Case Report: A longitudinal single-patient observation of metabolic changes during thyrotoxicosis due to toxic multinodular goiter in type 2 diabetes

Thyrotoxicosis can worsen glucose regulation and is also associated with lower circulating total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), a metabolic pattern that may be less readily recognized in routine diabetes care. We report a woman aged 51 years at first presentation, with approximately 20 years of type 2 diabetes mellitus and previously diagnosed thyrotoxicosis due to toxic multinodular goiter, who self-referred to our endocrine clinic on September 10, 2024 seeking help with poor glycemic control before planned thyroid surgery. A recent glycated hemoglobin (HbA1c) was 11.8% (105 mmol/mol), she had lost approximately 17 kg, and she reported marked hunger, frequent snacking, heat intolerance, sweating, tremor, insomnia, irritability, palpitations, polyuria, and polydipsia. Dietary contributors were addressed, glimepiride was replaced with pioglitazone, and metformin was increased. Before basal insulin was introduced, fasting plasma glucose (FPG) and HbA1c improved to 183.4 mg/dL (10.2 mmol/L) and 8.9% (74 mmol/mol) on May 6, 2025 while thyroid hormone concentrations also improved. When thyrotoxicosis subsequently worsened on September 15, 2025, free triiodothyronine (FT3) was 15.5 pmol/L and free thyroxine (FT4) was 3.8 ng/dL (48.9 pmol/L), FPG rose to 293.7 mg/dL (16.3 mmol/L) and HbA1c to 12.1% (109 mmol/mol), and TC and directly measured LDL-C were 121.9 mg/dL (3.2 mmol/L) and 45 mg/dL (1.2 mmol/L), respectively. With continued antithyroid treatment and later intensification of diabetes therapy, thyroid biochemistry and glycemia improved; by August 24, 2026, FT3 was 6.1 pmol/L, FT4 1.5 ng/dL (19.3 pmol/L), FPG 117.8 mg/dL (6.5 mmol/L), HbA1c 9.4% (79 mmol/mol), TC 151.4 mg/dL (3.9 mmol/L), and LDL-C 66 mg/dL (1.7 mmol/L). The patient preferred thyroidectomy and developed compressive symptoms, but surgery remained delayed because of glycemic concerns and long surgical appointment intervals. This longitudinal pattern suggests that thyrotoxicosis may have contributed to glycemic instability and the low LDL-C and TC pattern. Concurrent diabetes-treatment changes prevent attribution to thyroid status alone, but the case highlights that behavioral contributors and physiological drivers can coexist and that thyrotoxicosis should be considered when metabolic deterioration appears disproportionate to behavioral factors.