Neuroendocrine responses to levodopa in multiple system atrophy (MSA)

Hypothalamic dopaminergic pathways are involved in the regulation of growth hormone and prolactin release from the anterior pituitary. Neuroendocrine studies in patients with multiple system atrophy (MSA), in whom there is a reported loss of hypothalamic dopamine, are few and contradictory. We there...

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Veröffentlicht in:Movement disorders 1999-11, Vol.14 (6), p.981-987
Hauptverfasser: Kimber, Jeffery, Watson, Laura, Mathias, Christopher J.
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Watson, Laura
Mathias, Christopher J.
description Hypothalamic dopaminergic pathways are involved in the regulation of growth hormone and prolactin release from the anterior pituitary. Neuroendocrine studies in patients with multiple system atrophy (MSA), in whom there is a reported loss of hypothalamic dopamine, are few and contradictory. We therefore studied the neuroendocrine responses to 250 mg levodopa (plus 25 mg carbidopa) in subjects with MSA (n = 15), and compared them with age‐ and sex‐matched healthy control subjects (n = 8). There were no significant differences in basal or post‐levodopa levels of growth hormone (GH), growth hormone‐releasing hormone (GHRH), glucose, insulin‐like growth factor (IGF‐1), or thyroid‐stimulating hormone (TSH) between the groups. In patients with MSA, basal levels of prolactin were elevated (21.1 ± 5.2 ng/mL [mean ± standard error]) compared with control subjects (12.1 ± 1.7, p
doi_str_mv 10.1002/1531-8257(199911)14:6<981::AID-MDS1011>3.0.CO;2-W
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In conclusion, in patients with MSA, the GHRH and GH responses to l‐dopa were preserved and were similar to responses in age‐matched control subjects. In contrast, there was impaired dopaminergic suppression of prolactin secretion. In patients with MSA this may represent a selective dysfunction, rather than generalized loss, of tubero‐infundibular dopaminergic neurones.</description><identifier>ISSN: 0885-3185</identifier><identifier>EISSN: 1531-8257</identifier><identifier>DOI: 10.1002/1531-8257(199911)14:6&lt;981::AID-MDS1011&gt;3.0.CO;2-W</identifier><identifier>PMID: 10584673</identifier><language>eng</language><publisher>New York: John Wiley &amp; Sons, Inc</publisher><subject>Adult ; Aged ; Antiparkinson Agents - administration &amp; dosage ; Antiparkinson Agents - adverse effects ; Biological and medical sciences ; Blood Glucose - metabolism ; Carbidopa ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. 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Disord</addtitle><description>Hypothalamic dopaminergic pathways are involved in the regulation of growth hormone and prolactin release from the anterior pituitary. Neuroendocrine studies in patients with multiple system atrophy (MSA), in whom there is a reported loss of hypothalamic dopamine, are few and contradictory. We therefore studied the neuroendocrine responses to 250 mg levodopa (plus 25 mg carbidopa) in subjects with MSA (n = 15), and compared them with age‐ and sex‐matched healthy control subjects (n = 8). There were no significant differences in basal or post‐levodopa levels of growth hormone (GH), growth hormone‐releasing hormone (GHRH), glucose, insulin‐like growth factor (IGF‐1), or thyroid‐stimulating hormone (TSH) between the groups. In patients with MSA, basal levels of prolactin were elevated (21.1 ± 5.2 ng/mL [mean ± standard error]) compared with control subjects (12.1 ± 1.7, p &lt;0.05), and after l‐dopa there was increased variability in prolactin response with less suppression compared with control subjects. In conclusion, in patients with MSA, the GHRH and GH responses to l‐dopa were preserved and were similar to responses in age‐matched control subjects. In contrast, there was impaired dopaminergic suppression of prolactin secretion. 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Prion diseases</subject><subject>Dopamine - physiology</subject><subject>Drug Combinations</subject><subject>Female</subject><subject>Growth Hormone-Releasing Hormone - blood</subject><subject>Human Growth Hormone - physiology</subject><subject>Humans</subject><subject>Hypothalamo-Hypophyseal System - drug effects</subject><subject>Hypothalamo-Hypophyseal System - physiopathology</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>Levodopa</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Multiple system atrophy</subject><subject>Multiple System Atrophy - drug therapy</subject><subject>Multiple System Atrophy - physiopathology</subject><subject>Neuroendocrine</subject><subject>Neurology</subject><subject>Reference Values</subject><subject>Thyrotropin - blood</subject><issn>0885-3185</issn><issn>1531-8257</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkV1v0zAUQC0EYmXwF1AeENoeUnzt-CMFIXXdOiZtq9CA8nblJo7ISOJgNxv996RKGDzwwpMl6_j4-piQFOgUKGVvQHCINRPqCNI0BTiGZCbfpRpms_nFaXx1egMU4D2f0uli9ZbF60dk8nDmMZlQrUXMQYsD8iyEW9rDAuRTcgBU6EQqPiFn17bzzja5y3zZ2Mjb0Lom2BBtXVTZO5e71kRlE9VdtS3bykZhF7a2jszWu_bbLjq6upkfPydPClMF-2JcD8nn5dmnxYf4cnV-sZhfxlkiFMSMFpJrqjjliirNZC5FusmYogXbaF4InipGGeOZZDotcprkJuOWpRllGyUEPySvB2_r3Y_Ohi3WZchsVZnGui4gA5BUg-zBjwOYeReCtwW2vqyN3yFQ3LfFfSfcd8KhLUKCEvu2iH1bHNsiR4qLFTJc986X4-Xdprb5X8YhZg-8GgETMlMV3jRZGf5woBOQ-0eMce7Lyu7-Y7B_z_V7q_fGg7fsP-jng9f479hPpwSur89xufyilif0K57wXz18rAI</recordid><startdate>199911</startdate><enddate>199911</enddate><creator>Kimber, Jeffery</creator><creator>Watson, Laura</creator><creator>Mathias, Christopher J.