Alterations of bone mineral density and bone turnover in patients with Cushing's syndrome.
- Author:
Sun Hee PARK
1
;
Sun Wook KIM
;
Seon Hwa LEE
;
Do Joon PARK
;
Kyong Soo PARK
;
Seong Yeon KIM
;
Bo Youn CHO
;
Hong Kyu LEE
Author Information
1. Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Cushing's syndrome;
Bone mineral density;
Biochemical bone marker
- MeSH:
Bone Density*;
Bone Diseases, Metabolic;
Bone Resorption;
Cushing Syndrome*;
Female;
Femur;
Femur Neck;
Gonads;
Humans;
Osteoblasts;
Osteocalcin;
Osteogenesis;
Osteoporosis;
Skeleton;
Spine
- From:Korean Journal of Medicine
2000;58(5):560-567
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Although it is generally accepted that high serum glucocorticoid levels causes osteoporosis by suppressing the bone formation, conflicting results have reported on bone resorption. But, previous studies have been carried out in patients with glucocorticoid excess secondary to exogenous glucocorticoid treatment of disorders, which also affect bone turnover and mass by themselves. The purpose of this study were to assess the effect of glucocorticoid excess on bone mass and turnover not influenced by other diseases known to affect skeleton and by different gonadal status and sex and to study the reversibility of osteopenia after cure of Cushing's syndrome. METHODS: We measured bone mineral density using dual energy X-ray absorptiometry(DEXA) in 28 patients with Cushing's syndrome before and after surgical cure. In addition, in the patients with Cushing's syndrome and 21 healthy premenopausal women matched for age, we measured biochemical bone markers. RESULTS: 1) Marked osteopenia was present in most patients with active Cushing's syndrome. Lumbar spine BMD and Ward's triangle BMD were significantly lower than femoral neck BMD and femoral great trochanter BMD.(Z-score: lumbar spine -2.22+/-1.17, femoral neck -0.71+/-1.08, Ward's triangle -1.77+/-0.97, femoral great trochanter -0.64+/-0.71; mean+/-SD, p< 0.05). In patients with active Cushing's syndrome, serum osteocalcin, a marker of osteoblastic function, was reduced(p< 0.05), and bone resorption was increased, as indicated by increased urinary N-telopeptide(p< 0.05). 2) Osteopenia was still in patients after surgical cure.(Z-score: lumbar spine -1.59+/-1.01, femoral neck -0.47+/-0.58, Ward's triangle -1.44+/-0.77, femoral great trochanter -0.42+/-0.61). In Cushing's syndrome patients after surgical cure, serum osteocalcin and urinary N-telopeptide were higher compared to controls but not stastistically significant(p> 0.05). 3) When compared with pretreatment values, BMD after surgical cure of Cushing's syndrome was increased significantly(p< 0.05). Serum osteocalcin was increased and urinary N-telopeptide was decreased significantly(p< 0.05). CONCLUSION: These results show that compared to age matched control, premenopausal Cushing's syndrome patients have reduced bone formation, increased bone resorption, and reduced BMD, especially trabecular bone and that these abnormalities are improved after surgical cure.
