intestinal bypass surgery: a bone histomorphometric study. 384 Mar 79

A 25-yr-old black man with cystic fibrosis and cirrhosis developed symptoms of osteomalacia and hypocalcemia, hypophosphatemia, secondary hyperparathyroidism, and low circulating 25-hydroxyvitamin D (25-OHD). Serum 1,25-dihydroxyvitamin D (1,25-[OH]2D) was within the normal range. Iliac crest bone biopsy confirmed the diagnosis of osteomalacia. Oral administration of 50,000 IU of vitamin D2 failed to relieve symptoms or raise serum 25-OHD levels to normal. Intramuscular vitamin D2, 10,000 IU every 8-12 week, improved symptoms, raised serum 25-OHD to normal, and increased circulating 1,25-[OH]2D to values five times normal. Over the next 10 mo circulating 1,25-[OH]2D remained elevated despite normalization of serum calcium, phosphorus, and parathyroid hormone. Repeat bone biopsy 1 yr after parenteral vitamin D showed healing of the osteomalacia. Malabsorption of vitamin D appears secondary to profound steatorrhea due to pancreatic insufficiency and secondary biliary cirrhosis. Although extensive hepatocellular disease was present, hepatic conversion of vitamin D to 25-OHD was intact. Both high and low circulating 1,25-[OH]2D levels during active osteomalacia have been reported; initially, the level was in the normal range and higher values in this patient occurred with repletion of 25-OHD substrate. This study shows that symptomatic osteomalacia may be a major manifestation of cystic fibrosis in those patients surviving into adulthood. Measurements of serum 25-OHD in cystic fibrosis patients may identify those who should receive supplemental vitamin D.
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PMID:Vitamin D metabolism and osteomalacia in cystic fibrosis. 387 14

Seven patients (five male and two female) with chronic renal failure (CRF) treated by periodical haemodialysis presented with swelling and effusion of more than three months' duration in knees (four bilateral), shoulders (two, one of them bilateral), elbow (one), and ankle (one). Four had a carpal tunnel syndrome both clinically and electromyographically (three bilateral). All patients had hyperparathyroidism secondary to their CRF, which was not due to amyloidosis in any of them. The dialysis duration period varied from five to 14 years, with an average of 8.6 years. Amyloid deposits (Congo red positive areas with green birefringence under polarising microscopy) were shown in six of the seven synovial biopsy specimens of the knee, in five of the sediments of the synovial fluids, and in specimens removed during carpal tunnel syndrome surgery. No amyloid was found in the biopsy specimen of abdominal fat of six of the patients. The finding of amyloid only in the synovial membrane and fluid, and carpal tunnel, its absence in abdominal fat, and the lack of other manifestations of generalised amyloidosis (cardiomyopathy, malabsorption syndrome, macroglossia, etc.) and of Bence Jones myeloma (protein immunoelectrophoresis normal) raises the possibility that this is a form of amyloidosis which is peculiar to CRF treated by periodical haemodialysis.
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PMID:Amyloid arthropathy in patients undergoing periodical haemodialysis for chronic renal failure: a new complication. 406 86

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

The pathology of the parathyroid glands in two cases in which hyperparathyroidism was associated with chronic renal disease and 10 in which the association was with the malabsorption syndrome is described. It is concluded that whereas in chronic renal disease the development of an autonomous adenoma may be preceded by anatomical secondary diffuse hyperplasia such a stage is not proven when the adenomas develop against a background of the malabsorption syndrome. The importance of this latter association is stressed.
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PMID:Parathyroid adenomas associated with the malabsorption syndrome and chronic renal disease. 543 Apr 25

In our first 200 cases of primary hyperparathyroidism confirmed by operation 12 were also shown to have a long history either of a malabsorption syndrome or of chronic renal-glomerular failure. We consider that they first went through a phase of secondary hyperparathyroidism, during which one or more of the glands became autonomous adenamata. This then produced the biochemical changes of "primary" hyperparathyroidism, necessitating excision of the adenoma. This condition is best described as "tertiary" hyperparathyroidism. The transition from secondary to tertiary hyperparathyroidism occurred in four of the 12 patients while under our observation. We think the same process can be traced retrospectively in the other eight cases. The concept of tertiary hyperparathyroidism may help to explain the high incidence of other diseases in association with primary hyperparathyroidism.The behaviour of the parathyroid glands provides a valuable model for the investigation of tumour formation in man. All states occurred in our patients with primary hyperparathyroidism, from normal through hyperplasia to adenoma formation and finally to parathyroid carcinoma.
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PMID:Tertiary hyperparathyroidism. 569 Dec

A survey of vitamin D status in 152 patients with chronic gastrointestinal conditions and 104 patients with chronic liver diseases is presented. Mild deficiency was common and severe deficiency, as judged by plasma 25-OHD levels less than 8 nmol/l, was encountered in every disease category tested. In the gastrointestinal disease patients, deficiency was significantly more common in patients following gastroenterostomy than other gastric surgery, in patients with active Crohn's disease than in those with inactive disease and in patients with chronic pancreatitis or pancreatic carcinoma with cholestatic features than in those without cholestatic features. Deficiency was as common in patients with Crohn's disease who had not been treated surgically as in those who had. There was no significant correlation between plasma 25-OHD levels and any laboratory index of malabsorption or malnutrition except for serum albumin in the gastric surgery patients, haemoglobin and ESR in the Crohn's disease patients and albumin and vitamin E in the group of patients with gastrointestinal disorders taken as a whole. In the chronic liver disease patients, those with late primary biliary cirrhosis had lower plasma 25-OHD levels than those with histological Stage I and II disease who all had normal levels, and those with pruritus and jaundice were more commonly severely deficient. Whatever the underlying disease process, patients with other coincidental medical conditions were much more likely to be deficient as were patients with cholestasis. Evidence of secondary hyperparathyroidism and osteomalacia on bone histology indicated the clinical relevance of the vitamin D deficiency. This study showed no relationship between abnormal plasma vitamin D binding protein levels and vitamin deficiency.
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PMID:A survey of vitamin D deficiency in gastrointestinal and liver disorders. 654


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