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Complex dyslipidemia induced by lorlatinib therapy: A case study
Julianna West1, Abhimanyu Garg2
1Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA (Dr West).
Context:
Lorlatinib is an anaplastic lymphoma kinase (ALK) inhibitor, which is currently used for the treatment of ALK-positive metastatic non-small cell lung cancer (NSCLC). Previous reports have noticed an association between lorlatinib and hyperlipidemia, however the specific mechanisms for this side effect remain unknown. Some investigators have reported nephrotic syndrome to be the underlying cause of lorlatinib-induced hyperlipidemia.
Case Report:
A 59-year-old female with NSCLC presented with marked elevation of lipid levels, including total cholesterol, triglycerides, low-density lipoprotein-cholesterol (LDL-C), and high-density lipoprotein-cholesterol (HDL-C), after initiation of lorlatinib therapy. Despite high dose atorvastatin and ezetimibe, lipid levels remained elevated. A 24-hour urine collection revealed only 226 mg of protein excretion.
Conclusions:
Lorlatinib induced a complex dyslipidemia in our patient with elevations of both LDL-C and HDL-C. The underlying mechanism of lorlatinib-induced hyperlipidemia remains unknown and is unlikely to be secondary to nephrotic syndrome in many patients.
Insights
Lorlatinib can cause complex hyperlipidemia in non-small cell lung cancer (NSCLC) patients. This side effect is unlikely due to nephrotic syndrome, as indicated by low urine protein levels.
Area of Science:
- Oncology
- Pharmacology
- Nephrology
Background:
- Lorlatinib is an anaplastic lymphoma kinase (ALK) inhibitor for ALK-positive metastatic non-small cell lung cancer (NSCLC).
- Hyperlipidemia is a known side effect of lorlatinib, but its mechanisms are unclear.
- Nephrotic syndrome has been proposed as a cause for lorlatinib-induced hyperlipidemia.
Purpose of the Study:
- To investigate the potential link between lorlatinib and hyperlipidemia.
- To explore the underlying mechanisms of lorlatinib-induced dyslipidemia.
- To assess the role of nephrotic syndrome in lorlatinib-associated hyperlipidemia.
Main Methods:
- A case report of a 59-year-old female NSCLC patient treated with lorlatinib.
- Monitoring of lipid levels (total cholesterol, triglycerides, LDL-C, HDL-C) during lorlatinib therapy.
- Assessment of renal function via 24-hour urine protein excretion.
Main Results:
- The patient experienced marked elevation in all measured lipid parameters after starting lorlatinib.
- Aggressive lipid-lowering therapy with atorvastatin and ezetimibe was ineffective.
- Urine protein excretion was minimal (226 mg/24h), ruling out nephrotic syndrome.
Conclusions:
- Lorlatinib induced a complex dyslipidemia characterized by elevated LDL-C and HDL-C.
- The mechanism of lorlatinib-induced hyperlipidemia remains undetermined.
- Nephrotic syndrome is unlikely to be the cause of hyperlipidemia in many patients receiving lorlatinib.
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