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Responses of Urinary N-Telopeptide and Renal Calcium Handling to PTH Infusion after Treatment with Estrogen, Raloxifene, and Tamoxifen
This prospective, randomized, placebo-controlled study investigated whether estrogen, tamoxifen, and raloxifene protect the skeleton from the acute catabolic effects of continuous PTH(1–34) infusion. It was infused over 24 h in 25 postmenopausal women both before and while on medication for 16–20 we...
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Published in: | Calcified tissue international 2012-04, Vol.90 (4), p.263-271 |
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description | This prospective, randomized, placebo-controlled study investigated whether estrogen, tamoxifen, and raloxifene protect the skeleton from the acute catabolic effects of continuous PTH(1–34) infusion. It was infused over 24 h in 25 postmenopausal women both before and while on medication for 16–20 weeks (estrogen
n
= 7, raloxifene
n
= 5, tamoxifen
n
= 7, placebo
n
= 6). Blood and urine samples were collected at baseline and every 4 h during the PTH(1–34) infusion and analyzed for calcium homeostasis, bone remodeling, and specific cytokines. Data for the premedication PTH(1–34) infusions were pooled. During the premedication PTH(1–34) infusions, serum calcium and urine phosphorus increased, while serum phosphorus and urine calcium declined. Osteocalcin decreased (mean 18%), while urine NTX increased (mean 315%). Serum IL-6 increased 260%, but there were no other cytokine changes as a result of the PTH(1–34) infusion. On medication, the mean peak change in NTX with PTH(1–34) infusion was less (77, 59, and 31 nM/mM with raloxifene, tamoxifen, and estrogen, respectively). The reduction in urine calcium excretion was prolonged with each agent but only significantly with estrogen. There was no reduction in the IL-6 elevation induced by PTH(1–34) with any medication. The differential skeletal resorption response to PTH(1–34) infusion after the treatments may reflect different potencies of these agents or variability in interaction with the estrogen receptor. Renal calcium conservation and the blunted response of bone resorption to PTH(1–34) infusion may be mechanisms by which estrogen and estrogen agonist/antagonist agents preserve bone mass. |
doi_str_mv | 10.1007/s00223-012-9572-y |
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= 7, placebo
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= 6). Blood and urine samples were collected at baseline and every 4 h during the PTH(1–34) infusion and analyzed for calcium homeostasis, bone remodeling, and specific cytokines. Data for the premedication PTH(1–34) infusions were pooled. During the premedication PTH(1–34) infusions, serum calcium and urine phosphorus increased, while serum phosphorus and urine calcium declined. Osteocalcin decreased (mean 18%), while urine NTX increased (mean 315%). Serum IL-6 increased 260%, but there were no other cytokine changes as a result of the PTH(1–34) infusion. On medication, the mean peak change in NTX with PTH(1–34) infusion was less (77, 59, and 31 nM/mM with raloxifene, tamoxifen, and estrogen, respectively). The reduction in urine calcium excretion was prolonged with each agent but only significantly with estrogen. There was no reduction in the IL-6 elevation induced by PTH(1–34) with any medication. The differential skeletal resorption response to PTH(1–34) infusion after the treatments may reflect different potencies of these agents or variability in interaction with the estrogen receptor. Renal calcium conservation and the blunted response of bone resorption to PTH(1–34) infusion may be mechanisms by which estrogen and estrogen agonist/antagonist agents preserve bone mass.</description><identifier>ISSN: 0171-967X</identifier><identifier>EISSN: 1432-0827</identifier><identifier>DOI: 10.1007/s00223-012-9572-y</identifier><identifier>PMID: 22311517</identifier><language>eng</language><publisher>New York: Springer-Verlag</publisher><subject>Biochemistry ; Biomedical and Life Sciences ; Calcium - metabolism ; Cell Biology ; Chemotherapy ; Collagen Type I - urine ; Endocrinology ; Estrogens ; Estrogens - therapeutic use ; Female ; Humans ; Interleukin-6 - metabolism ; Kidney - metabolism ; Life Sciences ; Middle Aged ; Original Research ; Orthopedics ; Parathyroid Hormone - administration & dosage ; Peptides ; Peptides - urine ; Prospective Studies ; Raloxifene Hydrochloride - therapeutic use ; Tamoxifen - therapeutic use ; Urine</subject><ispartof>Calcified tissue international, 2012-04, Vol.90 (4), p.263-271</ispartof><rights>Springer Science+Business Media, LLC 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c403t-2dc7f16d5369f74401e2c7c9385ef3f52188766d512113a79159baf46cad21173</citedby><cites>FETCH-LOGICAL-c403t-2dc7f16d5369f74401e2c7c9385ef3f52188766d512113a79159baf46cad21173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22311517$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kulak, Carolina A. M.