RESUMO
Since December 2019 SARS-CoV-2 infections have affected millions of people worldwide. Along with the increasing number of COVID-19 patients, the number of cases of opportunistic fungal infections among the COVID-19 patients is also increasing. There have been reports of the cases of aspergillosis and candidiasis in the COVID-19 patients. The COVID-19 patients have also been affected by rare fungal infections such as histoplasmosis, pneumocystosis, mucormycosis and cryptococcosis. These fungal infections are prolonging the stay of COVID-19 patients in hospital. In this study several published case reports, case series, prospective and retrospective studies were investigated to explore and report the updated information regarding candidiasis, crytptococcosis, aspergillosis, mucormycosis, histoplasmosis, and pneumocystosis infections in COVID-19 patients. In this review, the risk factors of these co-infections in COVID-19 patients have been reported. There have been reports that the comorbidities and the treatment with corticoids, monoclonal antibodies, use of mechanical ventilation, and use of antibiotics during COVID-19 management are associated with the emergence of fungal infections in the COVID-19 patients. Hence, this review analyses the role of these therapies and comorbidities in the emergence of these fungal infections among COVID-19 patients. This review will help to comprehend if these fungal infections are the result of the co-morbidities, and treatment protocol followed to manage COVID-19 patients or directly due to the SARS-CoV-2 infection. The analysis of all these factors will help to understand their role in fungal infections among COVID-19 patients which can be valuable to the scientific community.
RESUMO
BACKGROUND: Targeted therapy in adenocarcinoma is recommended. The use of immune check point inhibitors for the treatment of Non-small cell lung carcinoma (NSCLC) is used as both first-line and the second-line treatment strategy. The current study was undertaken to assess the frequency of programmed cell death ligand-1 (PD-L1) expression with anaplastic lymphoma kinase (ALK), proto-oncogene 1, receptor tyrosine kinase (ROS), epidermal growth factor receptor (EGFR), Kirsten rat sarcoma (KRAS), and v-Raf murine sarcoma viral oncogene homolog B (BRAF)V600E driver gene mutations in NSCLC adenocarcinoma phenotype. It assesses the frequencies of all markers in the cases where both treatment strategies can be implemented. Expression of the all markers was further compared with demographic, clinical parameters, and overall survival rate. MATERIALS AND METHODS: The formalin-fixed paraffin-embedded (FFPE) tissue blocks were used in immunohistochemistry (IHC) staining and real-time polymerase chain reaction (RT-PCR) for determining the driver genes and PD-L1 expression in the 100 NSCLC-Adenocarcinoma cases. RESULTS: PD-L1 positivity was observed in 26.36% (n=29/110) cases in adenocarcinoma. No significant differences in PD-L1 expression were observed among patients harboring ALK, ROS1, EGFR, KRAS, and BRAF mutations EGFR mutations had significant association with smoking status. (p= 0.008), Thyroid transcription factor 1 (TTF1) (p=0.0005) and Napsin (p=0.002) expression. ALK gene re-arrangement was significantly related to age (p= 0.001), gender (p= 0.009) and smoking status (p= 0.043). The single versus multiple driver mutations were significantly correlated with smoking status (p=0.005). In the survival rate analysis, EGFR (p=0.058), KRAS (p=0.021), and PD-L1 (p=0.039) were significantly high with the positive versus negative group. CONCLUSIONS: The current study is a novel attempt to document the co-expression of multiple driver mutations in the NSCLC-adenocarcinoma phenotype. PD-L1 immunopositivity in NSCLC-adenocarcinoma was higher with EGFR mutation as compared to those of KRAS, ALK, ROS, and BRAF driver genes.
