Abstract
Endogenous Cushing's syndrome (CS) is a rare cause of secondary osteoporosis. The long-term consequences for bone metabolism after successful surgical treatment remain largely unknown. We assessed bone mineral density and fracture rates in 89 patients with confirmed Cushing's syndrome at the time of diagnosis and 2 years after successful tumor resection. We determined five bone turnover markers at the time of diagnosis, 1 and 2 years postoperatively. The bone turnover markers osteocalcin, intact procollagen-IN-propeptide (PINP), alkaline bone phosphatase, CTX-I, and TrAcP 5b were measured in plasma or serum by chemiluminescent immunoassays. For comparison, 71 sex-, age-, and body mass index (BMI)-matched patients in whom Cushing's syndrome had been excluded were studied. None of the patients received specific osteoanabolic treatment. At time of diagnosis, 69% of the patients had low bone mass (mean T-score = -1.4 ± 1.1). Two years after successful surgery, the T-score had improved in 78% of patients (mean T-score 2 years postoperatively -1.0 ± 0.9). The bone formation markers osteocalcin and intact PINP were significantly decreased at time of diagnosis (p ≤ 0.001 and p = 0.03, respectively), and the bone resorption marker CTX-I and TrAcP 5b increased. Postoperatively, the bone formation markers showed a three- to fourfold increase 1 year postoperatively, with a moderate decline thereafter. The bone resorption markers showed a similar but less pronounced course. This study shows that the phase immediately after surgical remission from endogenous CS is characterized by a high rate of bone turnover resulting in a striking net increase in bone mineral density in the majority of patients. © 2020 The Authors. Journal of Bone and Mineral Research published by American Society for Bone and Mineral Research.
Highlights
Cushing’s syndrome (CS) is a rare disease with approximately 0.7 to 2.4 new cases per 1 million per year.[1]
Guidelines for the management of osteoporosis due to endogenous CS are still missing.[5]. In terms of risk assessment, the subtype of CS does not seem to influence osteoporosis risk,(6) whereas the morning cortisol levels are negatively correlated with lumbar bone mineral density.[6]. The duration of endogenous Cushing’s syndrome obviously affects bone mineral density.[7]. Whether the T-score is the best predictor for fracture risk is not quite clear.[2]
The mean levels of bone formation markers osteocalcin and intact PINP were significantly decreased compared with the controls, and the bone formation marker bone alkaline phosphatase was increased (Table 1; Fig. 2)
Summary
Cushing’s syndrome (CS) is a rare disease with approximately 0.7 to 2.4 new cases per 1 million per year.[1]. Guidelines for the management of osteoporosis due to endogenous CS are still missing.[5] In terms of risk assessment, the subtype of CS does not seem to influence osteoporosis risk,(6) whereas the morning cortisol levels are negatively correlated with lumbar bone mineral density.[6] The duration of endogenous Cushing’s syndrome (or the duration of exogenous replacement therapy after successful surgery) obviously affects bone mineral density.[7] Whether the T-score is the best predictor for fracture risk is not quite clear.[2] Another area of uncertainty is the natural course of osteoporosis and bone turnover markers once the diagnosis of Cushing’s syndrome has been established. To the best of our knowledge, this is the first such study, and the data obtained will be instrumental for clinicians who care for patients with Cushing’s syndrome
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