Persistent atherogenic lipoprotein changes during lorlatinib therapy.
- 1Department of Diabetes and Endocrinology, Medical Research Institute KITANO HOSPITAL, PIIF Tazuke-Kofukai, Osaka 530-8480, Japan.
- 2Department of Thoracic Oncology, Osaka International Cancer Institute, Osaka 541-8567, Japan.
Abstract
Lorlatinib, a third-generation anaplastic lymphoma kinase (ALK)/ROS1 tyrosine kinase inhibitor, frequently induces hypercholesterolemia and hypertriglyceridemia, but longitudinal qualitative lipoprotein changes remain incompletely characterized. We describe a 52-year-old woman with ALK-rearranged non-small cell lung cancer who developed persistent dyslipidemia despite lipid-lowering therapy. Before lorlatinib, total cholesterol was 164 mg/dL (SI [International System of Units]: 4.24 mmol/L) (reference range, 148-248 mg/dL [SI: 3.83-6.41 mmol/L]), low-density lipoprotein (LDL) cholesterol was 52 mg/dL (SI: 1.34 mmol/L) (reference range, 65-139 mg/dL [SI: 1.68-3.59 mmol/L]), and triglycerides were 54 mg/dL (SI: 0.61 mmol/L) (reference range, 30-117 mg/dL [SI: 0.34-1.32 mmol/L]). Within 3 weeks after lorlatinib initiation, these increased to 340, 245, and 166 mg/dL, respectively. Longitudinal profiling showed persistent apolipoprotein B (ApoB) elevation, increased oxidized LDL, and a prominent pre-β-lipoprotein fraction. Subclinical hypothyroidism was later detected, and pitavastatin was switched to rosuvastatin. This case highlights the potential value of ApoB and qualitative lipid assessment during prolonged lorlatinib therapy.
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BibTeX
@article{shibue2026persistent,
title = {{Persistent atherogenic lipoprotein changes during lorlatinib therapy.}},
author = {Kimitaka Shibue and Kei Kunimasa and Akihiro Hamasaki},
journal = {JCEM case reports},
year = {2026},
month = oct,
doi = {10.1210/jcemcr/luag324},
url = {https://europepmc.org/article/MED/42923625},
note = {CC BY},
}
RIS
TY - JOUR
TI - Persistent atherogenic lipoprotein changes during lorlatinib therapy.
AU - Kimitaka Shibue
AU - Kei Kunimasa
AU - Akihiro Hamasaki
PY - 2026
DA - 2026/10/22
JO - JCEM case reports
DO - 10.1210/jcemcr/luag324
UR - https://europepmc.org/article/MED/42923625
AB - Lorlatinib, a third-generation anaplastic lymphoma kinase (ALK)/ROS1 tyrosine kinase inhibitor, frequently induces hypercholesterolemia and hypertriglyceridemia, but longitudinal qualitative lipoprotein changes remain incompletely characterized. We describe a 52-year-old woman with ALK-rearranged non-small cell lung cancer who developed persistent dyslipidemia despite lipid-lowering therapy. Before lorlatinib, total cholesterol was 164 mg/dL (SI [International System of Units]: 4.24 mmol/L) (reference range, 148-248 mg/dL [SI: 3.83-6.41 mmol/L]), low-density lipoprotein (LDL) cholesterol was 52 mg/dL (SI: 1.34 mmol/L) (reference range, 65-139 mg/dL [SI: 1.68-3.59 mmol/L]), and triglycerides were 54 mg/dL (SI: 0.61 mmol/L) (reference range, 30-117 mg/dL [SI: 0.34-1.32 mmol/L]). Within 3 weeks after lorlatinib initiation, these increased to 340, 245, and 166 mg/dL, respectively. Longitudinal profiling showed persistent apolipoprotein B (ApoB) elevation, increased oxidized LDL, and a prominent pre-β-lipoprotein fraction. Subclinical hypothyroidism was later detected, and pitavastatin was switched to rosuvastatin. This case highlights the potential value of ApoB and qualitative lipid assessment during prolonged lorlatinib therapy.
SN - 2755-1520
ER -