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 patient had systemic mastocytosis of 16 years' duration, with urticaria pigmentosa, osteopetrosis with severe bone pain, mastocytosis of the bone marrow with myeloid metaplasia, gastrointestinal malabsorption, and Cushingold features associated with prolonged usage of corticosteroids. Treatment with a single dose of mithramycin resulted in an abrupt disappearance of the patient's generalized bone pain, but it had little effect on his histamine release-type symptomatology.
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PMID:Mithramycin in the treatment of systemic mastocytosis. 12 7

Osteomalacia is characterized by large osteoid seams and a preserved volume of bone trabeculae. The mineralization of newly formed bone requires adequate concentrations of calcium and phosphate: the Ca.P product has been regarded as a useful, empirical diagnostic test of osteomalacia. It decreases in patients with osteomalacia mainly because they have very low plasma phosphate levels. At present total body bone mineral and total body bone density can be directly measured by whole body absorptiometry, which indicates the lowest total mineral content of the skeleton which can increase quickly after adequate treatment. The main symptoms of osteomalacia are: bone pain; muscular weakness (commonly as pelvic girdle myopathy); Looser-Milkman pseudofractures or more often a pattern of generalized demineralization at X-ray. The main biochemical parameters in osteomalacia include: defective calcium absorption with hypocalcemia and hypocalciuria; defective intestinal phosphate absorption with hypophosphatemia; there is often increased renal phosphate clearance due to hypocalcemia and secondary hyperparathyroidism; elevated alkaline phosphatase and osteocalcin levels; high bone turnover confirmed by kinetic studies carried out with radiocalcium or 99mTc-MDP. An etiological classification of the osteomalacias includes: 1) nutritional osteomalacia: a) inadequate exposure to sunlight and/or insufficient vitamin D intake; b) defective intestinal absorption of vitamin D because of malabsorption syndromes (e.g. jejuno-ileal bypass for obesity).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The osteomalacias. 166 41

D-lactate accumulates in some patients with malabsorption who continue oral intake of carbohydrate leading to a clinical syndrome of acidosis and encephalopathy. To assess the possibility that D-lactate contributes to acidosis and/or metabolic bone disease in patients with malabsorption receiving long-term parenteral nutrition yet maintaining oral intake, D-lactate levels in serum and urine were measured in 14 long-term parenteral nutrition subjects (average duration of support 74 months) and 27 control subjects. Significant elevations in both serum and urine D-lactate were found in only two parenteral nutrition subjects. Both subjects with elevated D-lactate levels had bone pain, x-ray evidence of fractures, and biopsy evidence of osteomalacia. These studies suggest that D-lactate accumulation may be a heretofore unappreciated metabolic abnormality associated with metabolic bone disease and acidosis in patients with malabsorption who are supported by long-term parenteral nutrition.
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PMID:D-lactate and metabolic bone disease in patients receiving long-term parenteral nutrition. 249 43

Mg deficiency is a frequent complication of inflammatory bowel disease (IBD) demonstrated in 13-88% of patients. Decreased oral intake, malabsorption and increased intestinal losses are the major causes of Mg deficiency. The complications of Mg deficiency include: cramps, bone pain, delirium, acute crises of tetany, fatigue, depression, cardiac abnormalities, urolithiasis, impaired healing and colonic motility disorders. Serum Mg is an insensitive index of Mg status in IBD. Twenty-four-hour urinary excretion of Mg is a sensitive index and should be monitored periodically. Parenteral Mg requirements in patients with IBD are at least 120 mg/day or more depending upon fecal or stomal losses. Oral requirements may be as great as 700 mg/day depending on the severity of malabsorption.
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PMID:Magnesium and inflammatory bowel disease. 329 19

