Hypofunction of the stress axis in Sjogren's syndrome

dc.contributor.authorJohnson, E. O.en
dc.contributor.authorVlachoyiannopoulos, P. G.en
dc.contributor.authorSkopouli, F. N.en
dc.contributor.authorTzioufas, A. G.en
dc.contributor.authorMoutsopoulos, H. M.en
dc.date.accessioned2015-11-24T19:12:40Z
dc.date.available2015-11-24T19:12:40Z
dc.identifier.issn0315-162X-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/21099
dc.rightsDefault Licence-
dc.subjectAdrenocorticotropic Hormone/metabolismen
dc.subjectAdulten
dc.subjectAnimalsen
dc.subjectAutoantibodies/immunologyen
dc.subjectCorticotropin-Releasing Hormone/metabolismen
dc.subjectFemaleen
dc.subjectHumansen
dc.subjectHydrocortisone/metabolismen
dc.subjectHypothalamo-Hypophyseal System/*physiopathologyen
dc.subjectMiddle Ageden
dc.subjectPituitary-Adrenal System/*physiopathologyen
dc.subjectSheepen
dc.subjectSjogren's Syndrome/immunology/metabolism/*physiopathology/psychologyen
dc.subjectStress, Physiological/immunology/*metabolism/*physiopathology/psychologyen
dc.subjectThyrotropin/metabolismen
dc.subjectThyrotropin-Releasing Hormone/metabolismen
dc.titleHypofunction of the stress axis in Sjogren's syndromeen
heal.abstractOBJECTIVE: To examine the functional integrity of the hypothalamic-pituitary-adrenal (HPA) and thyroid axes in Sjogren's syndrome (SS) via the assessment of basal and stimulated adrenocorticotropin (ACTH), cortisol, thyroid stimulating hormone (TSH), and prolactin levels. METHODS: Pituitary function of the HPA axis was assessed by determining the basal plasma levels of ACTH in the late afternoon, as well as the ACTH released to ovine corticotropin releasing hormone (oCRH) stimulation; adrenal function was assessed by measuring plasma cortisol levels in the late afternoon at baseline and after release of the endogenous ACTH during oCRH stimulation. Basal and thyrotropin releasing hormone (TRH) stimulated levels of TSH and prolactin were also assessed. Healthy volunteers were used as controls. RESULTS: Patients with SS, compared to controls, were characterized by significantly lower ACTH levels (pg/ml), (5.1 +/- 0.5 vs 11.4 +/- 1.5, respectively; p < 0.05) and cortisol levels (microg/ml), (2.4 +/- 0.6 vs 5.9 +/- 1.2, respectively; p < 0.05). Furthermore, a blunted pituitary and adrenal response to oCRH compared to controls was observed: peak plasma ACTH and cortisol levels for patients with SS were 46.2 +/- 5.4 pg/ml and 15.7 +/- 1.6 microg/ml, respectively, and for controls 61.5 +/- 3.8 and 19.6 +/- 0.7, respectively (p < 0.05). Basal TSH levels were significantly elevated in patients (1.3 +/- 0.3 microIU/ml vs 0.9 +/- 0.05 microIU/ml; p < 0.05). CONCLUSION: The above findings indicate hypoactivity of the HPA axis in patients with SS. Further studies are needed to definitively identify the locus of the defects and assess the significance of the pattern of the perturbations to the pathogenesis and expression of SS.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/9712092-
heal.journalNameJ Rheumatolen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate1998-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

Αρχεία

Φάκελος/Πακέτο αδειών

Προβολή: 1 - 1 of 1
Φόρτωση...
Μικρογραφία εικόνας
Ονομα:
license.txt
Μέγεθος:
1.74 KB
Μορφότυπο:
Item-specific license agreed upon to submission
Περιγραφή: