ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2011) 25 P219

Low bone mass is an infrequent long-term sequelea of pituitary disease

Julie Lynch & Robert Murray

Leeds Teaching Hospitals NHS Trust, Leeds, West Yorkshire, UK.

Introduction: Within the setting of putative or established pituitary disease the primary disease process (i.e. Cushing’s disease), hormone deficits (i.e. sex steroids, GH), and inappropriate replacement therapy (i.e. glucocorticoids) are reputed to predispose to low bone mass.

Patients and Methods: We examined bone mass at the lumbar spine (LS) and total hip (TH) using DXA in 259 patients with an insult to the hypothalamo–pituitary axis (51.6±15.7 years; 133F; BMI 29.3±5.5 kg/m2). Mean duration of follow-up 11.4±9.5 years. In patients who were receiving treatment for osteoporosis the scan result immediately before therapeutic intervention was used in this analysis.

Results: In the cohort overall Z-scores at the LS and TH were +0.09±1.81 and +0.54±1.21 respectively. A Z-score of less than −2.0 was observed at the LS in 10.4% and at the TH in 2.2% of individuals. No difference was observed in bone mass between subgroups at either the LS or TH following stratification for the primary pathology (Table). Further analysis of bone mass (Z-scores) by the number of additional anterior pituitary hormone deficits revealed no evidence of a trend towards lower bone mass with greater degree of hypopituitarism.

Table 1
n=Lumbar spine (Z-score)Total hip (Z-score)
Cushing’s Dis21+0.305±1.879+0.900±0.923

Conclusion: The impact of hypopituitarism and hormone replacement therapy has negligible impact on bone mass in long-term survivors of patients with a putative or established insult to the hypothalamo–pituitary axis.

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