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 small intestinal bacterial flora of 15 patients with chronic renal insufficiency was compared with that of subjects with blind loop synDROME. 9 patients were on regular hemodialysis with high protein intake and 6 (serum creatinine 7.5 to 12.5 mg/dl) were maintained on low protein diet. The chronic renal patients harbored a greatly increased microbial flora of both anaerobes and aerobes in the duodenum and jejunum, quantitatively comparable to those in blind loop subjects. The composition did not differ significantly in the two groups. Some organisms may have the potential to metabolize substrates which reach the intestinal lumen from the diet and bile, and perhaps to generate toxic metabolites that could contribute to uremic toxicity or malabsorption.
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PMID:Bacterial populations of the small intestine in uremia. 74 39

The pathogenesis, clinical course and treatment of senile-postmenopausal osteoporosis are reviewed. It is likely that several factors, including genetic and racial determinants as well as nutritional calcium and/or vitamin D deficiency in the elderly play a pathogenic role. Available data are consistent with the possibility that the primary alteration of bone metabolism in senile-postmenopausal osteoporosis may be a decrease in de-novo bone formation below the level necessary to compensate for age-related bone loss. The second part of the study deals with the osteomalacia syndrome. The most common known causes of osteomalacia are vitamin D deficiency, especially secondary to malabsorption, and a defective vitamin D metabolism associated with chronic renal insufficiency or prolonged anticonvulsant therapy. The hypophosphatemic forms of osteomalacia may be induced by renal tubular dysfunction or by phosphate deficiency of other origin; in these disorders a pathogenic role of altered vitamin D metabolism has not yet been established.
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PMID:[Osteoporosis and osteomalacia]. 112 74

A 14-year-old boy presented with the clinical and radiological features of rickets. Serum inorganic phosphate levels were constantly low, whereas serum calcium and parathyroid hormone levels were within the normal range. Laboratory investigation did not show any evidence for vitamin-D deficiency, chronic renal insufficiency, Fanconi syndrome, tubular acidosis, hepatic disease or intestinal malabsorption. A family study comprising 34 members over four generations revealed 10 other individuals to be affected and the mode of inheritance to be autosomal dominant. In addition to hypophosphataemia and normocalcaemia, the disease is characterized by elevated serum 1,25 dihydroxyvitamin D levels and hypercalciuria. This hereditary syndrome of renal hypophosphataemia differs from the common familial X-linked hypophosphataemia and the recently described autosomal recessive hypophosphataemic rickets with hypercalciuria by its dominant mode of inheritance; it differs from hypophosphataemic non-rachitic bone disease by the elevated serum 1,25 dihydroxyvitamin D levels and hypercalciuria.
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PMID:Autosomal dominant hypophosphataemia with elevated serum 1,25 dihydroxyvitamin D and hypercalciuria. 315 20

The hemodynamic effects induced by thiopental and a decrease in blood ionized calcium are uniform. This investigation was undertaken to show a possible decrease in ionized blood calcium during induction of general anesthesia with thiopental. Twenty-four patients aged 19-79 years (median 57) were studied. None had any known parathyroid disease, malabsorption, or chronic renal insufficiency, and none were receiving calcium channel blockers. For the analysis of blood Ca++, pH, and PCO2, blood samples were drawn anaerobically into a heparinized syringe from an i.v. cannula. A special heparin solution was used (S4500 Radiometer, Copenhagen) to avoid the influence of heparin on the Ca++ determination. The initial 2 ml were discarded. No samples were drawn in the first 3 min after removal of the tourniquet. A maximum of 100 ml isotonic saline was infused between the two samplings. The infusion was stopped for at least 30 s before sampling. PCO2, B-Ca++, and pH were measured directly using the ABL 4 (Radiometer, Copenhagen) and the ICA 1 ionized calcium analyzer (Radiometer, Copenhagen). The standard deviation of repeated measurements of B-Ca++ within a short time using the same sample is 0.01 mmol/l on the ICA 1. The samples were drawn just before and 2 min after thiopental injection (median 5.9 mg/kg) was started. The pulse and blood pressure were simultaneously measured. The individual Ca++ measurements are shown in Table 1. The results of the investigation are shown in Table 2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of thiopental Na on the concentration of calcium ions in blood]. 366 52

The intestinal absorption of calcium is often depressed in patients with chronic renal insufficiency. Furthermore, the malabsorption of calcium and the osteodystrophy which occur in association with chronic renal disease are often "resistant" to vitamin D; the basis for this resistance remains uncertain however. Recent studies by others have emphasized the role of an abnormality in the metabolism of vitamin D in accounting for the alterations in the calcium absorption and the apparent vitamin D-resistance which accompany the uremic syndrome. The present studies with an experimentally uremic animal model demonstrate a defect in the active transport of calcium by duodenal gut sacs in vitro. This abnormality is not due to the semistarvation associated with renal insufficiency and cannot be corrected by the administration of physiologic amounts of vitamin D(3): it is reversed by massive doses of the vitamin. Neither the metabolism of vitamin D(3) nor the levels of calcium binding protein activity in the duodenal mucosa are affected by renal insufficiency under the conditions employed in the present studies. The results of the present studies strongly suggest that in addition to the recently proposed mechanism involving an interference with the metabolism of vitamin D renal insufficiency also affects the cellular mechanisms for calcium transport in a manner which, while opposite in direction to that of vitamin D, is independent of a direct interaction with the vitamin or its metabolites.
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PMID:Effect of renal insufficiency on the active transport of calcium by the small intestine. 542 27

Severe osteomalacia of uncertain etiology was observed in a 44-year-old woman. There was no evidence of chronic renal insufficiency, malabsorption, or of the renal tubular defects classically associated with osteomalacia. However, the dietary history suggested vitamin D deficiency and most of the biochemical findings were compatible with this condition. The unusual feature of the case was a decrease in plasma bicarbonate levels which appeared to be due to a lowered renal tubular threshold for bicarbonate reabsorption. There was no renal tubular defect with respect to hydrogen ion excretion.Rapid symptomatic and radiologic improvement occurred when the dietary intake of vitamin D was increased to approximately 200 I.U. per day and the acidosis was simultaneously corrected with sodium bicarbonate. Although no firm conclusions could be drawn about the relative importance of vitamin D deficiency or chronic acidosis in the production of the osteomalacia, the possibility that the chronic acidosis may have been a major contributing factor is discussed.
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PMID:Osteomalacia associated with renal bicarbonate loss. 594 Jun 37