Effect of fenfluramine on episodic ACTH and cortisol secretion
Identifieur interne : 001449 ( PascalFrancis/Corpus ); précédent : 001448; suivant : 001450Effect of fenfluramine on episodic ACTH and cortisol secretion
Auteurs : T. H. Schürmeyer ; G. Brademann ; A. Von Zur MühlenSource :
- Clinical endocrinology : (Oxford) [ 0300-0664 ] ; 1996.
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- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
OBJECTIVE The central serotoninergic system is known to modulate the activity of the hypothalamic-pituitary-adrenal axis, but the effect of fenfluramine, a serotonin reuptake inhibitor, on ACTH and cortisol secretion is not well understood. We have therefore evaluated its effects on the hypothalamic-pituitary-adrenal axis in healthy controls. DESIGN Episodic secretion of ACTH and cortisol was investigated in 6 healthy volunteers under basal conditions and again during treatment with 20 and 60 mg fenfluramine given orally every 8 hours. On all occasions blood samples were obtained at 10-minute intervals for 24 hours and the mode of hormone secretion was analysed by three different methods (PULSAR, CLUSTER, DESADE). In addition ACTH and cortisol responses to CRH were tested at the end of the sampling period. RESULTS At the lower dose fenfluramine had no effect on ACTH and cortisol secretion. At the higher dose a signlficant increase of mean plasma ACTH (+85%) and cortisol (+129%) levels as well as of urinary free cortisol secretion (+44%) was observed. Fenfluramine did not modulate the frequency, but increased the amplitudes of ACTH and cortisol secretory episodes. ACTH and cortisol responses to CRH injection remained unchanged. Maximum plasma levels of d-fenfluramine and d-norfenfluramine were documented 2-4 hours after the ingestion of the drug. CONCLUSION Fenfluramine stimulates the activity of the hypothalamic-pituitary-adrenal axis at a suprapituitary level by modulating the amplitude of ACTH and cortisol secretory bursts.
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Format Inist (serveur)
| NO : | PASCAL 96-0370881 INIST |
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| ET : | Effect of fenfluramine on episodic ACTH and cortisol secretion |
| AU : | SCHÜRMEYER (T. H.); BRADEMANN (G.); VON ZUR MÜHLEN (A.) |
| AF : | Department of Endocrinology and Metabolism at the University, FPP/54286 Trier/Allemagne (1 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Clinical endocrinology : (Oxford); ISSN 0300-0664; Coden CLECAP; Royaume-Uni; Da. 1996; Vol. 45; No. 1; 39-46 [7 p.]; Bibl. 1 p.3/4 |
| LA : | Anglais |
| EA : | OBJECTIVE The central serotoninergic system is known to modulate the activity of the hypothalamic-pituitary-adrenal axis, but the effect of fenfluramine, a serotonin reuptake inhibitor, on ACTH and cortisol secretion is not well understood. We have therefore evaluated its effects on the hypothalamic-pituitary-adrenal axis in healthy controls. DESIGN Episodic secretion of ACTH and cortisol was investigated in 6 healthy volunteers under basal conditions and again during treatment with 20 and 60 mg fenfluramine given orally every 8 hours. On all occasions blood samples were obtained at 10-minute intervals for 24 hours and the mode of hormone secretion was analysed by three different methods (PULSAR, CLUSTER, DESADE). In addition ACTH and cortisol responses to CRH were tested at the end of the sampling period. RESULTS At the lower dose fenfluramine had no effect on ACTH and cortisol secretion. At the higher dose a signlficant increase of mean plasma ACTH (+85%) and cortisol (+129%) levels as well as of urinary free cortisol secretion (+44%) was observed. Fenfluramine did not modulate the frequency, but increased the amplitudes of ACTH and cortisol secretory episodes. ACTH and cortisol responses to CRH injection remained unchanged. Maximum plasma levels of d-fenfluramine and d-norfenfluramine were documented 2-4 hours after the ingestion of the drug. CONCLUSION Fenfluramine stimulates the activity of the hypothalamic-pituitary-adrenal axis at a suprapituitary level by modulating the amplitude of ACTH and cortisol secretory bursts. |
| CC : | 002B02B09C |
| FD : | Fenfluramine; Système hypothalamohypophysosurrénalien; Sérotonine; Hydrocortisone; Sécrétion; ACTH; Dosage; Urine; Homme; Amphétamine dérivé |
| FG : | Glucocorticoïde; Hormone surrénalienne; Hormone stéroïde |
