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Predicting the failure of disc surgery by a hypofunctional HPA axis: evidence from a prospective study on patients undergoing disc surgery

Identifieur interne : 000445 ( PascalFrancis/Curation ); précédent : 000444; suivant : 000446

Predicting the failure of disc surgery by a hypofunctional HPA axis: evidence from a prospective study on patients undergoing disc surgery

Auteurs : Andrea Geiss [Allemagne] ; Nicolas Rohleder [Allemagne] ; Clemens Kirschbaum [Allemagne] ; Klaus Steinbach [Allemagne] ; Heinz W. Bauer [Allemagne] ; Fernand Anton [Allemagne, Luxembourg (pays)]

Source :

RBID : Pascal:05-0374222

Descripteurs français

English descriptors

Abstract

Patients with postoperative ongoing sciatic pain have been shown to exhibit reduced cortisol levels along with enhanced IL-6 levels. The aim of the present study was to clarify the relationship between a reduced cortisol secretion and enhanced cytokine levels by performing a prospective study on patients with disc herniation. Twenty-two patients were examined before and after their disc surgery. Twelve healthy, pain-free subjects matched for age, education and gender constituted the control group. The preoperative examinations included the assessment of the diurnal pattern of cortisol secretion and the feedback sensitivity of the hypothalamus-pituitary-adrenal (HPA) axis. Patients' subjective stress levels also were assessed during the preoperative examination. The diurnal pattern of cortisol secretion was again assessed during the postoperative examination. Furthermore, blood samples were collected to measure catecholamine, adrenocorticotropic hormone (ACTH)- and interleukin-6 (IL-6) levels before and after measuring the pressure pain thresholds (PPTs). An assessment of the sensitivity of circulating monocytes to the immunosuppressive effects of glucocorticoids was further included in the postoperative examinations. Failed back syndrome (FBS) patients (n=12) showed a reduced cortisol secretion in the morning hours and enhanced feedback sensitivity of the HPA axis. Furthermore, FBS patients displayed an increased in-vitro production of proinflammatory cytokines and a relative glucocorticoid resistance of pro-inflammatory cytokine producing monocytes as compared to non-FBS patients (n=10) and controls. After PPT measurement FBS patients exhibited an increased norepinephrine but decreased epinephrine response, together with lower ACTH levels and a four times higher plasma IL-6 response. These findings suggest that chronically stressed patients are at a higher risk for a poor surgical outcome as their reduced cortisol secretion promotes the postoperative ongoing synthesis of proinflammatory cytokines.
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A08 01  1  ENG  @1 Predicting the failure of disc surgery by a hypofunctional HPA axis: evidence from a prospective study on patients undergoing disc surgery
A11 01  1    @1 GEISS (Andrea)
A11 02  1    @1 ROHLEDER (Nicolas)
A11 03  1    @1 KIRSCHBAUM (Clemens)
A11 04  1    @1 STEINBACH (Klaus)
A11 05  1    @1 BAUER (Heinz W.)
A11 06  1    @1 ANTON (Fernand)
A14 01      @1 Department of Psychobiology, University of Trier @2 54286 Trier @3 DEU @Z 1 aut. @Z 6 aut.
A14 02      @1 Biological Psychology, Technical University of Dresden @2 01062 Dresden @3 DEU @Z 2 aut. @Z 3 aut.
A14 03      @1 Klinik für Orthopädie und Sportmedizin der Hochwald Kliniken @2 66709 Weiskirchen/Saarr @3 DEU @Z 4 aut. @Z 5 aut.
A14 04      @1 Université du Luxembourg, 162A, avenue de la Faïbncerie @2 1511 Luxembourg @3 LUX @Z 6 aut.
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C01 01    ENG  @0 Patients with postoperative ongoing sciatic pain have been shown to exhibit reduced cortisol levels along with enhanced IL-6 levels. The aim of the present study was to clarify the relationship between a reduced cortisol secretion and enhanced cytokine levels by performing a prospective study on patients with disc herniation. Twenty-two patients were examined before and after their disc surgery. Twelve healthy, pain-free subjects matched for age, education and gender constituted the control group. The preoperative examinations included the assessment of the diurnal pattern of cortisol secretion and the feedback sensitivity of the hypothalamus-pituitary-adrenal (HPA) axis. Patients' subjective stress levels also were assessed during the preoperative examination. The diurnal pattern of cortisol secretion was again assessed during the postoperative examination. Furthermore, blood samples were collected to measure catecholamine, adrenocorticotropic hormone (ACTH)- and interleukin-6 (IL-6) levels before and after measuring the pressure pain thresholds (PPTs). An assessment of the sensitivity of circulating monocytes to the immunosuppressive effects of glucocorticoids was further included in the postoperative examinations. Failed back syndrome (FBS) patients (n=12) showed a reduced cortisol secretion in the morning hours and enhanced feedback sensitivity of the HPA axis. Furthermore, FBS patients displayed an increased in-vitro production of proinflammatory cytokines and a relative glucocorticoid resistance of pro-inflammatory cytokine producing monocytes as compared to non-FBS patients (n=10) and controls. After PPT measurement FBS patients exhibited an increased norepinephrine but decreased epinephrine response, together with lower ACTH levels and a four times higher plasma IL-6 response. These findings suggest that chronically stressed patients are at a higher risk for a poor surgical outcome as their reduced cortisol secretion promotes the postoperative ongoing synthesis of proinflammatory cytokines.
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C07 03  X  FRE  @0 Système ostéoarticulaire pathologie @5 22
C07 03  X  ENG  @0 Diseases of the osteoarticular system @5 22
C07 03  X  SPA  @0 Sistema osteoarticular patología @5 22
N21       @1 262

