Sensorineural hearing loss induced by gefitinib: A CARE-compliant case report and literature reviews.

RATIONALE: Gefitinib is a potent and selective orally active growth factor receptor (EGFR)-tyrosine kinase inhibitor that is commonly used to treat advanced non-small cell lung cancer patients with activating EGFR mutations. Hearing impairment with gefitinib was sparsely reported. In this report, we describe a case of sensorineural deafness associated with the administration of gefitinib, with a Naranjo score of 7. PATIENT CONCERNS: An 81-year-old female was diagnosed with lung adenocarcinoma with bone metastasis and an EGFR-activating mutation. The patient was prescribed gefitinib tablets at a daily dose of 250 mg for lung adenocarcinoma treatment. However, the patient experienced moderate to severe bilateral sensorineural deafness, primarily in her right ear, after taking gefitinib. Following the cessation of gefitinib administration, the patient exhibited partial restoration of auditory function. Upon resuming the medication, she experienced a worsening of deafness. DIAGNOSES: The otoscopic audiogram and hearing test indicated moderate to severe bilateral sensorineural deafness. INTERVENTIONS: The otolaryngologist recommended bilateral hearing aids to enhance hearing function. OUTCOMES: Throughout our follow-up period, the patient did not receive a hearing aid implant. LESSONS: This article first reported the ototoxicity caused by gefitinib. While rare, our report highlights that gefitinib-induced sensorineural deafness is possible and its mechanisms are still unclear. This adverse reaction should be monitored closely during clinical application of gefitinib to improve patient outcomes.

Imaging-Guided Drug Release from Glutathione-Responsive Supramolecular Porphysome Nanovesicles.

Drug delivery systems that can be employed to load anticancer drugs and release them triggered by a specific stimulus, such as glutathione, are of great importance in cancer therapy. In this study, supramolecular porphysome nanovesicles that were self-assembled by amphiphilic porphyrin derivatives were successfully constructed, mainly driven by the π-π stacking, hydrogen bonding, and hydrophobic interactions, and were used as carriers of anticancer drugs. The nanovesicles are monodispersed in shape and uniform in size. The drug loading and in vitro drug release investigations indicate that these nanovesicles are able to encapsulate doxorubicin (DOX) to achieve DOX-loaded nanovesicles, and the nanovesicles could particularly release the loaded drug triggered by a high concentration of glutathione (GSH). More importantly, the drug release in cancer cells could be monitored by fluorescent recovery of the porphyrin derivative. Cytotoxicity experiments show that the DOX-loaded nanovesicles possess comparable therapeutic effect to cancer cells as free DOX. This study presents a new strategy in the fabrication of versatile anticancer drug nanocarriers with stimuli-responsive properties. Thus, the porphysome nanovesicles demonstrated here might offer an opportunity to bridge the gap between intelligent drug delivery systems and imaging-guided drug release.