Endocrine Abstracts

JOINT2380

Introduction: Hashimoto’s thyroiditis and Graves’ disease are the most prevalent autoimmune thyroid disorders. Antibodies targeting the TSH receptor (TRAbs) may be either stimulatory (TSAbs), leading to hyperthyroidism, or blocking (TBAbs), resulting in hypothyroidism. In rare instances, patients may switch from TSAb to TBAb or vice versa, thereby exhibiting alternating hyper- and hypothyroidism. Although the shift from hyperthyroidism to hypothyroidism is commonly observed in clinical practice, progression from hypothyroidism to hyperthyroidism is notably uncommon. Herein, we describe a patient who presented initially with severe hypothyroidism and subsequently transitioned to hyperthyroidism following COVID-19 infection.

Case Presentation: A 57-year-old Caucasian female, smoker, with no previous history of thyroid disease, presented to the emergency department with profound fatigue, lethargy, weight gain, and diffuse edema. The patient reported mild proximal muscle weakness, hoarseness, and memory disturbances. Her medical history included obesity, hyperlipidemia, hypertension, and nephrolithiasis. On physical examination, she appeared myxedematous, with generalized edema, psychomotor retardation, hoarseness, and bradycardia. Laboratory investigations revealed markedly elevated TSH (83.93 μIU/ml), reduced free T4 (<0.42 ng/dl), high anti-TPO antibodies (>1,000 IU/ml), and elevated CPK (1106 U/L). Treatment with liquid levothyroxine was initiated, which resulted in rapid clinical improvement. Subsequently, the patient contracted COVID-19 infection and after a 13-day hospitalization, she was discharged with further clinical and biochemical improvement. One month later, at outpatient follow-up, she was euthyroid and in stable condition. However, two months post-COVID-19 infection, she developed clinical features indicative of hyperthyroidism, including weight loss, palpitations, nervousness, and fatigue in the absence of neck pain, tenderness, or fever. Laboratory evaluation showed a suppressed TSH level (0.011 μIU/ml; normal range: 0.25–3.43 μIU/ml). Despite the reduction of her levothyroxine dosage, her symptoms persisted. A subsequent workup revealed further TSH levels reduction <0.0083 μIU/ml, with normal FT3 and FT4 levels. Notably, thyroid-stimulating immunoglobulins (TSI) were tested positive, prompting initiation of thiamazole therapy alongside continued levothyroxine treatment, following a “block and replace” strategy. Under this combined regimen, the patient remains asymptomatic, euthyroid, and in good overall health.

Conclusions: This case underscores a rare instance of hypothyroidism transitioning to hyperthyroidism, highlighting the potential for alternating stimulatory and blocking TSH receptor antibodies. These findings may be particularly relevant following COVID-19 infection, suggesting that viral infections may trigger or exacerbate underlying autoimmune processes. Further research is warranted to elucidate the immunological mechanisms contributing to this unusual thyroid function shift and optimize management strategies for similar complex cases.