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)

Twenty-nine patients with chronic liver disease, nine of whom had symptoms suggesting bone disease, were studied by bone histology. Nine had osteomalacia; six associated with cholestatic liver disease and three with primarily hepatocellular disease. Two of these had clinical and biochemical features of cholestasis for at least a year and the other had alcoholic cirrhosis associated with severe malnutrition. Excluding the latter patient, histological osteomalacia was significantly associated with presence and duration of cholestasis. Plasma 25-hydroxyvitamin D was low and fasting urine hydroxyproline/creatinine ratio was high in all patients with osteomalacia but were abnormal also in some patients who did not have histological osteomalacia. Serum calcium, phosphate, alkaline phosphatase, vitamin D-binding protein and radiology were unhelpful in many patients with osteomalacia. Vitamin D-deficiency correlated significantly with deficiency of other fat-soluble vitamins and those patients with rachitic levels of plasma 25-hydroxyvitamin D showed no seasonal variation, suggesting a combination of malabsorption of vitamin D and reduced sunlight exposure. We suggest that patients with chronic liver disease with cholestasis for at least a year are at risk from osteomalacia and that those likely to have this complication may be identified by plasma 25-hydroxyvitamin D and/or fasting urine hydroxyproline/creatinine ratio measurements. The diagnosis can only be made with certainty by bone biopsy.
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PMID:Osteomalacia, vitamin D deficiency and cholestasis in chronic liver disease. 698 Nov 20

Patients with malabsorption syndromes have an increased risk of kidney stone formation. Those with cystic fibrosis (CF) suffer from extreme forms of steatorrhea, but they are not reported to be prone to kidney stone formation. Risk parameters for renal stone formation were studied in the urine of 43 patients with cystic fibrosis and compared to those of 5 patients with calcium oxalate nephrolithiasis and 21 healthy controls. Patients with CF showed increased urinary concentrations of oxalate, phosphate, xanthine and uric acid, and decreased concentrations of magnesium and citrate, comparable to concentrations found in patients with calcium oxalate stones. However, compared to stone bearing controls the calcium concentration was markedly decreased in the urine of CF patients. Our results suggest that hypocalciuria in CF seems to protect against nephrolithiasis despite the presence of lithogenic factors. Calcium supplementation instituted for clinical reasons may result in an increased risk for kidney stone formation. This risk may be diminished by additional administration of magnesium as well as allopurinol.
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PMID:Is there a risk for kidney stone formation in cystic fibrosis? 711 58

1. Intestinal phosphate absorption was measured in normal subjects, in patients with chronic renal failure, and in post-transplant patients, by a double isotope technique involving oral administration of 32P and simultaneous intravenous injection of 33P with subsequent deconvolution analysis. 2. By this technique intestinal phosphate absorption has been shown to have two components: an initial rapid phase, which is completed by 3 h, and a slower more prolonged phase, which continues beyond 7 1/2 h. 3. Phosphate malabsorption has been demonstrated in chronic renal failure and transplant patients, which is accounted for by impairment of the initial rapid phase of absorption. 4. Results obtained by deconvolution analysis have been compared with other estimates of phosphate absorption obtained from analysis of 32P radioactivity curves alone. 5. The fractional hourly rate of absorption and the plasma 32P radioactivity at 60 min corrected for extracellular fluid volume provided the best approximations to the result obtained by deconvolution analysis, with respect to both the maximal rate of phosphate absorption and cumulative percentage phosphate absorption.
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PMID:Comparison of radioisotope methods for the measurement of phosphate absorption in normal subjects and in patients with chronic renal failure. 723 25

