Endocrine Abstracts (2011) 26 MTE15

Cushing's

Susan Webb


Hospital Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain.


Cushing syndrome (CS) is associated with systemic complications, like central obesity, ‘moon’ face, limb atrophy, increased fat mass and reduced bone and lean body mass, excessive fatigue, purple striae, easy bruising and skin ulceration, hirsutism, hypogonadism and decreased libido. Morbidity like hypertension, insulin resistance and/or diabetes mellitus, dyslipidemia, prothrombotic state, vascular disease, atherosclerosis and increased cardiovascular risk, acquired metabolic syndrome, depression, loss of brain volume, cognitive decline and impaired health-related quality of life -HRQoL- may also occur. Mortality is higher than in age- and gender-matched subjects, due to complications directly and/or indirectly correlated with GC excess. Altogether, despite being a rare disease, difficulties in early diagnosis and residual morbidity represent a significant burden for the patients and for the health system.

Biochemical ‘cure’ of hypercortisolism is not followed by normalization of morbidity and mortality, which are still increased. Cardiovascular and metabolic risk, central fat and an unfavorable adipokine profile persist. Bone mass is reduced not only due to endogenous hypercortisolism, but also to duration and dose of exogenous glucocorticoid (GC) replacement therapy. Thus, therapy in operated patients with inhibition of the hypothalamic-pituitary-adrenal axis should be reduced to the lowest dose and minimum duration possible. Specific treatments should be considered in patients with decreased bone mass, aimed at reducing increased fracture incidence. Cognitive and health related quality of life impairments, described in active disease, are still present after endocrine remission. Thus, residual morbidity persists in cured CS, suggesting irreversibility of GC-induced phenomena typical of chronic hypercortisolism. Thus, the primary goal in the prevention and treatment of complications of Cushing’s syndrome is correction of hypercortisolism as soon as possible. Supported by FIS080302 and ERCUSYN 800200.

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