Mild hyperparathyroidism: a novel surgically correctable feature of primary aldosteronism
BACKGROUND:The parathyroid hormone (PTH) stimulates aldosterone secretion and cell proliferation in human adrenocortical cells; moreover, in rats hyperaldosteronism was associated with hyperparathyroidism. Hence, PTH could drive aldosterone excess in human primary aldosteronism. METHOD:To test this...
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| Veröffentlicht in: | Journal of hypertension 2012-02, Vol.30 (2), p.390-395 |
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| container_title | Journal of hypertension |
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| creator | Maniero, Carmela Fassina, Ambrogio Seccia, Teresa M Toniato, Antonio Iacobone, Maurizio Plebani, Mario De Caro, Raffaele Calò, Lorenzo A Pessina, Achille C Rossi, Gian P |
| description | BACKGROUND:The parathyroid hormone (PTH) stimulates aldosterone secretion and cell proliferation in human adrenocortical cells; moreover, in rats hyperaldosteronism was associated with hyperparathyroidism. Hence, PTH could drive aldosterone excess in human primary aldosteronism.
METHOD:To test this hypothesis, we recruited 105 consecutive hypertensive patients, of whom 44 had primary aldosteronism due to an aldosterone-producing adenoma (APA) and 61 had primary (essential) hypertension. We measured the plasma levels of (1-84)-PTH, 25(OH)D, 1,25(OH)2D, and serum Ca (total and ionized), inorganic P, Mg, K, and the 24-h urinary excretion of Ca, P, and deoxypyridinoline. In primary aldosteronism patients, these measurements were repeated after adrenalectomy or mineralocorticoid receptor blockade. We also sought for PTH receptor (PTHR-1) mRNA and protein in APA tissue.
RESULTS:Compared with primary (essential) hypertension patients, those with primary aldosteronism showed significantly higher plasma PTH (+31%), despite comparable urinary Ca excretion and similarly deficient 25(OH) vitamin D levels. In APA patients, who showed the PTHR-1 transcript and protein in tumor tissue, adrenalectomy normalized PTH levels (from 118 ± 13 to 76 ± 12 ng/l; P = 0.002) and increased ionized Ca(from 1.17 ± 0.04 to 1.22 ± 0.03 mmol/l; P |
| doi_str_mv | 10.1097/HJH.0b013e32834f0451 |
| format | Article |
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METHOD:To test this hypothesis, we recruited 105 consecutive hypertensive patients, of whom 44 had primary aldosteronism due to an aldosterone-producing adenoma (APA) and 61 had primary (essential) hypertension. We measured the plasma levels of (1-84)-PTH, 25(OH)D, 1,25(OH)2D, and serum Ca (total and ionized), inorganic P, Mg, K, and the 24-h urinary excretion of Ca, P, and deoxypyridinoline. In primary aldosteronism patients, these measurements were repeated after adrenalectomy or mineralocorticoid receptor blockade. We also sought for PTH receptor (PTHR-1) mRNA and protein in APA tissue.
RESULTS:Compared with primary (essential) hypertension patients, those with primary aldosteronism showed significantly higher plasma PTH (+31%), despite comparable urinary Ca excretion and similarly deficient 25(OH) vitamin D levels. In APA patients, who showed the PTHR-1 transcript and protein in tumor tissue, adrenalectomy normalized PTH levels (from 118 ± 13 to 76 ± 12 ng/l; P = 0.002) and increased ionized Ca(from 1.17 ± 0.04 to 1.22 ± 0.03 mmol/l; P < 0.001). The slope of the inverse PTH/ionized Ca relationship was steeper in primary aldosteronism than in primary (essential) hypertension, but normalized after adrenalectomy.
