Abstract
With great interest we read the article recently published in Thyroid regarding the exacerbation of autoimmune thyroiditis alter resolution of hypercortisolism (1). However, it was disappointing that the authors included the following sentence, “To our surprise, the literature on this matter seems quite scarce. Although other authors have reported a very few similar cases, to our knowledge there is only one study in which this issue was investigated in a population,” since we have already published, in the European Journal of Endocrinology (2), an article dealing with this topic. In fact, our group studied a population of 59 patients with Cushing's syndrome (CS) to investigate the prevalence of thyroid disorders, a number even bigger than the one published by Colao et al. (3). Among 41 patients, we have searched for the presence of anti-thyroid antibodies, and 56.1% had evidence of thyroid autoimmunity, compared with the 10% prevalence of a control group (p < 0.001). Moreover, 15 of these patients were evaluated before and after resolution of hypercortisolism. During the time they were suffering from CS, only 4 of them (26.7%) had positive titers of anti-thyroid antibodies. However, when the hypercortisolism was cured, 13 patients (86.7%) had shown high titers of the same circulating antibodies, indicating that resolution of the CS produced exacerbation of autoimmune thyroiditis.
As it can be seen, we have demonstrated a remarkably high prevalence of primary thyroid disorders in patients with endogenous CS, which strongly supports the contention that resolution of hypercortisolism triggers the development of autoimmune disorders in predisposed subjects. We have also suggested, following the rationale of Takasu et al. (4), that patients with thyroid autoimmunity may be “protected” from autoimmune thyroid disfunction by the development of CS, because of the immunosuppressor activity of hypercortisolism. We have also postulated that the development of autoimmune thyroid disorders, after the cure of patients with CS, could mimic what happens in postpartum thyroiditis, because pregnancy is a time of immune suppression, followed by a postpartum immunological rebound.
Finally, we agree with the authors of the Letter to the Editor (1) that thyroid autoimmunity (and function) needs to be accurately monitored in patients with CS after disease remission.