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)

Metabolic bone disease due to calcium and vitamin D malabsorption is a well-defined consequence of gastrectomy and to a lesser extent of pancreatic insufficiency. The diversity of its presentation, however, can be misleading, resulting in delayed diagnosis or a thorough investigation for possible underlying neoplasias being undertaken. We describe the case of a man with partial gastrectomy and pancreatectomy with osteomalacia and secondary hyperparathyroidism.
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PMID:Gastrectomy and osteomalacia: an association not to be forgotten. 1096 11

A component of ATP, phosphate is at the hub of the energy-related mechanisms operative in muscle cells. Together with calcium, phosphate is involved in bone tissue mineralization: thus, a chronic alteration in the metabolism of phosphate can induce bone and joint disorders. Diagnosis of chronic hypophosphatemia. Serum phosphate, calcium, and creatinine should be assayed simultaneously. Serum calcium is increased in hypophosphatemia caused by hyperparathyroidism and decreased in osteomalacia. Urinary phosphate excretion should be measured in patients with a normal serum calcium level and a serum phosphate level lower than 0.80 mmol/L. A decrease in urinary phosphate excretion to less than 10 mmol/24 h strongly suggests a gastrointestinal disorder, such as malabsorption, antacid use, or chronic alcohol abuse. In patients with a urinary phosphate excretion greater than 20 mmol/24 h, the maximal rate of tubular reabsorption of phosphate (TmPO4) and the ratio of TmPO4 over glomerular filtration rate (GFR) should be determined to look for phosphate diabetes. Manifestations and causes of phosphate diabetes in adults. Moderately severe phosphate diabetes in adults manifests as chronic fatigue, depression, spinal pain, and polyarthralgia, with osteoporosis ascribable to increased bone resorption. Although many cases are idiopathic, investigations should be done to look for X-linked vitamin D-resistant rickets missed during childhood, a mesenchymatous tumor, or Fanconi's syndrome with renal wasting of phosphate, glucose, and amino acids. Management of phosphate diabetes. Phosphate supplementation and, in patients with normal urinary calcium excretion, calcitriol produce some improvement in the symptoms and increase the bone mineral density. Whether dipyramidole is clinically effective remains unclear.
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PMID:Phosphate, the renal tubule, and the musculoskeletal system. 1139 20

The consequences of vitamin D deficiency upon the skeleton are well known and management in the absence of renal failure is relatively straightforward. Vitamin D, either by mouth or parenterally will correct the deficiency and heal the osteomalacia. The mechanisms underlying the causation of vitamin D deficiency are now better understood and indicate the importance of underlying calcium malabsorption and secondary hyperparathyroidism leading to 1,25(OH)2D-induced catabolism of 25(OH)D and possibly also of vitamin D itself. In such situations, e.g., gastrointestinal and pancreaticobiliary disease, calcium supplementation in addition to vitamin D is indicated. The reasons behind nutritional vitamin D deficiency and the possible role of meat in protecting from osteomalacia await further elucidation, but from epidemiological studies, calcium deficiency, per se, is not implicated in the etiopathogenesis. The concept of vitamin D insufficiency is poorly understood, and difficult to define since a single value or close range of serum 25(OH)D values is unlikely to predict the needs of all subjects. Oral calcium intake and renal function are also likely to be relevant to the level of 25(OH)D which is found to be sufficient or insufficient for any given individual to maintain a normal serum calcium level without secondary hyperparathyroidism. There is increasing evidence that vitamin D insufficiency, by leading to sustained hyperparathyroidism, is prejudicial to the skeleton, particularly cortical bone. Since it is without symptoms until fractures occur, it should be actively sought in those clinical situations now recognized as contributing to risk. It can only be identified by the periodic measurement of serum 25(OH)D and the calcitropic hormones PTH and 1,25(OH)2D. In addition, BMD should be measured in a predominantly cortical site such as the proximal forearm, as well as the more conventional sites of spine and hip. The implications of these recommendations are an increase in the use of assays for PTH and vitamin D metabolites in the groups of subjects discussed in this review. Patients with chronic malabsorption states might reasonably be expected to have measurements performed twice-yearly. When vitamin D insufficiency is found, treatment with either vitamin D, calcium or both will be necessary, depending on the etiology of the insufficiency state in the inividual. In some malabsorptive states, calcium malabsorption is the cause of hyperparathyroidism and oral calcium alone can be used to reverse excess PTH activity in those with an adequate state of vitamin D nutrition. However, even in those vitamin D replete individuals, vitamin D catabolism will be enhanced and a small additional oral dose of vitamin D can do no harm. Regular monitoring of PTH and vitamin D metabolites will remain a necessity to ensure continued efficacy of treatment. Current recommendations for dietary supplements of vitamin D are clearly inadequate [61]. There is compelling evidence for supplements of 800 IU per day in the elderly and other high risk populations. Such a dose is safe and without side effects. The available evidence suggests that this should be combined with calcium supplements of 1200 mg/day [19] and that the current UK recommendations for a daily calcium intake of 700 mg contrast with those from the USA at 1,200 mg for people over 50 years old. Physicians need to be aware of both the small but important problem of vitamin D depletion and osteomalacia with its sometimes ambiguous presentation, and the more common but covert vitamin D (and calcium) insufficiency with its widespread and varied clinical associations.
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PMID:Vitamin D nutrition and bone disease in adults. 1170 21

