Hypofunction of the stress axis in Sjogren's syndrome

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dc.contributor.author Johnson, EO en
dc.contributor.author Vlachoyiannopoulos, PG en
dc.contributor.author Skopouli, FN en
dc.contributor.author Tzioufas, AG en
dc.contributor.author Moutsopoulos, HM en
dc.date.accessioned 2014-03-01T01:47:36Z
dc.date.available 2014-03-01T01:47:36Z
dc.date.issued 1998 en
dc.identifier.issn 0315-162X en
dc.identifier.uri http://hdl.handle.net/123456789/25270
dc.subject stress axis en
dc.subject Sjogren's syndrome en
dc.subject cortisol en
dc.subject ACTH en
dc.subject.classification Rheumatology en
dc.subject.other PITUITARY-ADRENAL AXIS en
dc.subject.other RHEUMATOID-ARTHRITIS en
dc.subject.other BEHAVIORAL HOMEOSTASIS en
dc.subject.other CUSHINGS-DISEASE en
dc.subject.other LEWIS RATS en
dc.subject.other RESPONSES en
dc.subject.other SYSTEM en
dc.subject.other DEXAMETHASONE en
dc.subject.other ACTIVATION en
dc.title Hypofunction of the stress axis in Sjogren's syndrome en
heal.type journalArticle en
heal.language English en
heal.publicationDate 1998 en
heal.abstract Objective. 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 (mu g/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 mu g/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 mu IU/ml vs 0.9 +/- 0.05 mu IU/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.publisher J RHEUMATOL PUBL CO en
dc.identifier.isi ISI:000075104100012 en
dc.identifier.volume 25 en
dc.identifier.issue 8 en
dc.identifier.spage 1508 en
dc.identifier.epage 1514 en

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