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Sequential Occurrence of Thyroid Autoantibodies and Graves’ Disease after Immune Restoration in Severely Immunocompromised Human Immunodeficiency Virus-1-Infected Patients

Service d’Immunologie Clinique (V.J., J.T., J.-P.V.) and Laboratoire Central des Radio-Isotopes (M.I.), Hôpital Necker, 75743 Paris; Service d’Endocrinologie (A.P., F.S.) and Service de Maladies Infectieuses et Tropicales (B.H.), Centre Hospitalier Universitaire, 25030 Besançon; Service d’Immunologie Clinique, Hôpital Broussais (M.D.K.), 75674 Paris; and Unité de Maladies Infectieuses, Hôpital Saint-Joseph (J.G.), 75674 Paris, France

Address all correspondence and requests for reprints to: Jean-Paul Viard, M.D., Service d’Immunologie Clinique, Hôpital Necker, 149 rue de Sèvres, 75743 Paris Cedex 15, France.

We analyzed the kinetics of CD4 cells, human immunodeficiency virus (HIV) viral load, and autoantibodies in acquired immune deficiency syndrome patients with Graves’ disease (GD) after immune restoration on highly active antiretroviral therapy (HAART; retrospective study).

Five patients (median age, 41 yr) were diagnosed with GD after 20 (range, 14–22) months on HAART on the basis of clinical and biological hyperthyroidism, diffuse hyperfixation of thyroid scan, and the presence of anti-TSH receptor (anti-TSHR) antibodies (Ab). GD was diagnosed several months after the plasma HIV ribonucleic acid load became undetectable, when the CD4⁺ cell count had risen from 14 (range, 0–62) to 340 (range, 163–460) x 10⁶ cells/L. Antithyroid peroxidase (anti-TPO) and anti-TSHRAb appeared 14 (range, 9–18) and 14 (range, 11–20) months after starting HAART and 12 (range, 6–15) and 11 (range, 9–17) months after the increase in CD4⁺ cells. In 3 patients, TPOAb preceded TSHRAb by 3–10 months. No other autoantibodies were detected. Thyroid antibodies were absent in a group of 55 HIV-1-positive patients with comparable response to HAART and no symptoms of hyperthyroidism (cross-sectional study).

Thyroid-specific autoimmunity can occur upon immune restoration with HAART. Our observations suggest a relationship between thymus-dependent immune reconstitution after immunosuppression and autoimmunity and may provide insight into the pathophysiology of GD.

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