A 28-year-old woman with a history of Graves' disease presented with a two-month history of diarrhea, neck enlargement, tremor, and bilateral, pitting edema of the lower limbs. She had previously been diagnosed with Grave’s disease in 2017 and successfully treated with thirty-six months of carbimazole therapy (ceased in 2020). She had no other clinical signs of heart failure, and her chest radiograph did not demonstrate cardiomegaly or pulmonary edema. Laboratory tests revealed a free thyroxine (fT4) of 55.5 pmol/L (12-22), free triiodothyronine (fT3) of >30.7 pmol/L (3.1-6.8) and a thyroid-stimulating hormone (TSH) of <0.01 mIU/L (0.27-4.2). Thyroid receptor antibodies (TRAB) were positive at 9.5 IU/L (<1) supporting a relapse of Graves' disease. Her creatinine was normal and she did not have significant proteinuria. Her albumin was normal and her liver function tests were not notably impaired - Alanine aminotransferase was 61 U/L (10-35) and aspartate aminotransferase was 53 U/L (10-35). She was commenced on 20mg propranolol twice daily and re-commenced on carbimazole at 15mg three times daily. Within four weeks, she was clinically euthyroid and her lower limb edema had completely resolved. Repeat thyroid function tests demonstrated a TSH of <0.005 mIU/L, fT4 of 18.5 pmol/L, fT3 of 9.6 pmol/L and a TRAB of 9.5 IU/L.
This case highlights the rare presentation of bilateral, pitting lower limb edema in the context of hyperthyroidism without features of pretibial myxoedema, cardiac or renal involvement. The exact mechanism of pitting oedema in this context remains unclear but has been postulated to include impaired peripheral lymph drainage, local vascular mechanisms and thyroid hormone-induced activation of the renin-angiotensin-aldosterone system, causing to fluid retention. This case emphasizes the importance of considering hyperthyroidism in the differential diagnosis of unexplained bilateral pitting edema.