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)

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

The in vitro and in vivo production of hydrogen gas (H2) from various carbohydrates or proteins has been examined in normal rats and in rats infected with the nematode Nippostrongylus brasiliensis. Normal rat fecal homogenates were capable of producing H2 in vitro from glucose, sucrose, xylose, lactulose, bovine serum albumin, or casein hydrolysate. Direct injection of glucose, sucrose, xylose, lactulose, bovine serum albumin, or casein hydrolysate into the cecum of normal rats resulted in approximately twice as much H2 production in vivo than when these same carbohydrates or proteins were administered to the normal rats by gavage. Partial small intestinal villous atrophy was produced by infecting rats with the nematode N. brasiliensis. Impaired small intestinal cell function and evidence of malabsorption in the nematode-infected rats included: (a) decreased activity of intestinal cell lactase (-43%), sucrase (-33%), and alkaline phosphatase (-46%); (b) decreased gut sac uptake of 3-O-(methyl-3H]-D-glucose (-21%) or 1-[carboxyl-14C]-aminocyclopentane-1-carboxylic acid (-28%); and (c) increased (+ 64%-561%) 14CO2 production after D-[U-14C]xylose administration. These rats produced approximately twice as much H2 after gavage administration of glucose, sucrose, xylose, bovine serum albumin, or casein hydrolysate compared with normal rats. The present study suggests that H2 analysis may be useful in the evaluation of small intestinal malabsorption states in rats.
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PMID:Use of hydrogen gas (H2) analysis to assess intestinal absorption. Studies in normal rats and in rats infected with the nematode, Nippostrongylus brasiliensis. 728 87

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

One hundred and four children aged 0-15 years, with suspicion of malabsorption were studied. They had a proximal jejunal biopsy and, at the same time, the following measurements: 25-hydroxycholecalciferol (25-OH-CC), calcium, phosphorus and serum alkaline phosphatase, bone age on X-ray of the left hand and wrist, cortical thickness of the 2nd, 3rd, 4th metacarpal bones. For the analysis of the results, the patients were divided into two groups according to the season (winter vs. summer). None of the patients in either group had clinical or radiological signs of rickets. The following results were obtained: 1. The 25-OH-CC serum levels were significantly lower during the winter than during the summer months. This was observed more frequently in the cases with atrophy of the jejunal mucosa. 2. During the summer, the 25-OH-CC serum levels were not different in the cases with normal or pathological mucosa. This demonstrates the importance of the skin synthesis of vitamin D during the summer months. 3. The mean of the serum calcium levels was significantly lower in the group of children with atrophy of the jejunal mucosa than in children with normal intestinal biopsy. The serum calcium levels were not correlated with the serum 25-OH-CC levels. 4. The serum phosphorus levels were significantly lowered during the winter months in the children aged 0-3 years with pathological jejunal biopsy. 5. The serum alkaline phosphatase levels were lowered in cases of total atrophy of the jejunal epithelium cells. 6. Cortical thickness of the metacarpal bones becomes thinner with the progression of the alteration of the jejunal epithelium cells, independently of season or age. However, only the group of children aged 0-3 years studied during the winter months and with total atrophy of the jejunal mucosa have a significantly diminished cortical thickness of the metacarpal bones. The lowering of the calcium levels and the decrease of the cortical thickness are probably secondary to an impaired intestinal absorption of calcium. In the syndrome of malabsorption, the integrity of the jejunal epithelial cells seems to play a more important role than a vitamin D deficiency in the genesis of this calcium malabsorption.
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PMID:[Phosphorus-calcium metabolism and plasma 25-hydroxycholecalciferol in intestinal malabsorption]. 745 Dec 35

An experiment was performed to examine the interaction between Zn deficiency and lipid intake in carp. The carp were given a high-lipid diet that was either Zn-deficient (ZD) or Zn-supplemented (ZS), or were pair-fed (PF) the ZS diet to the intake of the ZD group. After 8 weeks the carp were killed and measurements were made of intestinal glucose uptake, levels of DNA, RNA and triacylglycerol, and alkaline phosphatase (EC 3.1.3.1) activity in liver and intestine samples. A further group of similar carp were given the same diets but at week 8 were transferred to low-lipid diets, with the exception of half the ZD group. After a further 8 weeks of treatment, carps were killed for biochemical studies. Intestinal [14C]glucose uptake, levels of DNA, RNA and alkaline phosphatase activity in intestine and liver were significantly (P < 0.05) lower in the high-lipid ZD group than in the high-lipid ZS and PF diet groups. The triacylglycerol concentration in the intestine was higher in the high-lipid ZD group than in the other two groups. When the carp were given the corresponding low-lipid diets, the variables measured in intestine and liver of the ZD group were close to those of the other groups. The results of this study demonstrate that lipid, when present in excess in the diet, accumulates in the intestine under Zn-deficient conditions and may reduce the absorption of glucose in carp. The reduced RNA and DNA levels and alkaline phosphatase activity in liver and intestine of ZD fish compared with those of ZS fish given high-lipid diets is proposed to be due to the malabsorption of nutrients linked with lipid deposition in the intestine, rather than their dependence on the level of Zn in the diet.
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PMID:Lipid deposition in intestine as a possible cause of malabsorption of nutrients in zinc-deficient common carp (Cyprinus carpio). 753 42

