{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,11]],"date-time":"2025-10-11T13:14:24Z","timestamp":1760188464917},"reference-count":17,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2004,12,16]],"date-time":"2004-12-16T00:00:00Z","timestamp":1103155200000},"content-version":"vor","delay-in-days":15,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Ther Apher Dial"],"published-print":{"date-parts":[[2004,12]]},"abstract":"<jats:p><jats:bold>Abstract:\u2002<\/jats:bold> The dose\u2013response relationships and the safety of administering 22\u2010oxacalcitriol (OCT) to patients with secondary hyperparathyroidism (2HPT) under regular three\u2010times\u2010weekly hemodialysis (HD) were evaluated by double\u2010blind parallel group design. A total of 203 patients with 2HPT were randomly allocated into four groups, and 5\u2003\u00b5g (Group L), 10\u2003\u00b5g (Group M), or 15\u2003\u00b5g (Group H) OCT, or placebo (Group P) was administrated at the end of every HD for 12\u2003weeks. Reductions of intact\u2010parathyroid hormone (iPTH) concentration greater than\u200330% from baseline were observed in 7.7% of Group P as compared to 77.3% of the pooled OCT groups after 12\u2003weeks of treatment (Mantel test: <jats:italic>P<\/jats:italic>\u2003&lt;\u20030.001). Time\u2010trends (slopes) of log\u2010iPTH concentration calculated by least\u2010squares line fitting to each patient's data during treatment differed between Group P and the pooled OCT groups (<jats:italic>t<\/jats:italic>\u2010test: <jats:italic>P<\/jats:italic>\u2003&lt;\u20030.001) and these iPTH slopes decreased dose\u2010dependently (linear trend by <jats:italic>t<\/jats:italic>\u2010test: <jats:italic>P<\/jats:italic>\u2003&lt;\u20030.001). Slopes of serum calcium corrected for albumin (corrected\u2010sCa) concentrations also differed between Group P and the pooled OCT groups (<jats:italic>t<\/jats:italic>\u2010test: <jats:italic>P<\/jats:italic>\u2003&lt;\u20030.001), and increased dose\u2010dependently (linear trend by <jats:italic>t<\/jats:italic>\u2010test: <jats:italic>P<\/jats:italic>\u2003&lt;\u20030.0001). Serum phosphorus and Ca\u2003\u00d7\u2003P product increased significantly only in high dose groups. Slopes of log(iPTH) and corrected\u2010sCa concentrations were reciprocally related. Most adverse events were hypercalcemia and dose\u2010related, but occasionally comprised pruritus or increased serum creatinine phosphokinase. These results indicate that OCT produced a strong and dose\u2010dependent suppression of PTH and an increase of corrected\u2010sCa concentration in patients with 2HPT. The recommended initial dosages of OCT would appear to be 5\u2003\u00b5g when pretreatment iPTH concentrations are less than\u2003500\u2003pg\/mL, and 10\u2003\u00b5g when greater than\u2003500\u2003pg\/mL for safe and effective treatment. As in the case of PTH, calcium and phosphorus showed dose\u2010dependent increases. It is therefore essential to take precautions as to possible increases in calcium and phosphorus.<\/jats:p>","DOI":"10.1111\/j.1774-9987.2004.00191.x","type":"journal-article","created":{"date-parts":[[2004,12,16]],"date-time":"2004-12-16T10:00:08Z","timestamp":1103191208000},"page":"480-491","source":"Crossref","is-referenced-by-count":18,"title":["Dose\u2010response Study of 22\u2010Oxacalcitriol in Patients with Secondary Hyperparathyroidism"],"prefix":"10.1111","volume":"8","author":[{"given":"Tadao","family":"Akizawa","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yasuo","family":"Ohashi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takashi","family":"Akiba","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masashi","family":"Suzuki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoshiki","family":"Nishizawa","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Etsuro","family":"Ogata","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eduardo","family":"Slatopolsky","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kiyoshi","family":"Kurokawa","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2004,12,16]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111639"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1159\/000186210"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1210\/endo-128-4-1687"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1248\/cpb.34.4410"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1248\/cpb.40.1494"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(87)80550-1"},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.3177\/jnsv.36.21"},{"key":"e_1_2_6_9_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114229"},{"key":"e_1_2_6_10_2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1991.110"},{"key":"e_1_2_6_11_2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1993.280"},{"key":"e_1_2_6_12_2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.283"},{"key":"e_1_2_6_13_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1797.1998.tb00377.x"},{"key":"e_1_2_6_14_2","doi-asserted-by":"publisher","DOI":"10.1093\/ndt\/11.supp3.121"},{"key":"e_1_2_6_15_2","doi-asserted-by":"publisher","DOI":"10.1136\/bmj.4.5893.643"},{"key":"e_1_2_6_16_2","first-page":"129","volume-title":"Renal Osteodystrophy","author":"Slatopolsky E","year":"1998"},{"issue":"3","key":"e_1_2_6_17_2","first-page":"S1","article-title":"K\/DOQI clinical practice guideline for bone metabolism and disease in chronic kidney disease","volume":"42","author":"National Kidney Foundation.","year":"2003","journal-title":"Am J Kidney Dis"},{"key":"e_1_2_6_18_2","doi-asserted-by":"publisher","DOI":"10.1159\/000054729"}],"container-title":["Therapeutic Apheresis and Dialysis"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1111%2Fj.1774-9987.2004.00191.x","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1111\/j.1774-9987.2004.00191.x","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,14]],"date-time":"2023-10-14T15:35:57Z","timestamp":1697297757000},"score":1,"resource":{"primary":{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/j.1774-9987.2004.00191.x"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2004,12]]},"references-count":17,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2004,12]]}},"alternative-id":["10.1111\/j.1774-9987.2004.00191.x"],"URL":"https:\/\/doi.org\/10.1111\/j.1774-9987.2004.00191.x","archive":["Portico"],"relation":{},"ISSN":["1744-9979","1744-9987"],"issn-type":[{"value":"1744-9979","type":"print"},{"value":"1744-9987","type":"electronic"}],"subject":[],"published":{"date-parts":[[2004,12]]}}}