A 68 year old man with prostatic carcinoma and extensive painful osteoblastic metastases was discovered to have hypocalcemia (serum calcium 7.1 mg/dl) without evidence of hypoalbuminemia, renal failure or malabsorption. Baseline studies revealed hypocalciuria (24 hour urine calcium less than 5 mg/day), normal serum phosphate (3.4 mg/dl), low tubular reabsorption of phosphate (68 percent), undetectable serum calcitonin, normal serum 25-hydroxyvitamin D, slightly elevated serum parathyroid hormone level and increased urinary cyclic AMP (8.87 mumol/g creatinine). These studies were compatible with secondary hyperparathyroidism. The intravenous administration of parathyroid extract produced no further change in urinary phosphate but a 25-fold increase in nephrogenous cyclic AMP. Three days administration of intramuscular parathyroid extract slowly and temporarily restored serum calcium to normal levels while increasing urinary cyclic AMP and phosphate. Chemotherapy with cyclophosphamide and 5-fluorouracil rendered the patient free of pain while reducing serum acid and alkaline phosphatase levels and restoring serum total and ionized calcium and urinary cyclic AMP excretion to normal.
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PMID:Hypocalcemia with osteoblastic metastases in patient with prostate carcinoma. A cause of secondary hyperparathyroidism. 724 80

Jejuno-ileostomy was performed in eight women because of severe alimentary obesity. Their calcium phosphate and bone metabolism was studied an average of 31 months post-operatively. This revealed secondary intestinal hyperparathyroidism due to an artificial malabsorption syndrome. While most of the significant metabolic factors were within normal limits, examination of calcium balance and kinetics indicated a marked disorder of calcium and bone metabolism. Calcium balance averaged-138 mg daily, corresponding to a yearly loss of skeletal mass of 4-5%.
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PMID:[Calcium and bone metabolism after jejunal bypass operation for alimentary obesity: model for a intestinally-conditioned disorder (author's transl)]. 734 80

Hypophosphatemic osteomalacia that remits after resection of a coexisting tumor has been described in 35 patients. Because the associated neoplasms have been of mesenchymal origin, it has been inferred that this tumor-induced osteomalacia syndrome is uniquely related to tumours of this derivation. However, in the present investigation we studied subjects with coincident hypophosphatemia and prostatic carcinoma to ascertain whether this endodermal malignancy causes the tumor-induced osteomalacia syndrome. The hypophosphatemic patients had renal phosphate wasting, gastrointestinal malabsorption of calcium and phosphate, and negative phosphate balance. Moreover, bone biopsies showed histomorphologic changes indicative of osteomalacia. Although widespread metastases precluded establishing the diagnosis of tumor-induced osteomalacia by resection of the tumor, a series of studied excluded alternate causes for the osteomalacia. Further, affected subjects had a normal serum concentration of 25-hydroxyvitamin D, 28.0 +/- 8.3 ng/mL, and serum 1,25-dihydroxyvitamin D levels were low, 15.0 +/- 1.0 pg/mL, characteristic of the tumor-induced osteomalacia syndrome. Thus, prostatic carcinoma, although an endodermal malignancy, may cause the tumor-induced osteomalacia syndrome.
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PMID:Hypophosphatemic osteomalacia: association with prostatic carcinoma. 740 80

A 60-year-old woman was evaluated for bone pain and incapacitating weakness. Initial laboratory studies showed a serum calcium level of 10.1 mg/dL, severe hypophosphatemia (1.1 mg/dL), and an elevated alkaline phosphatase level. X-ray films showed changes consistent with osteomalacia. Further studies revealed hypercalciuria (448 mg/24 hr) but absent urinary phosphorus. These data indicated phosphate malabsorption. Excessive use of an aluminum hydroxide-containing antacid was the cause of this patient's failure to absorb dietary phosphate. The features of this syndrome are reviewed to increase physicians' awareness of this illness, which occurs particularly in the elderly and is easily treated.
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PMID:Osteomalacia and weakness from excessive antacid ingestion. 743 92