</creatorcontrib><creatorcontrib>Baz-Hecht, Merav</creatorcontrib><creatorcontrib>Nieves, Jeri</creatorcontrib><creatorcontrib>Shen, Victor</creatorcontrib><creatorcontrib>Lindsay, Robert</creatorcontrib><creatorcontrib>Cosman, Felicia</creatorcontrib><title>Responses of Urinary N-Telopeptide and Renal Calcium Handling to PTH Infusion after Treatment with Estrogen, Raloxifene, and Tamoxifen</title><title>Calcified tissue international</title><addtitle>Calcif Tissue Int</addtitle><addtitle>Calcif Tissue Int</addtitle><description>This prospective, randomized, placebo-controlled study investigated whether estrogen, tamoxifen, and raloxifene protect the skeleton from the acute catabolic effects of continuous PTH(1–34) infusion. It was infused over 24 h in 25 postmenopausal women both before and while on medication for 16–20 weeks (estrogen
n
= 7, raloxifene
n
= 5, tamoxifen
n
= 7, placebo
n
= 6). Blood and urine samples were collected at baseline and every 4 h during the PTH(1–34) infusion and analyzed for calcium homeostasis, bone remodeling, and specific cytokines. Data for the premedication PTH(1–34) infusions were pooled. During the premedication PTH(1–34) infusions, serum calcium and urine phosphorus increased, while serum phosphorus and urine calcium declined. Osteocalcin decreased (mean 18%), while urine NTX increased (mean 315%). Serum IL-6 increased 260%, but there were no other cytokine changes as a result of the PTH(1–34) infusion. On medication, the mean peak change in NTX with PTH(1–34) infusion was less (77, 59, and 31 nM/mM with raloxifene, tamoxifen, and estrogen, respectively). The reduction in urine calcium excretion was prolonged with each agent but only significantly with estrogen. There was no reduction in the IL-6 elevation induced by PTH(1–34) with any medication. The differential skeletal resorption response to PTH(1–34) infusion after the treatments may reflect different potencies of these agents or variability in interaction with the estrogen receptor. Renal calcium conservation and the blunted response of bone resorption to PTH(1–34) infusion may be mechanisms by which estrogen and estrogen agonist/antagonist agents preserve bone mass.</description><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Calcium - metabolism</subject><subject>Cell Biology</subject><subject>Chemotherapy</subject><subject>Collagen Type I - urine</subject><subject>Endocrinology</subject><subject>Estrogens</subject><subject>Estrogens - therapeutic use</subject><subject>Female</subject><subject>Humans</subject><subject>Interleukin-6 - metabolism</subject><subject>Kidney - metabolism</subject><subject>Life Sciences</subject><subject>Middle Aged</subject><subject>Original Research</subject><subject>Orthopedics</subject><subject>Parathyroid Hormone - administration & dosage</subject><subject>Peptides</subject><subject>Peptides - urine</subject><subject>Prospective Studies</subject><subject>Raloxifene Hydrochloride - therapeutic use</subject><subject>Tamoxifen - therapeutic use</subject><subject>Urine</subject><issn>0171-967X</issn><issn>1432-0827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNp9kc9u1DAQhy0EokvhAbggiws91OBx_jg-VquWrVS1aJVK3CI3GS-pEjvYjui-QJ8btykgIcHJ8sw330jzI-Qt8I_AufwUOBciYxwEU4UUbP-MrCDPBOOVkM_JioMEpkr59YC8CuGWc8jLsnxJDtIUQAFyRe63GCZnAwbqDL32vdV-Ty9ZjYObcIp9h1Tbjm7R6oGu9dD280g3qTT0dkejo1_qDT23Zg69s1SbiJ7WHnUc0Ub6o4_f6GmI3u3QHtOtHtxdb9Di8aO11uPyf01eGD0EfPP0HpLrs9N6vWEXV5_P1ycXrM15FpnoWmmg7IqsVEbmOQcUrWxVVhVoMlMIqCpZpj4IgExLBYW60SYvW92liswOyYfFO3n3fcYQm7EPLQ6Dtujm0CihCp5nSiTy6L9kCqCqcq4KSOj7v9BbN_t0r0cfF0pUKkGwQK13IXg0zeT7MR07mR5kslnSbFKazUOazT7NvHsSzzcjdr8nfsWXALEAIbXsDv2fzf-2_gRw-anV</recordid><startdate>20120401</startdate><enddate>20120401</enddate><creator>Kulak, Carolina A. M.