Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

More than 250 patients with extreme obesity were treated at the Chir. Univ.-Klinik Erlangen by 30 + 20 cm jejunoileostomy. The patients lose overweight and reach nearly normal weight after 9-12 months. Carbohydrate intolerance and hypertriglyceridema disappear. Ensuing malabsorption and also the surgical procedure are responsible for complications like wound infection or intussuception. The resulting chronic vomitting causes hypoproteinemia, hypokaliemia and liver dysfunction. Continuous therapeutical substitution is necessary, especially of potassium, to avoid deficiency. The diarrhea is treated by drug administration, i.e Reasec. The long time results are not yet sufficiently known. Calcium deficiency may occur many years later. The rate of cholelithiasis and nephrolithiasis ranges from 2 to 10%. The over-all lethality over 5 years is 2,8% as seen in the patients of our clinic during the past 6 years.
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PMID:[Internal complications following jejunoileostomy in the treatment of extreme obesity]. 88 50

Calcium deficiency appears to play a central role in the development of involutional osteoporosis, especially in Japan, where calcium intake has been traditionally low, never reaching the current recommended daily allowance (RDA) of 600 mg/d. Compromised 1,25(OH)2 vitamin D synthesis in the aging kidney and age-bound changes of the intestine itself lead to calcium malabsorption; in addition, decreasing dietary intake of fat-soluble vitamins and reduced solar exposure associated with inadequate physical activity may contribute to calcium deficiency in old age. High salt intake and increasing protein and phosphate intake tend to aggravate such a tendency. These factors appear to underlie, in part, the widespread use of vitamin D derivatives for the treatment of osteoporosis in Japan. In 1981, a large-scale, double-blind clinical trial established the superior effect of 1 alpha(OH) vitamin D3 in maintaining bone density over that of placebo. The effect of 0.5 micrograms/d 1,25-(OH)2D3 (calcitriol) in two divided doses compared favorably with that of 1 micrograms/d of 1 alpha(OH) vitamin D3 in a recently conducted multicenter, double-blind study on 596 patients with involutional osteoporosis. Spinal fracture rate was also reduced to one-half by administration of the vitamin D derivative for 1 year to 800 patients with osteoporosis.
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PMID:Studies of osteoporosis in Japan. 232 70

Calcium deficiency causes osteoporosis in experimental animals because the skeleton is sacrificed for the preservation of the plasma (ionic) calcium and to meet obligatory calcium losses in the feces and urine. (Vitamin D deficiency, on the other hand, causes rickets and osteomalacia largely because of the loss of the calcemic action of vitamin D, which leads to hypocalcemia, secondary hyperparathyroidism, and hypophosphatemia.) The concept that human osteoporosis, particularly in postmenopausal women, results from negative calcium balance represents a working hypothesis that fits many, but not all of the available data. In normal women, the crucial event is a rise in obligatory urinary calcium loss, which may result from an increase in the complexed fraction of the plasma calcium, due in turn to an increase in plasma bicarbonate. Prospective trials with calcium supplements have, however, yielded conflicting results. In osteoporotic women, a further increase in urinary calcium combined with calcium malabsorption produces a further increase in bone resorption, but some impairment of bone formation due to declining androgens may constitute an additional risk factor with advancing age. The suppressibility of urinary hydroxyproline by calcium supplementation in those patients who can absorb calcium, and by calcitriol in those who cannot, supports the calcium deficiency model, but more trials are needed to establish its validity.
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PMID:The calcium deficiency model for osteoporosis. 264 3

It has become increasingly apparent that the pathogenesis of osteoporosis is complex, poorly understood, and ill-defined. Calcium deficiency and/or calcium malabsorption and the homeostatic response to this biological insult may ultimately prove to be one of the pivotal factors in conditioning or modulating the skeletal response to senescence. Until we know more about the prevention and potential reversibility of age-related changes in bone cell function, hormonal secretion and metabolism, and dietary patterns that prove deleterious to skeletal health, clinicians will be confronted with an ever-increasing population of aging, fracture-prone, osteoporotic patients. Because calcium supplements improve the calcium balance of perimenopausal and postmenopausal women and because improvements in calcium balance can be correlated with increased skeletal mass, it appears desirable to focus our efforts on diets and/or calcium supplements that guarantee an adequate supply of this essential mineral. Because calcium replacement may simply retard bone resorption and may not restore bone already lost by the fracture-prone, osteoporotic female, dietary analyses and appropriate modification of calcium intakes should be made at least in the third and fourth decades of life, with the goal of retarding the inexorable loss of skeletal tissue as early as possible.
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PMID:Calcium and osteoporosis. 638 May 41

Osteomalacia is a metabolic bone disease associated with impaired mineralization of the bone due to Vitamin D and Calcium deficiency that can develop in gastrointestinal disorders. Gastrointestinal malabsorption after surgery, in disorders of the small bowl, in diseases of the hepatobiliary tree and in pancreatic insufficiency can lead to decreased enteral resorption of the fat-soluble Vitamin D and/or depletion of endogenous Vitamin D stores due to abnormal enterohepatic circulation. As a consequence of the Vitamin D deficiency in combination with the underlying condition patients develop an impaired calcium absorption resulting in hypocalcaemia, which leads to defective bone mineralization. Additionally chronic gastrointestinal inflammation and corticosteroid therapy - which is often needed in these patients - have a negative effect on bone metabolism as well. The therapy consists of oral substitution of Vitamin D and Calcium as well as sufficient sun light exposure or in severe cases the use of artificial UVB-radiation.
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PMID:[Gastrointestinal diseases and osteomalacia]. 1871 73