Beyond ‘essential’ – progression from subclinical hyperthyroidism to T3-thyrotoxicosis presenting as refractory hypertension: a case report

Background : Subclinical hyperthyroidism is often considered a mild condition, yet it may progress to overt thyrotoxicosis with systemic consequences. Hypertension is a recognized though underappreciated cardiovascular complication of thyroid dysfunction. We report a case in which resistant hypertension was ultimately attributable to evolving thyroid disease and was controllable only after anti-thyroid therapy was introduced, emphasizing the need to consider secondary causes in refractory hypertension. Case Presentation : A 48-year-old Nigerian woman with a family history of hyperthyroidism presented with a diffuse anterior neck swelling and known hypertension. At baseline, she had subclinical hyperthyroidism and blood pressure of 140/90 mmHg while on amlodipine and losartan. Over 24 weeks, her thyroid status progressed to overt T3-predominant thyrotoxicosis, during which her blood pressure rose sharply to 170/120 mmHg despite intensifying of antihypertensive therapy. She also developed dyslipidaemia and impaired fasting glucose. Initiation of carbimazole 10–20 mg daily led to rapid blood pressure normalization (120/80 mmHg), improvement in glycaemia, and eventual restoration of euthyroidism by week 36, although mild dyslipidaemia persisted. Aetiology could not be definitively classified due to resource limitations, but the temporal association between thyroid correction and blood pressure improvement suggests that hyperthyroidism may have contributed to her hypertension. Conclusion : This case illustrates that hypertension may be secondary to thyroid dysfunction and remain resistant to conventional treatment until euthyroidism is achieved. It also highlights the cardiovascular potency of T3 thyrotoxicosis and its systemic effects on glucose and lipid metabolism. Clinicians should consider thyroid disease in patients with intractable hypertension, particularly when accompanied by metabolic derangements or family history. Early recognition and timely initiation of anti-thyroid therapy can be decisive in achieving clinical stability and preventing complications.