Table of Contents
Advances in Endocrinology
Volume 2014 (2014), Article ID 231432, 14 pages
http://dx.doi.org/10.1155/2014/231432
Review Article

Persistent Comorbidities in Cushing’s Syndrome after Endocrine Cure

Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBER-ER, Unidad 747), Instituto de Investigación Biomédica (IIB)-Sant Pau, ISCIII, Hospital Sant Pau, Endocrinology/Medicine Department and Universitat Autònoma de Barcelona, C. S. Antoni Maria Claret no. 167, 08025 Barcelona, Spain

Received 13 February 2014; Revised 15 April 2014; Accepted 15 April 2014; Published 4 May 2014

Academic Editor: Sarantis Livadas

Copyright © 2014 Eugenia Resmini. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

It was assumed that resolution of hypercortisolism in Cushing syndrome (CS) was followed by normalization of morbidity; however, in the last decade evidence is accumulating that patients with cured CS still have increased morbidity and mortality after the biochemical control of hypercortisolism. Patients with CS have an increased cardiovascular and metabolic risk and persistent accumulation of central fat, with an unfavorable adipokine profile, not only during the active phase of the disease but also long after biochemical remission. Clinical management should be particularly careful in identifying global cardiovascular risk, as a primary goal during the followup of these patients, aimed at improving global vascular morbidity. Moreover bone mass is reduced not only due to the endogenous hypercortisolism but also due to duration and dose of exogenous glucocorticoid (GC) replacement therapy after surgery. Thus, therapy in operated patients with inhibition of the hypothalamic-pituitary-adrenal axis should be reduced to the lowest dose and duration possible. Specific treatments should be considered in patients with decreased bone mass, aimed at reducing the increased fracture incidence. Finally, cognitive and health related quality of life impairments, described in active disease, are still abnormal after endocrine cure. Thus, residual morbidity persists in cured CS, suggesting irreversibility of GC-induced phenomena, typical of chronic hypercortisolism.