Primary Pulmonary Diffuse Large B Cell Lymphoma (PPDLBCL) is an extremely rare entity, which exhibits an aggressive behavior by compressing local blood vessels. It represents only 0.04% of all lymphoma cases and is extremely rare in young age. We present a case of a primary pulmonary lymphoma with superior vena cava syndrome (SVCS) in a young female. 27-year-old African American female presented with fever, cough, and facial puffiness for 2 weeks and unintentional weight loss. Chest examination showed decreased breath sounds and dullness on percussion on right side. Labs were normal except for mild leukocytosis, high lactate, and lactate dehydrogenase. Chest X-ray showed a large right side infiltrate with pleural effusion but chest CT showed 10 × 14 × 16 cm mass in the right lung without hilar and mediastinal lymphadenopathy. CT guided biopsy of the right lung mass was done and large B cell lymphoma was diagnosed. She received “involved field radiation” because of the bulky tumor size and superior vena cava involvement prior to R-CHOP to which she responded well. PPDLBCL should be considered as one of the differentials in a young patient with a large lung mass, which needs timely diagnosis and management.
PURPOSE: COPD is important cause of hospital admission and is associated with significant morbidity, mortality and healthcare cost. Centers for Medicare and Medicaid (CMS) has expanded its Hospital Readmissions Reduction Program to financially penalize hospitals with higher than expected all-cause 30-day readmission rates following a hospitalization for COPD exacerbation 1. The factors affecting COPD readmission is still poorly understood and vary in different patient population. This study aims to predict factors associated with 30 days readmission for COPD in African American (AA) patients. METHODS: This was a retrospective observational study performed in a community Hospital in Central Brooklyn. Data from 867 African American patients who were admitted with diagnosis of COPD exacerbation between the period of January 1, 2013 and December 31, 2015 were analyzed.
Background: Bruton’s tyrosine kinase (BTK), a kinase downstream of the B-cell receptor, involves in the B cell survival and proliferation and has become an attractive therapeutic target. Ibrutinib is an oral potent, covalent inhibitor of BTK and hence employed in many hematologic malignancies. We performed a systematic review and pooled analysis of randomized controlled trials (RCTs) to determine the risk of atrial fibrillation (AF) and pulmonary toxicities among patients treated with ibrutinib. Methods: We performed a comprehensive literature search using MEDLINE, EMBASE databases, and meeting abstracts through September 2018. Phase 3 RCTs that mention AF and pulmonary toxicities as adverse effects were incorporated in the analysis. Mantel-Haenszel method was used to calculate the estimated pooled risk ratio with 95% CI. Random effects model was applied. Results: 4 phase III RCTs with a total of 1,383 patients with chronic lymphocytic leukemia or small lymphocytic lymphoma were eligible. Studies comparing Ibrutinib (I) vs ofatumumab, I vs chlorambucil, I+ bendamustine (B)+ rituximab (R) vs placebo + B+ R, and I vs R were included in the analysis. The AF incidence was 41 (5.686%) in the ibrutinib group vs 8 (1.208%) in the control arm. The relative risk (RR) for AF was statistically significant at 3.825 (95% CI: 1.848–7.917; P<.0001) and RD was 0.041 (95% CI: 0.023–0.059; P<.0001). The RR of all-grade side effects was as follows: cough, 1.133 (95% CI: 0.724–1.773; P=.584); edema, 1.375 (95% CI: 0.943–2.006; P=.098); pneumonia, 1.227 (95% CI: 0.884–1.703; P=.221); and upper respiratory infections (URI), 1.075 (95% CI: 0.809–1.429; P=.616). The RR of high-grade side effects was as follows: cough, 0.373 (95% CI: 0.063–2.209; P=.277); edema, 1.232 (95% CI: 0.199–7.649; P=.822); pneumonia, 1.277 (95% CI: 0.847–1.926; P=.243); and URI, 1.555 (95% CI: 0.239–10.127; P=.644). Conclusion: Our meta-analysis demonstrated that patients on ibrutinib noted a significant increase in the risk of atrial fibrillation with a relative risk of 3.825. However, the risk of pulmonary toxicities was not statistically increased in the ibrutinib group.
Background: Due to limited access to leptomeningeal lesions, cerebrospinal fluid (CSF) may be the most representative liquid biopsy to get genomic information from leptomeningeal metastases (LM) in nonsmall-cell lung cancer (NSCLC). Loss of heterozygosity (LOH) is a common genetic event during cancer tumorigenesis. LOH of tumor suppressor gene in which loss-of-function occurs on alternative allele serves as "second hit" and leads to loss of the remaining functional allele. LOH of tumor suppressor gene, such as TP53, in CSF had been reported for its associated with EGFR-TKI resistance in LM. Here, through CSF derived liquid biopsy, we report a LOH of oncogene ERBB2 in LM of NSCLC patient. To the best of our knowledge, this is the first report of LOH of oncogene, no matter in a primary or metastatic tumor. Method: Three CSF biopsies and matched peripheral blood were collected within 6 months from one NSCLC patient with LM. Cell-free DNA (cfDNA) was extracted, and somatic mutations were examined using a designed lung cancer panel of 180 genes. SCNAs were further identified through 2x whole genome sequencing (WGS). Genomic alternations identified in all three matched biopsies were included in the subsequent analysis. Result: A rare oncogene ERBB2 activating mutation (V659E) was identified in CSF but not in plasma. V659E lies within the transmembrane domain and results in constitutive activation of Src and Akt signaling. Extreme high variants allele fraction (96.8%) of ERBB2 V659E in CSF implied the LOH of ERBB2 in LM. SNPs heterozygosity analysis and low pass WGS were further carried out and confirmed the LOH of entire chromosome 17, but not limited to ERBB2 region. Furthermore, A consecutive an amplification was observed on the remaining copy of chromosome 17q, on which the activated oncogene ERBB2 located. The amplification, following ERBB2 LOH with a concomitant activating mutation, may enhance constitutively active ERBB2 expression and drive the evolution of LM. Besides, there were two more unique mutations in CSF, TP53 T256fs (45.31%) and JAK3 R582Q (32.85%). Relatively Low variants allele fraction indicated that they were subclonal mutation occurring after ERBB2 activating mutation and LOH of chromosome 17. Conclusion: We first reported an oncogene ERBB2 LOH in CSF from one NSCLC patient with LM. Based on phylogeny inference, the ERBB2 activating mutation and LOH of chromosome 17 were likely to be the earliest driver event.
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