{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,6]],"date-time":"2026-04-06T16:32:40Z","timestamp":1775493160551,"version":"3.50.1"},"reference-count":36,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2004,6]]},"abstract":"<jats:p> Adult growth hormone deficiency (AGHD) is associated with osteoporosis. Previous reports have suggested that alterations in parathyroid gland responsiveness to changes in calcium concentration may play a role in the genesis of osteoporosis in untreated AGHD patients. We investigated the endogenous parathyroid hormone [PTH-(1\u201384)] response to hypocalcemic and hypercalcemic stimuli induced by sodium EDTA and calcium gluconate infusion, respectively, and to PTH-(1\u201334) infusion in AGHD patients before and during GH replacement (GHR). We have demonstrated that the maximum PTH-(1\u201384) stimulation and suppression occurred at significantly higher calcium concentrations and in response to smaller changes in calcium concentrations after GHR. The calcemic response to the effects of PTH-(1\u201334) infusion significantly increased after GHR. The calcium set point (the calcium concentration at which the rate of PTH secretion is one-half of its maximal value) significantly increased in all groups after 3 mo on GHR, and it increased further at 12 mo. Our results suggest increased parathyroid gland sensitivity to smaller changes in serum calcium and increased end-organ sensitivity to the effects of PTH in AGHD patients after GHR. These findings may help us to understand the mechanisms underlying the genesis of osteoporosis in AGHD patients. <\/jats:p>","DOI":"10.1152\/ajpendo.00325.2003","type":"journal-article","created":{"date-parts":[[2004,5,12]],"date-time":"2004-05-12T17:23:36Z","timestamp":1084382616000},"page":"E986-E993","source":"Crossref","is-referenced-by-count":14,"title":["Parathyroid responsiveness to hypocalcemic and hypercalcemic stimuli in adult growth hormone deficiency after growth hormone replacement"],"prefix":"10.1152","volume":"286","author":[{"given":"Aftab M.","family":"Ahmad","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marion T.","family":"Hopkins","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joegi","family":"Thomas","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brian H.","family":"Durham","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William D.","family":"Fraser","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jiten P.","family":"Vora","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.7.2732"},{"key":"R2","doi-asserted-by":"publisher","DOI":"10.1016\/S8756-3282(02)00952-3"},{"key":"R3","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2265.2001.01275.x"},{"key":"R4","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2002-021787"},{"key":"R5","unstructured":"Anonymous. 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