| ED : | Hypothalamohypophysoadrenal axis; Serotonin; Cortisol; Secretion; ACTH; Assay; Urine; Human; Amphetamine derivatives |
| EG : | Glucocorticoid; Adrenal hormone; Steroid hormone |
| GD : | Analytische Bestimmung |
| SD : | Sistema hipotalamohipofisosuprarrenal; Serotonina; Hidrocortisona; Secreción; Dosificación; Orina; Hombre; Amfetamina derivado |
| LO : | INIST-15568.354000060550740070 |
| ID : | 96-0370881 |
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Pascal:96-0370881Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Effect of fenfluramine on episodic ACTH and cortisol secretion</title><author><name sortKey="Schurmeyer, T H" sort="Schurmeyer, T H" uniqKey="Schurmeyer T" first="T. H." last="Schürmeyer">T. H. Schürmeyer</name><affiliation><inist:fA14 i1="01"><s1>Department of Endocrinology and Metabolism at the University, FPP</s1><s2>54286 Trier</s2><s3>DEU</s3><sZ>1 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Brademann, G" sort="Brademann, G" uniqKey="Brademann G" first="G." last="Brademann">G. Brademann</name></author><author><name sortKey="Von Zur Muhlen, A" sort="Von Zur Muhlen, A" uniqKey="Von Zur Muhlen A" first="A." last="Von Zur Mühlen">A. Von Zur Mühlen</name></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">96-0370881</idno><date when="1996">1996</date><idno type="stanalyst">PASCAL 96-0370881 INIST</idno><idno type="RBID">Pascal:96-0370881</idno><idno type="wicri:Area/PascalFrancis/Corpus">001449</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Effect of fenfluramine on episodic ACTH and cortisol secretion</title><author><name sortKey="Schurmeyer, T H" sort="Schurmeyer, T H" uniqKey="Schurmeyer T" first="T. H." last="Schürmeyer">T. H. Schürmeyer</name><affiliation><inist:fA14 i1="01"><s1>Department of Endocrinology and Metabolism at the University, FPP</s1><s2>54286 Trier</s2><s3>DEU</s3><sZ>1 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Brademann, G" sort="Brademann, G" uniqKey="Brademann G" first="G." last="Brademann">G. Brademann</name></author><author><name sortKey="Von Zur Muhlen, A" sort="Von Zur Muhlen, A" uniqKey="Von Zur Muhlen A" first="A." last="Von Zur Mühlen">A. Von Zur Mühlen</name></author></analytic><series><title level="j" type="main">Clinical endocrinology : (Oxford)</title><title level="j" type="abbreviated">Clin. endocrinol. : (Oxf.)</title><idno type="ISSN">0300-0664</idno><imprint><date when="1996">1996</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Clinical endocrinology : (Oxford)</title><title level="j" type="abbreviated">Clin. endocrinol. : (Oxf.)</title><idno type="ISSN">0300-0664</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>ACTH</term><term>Amphetamine derivatives</term><term>Assay</term><term>Cortisol</term><term>Human</term><term>Hypothalamohypophysoadrenal axis</term><term>Secretion</term><term>Serotonin</term><term>Urine</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Fenfluramine</term><term>Système hypothalamohypophysosurrénalien</term><term>Sérotonine</term><term>Hydrocortisone</term><term>Sécrétion</term><term>ACTH</term><term>Dosage</term><term>Urine</term><term>Homme</term><term>Amphétamine dérivé</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">OBJECTIVE The central serotoninergic system is known to modulate the activity of the hypothalamic-pituitary-adrenal axis, but the effect of fenfluramine, a serotonin reuptake inhibitor, on ACTH and cortisol secretion is not well understood. We have therefore evaluated its effects on the hypothalamic-pituitary-adrenal axis in healthy controls. DESIGN Episodic secretion of ACTH and cortisol was investigated in 6 healthy volunteers under basal conditions and again during treatment with 20 and 60 mg fenfluramine given orally every 8 hours. On all occasions blood samples were obtained at 10-minute intervals for 24 hours and the mode of hormone secretion was analysed by three different methods (PULSAR, CLUSTER, DESADE). In addition ACTH and cortisol responses to CRH were tested at the end of the sampling period. RESULTS At the lower dose fenfluramine had no effect on ACTH and cortisol secretion. At the higher dose a signlficant increase of mean plasma ACTH (+85%) and cortisol (+129%) levels as well as of urinary free cortisol secretion (+44%) was observed. Fenfluramine did not modulate the frequency, but increased the amplitudes of ACTH and cortisol secretory episodes. ACTH and cortisol responses to CRH injection remained unchanged. Maximum plasma levels of d-fenfluramine and d-norfenfluramine were documented 2-4 hours after the ingestion of the drug. CONCLUSION Fenfluramine stimulates the activity of the hypothalamic-pituitary-adrenal axis at a suprapituitary level by modulating the amplitude of ACTH and cortisol secretory bursts.