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This version published online on March 7, 2006
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2005-0860
A more recent version of this article appeared on May 1, 2006
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Submitted on April 20, 2005
Accepted on February 27, 2006

Estimated Risk for Developing Autoimmune Addison's Disease in Patients with Adrenal Cortex Autoantibodies

Graziella Coco MD, Chiara Dal Pra MD, Fabio Presotto MD, PhD, Maria Paola Albergoni BSc, Cristina Canova ScD, Beniamino Pedini BSc, Renato Zanchetta MD, Shu Chen MD, PhD, Jadwiga Furmaniak MD, PhD, Bernard Rees Smith PhD, DSc, Franco Mantero MD, and Corrado Betterle MD*

From the Endocrine Unit (GC, BP, RZ, FM, CB) and the 3Internal Medicine Unit (FP, CDP), Department of Medical and Surgical Sciences; and the Department of Medicine and Public Health (CC), University of Padua Medical School, Italy; Blood Bank, Padua General Hospital (MPA), Italy; FIRS Laboratories, RSR Ltd (SC, JF, BRS), Cardiff, United Kingdom

* To whom correspondence should be addressed. E-mail: corrado.betterle{at}unipd.it.

Context: Patients with adrenal-cortex autoantibodies (ACA) without overt autoimmune Addison's disease (AAD) are at risk of adrenal failure. To assess the contribution of different clinical, immunologic, genetic and functional factors in the progression to AAD we followed 100 ACA-positive and 63 ACA-negative patients without AAD for a maximum of 21 years (mean 6.0 years, median 4.8).

Design: ACA were measured by immunofluorescence and 21-OH autoantibodies (Abs) by radioimmunoassay. Adrenal function was assessed by measuring basal levels of cortisol, aldosterone, ACTH, renin activity and cortisol response to ACTH. The risk of developing AAD was calculated using survival and multivariate analyses.

Results: AAD developed in 31 ACA-positive patients and in 1 ACA-negative patient. The cumulative risk of disease in ACA-positive patients was 48.5% (95% CI = 40.8-56.1). The cumulative risk was higher in children than adults (100% vs. 31.9%; P < 0.0001), in males than females (68.6% vs. 42.7%; P = 0.006), in patients with subclinical rather than normal adrenal function at entry (87.4% vs. 30.1%; P < 0.0001), in patients with hypoparathyroidism and/or candidiasis than patients with other autoimmune or nonautoimmune diseases (100% vs. 29.7%; P < 0.0001), in patients with high rather than low-medium ACA-titers (62.8% vs. 41.2%; P = 0.12). The presence of HLA-DRB1 did not appear to contribute to the prediction of AAD. Adjusted hazard ratios by Cox model for the development of AAD were 3.37 for males (CI = 1.38-8.24), 5.23 for hypoparathyroidism and/or candidiasis (CI = 1.53-17.92), 3.33 for high antibody titers (CI = 1.43-7.78), and 6.15 for impaired adrenal function at entry (CI = 2.79-13.57). These results were used to construct a risk algorithm for estimating the probability of developing AAD from the combination of gender, age, adrenal function, antibody titer, and associated autoimmune disorders at entry.

Conclusions: The values of estimated risk could be used to decide appropriate follow-up intervals and future immunointervention strategies.
Key words: Addison's disease • adrenal autoimmunity • adrenal cortex autoantibodies




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