The potential role of hypocortisolism in the pathophysiology of stress-related bodily disorders.
Identifieur interne : 000816 ( PubMed/Checkpoint ); précédent : 000815; suivant : 000817The potential role of hypocortisolism in the pathophysiology of stress-related bodily disorders.
Auteurs : C. Heim [Allemagne] ; U. Ehlert ; D H HellhammerSource :
- Psychoneuroendocrinology [ 0306-4530 ] ; 2000.
English descriptors
- KwdEn :
- Adaptation, Psychological (physiology), Adrenal Glands (metabolism), Animals, Causality, Chronic Disease, Corticotropin-Releasing Hormone (secretion), Down-Regulation (physiology), Feedback, Female, Humans, Hydrocortisone (deficiency), Hypothalamo-Hypophyseal System (physiopathology), Male, Pituitary-Adrenal System (physiopathology), Psychophysiologic Disorders (physiopathology), Receptors, Corticotropin-Releasing Hormone (metabolism), Receptors, Glucocorticoid (metabolism), Sex Factors, Stress Disorders, Post-Traumatic (etiology), Stress Disorders, Post-Traumatic (physiopathology), Stress, Physiological (physiopathology).
- MESH :
- chemical , deficiency : Hydrocortisone.
- chemical , metabolism : Receptors, Corticotropin-Releasing Hormone, Receptors, Glucocorticoid.
- chemical , secretion : Corticotropin-Releasing Hormone.
- etiology : Stress Disorders, Post-Traumatic.
- metabolism : Adrenal Glands.
- physiology : Adaptation, Psychological, Down-Regulation.
- physiopathology : Hypothalamo-Hypophyseal System, Pituitary-Adrenal System, Psychophysiologic Disorders, Stress Disorders, Post-Traumatic, Stress, Physiological.
- Animals, Causality, Chronic Disease, Feedback, Female, Humans, Male, Sex Factors.
Abstract
Representing a challenge for current concepts of stress research, a number of studies have now provided convincing evidence that the adrenal gland is hypoactive in some stress-related states. The phenomenon of hypocortisolism has mainly been described for patients, who experienced a traumatic event and subsequently developed post-traumatic stress disorder (PTSD). However, as presented in this review, hypocortisolism does not merely represent a specific correlate of PTSD, since similar findings have been reported for healthy individuals living under conditions of chronic stress as well as for patients with several bodily disorders. These include chronic fatigue syndrome, fibromyalgia, other somatoform disorders, rheumatoid arthritis, and asthma, and many of these disorders have been related to stress. Although hypocortisolism appears to be a frequent and widespread phenomenon, the nature of the underlying mechanisms and the homology of these mechanisms within and across clinical groups remain speculative. Potential mechanisms include dysregulations on several levels of the hypothalamic-pituitary adrenal axis. In addition, factors such as genetic vulnerability, previous stress experience, coping and personality styles may determine the manifestation of this neuroendocrine abnormality. Several authors proposed theoretical concepts on the development or physiological meaning of hypocortisolism. Based on the reviewed findings, we propose that a persistent lack of cortisol availability in traumatized or chronically stressed individuals may promote an increased vulnerability for the development of stress-related bodily disorders. This pathophysiological model may have important implications for the prevention, diagnosis and treatment of the classical psychosomatic disorders.
PubMed: 10633533
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Heim</name><affiliation wicri:level="4"><nlm:affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Center for Psychobiological and Psychosomatic Research, University of Trier</wicri:regionArea><placeName><settlement type="city">Trèves (Allemagne)</settlement><region type="land" nuts="1">Rhénanie-Palatinat</region></placeName><orgName type="university">Université de Trèves</orgName></affiliation></author><author><name sortKey="Ehlert, U" sort="Ehlert, U" uniqKey="Ehlert U" first="U" last="Ehlert">U. Ehlert</name></author><author><name sortKey="Hellhammer, D H" sort="Hellhammer, D H" uniqKey="Hellhammer D" first="D H" last="Hellhammer">D H Hellhammer</name></author></analytic><series><title level="j">Psychoneuroendocrinology</title><idno type="ISSN">0306-4530</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptation, Psychological (physiology)</term><term>Adrenal Glands (metabolism)</term><term>Animals</term><term>Causality</term><term>Chronic Disease</term><term>Corticotropin-Releasing Hormone (secretion)</term><term>Down-Regulation (physiology)</term><term>Feedback</term><term>Female</term><term>Humans</term><term>Hydrocortisone (deficiency)</term><term>Hypothalamo-Hypophyseal System (physiopathology)</term><term>Male</term><term>Pituitary-Adrenal System (physiopathology)</term><term>Psychophysiologic Disorders (physiopathology)</term><term>Receptors, Corticotropin-Releasing Hormone (metabolism)</term><term>Receptors, Glucocorticoid (metabolism)</term><term>Sex Factors</term><term>Stress Disorders, Post-Traumatic (etiology)</term><term>Stress Disorders, Post-Traumatic (physiopathology)</term><term>Stress, Physiological (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Hydrocortisone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Receptors, Corticotropin-Releasing Hormone</term><term>Receptors, Glucocorticoid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="secretion" xml:lang="en"><term>Corticotropin-Releasing Hormone</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Stress Disorders, Post-Traumatic</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adrenal Glands</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Adaptation, Psychological</term><term>Down-Regulation</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Hypothalamo-Hypophyseal System</term><term>Pituitary-Adrenal System</term><term>Psychophysiologic Disorders</term><term>Stress Disorders, Post-Traumatic</term><term>Stress, Physiological</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Causality</term><term>Chronic Disease</term><term>Feedback</term><term>Female</term><term>Humans</term><term>Male</term><term>Sex Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Representing a challenge for current concepts of stress research, a number of