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0300-0664</s0></fA01><fA02 i1="01"><s0>CLECAP</s0></fA02><fA03 i2="1"><s0>Clin. endocrinol. : (Oxf.)</s0></fA03><fA05><s2>45</s2></fA05><fA06><s2>1</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Effect of fenfluramine on episodic ACTH and cortisol secretion</s1></fA08><fA11 i1="01" i2="1"><s1>SCHÜRMEYER (T. H.)</s1></fA11><fA11 i1="02" i2="1"><s1>BRADEMANN (G.)</s1></fA11><fA11 i1="03" i2="1"><s1>VON ZUR MÜHLEN (A.)</s1></fA11><fA14 i1="01"><s1>Department of Endocrinology and Metabolism at the University, FPP</s1><s2>54286 Trier</s2><s3>DEU</s3><sZ>1 aut.</sZ></fA14><fA20><s2>39-46 [7 p.]</s2></fA20><fA21><s1>1996</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>15568</s2><s5>354000060550740070</s5></fA43><fA44><s0>0000</s0><s1>© 1996 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.3/4</s0></fA45><fA47 i1="01" i2="1"><s0>96-0370881</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Clinical endocrinology : (Oxford)</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>OBJECTIVE The central serotoninergic system is known to modulate the activity of the hypothalamic-pituitary-adrenal axis, but the effect of fenfluramine, a serotonin reuptake inhibitor, on ACTH and cortisol secretion is not well understood. We have therefore evaluated its effects on the hypothalamic-pituitary-adrenal axis in healthy controls. DESIGN Episodic secretion of ACTH and cortisol was investigated in 6 healthy volunteers under basal conditions and again during treatment with 20 and 60 mg fenfluramine given orally every 8 hours. On all occasions blood samples were obtained at 10-minute intervals for 24 hours and the mode of hormone secretion was analysed by three different methods (PULSAR, CLUSTER, DESADE). In addition ACTH and cortisol responses to CRH were tested at the end of the sampling period. RESULTS At the lower dose fenfluramine had no effect on ACTH and cortisol secretion. At the higher dose a signlficant increase of mean plasma ACTH (+85%) and cortisol (+129%) levels as well as of urinary free cortisol secretion (+44%) was observed. Fenfluramine did not modulate the frequency, but increased the amplitudes of ACTH and cortisol secretory episodes. ACTH and cortisol responses to CRH injection remained unchanged. Maximum plasma levels of d-fenfluramine and d-norfenfluramine were documented 2-4 hours after the ingestion of the drug. CONCLUSION Fenfluramine stimulates the activity of the hypothalamic-pituitary-adrenal axis at a suprapituitary level by modulating the amplitude of ACTH and cortisol secretory bursts.</s0></fC01><fC02 i1="01" i2="X"><s0>002B02B09C</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Fenfluramine</s0><s2>NK</s2><s2>FR</s2><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Système hypothalamohypophysosurrénalien</s0><s5>04</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Hypothalamohypophysoadrenal axis</s0><s5>04</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Sistema hipotalamohipofisosuprarrenal</s0><s5>04</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Sérotonine</s0><s2>NK</s2><s2>FR</s2><s5>07</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Serotonin</s0><s2>NK</s2><s2>FR</s2><s5>07</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Serotonina</s0><s2>NK</s2><s2>FR</s2><s5>07</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Hydrocortisone</s0><s2>NK</s2><s2>FR</s2><s5>10</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Cortisol</s0><s2>NK</s2><s2>FR</s2><s5>10</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Hidrocortisona</s0><s2>NK</s2><s2>FR</s2><s5>10</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Sécrétion</s0><s5>11</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Secretion</s0><s5>11</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Secreción</s0><s5>11</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>ACTH</s0><s2>NK</s2><s2>FR</s2><s5>13</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>ACTH</s0><s2>NK</s2><s2>FR</s2><s5>13</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Dosage</s0><s5>14</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Assay</s0><s5>14</s5></fC03><fC03 