Bone density and microarchitecture in endogenous hypercortisolism
Summary Objective Osteoporosis is a serious and underestimated complication of endogenous hypercortisolism that results in an increased risk of fractures, even in patients with normal or slightly decreased bone mineral density (BMD). Alterations in bone microarchitecture, a very important component...
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Published in | Clinical endocrinology (Oxford) Vol. 83; no. 4; pp. 468 - 474 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Blackwell Publishing Ltd
01.10.2015
Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
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Summary: | Summary
Objective
Osteoporosis is a serious and underestimated complication of endogenous hypercortisolism that results in an increased risk of fractures, even in patients with normal or slightly decreased bone mineral density (BMD). Alterations in bone microarchitecture, a very important component of bone quality, may explain bone fragility. The aim of this study was to investigate bone density and microarchitecture in a cohort of patients with endogenous Cushing's syndrome (CS).
Design
Cross‐sectional study.
Patients
Thirty patients with endogenous active CS and fifty‐one age‐, sex‐ and body mass index‐matched controls were included.
Measurements
Participants were studied for areal BMD (dual‐energy X‐ray absorptiometry) of the lumbar spine (LS), femoral neck (FN), total femur (TF) and radius (33%), and for volumetric bone density (vBMD) and structure using high‐resolution peripheral quantitative computed tomography (HR‐pQCT) of the distal radius and distal tibia.
Results
Patients with active CS exhibited lower areal BMD and Z‐score values in the LS, FN and TF (P < 0·003 for all comparisons). At HR‐pQCT, the patients with CS also had lower cortical area (P = 0·009 at the radius and P = 0·002 at the tibia), lower cortical thickness (P = 0·02 at the radius and P = 0·002 at the tibia), lower cortical density (P = 0·008 at the tibia) and lower total vBMD (P = 0·002 at the tibia). After the exclusion of hypogonadal individuals, the patients with CS maintained the same microarchitectural and densitometric alterations described above.
Conclusions
Endogenous hypercortisolism has deleterious effects on bone, especially on cortical bone microstructure. These effects seem to be a more important determinant of bone impairment than gonadal status. |
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Bibliography: | ark:/67375/WNG-KXRKWGJL-1 istex:0B1D8634EA7A0B902B38B18DBB3D433C3D466B66 ArticleID:CEN12812 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0300-0664 1365-2265 |
DOI: | 10.1111/cen.12812 |