Israel Medical Association Journal

Background: No specific clinical or histological factors are recognized to be associated with the development of pericardial effusion in non-small cell lung cancer (NSCLC) other than a metastatic disease.

Objectives: To assess whether specific clinical and histological features are associated with development of pericardial effusion in patients with NSCLC.

Methods: A consecutive cohort of patients with NSCLC who presented with symptomatic pericardial effusion 2014–2017 was compared to a control group of patients with advanced NSCLC without pericardial effusion.

Results: The 27 patients in the effusion group were generally younger, more often female, and with a higher percentage of never-smokers, compared to the 54 patients of the control group. Epidermal growth factor receptor/anaplastic lymphoma kinase (EGFR/ALK) mutation tumors were found in 48% of patients in the effusion group vs. 25% in the control group. In the multivariate analysis, the unadjusted odds ratio (OR) for the development of pericardial effusion in patients with somatic mutations was significantly higher compared to wild type tumors (OR 2.65, 95% confidence interval 1.00–7.00). However, a suspected association between pericardial effusion and mutation status was found to be confounded by age. While a high rate of recurrence was observed when pericardiocentesis was initially performed (9/17, 53%), no recurrence was documented when pericardial window procedure was performed (total of 17 patients).

Conclusions: Patients with EGFR/ALK mutations may be at higher risk for the development of pericardial effusion; therefore, attending physicians need to be aware and have a high index of clinical suspicion

Background: The main acquired resistance mechanism to first- and second-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in EGFR mutant non-small cell lung cancer (NSCLC) is the propagation of T790M clones, which can be detected in circulating tumor DNA (ctDNA).

Objectives: To analyze osimertinib outcomes according to T790M testing method.

Methods: The study comprised 33 consecutive patients with advanced EGFR mutant NSCLC who were diagnosed with a T790M mutation after progression on first- or second-generation EGFR TKIs and treated with osimertinib. The patients were divided into groups A (diagnosed by tumor testing) and B (by ctDNA testing). Osimertinib outcomes were compared between the groups.

Results: Objective response rate with osimertinib comprised 54% and 62% in groups A and B, respectively (P = 0.58). Median progression-free survival (PFS) with osimertinib was 8.9 months (95% confidence interval [95%CI] 1.8–17.5) and 9.1 months (95%Cl 5.3–12.6) in groups A and B, respectively (log-rank test 0.12, P = 0.73). Median overall survival (OS) was 13.8 months (95%CI 4.9–25.5) and 13.8 months (95%Cl 7.7–27.7) in groups A and B, respectively (log-rank test 0.09, P = 0.75). T790M testing technique did not affect PFS (hazard ratio [HR] 1.16, 95%CI 0.50–2.69, P = 0.73) or OS (HR = 1.16, 95%CI 0.45–3.01, P = 0.76). The proportion of patients diagnosed by ctDNA grew from 56% in 2015 to 67% in 2016–2017.

Conclusions: Our study provides a ctDNA validation for the purpose of T790M testing in EGFR mutant NSCLC.

Objectives: To evaluate in a randomized control trial whether uninterrupted administration of angiotensin II (AngII) blockade medications influence estimated glomerular filtration rate (eGFR) in patients undergoing non-emergent coronary angiography.

Methods: Patients receiving treatment with angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACE-I/ARB) were recruited consecutively. The enrolled subjects were randomized into three groups at a 1:1:1 ratio: group A (ACE/ARB stopped 24 hours prior to the procedure and restarted immediately after the procedure), group B (ACE/ARB stopped 24 hours prior to the procedure and restarted 24 hours after the procedure), and group C (ACE/ARB continued throughout the study period). Plasma creatinine was measured and eGFR was calculated according to the Cockroft-Gault equation before and 48 hours after the coronary angiography. The primary endpoint was a change in eGFR at 48 hours.

Results: Groups A, B and C comprised 30, 31 and 33 patients respectively. The mean age of the study population was 65 ± 12 years and 67% were males. Fifty percent of the subjects had diabetes mellitus. The primary endpoint analysis showed that at 48 hours after the procedure there was no difference in ΔeGFR between groups A and C (4.25 ± 12.19 vs. 4.65 ± 11.76, P = 0.90) and groups B and C (3.72 ± 17.42 vs. 4.65 ± 11.76, P = 0.82). In post-hoc analysis the patients were clustered according to the following groups: medical alternation (group A and B) versus control (group C) and to baseline eGFR ≥ 60 ml/min vs. eGFR < 60 ml/min. In patients with baseline eGFR < 60 ml/min the ΔeGFR (baseline eGFR-eGFR 48 hours post-angiography) was significantly different between the intervention vs. control group (median 5.61 vs. median -2.19, P = 0.03 respectively). While in patients with baseline eGFR ≥ 60 ml/min there was no significant difference in ΔeGFR between the intervention and control groups.

Conclusions: ACE-I and ARB can safely be used before and after coronary angiography in patients with eGFR ≥ 60 ml/min.