Impaired Hypothalamo-pituitary-adrenal Axis in Patients with Ankylosing Spondylitis

Overview

Journal J Endocrinol Invest

Publisher Springer

Specialty Endocrinology

Date 2009 Jul 22

PMID 19620823

Citations 2

Authors

L Kebapcilar

O Bilgir

A Alacacioglu

Y Yildiz

A Taylan

R Gunaydin

A Yuksel

B Karaca

I Sari

Affiliations

Soon will be listed here.

Abstract

Background: To investigate the hypothalamic-pituitary- adrenal (HPA) axis in patients with ankylosing spondylitis (AS) and healthy controls.

Methods: Forty-nine AS patients and 20 healthy controls were included. Lowdose ACTH test (LDST) was used to assess the HPA axis. Basal cortisol, stimulated peak cortisol levels, and acutephase reactants [C-reactive protein (CRP), erythrocyte sedimentation rate, and fibrinogen] were studied. Bath Ankylosing Spondylitis Functional Index, Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and Bath Ankylosing Spondylitis Metrology Index were also evaluated.

Results: Patient and control groups were not different regarding age, sex, body mass index and waist circumference (WC). Basal cortisol levels did not show a significant difference between groups. However, cortisol increment after low-dose ACTH was significantly impaired in AS subjects with respect to controls (20.0+/-4.4 vs 24+/-2.2 microg/dl, p<0.001). Eleven AS patients had impaired cortisol peak after LDST when a cortisol cut-off is accepted as 500 nmol/l (18 microg/dl) and none of the controls exhibited a peak cortisol responses to LDST<500 nmol/l. Comparison of AS subjects who were receiving anti-tumor necrosis factor (TNF) (no.=23), and conventional therapy (no.=26) yielded similar basal and peak cortisol concentrations. Peak cortisol concentrations were associated with basal cortisol, impaired cortisol response, CRP, and fibrinogen. Impaired cortisol response (subjects with peak cortisol levels <18 microg/dl) was significantly correlated with basal and peak cortisol concentrations and BASDAI.

Conclusion: Our results indicate an increased prevalence of subclinical glucocorticoid deficiency in AS patients. Anti-TNF treatment seems not to have effect on HPA axis.

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Ankylosing spondylitis: etiology, pathogenesis, and treatments.

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