Marta Araujo-Castro1,2, Paola Parra Ramírez3, Cristina Robles Lázaro4, Rogelio García Centeno5, Paola Gracia Gimeno6, Mariana Tomé Fernández-Ladreda7, Miguel Antonio Sampedro Núñez8, Mónica Marazuela8, Héctor F Escobar-Morreale9,10, Pablo Valderrabano9. 1. Neuroendocrinology Unit, Department of Endocrinology & Nutrition, Instituto de Investigación Biomédica (IRYCIS), Hospital Universitario Ramón Y Cajal, Madrid, Spain. marta.araujo@salud.madrid.org. 2. Department of Health Science, Universidad de Alcalá, Madrid, Spain. marta.araujo@salud.madrid.org. 3. Endocrinology Department, Hospital La Paz, Madrid, Spain. 4. Endocrinology Department, Hospital Virgen de la Concha , Valladolid, Spain. 5. Endocrinology Department, Hospital Universitario Gregorio Marañón, Madrid, Spain. 6. Endocrinology Department, Hospital Royo Villanova, Zaragoza, Spain. 7. Endocrinology Department, Hospital Universitario de Puerto Real, Cádiz, Spain. 8. Endocrinology Department, Hospital Universitario de La Princesa, Madrid, Spain. 9. Department of Endocrinology & Nutrition, Hospital Universitario Ramón Y Cajal, Madrid, Spain. 10. Universidad de Alcalá & Instituto Ramón Y Cajal de Investigación Sanitaria & Centro de Investigación Biomédica en Red Diabetes Y Enfermedades Metabólicas Asociadas, Madrid, Spain.
Abstract
PURPOSE: The aim of this study was to evaluate the diagnostic accuracy of the 1 mg dexamethasone suppression test (DST) for the prediction of autonomous cortisol secretion (ACS)-related comorbidities in patients with adrenal incidentalomas (AIs). METHODS: This was a retrospective multicenter study. We recruited patients with AI/s ≥ 1 cm, excluding those who, during the study, were found during the extension study of an extra-adrenal cancer, with a known diagnosis of hereditary syndromes characterized by adrenal tumors, those presenting with overt hormonal excess syndromes, and those in whom the DST results were missing. RESULTS: A total of 823 patients met the inclusion criteria. Based on the 1.8, 3.0, and 5.0 µg/dl post-DST cortisol thresholds, the prevalence of ACS was 33.5%, 13.7%, and 5.6%, respectively. The prevalence of hypertension (OR = 1.8, 95% CI = 1.3-2.4), diabetes (OR = 1.6, 95% CI = 1.2-2.2), and dyslipidemia (OR = 1.4, 95% CI = 1.0-1.9) was higher with cortisol post-DST ≥ 1.8 µg/dl; the prevalence of hypertension (OR = 2.1, 95% CI = 1.4-3.3) and diabetes (OR = 1.7, 95% CI = 1.1-2.6) was higher with values ≥ 3.0 µg/dl; and the prevalence of hypertension (OR = 2.0, 95% CI = 1.0-3.7) was higher with levels ≥ 5.0 µg/dl. However, the diagnostic accuracy of the DST for the prediction of cardiometabolic comorbidities in patients with AIs was poor, with areas under the ROC curve < 0.61. CONCLUSIONS: The DST is a poor predictor of cardiometabolic comorbidities in patients with AIs regardless of the cortisol cut-off values applied. This finding suggests that the diagnosis of ACS should not be based solely on the results of the DST. Other clinical, metabolic, or imaging markers showing a better performance for the prediction of the development and progression of cardiometabolic comorbidities in AIs need to be identified.
PURPOSE: The aim of this study was to evaluate the diagnostic accuracy of the 1 mg dexamethasone suppression test (DST) for the prediction of autonomous cortisol secretion (ACS)-related comorbidities in patients with adrenal incidentalomas (AIs). METHODS: This was a retrospective multicenter study. We recruited patients with AI/s ≥ 1 cm, excluding those who, during the study, were found during the extension study of an extra-adrenal cancer, with a known diagnosis of hereditary syndromes characterized by adrenal tumors, those presenting with overt hormonal excess syndromes, and those in whom the DST results were missing. RESULTS: A total of 823 patients met the inclusion criteria. Based on the 1.8, 3.0, and 5.0 µg/dl post-DST cortisol thresholds, the prevalence of ACS was 33.5%, 13.7%, and 5.6%, respectively. The prevalence of hypertension (OR = 1.8, 95% CI = 1.3-2.4), diabetes (OR = 1.6, 95% CI = 1.2-2.2), and dyslipidemia (OR = 1.4, 95% CI = 1.0-1.9) was higher with cortisol post-DST ≥ 1.8 µg/dl; the prevalence of hypertension (OR = 2.1, 95% CI = 1.4-3.3) and diabetes (OR = 1.7, 95% CI = 1.1-2.6) was higher with values ≥ 3.0 µg/dl; and the prevalence of hypertension (OR = 2.0, 95% CI = 1.0-3.7) was higher with levels ≥ 5.0 µg/dl. However, the diagnostic accuracy of the DST for the prediction of cardiometabolic comorbidities in patients with AIs was poor, with areas under the ROC curve < 0.61. CONCLUSIONS: The DST is a poor predictor of cardiometabolic comorbidities in patients with AIs regardless of the cortisol cut-off values applied. This finding suggests that the diagnosis of ACS should not be based solely on the results of the DST. Other clinical, metabolic, or imaging markers showing a better performance for the prediction of the development and progression of cardiometabolic comorbidities in AIs need to be identified.
Authors: Martha A Zeiger; Geoffrey B Thompson; Quan-Yang Duh; Amir H Hamrahian; Peter Angelos; Dina Elaraj; Elliott Fishman; Julia Kharlip Journal: Endocr Pract Date: 2009 Jul-Aug Impact factor: 3.443
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Authors: G Osella; M Terzolo; G Borretta; G Magro; A Alí; A Piovesan; P Paccotti; A Angeli Journal: J Clin Endocrinol Metab Date: 1994-12 Impact factor: 5.958