The effect of thyrotoxicosis on adrenocortical reserve

dc.contributor.authorTsatsoulis, A.en
dc.contributor.authorJohnson, E. O.en
dc.contributor.authorKalogera, C. H.en
dc.contributor.authorSeferiadis, K.en
dc.contributor.authorTsolas, O.en
dc.date.accessioned2015-11-24T19:41:48Z
dc.date.available2015-11-24T19:41:48Z
dc.identifier.issn0804-4643-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/24537
dc.rightsDefault Licence-
dc.subjectAdrenal Cortex/*metabolismen
dc.subjectAdrenocorticotropic Hormone/administration & dosage/*metabolismen
dc.subjectAdulten
dc.subjectAntibodies/blooden
dc.subjectFemaleen
dc.subjectHumansen
dc.subjectHydrocortisone/*blooden
dc.subjectMaleen
dc.subjectMiddle Ageden
dc.subjectThyroid Gland/immunologyen
dc.subjectThyroid Hormones/blooden
dc.subjectThyrotoxicosis/*blood/etiologyen
dc.subjectThyrotropin/blooden
dc.subjectTime Factorsen
dc.titleThe effect of thyrotoxicosis on adrenocortical reserveen
heal.abstractOBJECTIVE: Variations in thyroid function are known to be associated with changes in adrenocortical activity. Previous studies in animals have suggested that long-standing hyperthyroidism may be associated with diminished adrenal functional reserve despite a continuing hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis. In humans, there has been no direct assessment of adrenal secretory reserve in clinical thyrotoxicosis. This study aimed to assess adrenocortical reserve in response to low-dose ACTH, following dexamethasone suppression, in patients with severe thyrotoxicosis. DESIGN AND METHODS: Ten patients (four men and six women, 30-45 years) with severe long-standing thyrotoxicosis due to Graves' disease (n=6) or toxic nodular goitre (n=4) were studied at diagnosis and again when in a stable euthyroid state following drug therapy for 8-12 months. All patients underwent ACTH stimulation tests at 0800h with ACTH(1-24) (Cortrosyn; 0.1microg/kg body weight, i.v.) following overnight suppression of the HPA axis with dexamethasone (1mg per os at 2300h). Serum cortisol was assayed at -15, 0, 15, 30, 60 and 90min after the administration of ACTH. RESULTS: The mean (+/-s.d.) peak and delta cortisol responses to ACTH (634.5+/-164nmol/l and 618+/- 196nmol/l respectively), as well as the net area under the response curve (36769+/-12188nmol/lx min) in the hyperthyroid patients were significantly lower compared with the values when the same patients were euthyroid (911+/-157nmol/l, 905+/-160nmol/l and 57652+/-10128nmol/lxmin respectively; P<0.005). Subnormal peak cortisol responses (<500nmol/l) were observed in two severely toxic patients. The findings were independent of the cause of thyrotoxicosis. CONCLUSION: In patients with severe thyrotoxicosis, cortisol secretion in response to low-dose ACTH stimulation, following dexamethasone suppression, is lower in the hyperthyroid than in the euthyroid state. It appears that thyrotoxicosis is associated with subtle impairment of adrenocortical reserve.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/10700716-
heal.identifier.secondaryhttp://www.eje-online.org/content/142/3/231.full.pdf-
heal.journalNameEuropean Journal of Endocrinologyen
heal.journalTypepeer-reviewed-
heal.languageen-
heal.publicationDate2000-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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