Increased calcium intake does not suppress circulating 1,25-dihydroxyvitamin D in normocalcemic patients with sarcoidosis.

Abstract

Ca absorption is regulated by 1,25(OH)2D, and serum values vary inversely with Ca intake. In sarcoidosis, 1,25(OH)2D is produced by alveolar macrophages in response to y-interferon, and patients may develop hypercalcemia after prolonged exposure to sunlight and increased dermal production of vitamin D3. To determine if increased Ca intake suppresses serum 1,25(OH)2D in normocalcemic patients and to identify those at risk, 17 normal subjects and 11 patients were studied on a metabolic 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 enzyme (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 were not different in the two groups. On the higher Ca intake, mean urinary Ca increased in both groups, but mean serum 1,25(OH)2D was suppressed only in the normal subjects. Thus, 1,25(OH)2D production is abnormally regulated, indicating that (a) normocalcemic patients with sarcoidosis are at risk for developing abnormal Ca metabolism, and (b) a better index of disease activity is provided by the oral Ca suppression test than by serum ACE. (J. Clin. Invest. 1993. 91:1396-1398

Effects of Mineral Composition of Drinking Water on Risk for Stone Formation and Bone Metabolism in Idiopathic Calcium Nephrolithiasis

“…Two factors explain this finding: first, only a fraction of the supplementary calcium supplied with drinking water appeared in the urine; second, these modest increases in calcium excretion were associated with corresponding decreases in oxalate excretion. Concerning the first point, in this study [24], and inverse relationships between calcium intake and calcitriol exist [25]. In this study, calcitriol levels decreased when the supplementary calcium of drinking water was added to a low-calcium diet, and this decrease may have played some part in the reduction of the fractional absorption and urinary excretion of calcium at higher calcium intakes.…”

Extrarenal 1α-Hydroxylase

“…First, hypercalcemic patients with sarcoidosis possess a frankly high or inappropriately elevated serum 1,25 (OH) 2 D concentration, although their serum PTH level is suppressed and their serum phosphate concentration is relatively elevated [21,22]. If 1,25(OH) 2 D synthesis were under the regulation of PTH, phosphate, and 1,25 (OH) 2 D itself, then 1,25(OH) 2 D concentrations in such patients should be low.…”

Ionized calcium and 1,25-dihydroxyvitamin D concentration in serum of patients with sarcoidosis

“…This extrarenal production of 1,25(OH) 2 D 3 , although not as tightly regulated as in the kidneys, occurs in a substrate-dependent manner [2,5]. A portion of extrarenally produced 1,25(OH) 2 D 3 , taken into systemic blood circulation, probably causes an excess of calcium transport at the small intestine and, at the same time, an excess of bone resorption, which is thought to bring on an imbalance of calcium, hypercalcaemia or hypercalciuria, in patients with sarcoidosis [6][7][8][9][10][11].…”