</creator><general>John Wiley &amp; Sons, Inc</general><general>Wiley</general><scope>BSCLL</scope><scope>IQODW</scope><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>7TK</scope></search><sort><creationdate>199911</creationdate><title>Neuroendocrine responses to levodopa in multiple system atrophy (MSA)</title><author>Kimber, Jeffery ; Watson, Laura ; Mathias, Christopher J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4571-20f63807303707826d659bc270f2b83f539720223c6289fd04dac3e29c02b7553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Antiparkinson Agents - administration &amp; dosage</topic><topic>Antiparkinson Agents - adverse effects</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - metabolism</topic><topic>Carbidopa</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Dopamine - physiology</topic><topic>Drug Combinations</topic><topic>Female</topic><topic>Growth Hormone-Releasing Hormone - blood</topic><topic>Human Growth Hormone - physiology</topic><topic>Humans</topic><topic>Hypothalamo-Hypophyseal System - drug effects</topic><topic>Hypothalamo-Hypophyseal System - physiopathology</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>Levodopa</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Multiple system atrophy</topic><topic>Multiple System Atrophy - drug therapy</topic><topic>Multiple System Atrophy - physiopathology</topic><topic>Neuroendocrine</topic><topic>Neurology</topic><topic>Reference Values</topic><topic>Thyrotropin - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kimber, Jeffery</creatorcontrib><creatorcontrib>Watson, Laura</creatorcontrib><creatorcontrib>Mathias, Christopher J.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><jtitle>Movement disorders</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kimber, Jeffery</au><au>Watson, Laura</au><au>Mathias, Christopher J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroendocrine responses to levodopa in multiple system atrophy (MSA)</atitle><jtitle>Movement disorders</jtitle><addtitle>Mov. Disord</addtitle><date>1999-11</date><risdate>1999</risdate><volume>14</volume><issue>6</issue><spage>981</spage><epage>987</epage><pages>981-987</pages><issn>0885-3185</issn><eissn>1531-8257</eissn><abstract>Hypothalamic dopaminergic pathways are involved in the regulation of growth hormone and prolactin release from the anterior pituitary. Neuroendocrine studies in patients with multiple system atrophy (MSA), in whom there is a reported loss of hypothalamic dopamine, are few and contradictory. We therefore studied the neuroendocrine responses to 250 mg levodopa (plus 25 mg carbidopa) in subjects with MSA (n = 15), and compared them with age‐ and sex‐matched healthy control subjects (n = 8). There were no significant differences in basal or post‐levodopa levels of growth hormone (GH), growth hormone‐releasing hormone (GHRH), glucose, insulin‐like growth factor (IGF‐1), or thyroid‐stimulating hormone (TSH) between the groups. In patients with MSA, basal levels of prolactin were elevated (21.1 ± 5.2 ng/mL [mean ± standard error]) compared with control subjects (12.1 ± 1.7, p &lt;0.05), and after l‐dopa there was increased variability in prolactin response with less suppression compared with control subjects. In conclusion, in patients with MSA, the GHRH and GH responses to l‐dopa were preserved and were similar to responses in age‐matched control subjects. In contrast, there was impaired dopaminergic suppression of prolactin secretion. In patients with MSA this may represent a selective dysfunction, rather than generalized loss, of tubero‐infundibular dopaminergic neurones.</abstract><cop>New York</cop><pub>John Wiley &amp; Sons, Inc</pub><pmid>10584673</pmid><doi>10.1002/1531-8257(199911)14:6&lt;981::AID-MDS1011&gt;3.0.CO;2-W</doi><tpages>7</tpages></addata></record>
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source MEDLINE; Wiley Online Library Journals Frontfile Complete
subjects Adult
Aged
Antiparkinson Agents - administration & dosage
Antiparkinson Agents - adverse effects
Biological and medical sciences
Blood Glucose - metabolism
Carbidopa
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Dopamine - physiology
Drug Combinations
Female
Growth Hormone-Releasing Hormone - blood
Human Growth Hormone - physiology
Humans
Hypothalamo-Hypophyseal System - drug effects
Hypothalamo-Hypophyseal System - physiopathology
Insulin-Like Growth Factor I - metabolism
Levodopa
Male
Medical sciences
Middle Aged
Multiple system atrophy
Multiple System Atrophy - drug therapy
Multiple System Atrophy - physiopathology
Neuroendocrine
Neurology
Reference Values
Thyrotropin - blood
title Neuroendocrine responses to levodopa in multiple system atrophy (MSA)
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