Thyrotoxicosis linked to unstable blood sugar and strikingly low cholesterol in one patient

A newly published case report describes a woman in her early fifties whose long-standing type 2 diabetes became markedly harder to control as her previously diagnosed thyrotoxicosis worsened, with her blood sugar and cholesterol levels tracking the swings in her thyroid hormones over nearly two years of follow-up. The report, published in Frontiers in Endocrinology, follows a single patient seen at an endocrine clinic in Saudi Arabia and documents a longitudinal pattern in which episodes of thyroid hormone excess coincided with sharp rises in fasting glucose and glycated hemoglobin, alongside unusually low concentrations of total cholesterol and low-density lipoprotein cholesterol.

The patient, aged 51 years at first presentation, had lived with type 2 diabetes for approximately 20 years and had already been diagnosed with thyrotoxicosis due to a toxic multinodular goiter. She self-referred to the endocrine clinic on September 10, 2024, seeking help with poor glycemic control ahead of planned thyroid surgery. At that visit, a recent glycated hemoglobin measurement stood at 11.8 percent (105 mmol/mol), and she had lost roughly 17 kilograms. She reported marked hunger, frequent snacking, heat intolerance, sweating, tremor, insomnia, irritability, palpitations, polyuria, and polydipsia, a symptom cluster consistent with both poorly controlled diabetes and excess circulating thyroid hormone.

Management began with attention to dietary contributors to her hyperglycemia. Her diabetes regimen was adjusted: glimepiride was replaced with pioglitazone, and metformin was increased. Before basal insulin was introduced, her fasting plasma glucose and HbA1c improved to 183.4 mg/dL (10.2 mmol/L) and 8.9 percent (74 mmol/mol) by May 6, 2025, a period during which her thyroid hormone concentrations also improved. This parallel movement between thyroid status and glycemia formed one thread of the longitudinal observation.

The pattern reversed when the thyrotoxicosis subsequently worsened. On September 15, 2025, her free triiodothyronine measured 15.5 pmol/L and her free thyroxine 3.8 ng/dL (48.9 pmol/L). At the same time, fasting plasma glucose rose to 293.7 mg/dL (16.3 mmol/L) and HbA1c climbed to 12.1 percent (109 mmol/mol). Strikingly, her lipid profile moved in the opposite direction: total cholesterol was 121.9 mg/dL (3.2 mmol/L) and directly measured LDL cholesterol was 45 mg/dL (1.2 mmol/L), both markedly low.

With continued antithyroid treatment and later intensification of her diabetes therapy, both thyroid biochemistry and glycemic control improved again. By August 24, 2026, free triiodothyronine had fallen to 6.1 pmol/L and free thyroxine to 1.5 ng/dL (19.3 pmol/L). Fasting plasma glucose reached 117.8 mg/dL (6.5 mmol/L) and HbA1c 9.4 percent (79 mmol/mol). Total cholesterol rose to 151.4 mg/dL (3.9 mmol/L) and LDL cholesterol to 66 mg/dL (1.7 mmol/L), mirroring the resolution of the thyrotoxic state.

The surgical side of the story remained unresolved. The patient preferred thyroidectomy and went on to develop compressive symptoms from her goiter, but the operation was delayed, in part because of concerns about her glycemic control and in part because of long surgical appointment intervals.

The author of the report is careful about what the single-patient data can and cannot show. The longitudinal pattern suggests that thyrotoxicosis may have contributed to the glycemic instability and to the low LDL cholesterol and total cholesterol pattern observed. However, concurrent changes in the diabetes treatment regimen prevent attribution of these metabolic shifts to thyroid status alone, since medication adjustments were happening on the same timeline. The case is presented as a hypothesis-generating observation rather than a test of causal mechanisms.

What the report does highlight is a diagnostic point for clinicians managing diabetes. Behavioral contributors to poor glycemic control, such as dietary habits, and physiological drivers, such as thyroid hormone excess, can coexist in the same patient. The author suggests that thyrotoxicosis should be considered when metabolic deterioration appears disproportionate to behavioral factors, particularly in patients with known thyroid disease. As a single-patient case report, the findings cannot establish how often this pattern occurs or how strongly thyrotoxicosis drives glycemic instability in the broader population of people with type 2 diabetes, but they document in detail how glucose and cholesterol measurements moved in relation to thyroid hormone concentrations over repeated clinical encounters.

Subject of Research: A longitudinal case report of metabolic changes during thyrotoxicosis in a patient with type 2 diabetes

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

Article References: Rajab, H. A. (2026). Case Report: A longitudinal single-patient observation of metabolic changes during thyrotoxicosis due to toxic multinodular goiter in type 2 diabetes. Frontiers in Endocrinology, 17, Article 1989874. https://doi.org/10.3389/fendo.2026.1989874

Image Credits: AI Generated

DOI: 10.3389/fendo.2026.1989874

Keywords: thyrotoxicosis, toxic multinodular goiter, type 2 diabetes, HbA1c, LDL cholesterol, total cholesterol, hyperglycemia, case report, endocrinology, thyroidectomy, free thyroxine, glycemic control