Friday, March 26, 2010

Effects of Cushing Disease on Bone Mineral Density in a Pediatric Population

Maya B. Lodish, MDabCorresponding Author Informationemail address, Hui-Pin Hsiao, MDac, Anastasios Serbis, MDa, Ninet Sinaii, PhD, MPHd, Anya Rothenbuhler, MDa, Margaret F. Keil, CRNPa, Sosipatros A. Boikos, MDa, James C. Reynolds, MDe, Constantine A. Stratakis, MD, DScab

Received 30 July 2009; received in revised form 19 October 2009; accepted 16 December 2009. published online 11 March 2010.
Corrected Proof

Objective

To evaluate bone mineral density (BMD) in children with Cushing disease before and after transphenoidal surgery (TSS).

Study design

Hologic dual-energy x-ray absorptiometry (DXA) scans of 35 children with Cushing disease were analyzed retrospectively. Sixteen of the 35 patients had follow-up DXA scans performed 13 to 18 months after TSS. BMD and bone mineral apparent density (BMAD) for lumbar spine (LS) L1 to L4 and femoral neck (FN) were calculated.

Results

Preoperatively, 38% and 23% of patients had osteopenia of the LS and FN, respectively. Both BMD and BMAD Z-scores of the LS were worse than those for the FN (–1.60 ± 1.37 versus –1.04 ± 1.19, P = .003), and (–1.90 ± 1.49 versus –0.06 ± 1.90, P < .001); postoperative improvement in BMD and BMAD were more pronounced in LS than in the FN (0.84 ± 0.88 versus 0.15 ± 0.62, P<.001; and 0.73 ± 1.13 versus –0.26 ± 1.21, P = .015). Pubertal stage, cortisol levels, and length of disease had no effect on BMD.

Conclusions

In children with Cushing disease, vertebral BMD was more severely affected than femoral BMD and this effect was independent of degree or duration of hypercortisolism. BMD for the LS improved significantly after TSS; osteopenia in this group may be reversible.

BMAD, Bone mineral apparent density, BMD, Bone mineral density, CS, Cushing syndrome, DXA, Dual-energy x-ray absorptiometry, FN, Femoral neck, GH, Growth hormone, GHD, Growth hormone deficiency, LS, Lumbar spine, TSS, Transphenoidal surgery, UFC, Urinary free cortisol

a Section on Endocrinology Genetics, Program on Developmental Endocrinology Genetics, National Institutes of Health, Bethesda, MD

b Pediatric Endocrinology Inter-Institute Training Program, National Institutes of Health, Bethesda, MD

c Department of Pediatrics, Kaohsiung Municipal HsiaoKang Hospital and College of Medicine, Kaohsiung Medical University, Taiwan

d Biostatistics and Clinical Epidemiology Service, National Institutes of Health Clinical Center, Bethesda, MD

e Department of Radiology, Nuclear Medicine Division, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, MD

Corresponding Author InformationReprint requests: Dr Maya Lodish, NICHD, NIH, Bldg 10, CRC (East Laboratories), Room 1-3330, 10 Center Dr, MSC 1103, Bethesda, MD 20892.

The authors have no financial relationships relevant to this article to disclose. Supported by the US National Institutes of Health, National Institute of Child Health and Human Development intramural project (Z01-HD-000642-04) (C.S.). The authors declare no conflicts of interest.

PII: S0022-3476(09)01256-6

doi:10.1016/j.jpeds.2009.12.027

© 2010 Mosby, Inc. All rights reserved.

Full Text at http://www.jpeds.com/article/PIIS0022347609012566/fulltext