{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T16:11:50Z","timestamp":1785773510322,"version":"3.56.0"},"reference-count":48,"publisher":"Oxford University Press (OUP)","issue":"5","content-domain":{"domain":["eje.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2011,5]]},"abstract":"<jats:sec><jats:title>Context<\/jats:title><jats:p>In healthy subjects and in patients with primary hyperparathyroidism (PH), the administration of a low dose of 25(OH)D (25\u200a\u03bcg\/day) increases the serum levels of both 25(OH)D and 1,25(OH)<jats:sub>2<\/jats:sub>D. It is unknown whether this relationship is present in patients affected by familial benign hypocalciuric hypercalcemia (FBH).<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective<\/jats:title><jats:p>To evaluate the different vitamin D substrate\u2013product relationship after oral vitamin D supplementation in familial benign hypercalcemia, PH, and healthy controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Design<\/jats:title><jats:p>We evaluated the main physiological regulators of 1\u03b1-hydroxylase and the substrate\u2013product relationship of 25(OH)D and 1,25(OH)<jats:sub>2<\/jats:sub>D in 20 patients with PH, 25 with FBH, and 122 healthy sex- and age-matched controls before and after administration of 25(OH)D for 2 weeks.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>25(OH)D increased significantly in all subjects, whereas 1,25(OH)<jats:sub>2<\/jats:sub>D serum levels increased significantly in PH patients and healthy controls but not in patients with FBH. Therefore, a significant positive substrate\u2013product relationship of 25(OH)D\u20131,25(OH)<jats:sub>2<\/jats:sub>D was found in PH and healthy controls, but not in FBH. Monomeric calcitonin (hCT-M) was significantly lower at baseline and after 25(OH)D supplementation in the FBH group compared with the other two groups.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The lack of 1,25(OH)<jats:sub>2<\/jats:sub>D increase in FBH may be due to a direct inhibitory effect on 1\u03b1-hydroxylase of hypercalcemia<jats:italic>per se<\/jats:italic>, increased metabolic clearance of 1,25(OH)<jats:sub>2<\/jats:sub>D, or a decreased stimulus of 1\u03b1-hydroxylase related to persistently low levels of hCT.<\/jats:p><\/jats:sec>","DOI":"10.1530\/eje-10-1053","type":"journal-article","created":{"date-parts":[[2011,2,11]],"date-time":"2011-02-11T03:39:24Z","timestamp":1297395564000},"page":"833-838","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":5,"title":["Different vitamin D substrate\u2013product relationship after oral vitamin D supplementation in familial benign 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