The case of a 49-year-old woman suffering from generalized skeletal pain and multiple fractures accompanied by severe hypophosphataemia and low urinary phosphorus excretion is reported. She had been taking large amounts of antacids containing aluminum hydroxide for many years. A diagnosis of antacid-induced osteomalacia was made. It was confirmed by biological work-up, radiographs and bone biopsy. A dramatic biological, osteodensitometric, and clinical improvement was achieved by withdrawal of antacids and phosphorus administration. The literature concerning this unusual condition has been reviewed.
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Antacid-induced osteomalacia.
Clin Rheumatol
January 1996
Department of Rheumatology, St-Luc University Hospital, Louvain University in Brussels, Belgium.
The case of a 49-year-old woman suffering from generalized skeletal pain and multiple fractures accompanied by severe hypophosphataemia and low urinary phosphorus excretion is reported. She had been taking large amounts of antacids containing aluminum hydroxide for many years. A diagnosis of antacid-induced osteomalacia was made.
View Article and Find Full Text PDFAntacid-induced osteomalacia: a case report with a histomorphometric analysis.
J Intern Med
March 1991
Department of Endocrinology and Metabolism, Aarhus Amtssygehus, Denmark.
The case of a 75-year-old woman with severe osteomalacia secondary to ingestion of large amounts of an aluminum-containing antacid is reported. Biochemical analysis revealed signs of phosphate malabsorption and increased levels of bone markers (S-alkaline phosphatase and U-hydroxyproline). A 99mTc-bone scan revealed multiple areas of increased uptake.
View Article and Find Full Text PDFHypophosphatemic rickets with hypocalciuria following long-term treatment with aluminum-containing antacid.
Bone
August 1991
Department of Medicine, Henry Ford Hospital, Detroit, Michigan.
We present what we believe is the first case of rickets following prolonged treatment with aluminum containing antacids that bind phosphate, in an 18-year-old mentally retarded boy with cerebral palsy and spastic quadriplegia. As expected, serum calcitriol was increased and urinary phosphate excretion was very low. However, in contrast to all published cases of antacid induced hypophosphatemic osteomalacia in adults, despite a substantial increase in bone resorption reflected by urinary total hydroxyproline excretion, urinary calcium excretion was low rather than high, and significant hypocalcemia occurred after antacids were ceased and a phosphate salt administered.
View Article and Find Full Text PDFA patient with hypophosphatemic osteomalacia secondary to ingestion of large amounts of phosphate-binding antacids is presented. Vitamin D metabolites were measured during the course of his illness and recovery and demonstrated an initially elevated concentration of 1,25-dihydroxyvitamin D, an undetectable level of 24,25-dihydroxyvitamin D, and a normal level of 25-hydroxyvitamin D. These metabolites returned to normal levels when the hypophosphatemia was corrected.
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