Successful treatment with alectinib after crizotinib-induced hepatitis in ALK-rearranged advanced lung cancer patient: a case report

• Autor(a) principal: Flávia Amaral Duarte
• Data de Publicação: 2021
• Outros Autores: Leonardo Brand Rodrigues, Flávia Rocha Paes, Paulo Henrique Costa Diniz, Helena Flávia Cuba de Almada Lima
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFMG
• Texto Completo: https://doi.org/10.1186/s12890-020-01390-6; http://hdl.handle.net/1843/54670; https://orcid.org/0000-0002-4647-9788; https://orcid.org/0000-0003-0948-1819; https://orcid.org/0000-0003-2016-5593
• topic: Crizotinib; Hepatotoxicity; Alectinib; Non-small cell lung cancer; Case report; Carcinoma pulmonar de células não pequenas; Toxicidade; Fígado; Quinase do linfoma anaplásico; Crizotinibe; Relatos de casos

Background: Besides the clinical beneft of crizotinib in ALK-rearranged metastatic non-small cell lung cancer (NSCLC), concerns about its hepatotoxicity have arisen. It is not clear whether this is a drug class side efect or if the use of other selective ALKs inhibitors is safe after this serious adverse event. While evidence from clinical trials is scarce, reports of treatment after crizotinib-induces hepatitis may add to clinical decision. Case presentation: Herein, we report a case of acute hepatitis induced by crizotinib in a 32-years-old female diagnosed with metastatic NSCLC, harboring the ALK-rearrangement. After 60 days of crizotinib therapy, the patient presented with acute hepatitis, diagnosed after investigation of non-specifc symptoms, such as nausea and fatigue. Serum aspartate aminotransferase and alanine aminotransferase levels had increased from baseline to 3010 IU/L and 9145 IU/L, respectively. Total bilirubin increased up to 7.91 mg/dL, but she did not develop liver failure. After crizotinib discontinuation, a gradual hepatic function recovery occurred. Unfortunately, during the period without specifc oncology treatment, her disease showed an unequivocal progression. Therefore, she started on alectinib with great response, and no liver function alteration recurred. Conclusions: This case suggests that alectinib, even belonging to the same drug class, could be used as an alternative agent when crizotinib is the etiology of liver damage, but more robust evidence has awaited.