Sixty-two outpatients were assessed and divided into the following groups: 20 patients who had had partial gastrectomy (PG group), 22 patients who had had truncal vagotomy and pyloroplasty (TV group) or high selective vagotomy (HSV group), and 20 patients who had had cholecystectomy (CH group). The patients' age ranged from 35 to 64 years (mean 45 years), and the average postoperative period was 9 years. None of the patients evidenced clinical or biochemical symptoms of malnutrition or malabsorption or of diseases affecting vitamin D metabolism. The function of the kidneys and the liver was normal. An age-matched group of volunteers served as a control group. The calcium dietary intake was determined using a standardized questionnaire; and the levels of serum calcium (Cas), phosphate (Ps), alkaline phosphatase (AP), and 25-hydroxyvitamin D [25(OH)D] and the excretion of Ca in a sample of fasting urine corrected for concurrent creatine excretion (FuCa/cr) were assessed by means of standard laboratory techniques. The bone mineral density (BMD) of the lumbar spine (L2-4) and femoral neck (neck-L) was determined by means of dual energy x-ray absorptiometry (DXA). The daily Ca dietary intake was lower than recommended (RDA) in 80% of the patients, with most of them ingesting less than 300 mg daily. The mean values of Cas, Ps, AP, and FuCa/cr did not differ from those in the controls. Significantly reduced 25(OH)D levels were observed in the PG group (7.0 ng/ml) (p < 0.001) and CH group (12.5 ng/ml) (p < 0.01) compared with the values in the control group (20.0 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium/phosphate/vitamin D homeostasis and bone mass in patients after gastrectomy, vagotomy, and cholecystectomy. 767 6

We previously showed that recurrent calcium renal stone formers have enhanced urinary excretions of calcium and oxalate resulting from malabsorption of citrate. In the present investigation, the mechanism of the citrate-induced increased calcium uptake was studied using guinea pig ileal brush border membrane vesicles. In this model, calcium is absorbed in a concentration dependent, single mechanism uptake with a Km of 275 +/- 30 umol/liter (SD) and a Vmax of 4.0 +/- 0.5 nmol/min.mg protein. Under conditions of maximal calcium uptake, both citrate and phosphate inhibited calcium absorption into brush border membrane vesicles (BBMVs). In contrast, when phosphate and citrate were added together, calcium absorption normalized. Citrate inhibition of calcium absorption appeared to be due to free citrate ions, and phosphate ions overcame this inhibition. Phosphate inhibition was mostly due to decreased concentrations of ionized calcium and partly to precipitation of insoluble calcium phosphate. These studies confirm that the effects of citrate in humans in enhancing calcium absorption occur in the lumen of the gut and are not related to further biochemical conversions of citrate by the gut cells, to effects of citrate on calcium-related hormones, or to the renal handling of calcium. Also, the effects of citrate on increasing calcium absorption should be increased or attenuated in patients who malabsorb citrate, and this explains the increased urinary calcium and oxalate excretions reported for recurrent calcium stone formers.
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PMID:Increased calcium absorption in nephrolithiasis explained by uptake studies in ileal brush border membrane vesicles. 804 3

Hypophosphatemia due to parenteral nutrition has been described frequently. It was attributed to the lack of phosphorus content in parenteral nutrition solutions. With modern parenteral nutrition regimens containing phosphorus, this problem has been virtually eliminated. Enteral nutrition solutions contain adequate phosphate for patients with normal phosphate stores. Hypophosphatemia has therefore rarely been reported in enteral nutrition. We describe two patients with protein-energy malnutrition who developed severe hypophosphatemia during tube feeding with phosphorus-containing formula diets. Chronic alcoholism and vitamin D deficiency due to malabsorption because of Crohn's disease were additional risk factors in these two patients. Patients with depleted phosphate stores and high metabolic demand have a higher daily requirement for phosphorus than is available in routine isotonic enteral formulas. This case report emphasizes the importance of monitoring serum phosphate concentration daily during the first week of refeeding.
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PMID:Enteral supplementation of phosphate does not prevent hypophosphatemia during refeeding of cachectic patients. 820 56


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