Endocrine Abstracts

Introduction: Thyrotropin receptor stimulating antibodies (TRAb) are responsible for Graves’ disease (GD) manifestations. Other thyroid antibodies, namely thyroperoxidase (TPOAb) and thyroglobulin (TGAb) antibodies are highly prevalent in GD, but their roles in GD presentation and evolution are controversial.

Methods: We retrospectively analysed TPOAb and TGAb levels and evolution in 88 consecutive patients with newly diagnosed GD between 2000 and 2018. The patients were treated with anti-thyroid drugs (ATD) in a block-and-replace regimen for at least 12 months and followed-up after ATD discontinuation for at least one year or until disease relapse.

Results: The mean age at diagnosis was 41.4±12 years, 67/88(76.1%) of patients were women and 16/88(18.2%) of patients were smokers. Thyroid eye disease (TED) was observed in 21/88 (24%) patients. Mean duration of medical treatment and follow-up were 24.6 ± 13.2 months and 80.3±58.2 months, respectively. During follow-up, 51/88 (58%) of patients relapsed. At diagnosis, 64/88 (73%) of patients were TPOAb positive and 45/88 (51%) of patients were TGAb positive. The presence of TPOAb or TgAb antibodies at diagnosis did not influence the relapse (P = 0.356 and P = 0.641, respectively). There was less TED in patients TgAb positive at diagnosis than in patients without TGAb (15.6% vs.32.6%, P = 0.061). Logistic regression showed that the absence of TGAb at diagnosis increased the risk of TED by a factor 2.6, without reaching statistical significance (P = 0.066). TPOAb and TGAb were both positive in 39/88 (44%) of patients, 25/88 (28.5%) of patients had only TPOAb, 6/88 (7%) of patients had only TGAb, and neither antibody was positive in 18/88 (20.5%) of patients. There was no difference in terms of GD relapse (56.4%, 65.4%, 40% and 55.6% respectively, P = 0.722) or TED occurence (P = 0.119) between the four groups. The positivity of TPOAb and/or TgAb at treatment discontinuation or at the last visit before relapse was not predictive of relapse. We observed lower titers of TGAb during treatment in patients who relapsed, however this difference was not significant (P = 0.076). In relapsing patients, TRAb, TPOAb and TGAb significantly decreased during the treatment and increased after ATD discontinuation until relapse.

Conclusion: TPOAb and/or TGAb positivity and evolution were not significantly associated with GD presentation or relapse after a first course of ATD. There is a non significant trend of more recurrence of GD in patients with low levels of TgAb but a slight non significant protection against TED in cases of TGAb positive at diagnosis.