Time course of 21-hydroxylase antibodies and long-term remission of subclinical autoimmune adrenalitis after corticosteroid therapy: Case report

Citation
A. De Bellis et al., Time course of 21-hydroxylase antibodies and long-term remission of subclinical autoimmune adrenalitis after corticosteroid therapy: Case report, J CLIN END, 86(2), 2001, pp. 675-678
Citations number
25
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
ISSN journal
0021972X → ACNP
Volume
86
Issue
2
Year of publication
2001
Pages
675 - 678
Database
ISI
SICI code
0021-972X(200102)86:2<675:TCO2AA>2.0.ZU;2-#
Abstract
Subclinical Addison's disease is characterized by the presence of adrenal a utoantibodies (ACA) and steroid 21-hydroxylase autoantibodies (21OHAb) with or without adrenal function failure. In our previous longitudinal study so me patients with high titers of ACA and at stage 2 of subclinical adrenocor tical failure showed disappearance of ACA with recovery of normal adrenocor tical function after corticosteroid treatment for Graves' ophthalmopathy. T o investigate whether corticosteroid-induced modification of the adrenal au toimmune markers can also involve 21OHAb and to evaluate whether the remiss ion of subclinical adrenocortical failure can persist over a long period of time, me followed-up for 100 months the levels of 21OHAb and ACA as well a s the metabolic markers of adrenal function in one patient with Graves' oph thalmopathy and at stage 2 of subclinical adrenocortical failure before and after corticosteroid therapy. A 34-yr-old woman with Graves' disease and a ctive ophthalmopathy who was found to be positive for ACA and to have high PRA, low aldosterone levels, and normal basal ACTH and cortisol levels, but impaired cortisol response to ACTH was studied. The patient was treated wi th oral corticosteroid therapy for 6 months. After corticosteroid therapy, 21OHAb, initially positive, became negative in concomitance with the disapp earance of ACA and the restoration of normal adrenal function. The disappea rance of both 21OHAb and ACA and their prolonged absence during the follow- up suggest that corticosteroid treatment can induce long-term remission of subclinical adrenal insufficiency and prevent the onset of the clinical pha se of the disease. Our pilot study may pave the way to future trials aimed at preventing the onset of the clinical signs of Addison's disease in ACA/2 1OHAb-positive patients.