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

Immunocytochemistry using a specific monoclonal antibody 9A7 gamma was used to identify receptors for calcitriol (1,25 (OH)2 D3), the active metabolite of vitamin D, in sections of duodenal mucosa. Specific staining for vitamin D receptors was largely restricted to nuclei of enterocytes lining crypts in duodenal biopsy specimens from normal mucosa. Vitamin D receptors were also abundant in crypts from duodenal mucosa in coeliac disease patients with mucosal damage and villous atrophy. In contrast, alkaline phosphatase, a vitamin D regulated protein, was absent from crypts but present on brush borders of normal villi, and on surface enterocytes in coeliac disease. Oestrogen receptor could not be identified in duodenal mucosa. These findings suggest that calcium malabsorption in coeliac disease does not result from the absence of vitamin D receptors, but rather from reduction in vitamin D regulated proteins and functions essential for active calcium absorption that are located in the enterocytes of the villi.
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PMID:Localisation of vitamin D receptor in normal human duodenum and in patients with coeliac disease. 795 27

A manifest clinical response has been achieved in 38 patients with chronic enteritis kept on apple diet in the form of apple powder produced from apple juice refuse. Carbohydrate loading with starch (polysaccharide), saccharose (disaccharide), glucose (monosaccharide), d-xylose made it clear that the apple powder improves hydrolysis and carbohydrate absorption: by 30%, 23%, 32% and 40% for starch, saccharose, glucose and d-xylose, respectively. Attenuation of the inflammation in the small intestine was also evident from the tendency to normalization of some fecal intestinal enzymes activity (entero-kinase, alkaline phosphatase). Changes in the systems PGE-cAMP and PGF-cGMP are suggested to play a role in the emergence of malabsorption syndrome, diarrhea, structural lesions in small intestinal mucosa.
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PMID:[Apple powder in the treatment of patients with chronic enteritis]. 797 20

Inflammatory bowel disease (Crohn's disease and ulcerative colitis) is associated with decreased bone mineral density and increased risk of osteoporosis. However, the pathogenesis of this bone loss is not yet fully understood. In the present study we measured lumbar bone mineral density (by dual photon absorptiometry), serum levels of parathyroid hormone (PTH) and vitamin D metabolites, and serum markers of bone turnover (alkaline phosphatase and osteocalcin) in 15 patients with Crohn's disease and in 4 patients with ulcerative colitis. The median duration of the disease was 4 years and the median lifetime steroid dose was 10g of prednisone. We compared our results to a control group of 19 normal persons, who were matched for age and sex to the patients. We found that lumbar bone density was reduced by 11% in patients compared with control persons (Z-score -0.6 +/- 0.6 versus -0.1 +/- 0.8; p < 0.05). In patients, the serum levels of PTH, 25-hydroxyvitamin D3, and calcitriol (1,25(OH)2D3) were significantly reduced compared with control persons. Serum alkaline phosphatase activity (AP) was significantly higher in the patients and was inversely related to lumbar bone density. Osteocalcin values were not different between patients and control persons. There was also no difference in serum levels of calcium between the two groups, whereas phosphorus levels were higher in patients. We conclude that malabsorption of calcium was not a primary cause of bone loss in our patients, because we did not find secondary hyperparathyroidism. Accordingly, we did not find a severe vitamin D deficiency, since 25-hydroxyvitamin D3 levels were within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bone mineral density and calcium regulating hormones in patients with inflammatory bowel disease (Crohn's disease and ulcerative colitis). 800 8

A 45-year-old woman reported the development of thigh pain followed within a year by proximal muscle weakness. Clinical findings included short stature, prominent kyphoscoliosis, proximal weakness, and brisk reflexes. Recognition of an increased level of serum alkaline phosphatase and hypophosphatemia led to the diagnosis of osteomalacia. Identification of iron deficiency anemia and hypocholesterolemia implicated previously unrecognized gluten-sensitive enteropathy with associated vitamin D malabsorption as the cause of the osteomalacia. Adherence to a gluten-free diet and treatment with vitamin D2 resulted in weight gain, resolution of pain, and improvement in strength within 3 months. Painful proximal weakness and hyperreflexia may be the initial and primary manifestations of osteomalacia, a readily treatable cause of muscle and bone disease.
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PMID:Osteomalacic myopathy. 787 Jan 21


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