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

The classical symptoms of malabsorption syndrome are diarrhea, steatorrhea, weight loss, and fatigue. Tetany, ecchymosis, anorexia, bone pain, pallor, muscle wasting, hyperpigmentation, apathy, digital clubbing, abdominal distention which contrasts in view of the reduced common statement are other signs of malabsorption. Long before the onset of these symptoms there may be a disinterest in regular daily activities often associated with the passage of three soft stools per day and with the remarkable sign of difficulties in flushing bulky stools. Anamnesia, clinical examination in connection with common laboratory findings, small intestinal x-rays and endoscopic investigations associated with biopsies of the small (and large) bowel as well as estimation of stool fat excretion, xylose- and Schilling-test allow the diagnosis in most of the cases.
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PMID:[Clinical aspects and differential diagnosis of malabsorption]. 684 29

The intestinal absorption and hepatic metabolism of vitamin D were studied in a woman with icteric primary biliary cirrhosis (PBC) complicated by pronounced bone pain and muscle weakness due to vitamin-D deficiency. The patient had a markedly reduced intestinal absorption of vitamin D, while the 25-hydroxylation of this vitamin was found to be normal despite the presence of longstanding icterus. The malabsorption of fat-soluble compounds secondary to the cholestasis was probably further impaired by several years of cholestyramine treatment. Administration of 1.25-(OH)2D3 increased intestinal calcium absorption, normalized serum calcium and increased bone mineral content of the proximal tibia. Furthermore, drastic improvement of muscle weakness and relief of bone pain were observed. It is recommended that repeated measurements of serum 25-(OH)D should be carried out in patients with PBC, and especially in those treated with cholestyramine. In certain vitamin D deficient patients, studies using radio-labelled vitamin D may provide clinically valuable information as to the exact site of the underlying disturbances.
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PMID:Normal hepatic vitamin-D metabolism in icteric primary biliary cirrhosis associated with pronounced vitamin-D deficiency symptoms. 709 38

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

Gluten-induced enteropathy or coeliac disease is a condition characterized by malabsorption and a variety of clinical manifestations. In adults, coeliac disease may be discovered while investigating iron-deficient anemia, bone pain or unexplained weight loss. We have recently diagnosed a case of gluten-induced enteropathy in an elderly woman whose symptoms were unusual. The patient had episodes of laryngospasm secondary to severe hypocalcemia and hypomagnesemia. The malabsorption syndrome was responsible for low levels of vitamin D, causing the electrolytic imbalance. Laryngospasm is a rare symptom of hypocalcemia and has not, to our knowledge, been described in the context of coeliac disease.
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PMID:[Laryngospasm: unusual manifestation of celiac disease]. 845 63

In 1990 Scopinaro's technique of biliopancreatic diversion with distal gastrectomy (DG) and gastroileostomy was modified. A sleeve gastrectomy with duodenal switch (DS) was used instead of the distal gastrectomy; and the length of the common channel was made 100 cm instead of 50 cm. A questionnaire and a prescription for blood work were sent to 252 patients who underwent DG a mean 8.3 years ago (range 6-13 years) and 465 patients who underwent DS 4.1 years ago (range 1.7-6.0 years). The questionnaire response rate was 93%, and laboratory work was completed for 65% of both groups. The mean weight loss after DG was 37 +/- 21 kg and after DS 46 +/- 20 kg. There were fewer side effects after DS: The number of daily stools was lower (p < 0.0002), as was the prevalence of diarrhea (p < 0.01), vomiting (p < 0.001), and bone pain (p < 0.001). Greater benefits related to several aspects of life were reported after DS than DG (p < 0.0001). The mean serum levels of ferritin, calcium, and vitamin A were higher (p < 0.001), and parathyroid hormone was lower. The yearly revision rate for excessive malabsorption was 1.7% per year after DG and 0.1% per year after DS. The two procedures were equally efficient for treating co-morbid conditions such as diabetes, hypertension, and hypercholesterolemia. Biliopancreatic diversion with sleeve gastrectomy/duodenal switch and a 100-cm common limb was shown to produce greater weight loss with fewer side effects.
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PMID:Biliopancreatic diversion with duodenal switch. 971 20


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