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DOI: 10.1530/eje.1.02045
European Journal of Endocrinology, Vol 153, Issue 6, 837-844
Copyright © 2005 by European Society of Endocrinology
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CLINICAL STUDY

Association of subclinical hypercortisolism with type 2 diabetes mellitus: a case-control study in hospitalized patients

Iacopo Chiodini1, Massimo Torlontano2, Alfredo Scillitani2, Maura Arosio1,3, Simonetta Bacci2, Sergio Di Lembo1, Paolo Epaminonda1, Giovanni Augello2, Riccardo Enrini4, Bruno Ambrosi4, Guido Adda1 and Vincenzo Trischitta2,5

1 Unit of Endocrinology ‘San Giuseppe-Fatebenefratelli’ Hospital, A.Fa.R. Milano, via San Vittore 12 20123 Milan, Italy, 2 Unit of Endocrinology, Scientific Institute ‘Casa Sollievo della Sofferenza’, S Giovanni Rotondo, Italy, 3 Institute of Endocrine Sciences, University of Milan, Fondazione Policlinico IRCCS, Milan, Italy, 4 Unit of Endocrinology, Department of Medical and Surgical Sciences, University of Milan, ‘Policlinico San Donato’ Institute, San Donato Milanese, Milan, Italy and 5 Department of Clinical Sciences, ‘La Sapienza’ University, Rome, Italy

(Correspondence should be addressed to I Chiodini; Email: ichiodini{at}katamail.com)

Objective: Subclinical hypercortisolism (SH) may play a role in several metabolic disorders, including diabetes. No data are available on the relative prevalence of SH in type 2 diabetes (T2D). In order to compare the prevalence of SH in T2D and matched non-diabetic control individuals, we performed a case-controlled, multicenter, 12-month study, enrolling 294 consecutive T2D inpatients (1.7% dropped out the study) with no evidence of clinical hypercortisolism and 189 consecutive age- and body mass index-matched non-diabetic inpatients (none of whom dropped out).

Design and methods: Ascertained SH (ASH) was diagnosed in individuals (i) with plasma cortisol after 1 mg overnight dexamethasone suppression >1.8 µg/dl (50 nmol/l), (ii) with more than one of the following: (a) urinary free cortisol >60.0 µg/24 h (165.6 nmol/24 h), (b) plasma ACTH <10.0 pg/ml (2.2 pmol/l) or (c) plasma cortisol >7.5 µg/dl (207 nmol/l) at 24:00 h or >1.4 µg/dl (38.6 nmol/l) after dexamethasone-CRH (serum cortisol after corticotrophin-releasing hormone stimulus during dexamethasone administration) test, and (iii) in whom the source of glucocorticoid excess was suggested by imaging and by additional biochemical tests (for ACTH-dependent ASH).

Results: Prevalence of ASH was higher in diabetic individuals than in controls (9.4 versus 2.1%; adjusted odds ratio, 4.8; 95% confidence interval, 1.6–14.1; P = 0.004). In our population the proportion of T2D which is statistically attributable to ASH was approx. 7%. Among diabetic patients, the presence of severe diabetes (as defined by the coexistence of hypertension, dyslipidaemia and insulin treatment) was significantly associated with SH (adjusted odds ratio, 3.8; 95% confidence interval, 1.4–10.2; P = 0.017).

Conclusions: In hospitalized patients, SH is associated with T2D.




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