</creator><creator>Baz-Hecht, Merav</creator><creator>Nieves, Jeri</creator><creator>Shen, Victor</creator><creator>Lindsay, Robert</creator><creator>Cosman, Felicia</creator><general>Springer-Verlag</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20120401</creationdate><title>Responses of Urinary N-Telopeptide and Renal Calcium Handling to PTH Infusion after Treatment with Estrogen, Raloxifene, and Tamoxifen</title><author>Kulak, Carolina A. M. ; Baz-Hecht, Merav ; Nieves, Jeri ; Shen, Victor ; Lindsay, Robert ; Cosman, Felicia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c403t-2dc7f16d5369f74401e2c7c9385ef3f52188766d512113a79159baf46cad21173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Calcium - metabolism</topic><topic>Cell Biology</topic><topic>Chemotherapy</topic><topic>Collagen Type I - urine</topic><topic>Endocrinology</topic><topic>Estrogens</topic><topic>Estrogens - therapeutic use</topic><topic>Female</topic><topic>Humans</topic><topic>Interleukin-6 - metabolism</topic><topic>Kidney - metabolism</topic><topic>Life Sciences</topic><topic>Middle Aged</topic><topic>Original Research</topic><topic>Orthopedics</topic><topic>Parathyroid Hormone - administration & dosage</topic><topic>Peptides</topic><topic>Peptides - urine</topic><topic>Prospective Studies</topic><topic>Raloxifene Hydrochloride - therapeutic use</topic><topic>Tamoxifen - therapeutic use</topic><topic>Urine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kulak, Carolina A. M.</creatorcontrib><creatorcontrib>Baz-Hecht, Merav</creatorcontrib><creatorcontrib>Nieves, Jeri</creatorcontrib><creatorcontrib>Shen, Victor</creatorcontrib><creatorcontrib>Lindsay, Robert</creatorcontrib><creatorcontrib>Cosman, Felicia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Nursing & Allied Health Database</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Calcified tissue international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kulak, Carolina A. M.</au><au>Baz-Hecht, Merav</au><au>Nieves, Jeri</au><au>Shen, Victor</au><au>Lindsay, Robert</au><au>Cosman, Felicia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Responses of Urinary N-Telopeptide and Renal Calcium Handling to PTH Infusion after Treatment with Estrogen, Raloxifene, and Tamoxifen</atitle><jtitle>Calcified tissue international</jtitle><stitle>Calcif Tissue Int</stitle><addtitle>Calcif Tissue Int</addtitle><date>2012-04-01</date><risdate>2012</risdate><volume>90</volume><issue>4</issue><spage>263</spage><epage>271</epage><pages>263-271</pages><issn>0171-967X</issn><eissn>1432-0827</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><notes>ObjectType-Article-2</notes><notes>ObjectType-News-1</notes><notes>ObjectType-Feature-3</notes><abstract>This prospective, randomized, placebo-controlled study investigated whether estrogen, tamoxifen, and raloxifene protect the skeleton from the acute catabolic effects of continuous PTH(1–34) infusion. It was infused over 24 h in 25 postmenopausal women both before and while on medication for 16–20 weeks (estrogen
n
= 7, raloxifene
n
= 5, tamoxifen
n
= 7, placebo
n
= 6). Blood and urine samples were collected at baseline and every 4 h during the PTH(1–34) infusion and analyzed for calcium homeostasis, bone remodeling, and specific cytokines. Data for the premedication PTH(1–34) infusions were pooled. During the premedication PTH(1–34) infusions, serum calcium and urine phosphorus increased, while serum phosphorus and urine calcium declined. Osteocalcin decreased (mean 18%), while urine NTX increased (mean 315%). Serum IL-6 increased 260%, but there were no other cytokine changes as a result of the PTH(1–34) infusion. On medication, the mean peak change in NTX with PTH(1–34) infusion was less (77, 59, and 31 nM/mM with raloxifene, tamoxifen, and estrogen, respectively). The reduction in urine calcium excretion was prolonged with each agent but only significantly with estrogen. There was no reduction in the IL-6 elevation induced by PTH(1–34) with any medication. The differential skeletal resorption response to PTH(1–34) infusion after the treatments may reflect different potencies of these agents or variability in interaction with the estrogen receptor. Renal calcium conservation and the blunted response of bone resorption to PTH(1–34) infusion may be mechanisms by which estrogen and estrogen agonist/antagonist agents preserve bone mass.</abstract><cop>New York</cop><pub>Springer-Verlag</pub><pmid>22311517</pmid><doi>10.1007/s00223-012-9572-y</doi><tpages>9</tpages></addata></record> |
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subjects | Biochemistry Biomedical and Life Sciences Calcium - metabolism Cell Biology Chemotherapy Collagen Type I - urine Endocrinology Estrogens Estrogens - therapeutic use Female Humans Interleukin-6 - metabolism Kidney - metabolism Life Sciences Middle Aged Original Research Orthopedics Parathyroid Hormone - administration & dosage Peptides Peptides - urine Prospective Studies Raloxifene Hydrochloride - therapeutic use Tamoxifen - therapeutic use Urine |
title | Responses of Urinary N-Telopeptide and Renal Calcium Handling to PTH Infusion after Treatment with Estrogen, Raloxifene, and Tamoxifen |
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