CONCLUSION:Hence, in primary aldosteronism an increased sensitivity of parathyroid cells to Ca lowering leads to an increase of PTH. This subtle hyperparathyroidism by acting on PTHR-1 in APA might contribute to maintaining hyperaldosteronism despite suppression of angiotensin II formation.</description><identifier>ISSN: 0263-6352</identifier><identifier>EISSN: 1473-5598</identifier><identifier>DOI: 10.1097/HJH.0b013e32834f0451</identifier><identifier>PMID: 22179087</identifier><language>eng</language><publisher>England: Lippincott Williams & Wilkins, Inc</publisher><subject>Adrenalectomy ; Adult ; Blood Pressure ; Calcium - metabolism ; Female ; Humans ; Hyperaldosteronism - complications ; Hyperparathyroidism - etiology ; Hyperparathyroidism - surgery ; Male ; Middle Aged ; Parathyroid Hormone - blood</subject><ispartof>Journal of hypertension, 2012-02, Vol.30 (2), p.390-395</ispartof><rights>2012 Lippincott Williams & Wilkins, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3511-bd938c1e06ff0a94e0e446a138f41dd99954298fb0cf28097e8cfced5f4081963</citedby><cites>FETCH-LOGICAL-c3511-bd938c1e06ff0a94e0e446a138f41dd99954298fb0cf28097e8cfced5f4081963</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22179087$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Maniero, Carmela</creatorcontrib><creatorcontrib>Fassina, Ambrogio</creatorcontrib><creatorcontrib>Seccia, Teresa M</creatorcontrib><creatorcontrib>Toniato, Antonio</creatorcontrib><creatorcontrib>Iacobone, Maurizio</creatorcontrib><creatorcontrib>Plebani, Mario</creatorcontrib><creatorcontrib>De Caro, Raffaele</creatorcontrib><creatorcontrib>Calò, Lorenzo A</creatorcontrib><creatorcontrib>Pessina, Achille C</creatorcontrib><creatorcontrib>Rossi, Gian P</creatorcontrib><title>Mild hyperparathyroidism: a novel surgically correctable feature of primary aldosteronism</title><title>Journal of hypertension</title><addtitle>J Hypertens</addtitle><description>BACKGROUND:The parathyroid hormone (PTH) stimulates aldosterone secretion and cell proliferation in human adrenocortical cells; moreover, in rats hyperaldosteronism was associated with hyperparathyroidism. Hence, PTH could drive aldosterone excess in human primary aldosteronism.
METHOD:To test this hypothesis, we recruited 105 consecutive hypertensive patients, of whom 44 had primary aldosteronism due to an aldosterone-producing adenoma (APA) and 61 had primary (essential) hypertension. We measured the plasma levels of (1-84)-PTH, 25(OH)D, 1,25(OH)2D, and serum Ca (total and ionized), inorganic P, Mg, K, and the 24-h urinary excretion of Ca, P, and deoxypyridinoline. In primary aldosteronism patients, these measurements were repeated after adrenalectomy or mineralocorticoid receptor blockade. We also sought for PTH receptor (PTHR-1) mRNA and protein in APA tissue.
RESULTS:Compared with primary (essential) hypertension patients, those with primary aldosteronism showed significantly higher plasma PTH (+31%), despite comparable urinary Ca excretion and similarly deficient 25(OH) vitamin D levels. In APA patients, who showed the PTHR-1 transcript and protein in tumor tissue, adrenalectomy normalized PTH levels (from 118 ± 13 to 76 ± 12 ng/l; P = 0.002) and increased ionized Ca(from 1.17 ± 0.04 to 1.22 ± 0.03 mmol/l; P < 0.001). The slope of the inverse PTH/ionized Ca relationship was steeper in primary aldosteronism than in primary (essential) hypertension, but normalized after adrenalectomy.
CONCLUSION:Hence, in primary aldosteronism an increased sensitivity of parathyroid cells to Ca lowering leads to an increase of PTH. This subtle hyperparathyroidism by acting on PTHR-1 in APA might contribute to maintaining hyperaldosteronism despite suppression of angiotensin II formation.</description><subject>Adrenalectomy</subject><subject>Adult</subject><subject>Blood Pressure</subject><subject>Calcium - metabolism</subject><subject>Female</subject><subject>Humans</subject><subject>Hyperaldosteronism - complications</subject><subject>Hyperparathyroidism - etiology</subject><subject>Hyperparathyroidism - surgery</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Parathyroid Hormone - blood</subject><issn>0263-6352</issn><issn>1473-5598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkE1PGzEQhq2qqAkf_6CqfOtpw_hjd21uCAEBUXFpDz1ZXu-42daJg71LlH9fI1KQehiNRpr3nXkfQj4zWDDQ7fnyfrmADphAwZWQHmTNPpA5k62o6lqrj2QOvBFVI2o-I8c5_wYApVvxicw4Z60G1c7Jz29D6Olqv8W0tcmOq32KQz_k9QW1dBOfMdA8pV-DsyHsqYspoRttF5B6tOOUkEZPt2lY27SnNvQxj5jiphickiNvQ8azQz8hP26uv18tq4fH27ury4fKiZqxquu1UI4hNN6D1RIBpWwsE8pL1vda61pyrXwHznNVgqNy3mFfewmK6UackK-vvtsUnybMo1kP2WEIdoNxykazptENr6FsytdNl2LOCb05PG4YmBempjA1_zMtsi-HA1O3xv5N9A_iu-8uhpI-_wnTDpNZoQ3jyhTqIFXLKw6MAy9TVYoz8RfnG4Qf</recordid><startdate>201202</startdate><enddate>201202</enddate><creator>Maniero, Carmela</creator><creator>Fassina, Ambrogio</creator><creator>Seccia, Teresa