Profound Hypothyroidism as a Reversible Cause of Severe Low-Density Lipoprotein Cholesterol (LDL-C) Elevation: A Case Report

Thyroid hormone plays a central role in regulating lipid metabolism. In states of profound hypothyroidism, impaired triiodothyronine (T3)-mediated regulation of hepatic LDL (low-density lipoprotein) receptor expression results in decreased clearance of apolipoprotein B-containing lipoproteins. These physiologic disturbances can lead to substantial low-density lipoprotein cholesterol (LDL-C) elevation, which can mimic primary genetic lipid disorders and complicate the clinical evaluation of severe hypercholesterolemia. Herein, we describe a patient with autoimmune thyroid disease status post total thyroidectomy who demonstrated marked, reproducible LDL-C elevations during periods of profound hypothyroidism, with substantial improvement upon restoration of euthyroidism. These fluctuations occurred in the absence of lipid-lowering therapy. This case highlights the importance of assessing thyroid function in patients with severe LDL-C elevation. Recognition and treatment of hypothyroidism can substantially improve lipid abnormalities and reveal a reversible endocrine-mediated contributor to marked hypercholesterolemia.

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Publication Details

Journal
Cureus
Published
2026-07-25
DOI
https://doi.org/10.7759/cureus.113365
Primary Topic
Thyroid Disorders and Treatments
Type
article
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article

Profound Hypothyroidism as a Reversible Cause of Severe Low-Density Lipoprotein Cholesterol (LDL-C) Elevation: A Case Report

Shalini Bhat, Nirosh E Mataraarachchi
Cureus
Thyroid Disorders and Treatments
article

Profound Hypothyroidism as a Reversible Cause of Severe Low-Density Lipoprotein Cholesterol (LDL-C) Elevation: A Case Report

Shalini Bhat, Nirosh E Mataraarachchi
article en

Abstract

Thyroid hormone plays a central role in regulating lipid metabolism. In states of profound hypothyroidism, impaired triiodothyronine (T3)-mediated regulation of hepatic LDL (low-density lipoprotein) receptor expression results in decreased clearance of apolipoprotein B-containing lipoproteins. These physiologic disturbances can lead to substantial low-density lipoprotein cholesterol (LDL-C) elevation, which can mimic primary genetic lipid disorders and complicate the clinical evaluation of severe hypercholesterolemia. Herein, we describe a patient with autoimmune thyroid disease status post total thyroidectomy who demonstrated marked, reproducible LDL-C elevations during periods of profound hypothyroidism, with substantial improvement upon restoration of euthyroidism. These fluctuations occurred in the absence of lipid-lowering therapy. This case highlights the importance of assessing thyroid function in patients with severe LDL-C elevation. Recognition and treatment of hypothyroidism can substantially improve lipid abnormalities and reveal a reversible endocrine-mediated contributor to marked hypercholesterolemia.

Cureus
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Thyroid Disorders and Treatments
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