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<s0>Patients with postoperative ongoing sciatic pain have been shown to exhibit reduced cortisol levels along with enhanced IL-6 levels. The aim of the present study was to clarify the relationship between a reduced cortisol secretion and enhanced cytokine levels by performing a prospective study on patients with disc herniation. Twenty-two patients were examined before and after their disc surgery. Twelve healthy, pain-free subjects matched for age, education and gender constituted the control group. The preoperative examinations included the assessment of the diurnal pattern of cortisol secretion and the feedback sensitivity of the hypothalamus-pituitary-adrenal (HPA) axis. Patients' subjective stress levels also were assessed during the preoperative examination. The diurnal pattern of cortisol secretion was again assessed during the postoperative examination. Furthermore, blood samples were collected to measure catecholamine, adrenocorticotropic hormone (ACTH)- and interleukin-6 (IL-6) levels before and after measuring the pressure pain thresholds (PPTs). An assessment of the sensitivity of circulating monocytes to the immunosuppressive effects of glucocorticoids was further included in the postoperative examinations. Failed back syndrome (FBS) patients (n=12) showed a reduced cortisol secretion in the morning hours and enhanced feedback sensitivity of the HPA axis. Furthermore, FBS patients displayed an increased in-vitro production of proinflammatory cytokines and a relative glucocorticoid resistance of pro-inflammatory cytokine producing monocytes as compared to non-FBS patients (n=10) and controls. After PPT measurement FBS patients exhibited an increased norepinephrine but decreased epinephrine response, together with lower ACTH levels and a four times higher plasma IL-6 response. These findings suggest that chronically stressed patients are at a higher risk for a poor surgical outcome as their reduced cortisol secretion promotes the postoperative ongoing synthesis of proinflammatory cytokines.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002A26N03B</s0>
</fC02>
<fC02 i1="02" i2="X">
<s0>002B15F</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Prospective</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Prospective</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Prospectiva</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Postopératoire</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Postoperative</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Postoperatorio</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Douleur</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Pain</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Dolor</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Hydrocortisone</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Hydrocortisone</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Hidrocortisona</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Interleukine 6</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Interleukin 6</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Interleuquina 6</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Cytokine</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Cytokine</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Citoquina</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Sexe</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Sex</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Sexo</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Préopératoire</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Preoperative</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Preoperatorio</s0>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Hernie discale</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Intervertebral disk displacement</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Hernia disco intervertebral</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Sensibilité</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Sensitivity</s0>
<s5>10</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Sensibilidad</s0>
<s5>10</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE">
<s0>Stress</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG">
<s0>Stress</s0>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA">
<s0>Estrés</s0>
<s5>11</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE">
<s0>Catécholamine</s0>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG">
<s0>Catecholamine</s0>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA">
<s0>Catecolamina</s0>
<s5>13</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE">
<s0>Glucocorticoïde</s0>
<s5>14</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG">
<s0>Glucocorticoid</s0>
<s5>14</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA">
<s0>Glucocorticoide</s0>
<s5>14</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE">
<s0>Homme</s0>
<s5>54</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG">
<s0>Human</s0>
<s5>54</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA">
<s0>Hombre</s0>
<s5>54</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE">
<s0>Système hypothalamohypophysosurrénalien</s0>
<s5>57</s5>
</fC03>
<fC03 i1="15" i2="X" l="ENG">
<s0>Hypothalamohypophysoadrenal axis</s0>
<s5>57</s5>
</fC03>
<fC03 i1="15" i2="X" l="SPA">
<s0>Sistema hipotalamohipofisosuprarrenal</s0>
<s5>57</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Hormone surrénalienne</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Adrenal hormone</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Hormona suprarrenal</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Rachis pathologie</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Spine disease</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Raquis patología</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Système ostéoarticulaire pathologie</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Diseases of the osteoarticular system</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Sistema osteoarticular patología</s0>
<s5>22</s5>
</fC07>
<fN21>
<s1>262</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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