Life sciences · Journal article
Frontiers in Pharmacology · November 2, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
In the era of precision targeted therapy, anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors (TKIs) have significantly improved survival outcomes for patients with ALK -positive non-small cell lung cancer (NSCLC). The third-generation ALK inhibitor lorlatinib, characterized by superior antitumor activity, a broader spectrum of ALK mutation sites and enhanced central nervous system (CNS) penetrability, has yielded breakthrough clinical benefits. However, lorlatinib has a distinct adverse event profile, with edema, dyslipidemia, central and peripheral nervous system toxicities, posing key clinical management challenges. Herein, we report the first case of an ALK -fusion NSCLC patient who developed peripheral neuropathy, dysarthria, and sensorineural deafness following lorlatinib treatment. While dysarthria and peripheral neuropathy have been previously documented, sensorineural deafness is extremely rare, and no prior reports describe the concurrent and persistent onset of all three symptoms, underscoring the need for enhanced toxicity monitoring and patient education.