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Bone turnover in patients with endogenous Cushing's syndrome before and after successful treatment
A Szappanos1, J Toke, D Lippai
12nd Department of Medicine, Semmelweis University, Budapest, Hungary.
Unlabelled:
We investigated bone turnover and its restoration in a large number of patients in the active phase and after cure of endogenous Cushing's syndrome. Furthermore, the usefulness of serum osteocalcin and collagen breakdown products as potential markers of active Cushing's syndrome was also evaluated.
Introduction:
Suppressed bone formation is one of the most characteristic features of Cushing's syndrome (CS). Despite numerous previous reports, many aspects of the disturbed bone metabolism of these patients are unexplored. In this study, we investigated the time course of bone marker changes after the cure of CS as well as correlations between bone markers and serum cortisol concentrations.
Methods:
Eighty-seven patients with CS were studied. Patients were followed up to 48 months after surgical cure. Serum osteocalcin (OC) and collagen breakdown products (CTX) were measured with immunochemiluminescence method and compared to the results of 161 healthy controls.
Results:
OC showed a negative, while CTX displayed a positive correlation with serum cortisol. Patients with diabetes mellitus and myopathy had significantly lower serum OC levels compared to those without these complications. The area under the curve of OC obtained by receiver-operating characteristics analysis for the discrimination of patients with CS from healthy controls was 0.9227. Postoperative OC increased rapidly from the first few days or weeks reaching its maximum at the sixth month and remained stable after the 24th postoperative month.
Conclusions:
Our study demonstrated significant correlations between serum cortisol and both bone formation and resorption markers in the active phase of CS. We propose that OC may serve as a sensitive biologic marker of glucocorticoid activity in endogenous CS during its active phase and it may reflect the clinical cure of the disease.
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