studies have now provided convincing evidence that the adrenal gland is hypoactive in some stress-related states. The phenomenon of hypocortisolism has mainly been described for patients, who experienced a traumatic event and subsequently developed post-traumatic stress disorder (PTSD). However, as presented in this review, hypocortisolism does not merely represent a specific correlate of PTSD, since similar findings have been reported for healthy individuals living under conditions of chronic stress as well as for patients with several bodily disorders. These include chronic fatigue syndrome, fibromyalgia, other somatoform disorders, rheumatoid arthritis, and asthma, and many of these disorders have been related to stress. Although hypocortisolism appears to be a frequent and widespread phenomenon, the nature of the underlying mechanisms and the homology of these mechanisms within and across clinical groups remain speculative. Potential mechanisms include dysregulations on several levels of the hypothalamic-pituitary adrenal axis. In addition, factors such as genetic vulnerability, previous stress experience, coping and personality styles may determine the manifestation of this neuroendocrine abnormality. Several authors proposed theoretical concepts on the development or physiological meaning of hypocortisolism. Based on the reviewed findings, we propose that a persistent lack of cortisol availability in traumatized or chronically stressed individuals may promote an increased vulnerability for the development of stress-related bodily disorders. This pathophysiological model may have important implications for the prevention, diagnosis and treatment of the classical psychosomatic disorders.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10633533</PMID><DateCreated><Year>2000</Year><Month>01</Month><Day>27</Day></DateCreated><DateCompleted><Year>2000</Year><Month>01</Month><Day>27</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0306-4530</ISSN><JournalIssue CitedMedium="Print"><Volume>25</Volume><Issue>1</Issue><PubDate><Year>2000</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Psychoneuroendocrinology</Title><ISOAbbreviation>Psychoneuroendocrinology</ISOAbbreviation></Journal><ArticleTitle>The potential role of hypocortisolism in the pathophysiology of stress-related bodily disorders.</ArticleTitle><Pagination><MedlinePgn>1-35</MedlinePgn></Pagination><Abstract><AbstractText>Representing a challenge for current concepts of stress research, a number of studies have now provided convincing evidence that the adrenal gland is hypoactive in some stress-related states. The phenomenon of hypocortisolism has mainly been described for patients, who experienced a traumatic event and subsequently developed post-traumatic stress disorder (PTSD). However, as presented in this review, hypocortisolism does not merely represent a specific correlate of PTSD, since similar findings have been reported for healthy individuals living under conditions of chronic stress as well as for patients with several bodily disorders. These include chronic fatigue syndrome, fibromyalgia, other somatoform disorders, rheumatoid arthritis, and asthma, and many of these disorders have been related to stress. Although hypocortisolism appears to be a frequent and widespread phenomenon, the nature of the underlying mechanisms and the homology of these mechanisms within and across clinical groups remain speculative. Potential mechanisms include dysregulations on several levels of the hypothalamic-pituitary adrenal axis. In addition, factors such as genetic vulnerability, previous stress experience, coping and personality styles may determine the manifestation of this neuroendocrine abnormality. Several authors proposed theoretical concepts on the development or physiological meaning of hypocortisolism. Based on the reviewed findings, we propose that a persistent lack of cortisol availability in traumatized or chronically stressed individuals may promote an increased vulnerability for the development of stress-related bodily disorders. This pathophysiological model may have important implications for the prevention, diagnosis and treatment of the classical psychosomatic disorders.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Heim</LastName><ForeName>C</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ehlert</LastName><ForeName>U</ForeName><Initials>U</Initials></Author><Author ValidYN="Y"><LastName>Hellhammer</LastName><ForeName>D H</ForeName><Initials>DH</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType 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Disorders</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018019" MajorTopicYN="N">Receptors, Corticotropin-Releasing Hormone</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011965" MajorTopicYN="N">Receptors, Glucocorticoid</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012737" MajorTopicYN="N">Sex Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013313" MajorTopicYN="N">Stress Disorders, Post-Traumatic</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013312" MajorTopicYN="N">Stress, Physiological</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>210</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year><Month>1</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2000</Year><Month>1</Month><Day>14</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2000</Year><Month>1</Month><Day>14</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10633533</ArticleId><ArticleId IdType="pii">S0306-4530(99)00035-9</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country><region><li>Rhénanie-Palatinat</li></region><settlement><li>Trèves (Allemagne)</li></settlement><orgName><li>Université de Trèves</li></orgName></list><tree><noCountry><name sortKey="Ehlert, U" sort="Ehlert, U" uniqKey="Ehlert U" first="U" last="Ehlert">U. Ehlert</name><name sortKey="Hellhammer, D H" sort="Hellhammer, D H" uniqKey="Hellhammer D" first="D H" last="Hellhammer">D H Hellhammer</name></noCountry><country name="Allemagne"><region name="Rhénanie-Palatinat"><name sortKey="Heim, C" sort="Heim, C" uniqKey="Heim C" first="C" last="Heim">C. Heim</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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