SUN-369 Unmasking Hyperlipidemia After Graves’ Disease Remission: A Triglyceride Problem

Abstract Disclosure: P.J. Bhatt: None. S.S. Chaidarun: None. Hypothyroidism is a common cause of dyslipidemia and a significant risk factor for atherosclerotic cardiovascular disease. Thyroid hormones affect the production, clearance and transformation of cholesterol but it has been found that thyroid stimulating hormone (TSH) is independently associated with lipid metabolism [1]. In fact, a linear increase in total cholesterol (TC), low density lipoprotein (LDL) and triglyceride (TG) levels and decrease in high density lipoprotein (HDL) levels have been seen with increasing TSH values even within the normal range [2-3]. A 38 year old female with a history of Graves’ disease in remission, type 2 diabetes (A1c 5.3%), depression and hypertriglyceridemia, presented with sudden severe hyperlipidemia with TG >4,425mg/dL [<150], LDL 35mg/dL [<130], HDL 14mg/dL [>50], TC 816mg/dL [<200] with TSH of 2.31mcIU/mL [0.27-4.20]. She had no history of alcohol use or pancreatitis, family history of dyslipidemia, or xanthelasmas on exam. A year ago, her TG level was 1,351mg/dL and TSH was 1.65mcIU/mL. Statin and fibrate medications were not initiated at the time as she was actively trying to conceive. She was started on a low-fat diet, omega 3 fatty acid supplements, 25mcg levothyroxine with goal TSH 0.3-2.0mcIU/mL and statin later switched to fenofibrate to improve her TG levels. After 1 month, TG level was 1,258mg/dL with TSH 1.63mcIU/mL. 3 months after initial presentation, labs again showed TG>4,425mg/dL, LDL 43mg/dL, HDL 8mg/dL, TC of 981 mg/dL, TSH of 1.69mcIU/mL prompting an increase of her levothyroxine dose to 50mcg daily. 3 weeks later, her labs showed improved levels of TG 2,873mg/dL with TSH 1.05mcIU/mL, and 5mcg liothyronine was added. After 2 months, TSH was 0.26mcIU/mL, free T4 was 1.36ng/dL [0.93-1.70] and lipids improved to TG 995mg/dL, LDL 87mg/dL, HDL 26mg/dL and TC 221mg/dL. In overt hypothyroidism, decreased lipoprotein lipase activity reduces clearance of TG and LDL particles and increases absorption of cholesterol from the intestines [1,3]. Studies in patients with subclinical hypothyroidism show an association with dyslipidemia, improved with thyroid supplementation [4,5]. Effects of lipid levels with mild elevation and depression of TSH values, however, have not been well documented. In our patient, TG levels were stable in a more hyperthyroid state. Once TSH values exceeded 2, her TGs suddenly increased 4X her baseline and only began to decrease after treatment with thyroid hormones and return of TSH to a subclinical hyperthyroid state. Despite not meeting criteria for overt or subclinical hypothyroidism, treatment with thyroid hormones helped decrease her TG levels substantially from >4,000mg/dL to <1000mg/dL. Our case highlights the prominent role that TSH and thyroid hormones play in maintaining lipid homeostasis to prevent lipid associated comorbidities and the potential masking of dyslipidemia in a hyperthyroid state. Presentation: Sunday, July 13, 2025

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Journal
Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.2379
Primary Topic
Academic Writing and Publishing
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article
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article

SUN-369 Unmasking Hyperlipidemia After Graves’ Disease Remission: A Triglyceride Problem

Journal of the Endocrine Society
Academic Writing and Publishing
article

SUN-369 Unmasking Hyperlipidemia After Graves’ Disease Remission: A Triglyceride Problem

article en

Abstract

Abstract Disclosure: P.J. Bhatt: None. S.S. Chaidarun: None. Hypothyroidism is a common cause of dyslipidemia and a significant risk factor for atherosclerotic cardiovascular disease. Thyroid hormones affect the production, clearance and transformation of cholesterol but it has been found that thyroid stimulating hormone (TSH) is independently associated with lipid metabolism [1]. In fact, a linear increase in total cholesterol (TC), low density lipoprotein (LDL) and triglyceride (TG) levels and decrease in high density lipoprotein (HDL) levels have been seen with increasing TSH values even within the normal range [2-3]. A 38 year old female with a history of Graves’ disease in remission, type 2 diabetes (A1c 5.3%), depression and hypertriglyceridemia, presented with sudden severe hyperlipidemia with TG >4,425mg/dL [<150], LDL 35mg/dL [<130], HDL 14mg/dL [>50], TC 816mg/dL [<200] with TSH of 2.31mcIU/mL [0.27-4.20]. She had no history of alcohol use or pancreatitis, family history of dyslipidemia, or xanthelasmas on exam. A year ago, her TG level was 1,351mg/dL and TSH was 1.65mcIU/mL. Statin and fibrate medications were not initiated at the time as she was actively trying to conceive. She was started on a low-fat diet, omega 3 fatty acid supplements, 25mcg levothyroxine with goal TSH 0.3-2.0mcIU/mL and statin later switched to fenofibrate to improve her TG levels. After 1 month, TG level was 1,258mg/dL with TSH 1.63mcIU/mL. 3 months after initial presentation, labs again showed TG>4,425mg/dL, LDL 43mg/dL, HDL 8mg/dL, TC of 981 mg/dL, TSH of 1.69mcIU/mL prompting an increase of her levothyroxine dose to 50mcg daily. 3 weeks later, her labs showed improved levels of TG 2,873mg/dL with TSH 1.05mcIU/mL, and 5mcg liothyronine was added. After 2 months, TSH was 0.26mcIU/mL, free T4 was 1.36ng/dL [0.93-1.70] and lipids improved to TG 995mg/dL, LDL 87mg/dL, HDL 26mg/dL and TC 221mg/dL. In overt hypothyroidism, decreased lipoprotein lipase activity reduces clearance of TG and LDL particles and increases absorption of cholesterol from the intestines [1,3]. Studies in patients with subclinical hypothyroidism show an association with dyslipidemia, improved with thyroid supplementation [4,5]. Effects of lipid levels with mild elevation and depression of TSH values, however, have not been well documented. In our patient, TG levels were stable in a more hyperthyroid state. Once TSH values exceeded 2, her TGs suddenly increased 4X her baseline and only began to decrease after treatment with thyroid hormones and return of TSH to a subclinical hyperthyroid state. Despite not meeting criteria for overt or subclinical hypothyroidism, treatment with thyroid hormones helped decrease her TG levels substantially from >4,000mg/dL to <1000mg/dL. Our case highlights the prominent role that TSH and thyroid hormones play in maintaining lipid homeostasis to prevent lipid associated comorbidities and the potential masking of dyslipidemia in a hyperthyroid state. Presentation: Sunday, July 13, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
Dartmouth–Hitchcock Medical Center (US)
Albert Einstein Healthcare Network
Good health and well-being
Openalex Percentile: Top 31%
Academic Writing and Publishing
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