Endocrine Abstracts

Introduction: Increased prevalence of thyroid autoimmunity has been described in few cases after successful treatment for Cushing’s syndrome. In De Quervain’s thyroiditis (DQT) autoimmunity does not seem to play a primary pathogenetic role.

We describe two cases of DQT coinciding with the resolution of hypercortisolism, after successful treatment of Cushing’s syndrome/disease.

Case 1: A 41-year-old female with Cushing’s disease who refused neurosurgery was started on SOM230. On the third month of successful treatment (UFC=4 μg/24 h), she experienced a febrile state accompanied by malaise and severe neck pain. Clinically, thyroid was tender at palpation and tachycardia was noted. Laboratory tests revealed thyrotoxicosis (TSH=0.065 mU/l, FT₄=2 ng/dl), and elevated ESR (110 mm/h). Thyroid uptake was absent on a technetium thyroid scan and thyroid ultrasonography was indicative of DQT. SOM 230 was temporarily discontinued, but due to persistence of fever and pain, despite non-steroidal anti-inflammatory medication, glucocorticoid treatment with methylprednisolone was initiated, resulting to a dramatic clinical improvement.

Case 2: A 50-year-old female patient with Cushing’s syndrome due to a cortisol secreting adenoma had undergone unilateral adrenalectomy and been placed on glucocorticoid substitution due to HPA axis suppression. Five months post-operatively, at an attempt to taper hydrocortisone dose, she developed left sided neck pain, irradiating to jaw and ear, accompanied by low grade fever and malaise. Laboratory tests showed thyrotoxicosis, high ESR and negative thyroid auto-antibodies. Thyroid ultrasonography and scintigraphy confirmed the diagnosis of DQT. She was treated with prednisolone resulting in immediate symptomatic relief.

Conclusions: The incidence of DQT upon successful therapy of hypercortisolism, either medical or surgical has not been previously described. The exact pathogenetic mechanism could only be speculated. Perhaps the relative or absolute glucocorticoid deficiency, after effective treatment of hypercortisolism, alters immunologic responses and renders patients more vulnerable to thyrolytic processes.