Cortisol, ACTH, and beta-endorphin after dexamethasone administration in Parkinson's dementia
Identifieur interne : 001402 ( Main/Corpus ); précédent : 001401; suivant : 001403Cortisol, ACTH, and beta-endorphin after dexamethasone administration in Parkinson's dementia
Auteurs : J. M. Rabey ; M. Scharf ; Z. Oberman ; M. Zohar ; E. GraffSource :
- Biological Psychiatry [ 0006-3223 ] ; 1988.
Abstract
The dexamethasone suppression test (DST) has been suggested as an effective tool for differentiating between depression and dementia. After administering 1 mg dexamethasone, we measured cortisol, ACTH, and beta-endorphin levels in 32 nondepressed patients with idiopathic Parkinson's disease (PD) (14 also with dementia) and 20 healthy, age-matched controls. Four of the 20 controls, 9 of the 18 with PD alone, and 8 of the 14 with PD and dementia were dexamethasone nonsuppressors (cortisol value ≥ 5 μg/100 ml). Plasma ACTH and beta-endorphin responded in a coupled way to dexamethasone challenge. Higher basal levels of both peptides were found among PD patients (demented and nondemented), nonresponders to DST. Thus, the DST does not appear to be effective in differentiating between depression and dementia in PD. In addition, PD nonsuppressors showed higher basal values of plasma ACTH, beta-endorphin, and cortisol (similar to patients with major depression). This suggests that although the depression is clinically undetectable, both disorders may share some pathophysiological features at the hypothalamic hypophyseal adrenal level.
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DOI: 10.1016/0006-3223(90)90525-7
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Rabey</name><affiliation><mods:affiliation>From the Department of Neurology and Clinical Chemistry, Tel-Aviv Medical Center, Sackler School of Medicine, Tel-Aviv University, Israel</mods:affiliation></affiliation></author><author><name sortKey="Scharf, M" sort="Scharf, M" uniqKey="Scharf M" first="M." last="Scharf">M. Scharf</name><affiliation><mods:affiliation>From the Department of Neurology and Clinical Chemistry, Tel-Aviv Medical Center, Sackler School of Medicine, Tel-Aviv University, Israel</mods:affiliation></affiliation></author><author><name sortKey="Oberman, Z" sort="Oberman, Z" uniqKey="Oberman Z" first="Z." last="Oberman">Z. Oberman</name><affiliation><mods:affiliation>From the Department of Neurology and Clinical Chemistry, Tel-Aviv Medical Center, Sackler School of Medicine, Tel-Aviv University, Israel</mods:affiliation></affiliation></author><author><name sortKey="Zohar, M" sort="Zohar, M" uniqKey="Zohar M" first="M." last="Zohar">M. 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Graff</name><affiliation><mods:affiliation>From the Department of Neurology and Clinical Chemistry, Tel-Aviv Medical Center, Sackler School of Medicine, Tel-Aviv University, Israel</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Biological Psychiatry</title><title level="j" type="abbrev">BPS</title><idno type="ISSN">0006-3223</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1988">1988</date><biblScope unit="volume">27</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="581">581</biblScope><biblScope unit="page" to="591">591</biblScope></imprint><idno type="ISSN">0006-3223</idno></series><idno type="istex">59924452D39CAE1B18F56DF4CD4481690B4055F6</idno><idno type="DOI">10.1016/0006-3223(90)90525-7</idno><idno type="PII">0006-3223(90)90525-7</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-3223</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The dexamethasone suppression test (DST) has been suggested as an effective tool for differentiating between depression and dementia. After administering 1 mg dexamethasone, we measured cortisol, ACTH, and beta-endorphin levels in 32 nondepressed patients with idiopathic Parkinson's disease (PD) (14 also with dementia) and 20 healthy, age-matched controls. Four of the 20 controls, 9 of the 18 with PD alone, and 8 of the 14 with PD and dementia were dexamethasone nonsuppressors (cortisol value ≥ 5 μg/100 ml). Plasma ACTH and beta-endorphin responded in a coupled way to dexamethasone challenge. Higher basal levels of both peptides were found among PD patients (demented and nondemented), nonresponders to DST. Thus, the DST does not appear to be effective in differentiating between depression and dementia in PD. In addition, PD nonsuppressors showed higher basal values of plasma ACTH, beta-endorphin, and cortisol (similar to patients with major depression). This suggests that although the depression is clinically undetectable, both disorders may share some pathophysiological features at the hypothalamic hypophyseal adrenal level.