Epidermal growth factor receptor-mutant pulmonary adenocarcinoma coexisting with tuberculosis

Abstract

Rationale: Lung cancer and pulmonary infections can have similar clinical and radiographic manifestations. Treatment for the coexistence of epidermal growth factor receptor (EGFR)-mutant pulmonary adenocarcinoma and tuberculosis remains unclear. Patient concerns: We reported a case of EGFR-mutant lung adenocarcinoma (mimicking pulmonary infections) that coexisted with pulmonary tuberculosis during the course of the disease. Diagnoses: The patient was initially diagnosed with pneumonia-like pulmonary adenocarcinoma with EGFR exon 19 deletions based on computed tomography scan, fiberoptic bronchoscopy, pathology, and genetic analysis, and then coexistence with active tuberculosis (TB) was confirmed via laboratory examinations and TB-DNA polymerase chain reaction. Interventions: Antibiotics and gefitinib were administered initially. A combination of gefitinib and anti-TB treatment was then administered when active TB was confirmed, and osimertinib was then prescribed because the disease was progressive and EGFR T790 M mutation was detected. Outcomes: The patient has survived with a stable disease status to date. Lessons: Exploring and ruling out differential diagnoses between pulmonary malignancies and infectious diseases is vital for treatment decisions and outcomes. The combined gefitinib-anti-TB regimen was safe, though it needed modification.

Visualization analysis of research progress and trends in coexistence of lung cancer and pulmonary tuberculosis using bibliometrics

“…Patients with drugresistant TB or with LC often exhibit gene mutations associated with drug resistance, which may promote the occurrence of LC-PTB comorbidity. For instance, previous studies have revealed a potential link between TB and EGFR gene mutations leading to LC drug resistance [73,74]. In drug-resistant populations, significant increases in phosphatase and tensin homolog mutations, which inhibit the tumor suppressor phosphatidylinositol 3-kinase (PI3K) pathway, have been observed.…”