i1="07" i2="X" l="GER"><s0>Analytische Bestimmung</s0><s5>14</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Dosificación</s0><s5>14</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Urine</s0><s5>15</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Urine</s0><s5>15</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Orina</s0><s5>15</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Homme</s0><s5>20</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Human</s0><s5>20</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Hombre</s0><s5>20</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Amphétamine dérivé</s0><s5>25</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Amphetamine derivatives</s0><s5>25</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Amfetamina derivado</s0><s5>25</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Glucocorticoïde</s0><s5>61</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Glucocorticoid</s0><s5>61</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Glucocorticoide</s0><s5>61</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Hormone surrénalienne</s0><s5>62</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Adrenal hormone</s0><s5>62</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Hormona suprarrenal</s0><s5>62</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Hormone stéroïde</s0><s5>63</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Steroid hormone</s0><s5>63</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Hormona esteroide</s0><s5>63</s5></fC07><fN21><s1>253</s1></fN21></pA></standard><server><NO>PASCAL 96-0370881 INIST</NO><ET>Effect of fenfluramine on episodic ACTH and cortisol secretion</ET><AU>SCHÜRMEYER (T. H.); BRADEMANN (G.); VON ZUR MÜHLEN (A.)</AU><AF>Department of Endocrinology and Metabolism at the University, FPP/54286 Trier/Allemagne (1 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Clinical endocrinology : (Oxford); ISSN 0300-0664; Coden CLECAP; Royaume-Uni; Da. 1996; Vol. 45; No. 1; 39-46 [7 p.]; Bibl. 1 p.3/4</SO><LA>Anglais</LA><EA>OBJECTIVE The central serotoninergic system is known to modulate the activity of the hypothalamic-pituitary-adrenal axis, but the effect of fenfluramine, a serotonin reuptake inhibitor, on ACTH and cortisol secretion is not well understood. We have therefore evaluated its effects on the hypothalamic-pituitary-adrenal axis in healthy controls. DESIGN Episodic secretion of ACTH and cortisol was investigated in 6 healthy volunteers under basal conditions and again during treatment with 20 and 60 mg fenfluramine given orally every 8 hours. On all occasions blood samples were obtained at 10-minute intervals for 24 hours and the mode of hormone secretion was analysed by three different methods (PULSAR, CLUSTER, DESADE). In addition ACTH and cortisol responses to CRH were tested at the end of the sampling period. RESULTS At the lower dose fenfluramine had no effect on ACTH and cortisol secretion. At the higher dose a signlficant increase of mean plasma ACTH (+85%) and cortisol (+129%) levels as well as of urinary free cortisol secretion (+44%) was observed. Fenfluramine did not modulate the frequency, but increased the amplitudes of ACTH and cortisol secretory episodes. ACTH and cortisol responses to CRH injection remained unchanged. Maximum plasma levels of d-fenfluramine and d-norfenfluramine were documented 2-4 hours after the ingestion of the drug. CONCLUSION Fenfluramine stimulates the activity of the hypothalamic-pituitary-adrenal axis at a suprapituitary level by modulating the amplitude of ACTH and cortisol secretory bursts.</EA><CC>002B02B09C</CC><FD>Fenfluramine; Système hypothalamohypophysosurrénalien; Sérotonine; Hydrocortisone; Sécrétion; ACTH; Dosage; Urine; Homme; Amphétamine dérivé</FD><FG>Glucocorticoïde; Hormone surrénalienne; Hormone stéroïde</FG><ED>Hypothalamohypophysoadrenal axis; Serotonin; Cortisol; Secretion; ACTH; Assay; Urine; Human; Amphetamine derivatives</ED><EG>Glucocorticoid; Adrenal hormone; Steroid hormone</EG><GD>Analytische Bestimmung</GD><SD>Sistema hipotalamohipofisosuprarrenal; Serotonina; Hidrocortisona; Secreción; Dosificación; Orina; Hombre; Amfetamina derivado</SD><LO>INIST-15568.354000060550740070</LO><ID>96-0370881</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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