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>J.M. Rabey</name><affiliations><json:string>From the Department of Neurology and Clinical Chemistry, Tel-Aviv Medical Center, Sackler School of Medicine, Tel-Aviv University, Israel</json:string></affiliations></json:item><json:item><name>M. Scharf</name><affiliations><json:string>From the Department of Neurology and Clinical Chemistry, Tel-Aviv Medical Center, Sackler School of Medicine, Tel-Aviv University, Israel</json:string></affiliations></json:item><json:item><name>Z. Oberman</name><affiliations><json:string>From the Department of Neurology and Clinical Chemistry, Tel-Aviv Medical Center, Sackler School of Medicine, Tel-Aviv University, Israel</json:string></affiliations></json:item><json:item><name>M. Zohar</name><affiliations><json:string>From the Department of Neurology and Clinical Chemistry, Tel-Aviv Medical Center, Sackler School of Medicine, Tel-Aviv University, Israel</json:string></affiliations></json:item><json:item><name>E. Graff</name><affiliations><json:string>From the Department of Neurology and Clinical Chemistry, Tel-Aviv Medical Center, Sackler School of Medicine, Tel-Aviv University, Israel</json:string></affiliations></json:item></author><language><json:string>eng</json:string></language><abstract>The dexamethasone suppression test (DST) has been suggested as an effective tool for differentiating between depression and dementia. After administering 1 mg dexamethasone, we measured cortisol, ACTH, and beta-endorphin levels in 32 nondepressed patients with idiopathic Parkinson's disease (PD) (14 also with dementia) and 20 healthy, age-matched controls. Four of the 20 controls, 9 of the 18 with PD alone, and 8 of the 14 with PD and dementia were dexamethasone nonsuppressors (cortisol value ≥ 5 μg/100 ml). Plasma ACTH and beta-endorphin responded in a coupled way to dexamethasone challenge. Higher basal levels of both peptides were found among PD patients (demented and nondemented), nonresponders to DST. Thus, the DST does not appear to be effective in differentiating between depression and dementia in PD. In addition, PD nonsuppressors showed higher basal values of plasma ACTH, beta-endorphin, and cortisol (similar to patients with major depression). 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After administering 1 mg dexamethasone, we measured cortisol, ACTH, and beta-endorphin levels in 32 nondepressed patients with idiopathic Parkinson's disease (PD) (14 also with dementia) and 20 healthy, age-matched controls. Four of the 20 controls, 9 of the 18 with PD alone, and 8 of the 14 with PD and dementia were dexamethasone nonsuppressors (cortisol value ≥ 5 μg/100 ml). Plasma ACTH and beta-endorphin responded in a coupled way to dexamethasone challenge. Higher basal levels of both peptides were found among PD patients (demented and nondemented), nonresponders to DST. Thus, the DST does not appear to be effective in differentiating between depression and dementia in PD. In addition, PD nonsuppressors showed higher basal values of plasma ACTH, beta-endorphin, and cortisol (similar to patients with major depression). This suggests that although the depression is clinically undetectable, both disorders may share some pathophysiological features at the hypothalamic hypophyseal adrenal level.</p></abstract></profileDesc><revisionDesc><change when="1988-12-07">Received</change><change when="1989-06-08">Modified</change><change when="1988">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" </istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>BPS</jid><aid>90525</aid><ce:pii>0006-3223(90)90525-7</ce:pii><ce:doi>10.1016/0006-3223(90)90525-7</ce:doi><ce:copyright type="unknown" year="1990"></ce:copyright></item-info><head><ce:title>Cortisol, ACTH, and beta-endorphin after dexamethasone administration in Parkinson's dementia</ce:title><ce:author-group><ce:author><ce:given-name>J.M.</ce:given-name><ce:surname>Rabey</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>M.</ce:given-name><ce:surname>Scharf</ce:surname></ce:author><ce:author><ce:given-name>Z.</ce:given-name><ce:surname>Oberman</ce:surname></ce:author><ce:author><ce:given-name>M.</ce:given-name><ce:surname>Zohar</ce:surname></ce:author><ce:author><ce:given-name>E.</ce:given-name><ce:surname>Graff</ce:surname></ce:author><ce:affiliation><ce:textfn>From the Department of Neurology and Clinical Chemistry, Tel-Aviv Medical Center, Sackler School of Medicine, Tel-Aviv University, Israel</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Address reprint requests to Dr. Jose Martin Rabey, Department of Neurology, Ichilov Hospital, 6 Weizman Street, Tel-Aviv 64239, Israel.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="7" month="12" year="1988"></ce:date-received><ce:date-revised day="8" month="6" year="1989"></ce:date-revised><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para id="SP0005">The dexamethasone suppression test (DST) has been suggested as an effective tool for differentiating between depression and dementia. After administering 1 mg dexamethasone, we measured cortisol, ACTH, and beta-endorphin levels in 32 nondepressed patients with idiopathic Parkinson's disease (PD) (14 also with dementia) and 20 healthy, age-matched controls. Four of the 20 controls, 9 of the 18 with PD alone, and 8 of the 14 with PD and dementia were dexamethasone nonsuppressors (cortisol value ≥ 5 μg/100 ml). Plasma ACTH and beta-endorphin responded in a coupled way to dexamethasone challenge. Higher basal levels of both peptides were found among PD patients (demented and nondemented), nonresponders to DST. Thus, the DST does not appear to be effective in differentiating between depression and dementia in PD. In addition, PD nonsuppressors showed higher basal values of plasma ACTH, beta-endorphin, and cortisol (similar to patients with major depression). 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