M</creator><creator>Toniato, Antonio</creator><creator>Iacobone, Maurizio</creator><creator>Plebani, Mario</creator><creator>De Caro, Raffaele</creator><creator>Calò, Lorenzo A</creator><creator>Pessina, Achille C</creator><creator>Rossi, Gian P</creator><general>Lippincott Williams & Wilkins, Inc</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>7X8</scope></search><sort><creationdate>201202</creationdate><title>Mild hyperparathyroidism: a novel surgically correctable feature of primary aldosteronism</title><author>Maniero, Carmela ; Fassina, Ambrogio ; Seccia, Teresa M ; Toniato, Antonio ; Iacobone, Maurizio ; Plebani, Mario ; De Caro, Raffaele ; Calò, Lorenzo A ; Pessina, Achille C ; Rossi, Gian P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3511-bd938c1e06ff0a94e0e446a138f41dd99954298fb0cf28097e8cfced5f4081963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adrenalectomy</topic><topic>Adult</topic><topic>Blood Pressure</topic><topic>Calcium - metabolism</topic><topic>Female</topic><topic>Humans</topic><topic>Hyperaldosteronism - complications</topic><topic>Hyperparathyroidism - etiology</topic><topic>Hyperparathyroidism - surgery</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Parathyroid Hormone - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Maniero, Carmela</creatorcontrib><creatorcontrib>Fassina, Ambrogio</creatorcontrib><creatorcontrib>Seccia, Teresa M</creatorcontrib><creatorcontrib>Toniato, Antonio</creatorcontrib><creatorcontrib>Iacobone, Maurizio</creatorcontrib><creatorcontrib>Plebani, Mario</creatorcontrib><creatorcontrib>De Caro, Raffaele</creatorcontrib><creatorcontrib>Calò, Lorenzo A</creatorcontrib><creatorcontrib>Pessina, Achille C</creatorcontrib><creatorcontrib>Rossi, Gian P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Maniero, Carmela</au><au>Fassina, Ambrogio</au><au>Seccia, Teresa M</au><au>Toniato, Antonio</au><au>Iacobone, Maurizio</au><au>Plebani, Mario</au><au>De Caro, Raffaele</au><au>Calò, Lorenzo A</au><au>Pessina, Achille C</au><au>Rossi, Gian P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mild hyperparathyroidism: a novel surgically correctable feature of primary aldosteronism</atitle><jtitle>Journal of hypertension</jtitle><addtitle>J Hypertens</addtitle><date>2012-02</date><risdate>2012</risdate><volume>30</volume><issue>2</issue><spage>390</spage><epage>395</epage><pages>390-395</pages><issn>0263-6352</issn><eissn>1473-5598</eissn><abstract>BACKGROUND:The parathyroid hormone (PTH) stimulates aldosterone secretion and cell proliferation in human adrenocortical cells; moreover, in rats hyperaldosteronism was associated with hyperparathyroidism. Hence, PTH could drive aldosterone excess in human primary aldosteronism.
METHOD:To test this hypothesis, we recruited 105 consecutive hypertensive patients, of whom 44 had primary aldosteronism due to an aldosterone-producing adenoma (APA) and 61 had primary (essential) hypertension. We measured the plasma levels of (1-84)-PTH, 25(OH)D, 1,25(OH)2D, and serum Ca (total and ionized), inorganic P, Mg, K, and the 24-h urinary excretion of Ca, P, and deoxypyridinoline. In primary aldosteronism patients, these measurements were repeated after adrenalectomy or mineralocorticoid receptor blockade. We also sought for PTH receptor (PTHR-1) mRNA and protein in APA tissue.
RESULTS:Compared with primary (essential) hypertension patients, those with primary aldosteronism showed significantly higher plasma PTH (+31%), despite comparable urinary Ca excretion and similarly deficient 25(OH) vitamin D levels. In APA patients, who showed the PTHR-1 transcript and protein in tumor tissue, adrenalectomy normalized PTH levels (from 118 ± 13 to 76 ± 12 ng/l; P = 0.002) and increased ionized Ca(from 1.17 ± 0.04 to 1.22 ± 0.03 mmol/l; P < 0.001). The slope of the inverse PTH/ionized Ca relationship was steeper in primary aldosteronism than in primary (essential) hypertension, but normalized after adrenalectomy.
CONCLUSION:Hence, in primary aldosteronism an increased sensitivity of parathyroid cells to Ca lowering leads to an increase of PTH. This subtle hyperparathyroidism by acting on PTHR-1 in APA might contribute to maintaining hyperaldosteronism despite suppression of angiotensin II formation.</abstract><cop>England</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>22179087</pmid><doi>10.1097/HJH.0b013e32834f0451</doi><tpages>6</tpages></addata></record> |
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| source | MEDLINE; Journals@Ovid Complete |
| subjects | Adrenalectomy Adult Blood Pressure Calcium - metabolism Female Humans Hyperaldosteronism - complications Hyperparathyroidism - etiology Hyperparathyroidism - surgery Male Middle Aged Parathyroid Hormone - blood |
| title | Mild hyperparathyroidism: a novel surgically correctable feature of primary aldosteronism |
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