Etiology of hypercalcemia in a patient with Addison's disease.
A case is reported of a hypercalcemic patient with primary Addison's disease. A combination of increased calcium input into the extracellular space and reduced calcium removal by the kidney accounted for the hypercalcemia. The mechanisms responsible for the reduction in calcium removal were decreased glomerular filtration and increased tubular calcium reabsorption. Both renal factors were secondary to volume depletion and improved rapidly during rehydration with saline infusion. The enhanced calcium mobilization was probably of skeletal origin. It persisted irrespective of volume status until hydrocortisone treatment was instituted. Serum 1,25-dihydroxyvitamin D3 levels were below 10 pg/ml, even after normalization of the glomerular filtration rate, but returned slowly to the normal range during corticosteroid substitution. Serum 25-hydroxyvitamin D3 and parathyroid hormone levels were within the normal range. Our case report therefore demonstrates that physiological amounts of glucocorticoids reduce bone resorption, normalize serum calcium, and restore the production of 1,25-dihydroxyvitamin D3.
D000224:Addison Disease / Q000097:blood / Q000150:complications* / Q000378:metabolism; D002112:Calcifediol / Q000097:blood; D002117:Calcitriol / Q000097:blood; D002118:Calcium / Q000652:urine; D002352:Carrier Proteins / Q000097:blood; D005260:Female; D006801:Humans; D006934:Hypercalcemia / Q000097:blood / Q000209:etiology*; D007668:Kidney / Q000378:metabolism; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000097:blood / Q000276:immunology; D014809:Vitamin D-Binding Protein
D002352:Carrier Proteins; D010281:Parathyroid Hormone; D014809:Vitamin D-Binding Protein; D002117:Calcitriol; D002112:Calcifediol; D002118:Calcium