Children with cholestatic liver disease have been thought to develop hepatic osteodystrophy resulting from vitamin D and calcium malabsorption, resulting in secondary hyperparathyroidism and osteomalacia or rickets. However, treatment with vitamin D has not always proven successful in improving the bone disturbance. The aim of our study was to determine the role of vitamin D deficiency in the pathogenesis of hepatic osteodystrophy. We studied five patients, three female and two male, ages 0.9-19 yr, with biopsy-proven chronic cholestatic liver disease and previously low serum levels of vitamin D despite oral intake of vitamin D preparations. Patients were admitted to the Clinical Research Center for 8 days for sunlight deprivation and ultraviolet light substitution and for determinations of serum 25-hyroxyvitamin D(25(OH)) D2 and -D3, osteocalcin, and type I collagen telopeptide (ICTP), the last two being markers of bone formation and resorption, respectively. Samples were taken on admission, at discharge, and 1 month later. Results demonstrated low serum levels of osteocalcin and normal circulating levels of ICTP. Admission serum 25(OH)D2 levels were uniformly low or undetectable and remained so. Admission levels of circulating 25(OH)D3 were normal or low and did not rise during ultraviolet light therapy or subsequent resumption of oral vitamin D therapy and remained low 1 month later. These results indicate that in the face of low-normal to low total 25(OH)D levels, the low osteocalcin and normal ICTP levels suggest that decreased bone formation and not increased bone resorption is the main determinant of bone loss in a subset of children with chronic cholestatic liver disease.
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PMID:Hepatic osteodystrophy in chronic cholestasis: evidence for a multifactorial etiology. 1200 Apr 70

There is no one cause of bone fragility; genetic and environmental factors play a part in development of smaller bones, fewer or thinner trabeculae, and thin cortices, all of which result in low peak bone density. Material and structural strength is maintained in early adulthood by remodelling; the focal replacement of old with new bone. However, as age advances less new bone is formed than resorbed in each site remodelled, producing bone loss and structural damage. In women, menopause-related oestrogen deficiency increases remodelling, and at each remodelled site more bone is resorbed and less is formed, accelerating bone loss and causing trabecular thinning and disconnection, cortical thinning and porosity. There is no equivalent midlife event in men, though reduced bone formation and subsequent trabecular and cortical thinning do result in bone loss. Hypogonadism contributes to bone loss in 20-30% of elderly men, and in both sexes hyperparathyroidism secondary to calcium malabsorption increases remodelling, worsening the cortical thinning and porosity and predisposing to hip fractures. Concurrent bone formation on the outer (periosteal) cortical bone surface during ageing partly compensates for bone loss and is greater in men than in women, so internal bone loss is better offset in men. More women than men sustain fractures because their smaller skeleton incurs greater architectural damage and adapts less effectively by periosteal bone formation. The structural basis of bone fragility is determined before birth, takes root during growth, and gains full expression during ageing in both sexes.
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PMID:Pathogenesis of bone fragility in women and men. 1204 92

In patients with secondary hyperparathyroidism (HPT), increased parathyroid hormone (PTH) secretion is triggered by low plasma calcitriol levels, hypocalcemia, and hyperphosphatemia. Vitamin D analogues have been used successfully to reduce PTH levels, but increases in serum calcium, phosphorus, and calcium x phosphorus ion product levels may occur. Second-generation calcimimetics have been shown to suppress PTH levels and also reduce calcium x phosphorus ion product. Potential indications are patients with secondary HPT, particularly those who respond to calcitriol therapy with an increase in calcium x phosphorus ion product. Coadministration of active vitamin D compounds may be necessary to overcome intestinal malabsorption of calcium and maintain normocalcemia in patients on long-term treatment with calcimimetics.
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PMID:Renal osteodystrophy: role of calcimimetics. 1261 64

