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Afatinib-Induced Acute Fatal Pneumonitis in Metastatic Lung Adenocarcinoma / 가정의학회지
Article in English | WPRIM (Western Pacific) | ID: wpr-137669
Responsible library: WPRO
ABSTRACT
Afatinib is an oral tyrosine kinase inhibitor (TKI) that inhibit Endothelial Growth Factor Receptor (EGFR), Human Epidermal Growth Factor Receptor 2 (HER2), and HER4. The common side effects of EGFR TKI are rash, acne, diarrhea, stomatitis, pruritus, nausea, and loss of appetite. Drug induced pneumonitis is the less common adverse effects of EGFR TKI. Afatinib, 2nd generation EGFR TKI is anticipated to overcome drug resistance from 1st generation EGFR TKI according to preclinical study, and several studies are being conducted to compare clinical efficacy between 1st and 2nd EGFR TKI. Several cases of rug induced acute fatal pneumonitis were reported after use of erlotinib or gefitinib. However, a case of acute fatal pneumonitis associated with afatinib was note reported except drug induced pneumonitis in other clinical study. Here, we present a cases of acute severe pneumonitis related with afatinib in metastatic lung adenocarcinoma with literature review.
Subject(s)

Full text: Available Health context: Neglected Diseases Health problem: Diarrhea / Neglected Diseases Database: WPRIM (Western Pacific) Main subject: Appetite / Pneumonia / Pruritus / Stomatitis / Protein-Tyrosine Kinases / Drug Resistance / Adenocarcinoma / Treatment Outcome / Acne Vulgaris / Receptors, Vascular Endothelial Growth Factor Limits: Humans Language: English Journal: Korean Journal of Family Medicine Year: 2016 Document type: Article
Full text: Available Health context: Neglected Diseases Health problem: Diarrhea / Neglected Diseases Database: WPRIM (Western Pacific) Main subject: Appetite / Pneumonia / Pruritus / Stomatitis / Protein-Tyrosine Kinases / Drug Resistance / Adenocarcinoma / Treatment Outcome / Acne Vulgaris / Receptors, Vascular Endothelial Growth Factor Limits: Humans Language: English Journal: Korean Journal of Family Medicine Year: 2016 Document type: Article
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