Marked recovery of bone mineral density following cure of Cushing's syndrome
Katsuhito NishiyamaToshitsugu SugimotoHiroshi KajiRiko KitazawaToru YamaguchiYasuo ImaiMasaaki FukaseKazuo Chihara
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Objective To investigate the effects of Cushing’s disease (CD) and adrenal-dependent Cushing’s syndrome (ACS) on bone mineral density (BMD) and bone metabolism. Methods Data were retrospectively collected for 55 patients with hypercortisolism (CD, n = 34; ACS n = 21) from January 1997 to June 2014. BMD was examined in all patients, and bone turnover markers were tested in some patients. Healthy controls (n = 18) were also recruited. Results The lumbar spine and femoral neck BMD were significantly lower in the ACS and CD groups than in the control group. Lumbar BMD was significantly lower in the ACS than CD group. The collagen breakdown product (CTX) concentrations were significantly higher while the osteocalcin and procollagen type I N-terminal propeptide (PINP) concentrations were significantly lower in the ACS and CD groups than in the control group. The PINP concentration was significantly lower while the CTX concentration was significantly higher in the ACS than CD group. In the CD group only, lumbar BMD and serum adrenocorticotropic hormone had a significant positive correlation. Conclusions Bone turnover markers indicated suppressed osteoblast and enhanced osteoclast activities. PINP and CTX changes might indicate bone mass deterioration. Adrenocorticotropic hormone might be protective for lumbar BMD in patients with CD.
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Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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The mineral density of bone was measured in 45 patients with primary hyperparathyroidism before surgical treatment and during follow-up averaging 6.5 years, using the Am241 gamma transmission method. Statistically significant demineralization was found at the time of surgery. Removal of pathologic gland(s) was followed by healing of bone density during periods up to 4-5 years. Thereafter bone loss was again faster than in controls. The cause may be a persistent disturbance in the bone-remodelling process.
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