INCREASED CALCIUM INTAKE DOES NOT SUPPRESS CIRCULATING 1,25-DIHYDROXYVITAMIN-D IN NORMOCALCEMIC PATIENTS WITH SARCOIDOSIS

Ca absorption is regulated by 1,25(OH)2D, and serum values vary invers ely with Ca intake. In sarcoidosis, 1,25(OH)2D is produced by alveolar macrophages in response to gamma-interferon, and patients may develop hypercalcemia after prolonged exposure to sunlight and increased derm al production of vitamin D3. To determine if increased Ca intake suppr esses serum 1,25(OH)2D in normocalcemic patients and to identify those at risk, 17 normal subjects and 11 patients were studied on a metabol ic ward for two and one-half days while receiving first 400 and then 1 ,000 mg/d of Ca. On the low Ca intake, serum angiotensin-converting en zyme (ACE), an index of disease activity, was higher in only three of the patients than in the controls, mean serum 1,25(OH)2D was higher in the patients, and mean serum total Ca, serum Ca++, and urinary Ca wer e not different in the two groups. On the higher Ca intake, mean urina ry Ca increased in both groups, but mean serum 1,25(OH)2D was suppress ed only in the normal subjects. Thus, 1,25(OH)2D production is abnorma lly regulated, indicating that (a) normocalcemic patients with sarcoid osis are at risk for developing abnormal Ca metabolism, and (b) a bett er index of disease activity is provided by the oral Ca suppression te st than by serum ACE.