Nutritional disorders that cause bone loss in adults include disordered eating behaviors (female athlete triad and anorexia nervosa), gastrointestinal diseases (celiac sprue, inflammatory bowel disease, and other malabsorption syndromes), alcoholism, and hypervitaminosis A. These disorders exert their effects on bone through a number of mechanisms, including estrogen deficiency. Deficiencies of anabolic hormones may also be important, including insulin-like growth factor I (IGF-I), a nutritionally regulated bone trophic factor. In addition, low weight itself is a risk factor for bone loss and decreased bone formation. Reduced calcium and vitamin D availability, with resultant secondary hyperparathyroidism, is another important mechanism of bone loss in nutritional disorders. This review discusses nutritional causes of reduced bone mass in adults and how nutritional disorders exert deleterious effects on the skeleton.
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PMID:Mechanisms by which nutritional disorders cause reduced bone mass in adults. 1273 12

The causes and clinical picture of osteopenia and osteoporosis were analyzed in 13 children (7 girls and 6 boys aged 6-15 years of life, mean age 10.2 years). The diagnosis was based on X-ray and densitometric studies. Upper gastrointestinal tract diseases were noted in 7 patients (one child received additional anti-epileptic drugs) and 5 had juvenile osteoporosis. Children with Gl tract diseases and these on anti-epileptic management may develop osteoporosis and osteopenia as a consequence of vitamin D3 deficit and calcium malabsorption leading to hypocalcemia and secondary hyperparathyroidism.
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PMID:[Causes and clinical picture of osteopenia and osteoporosis in children]. 1281 89

In this case report, a 56-year-old woman with a reversible multiple organ disease with septic fever, arthritis, rash, weight loss, thrombocytopenia, severe disturbance of liver function, renal tubular dysfunction, general muscular weakness, pleural and pericardial effusions and elevated CRP, leukocytosis and a striking hyperferritinemia is presented. An autoimmune disease and a septic process were excluded. Because of the significantly decreased plasma phosphorus concentration (0.2 mmol/l), caused by malabsorption after Whipple's operation with lowered vitamin D and secondary hyperparathyroidism and by chronic alcoholism, severe phosphate deficiency was diagnosed. By substitution of phosphorus, all symptoms disappeared and laboratory findings normalized. Except for the patient's age, all criteria for the diagnosis of Still's disease were fulfilled. So we reflected upon Still's disease to be rather a disturbance of energy metabolism with secondary immunologic changes than an inflammatory rheumatic disease. Significant weight loss in Still's disease and osteopenia might be signs of decreased energy supply. Besides hypophosphatemia, deficiency of magnesium, which is involved in all ATP-dependent processes, and mitochondrial diseases cause disturbances of energy metabolism.
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PMID:[Adult Still's disease as a manifestation of severe hypophosphatemia. Still's disease--a disturbance of energy metabolism?]. 1282 5

Patients with fragility fractures may have abnormalities in bone structural and material properties such as larger or smaller bone size, fewer and thinner trabeculae, thinned and porous cortices, and tissue mineral content that is either too high or too low. Bone models and remodels throughout life; however, with advancing age, less bone is replaced than was resorbed within each remodeling site. Estrogen deficiency at menopause increases remodeling intensity: a greater proportion of bone is remodeled on its endosteal (inner) surface, and within each of the many sites even more bone is lost as more bone is resorbed while less is replaced, accelerating architectural decay. In men, there is no midlife increase in remodeling. Bone loss within each remodeling site proceeds by reduced bone formation, producing trabecular and cortical thinning. Hypogonadism in 20-30% of elderly men contributes to bone loss. In both sexes, calcium malabsorption and secondary hyperparathyroidism increase remodeling: more bone is removed from an ever-diminishing bone mass. As bone is removed from the endosteal envelope, concurrent bone formation on the periosteal (outer) bone surface during aging partly offsets bone loss and increases bone's cross-sectional area. Periosteal apposition is less in women than in men; therefore, women have more net bone loss because they gain less on the periosteal surface, not because they resorb more on the endosteal surface. More women than men experience fractures because their smaller skeleton incurs greater architectural damage and adapts less by periosteal apposition.
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PMID:Invited Review: Pathogenesis of osteoporosis. 1455 75


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