Surgicel® (Ethicon, North Ryde, NSW, Australia) is an absorbable sheet of oxidized cellulose polyanhydroglucuronic acid polymer used as an hemostatic in cardiovascular and thoracic surgery. In some cases, the retained material may cause foreign body granulomatous reactions and simulate tumor recurrence, an abscess, an hematoma, or an infection. We report the case of a 55-year-old patient who was operated of a lung adenocarcinoma. In the thoracic computed tomography scan 1 year after the surgery, a right paratracheal lymph node was detected, so endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) was performed suspecting recurrence of the tumor. The cytology results of the lymph node showed a nonnecrotizing granulomatous reaction secondary to Surgicel®, used as an hemostatic during the surgery. The objective of presenting this case is to consider foreign body reaction to Surgicel® in the differential diagnosis of postoperative suspicion of neoplastic recurrence, and on the other hand, to note that EBUS-TBNA enables diagnosis.

Endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) is a minimally invasive procedure for the diagnosis of mediastinal lymph nodes and masses. Its complications are rare and include hemorrhage, pneumothorax and infections such as mediastinitis. We report the case of a 51-year-old patient who presented with a localized subcarinal adenitis after EBUS-TBNA. Germs colonizing the oropharynx may have been dragged along by the echobronchoscope, inoculating the punctured mediastinal lymph node.

Tumor recurrence is frequent and survival rates remain extremely low in lung adenocarcinoma (ADC). We hypothesize that carcinogenic factors will promote loco-regional modifications not only in the future tumor, but throughout the exposed lung. Objective: To analyze whether the most prevalent mutations observed in ADC can also be observed in the non-neoplastic lung tissue, as well as the short-term prognosis implications of this finding. Methods: Non-tumoral lung parenchyma specimens obtained during surgery from 47 patients with EGFR and/or KRAS abnormalities in their ADC tumors underwent similar genomic testing. Short-term outcomes were also recorded. Results: The same mutations were present in the tumor and the histologically normal tissue in 21.3% of patients (SM group). Although local recurrences were similar in both groups, distant metastases were more frequent in the former (60 vs. 5.4%, p < 0.001). Moreover, SM patients showed lower time-to-progression (8.5 vs. 11.7 months, p < 0.001) and disease-free survival (8.5 vs. 11.2 months, p < 0.001). COX regression showed a higher risk of progression or death (DFS) in the SM group (HR 5.94, p < 0.01]. Similar results were observed when adjusting for potential confounding variables. Conclusions: These results confirm that genetic changes are present in the apparently normal lung in many ADC patients, and this finding has prognostic implications.

Lung cancer (LC) risk increases in patients with chronic respiratory diseases (COPD). MicroRNAs and redox imbalance are involved in lung tumorigenesis in COPD patients. Whether systemic alterations of those events may also take place in LC patients remains unknown. Our objectives were to assess the plasma levels of microRNAs, redox balance, and cytokines in LC patients with/without COPD. MicroRNAs (RT-PCR) involved in LC, oxidized DNA, MDA-protein adducts, GSH, TEAC, VEGF, and TGF-beta (ELISA) were quantified in plasma samples from non-LC controls (n = 45), LC-only patients (n = 32), and LC-COPD patients (n = 91). In LC-COPD patients compared to controls and LC-only, MDA-protein adduct levels increased, while those of GSH decreased, and two patterns of plasma microRNA were detected. In both LC patient groups, miR-451 expression was downregulated, while those of microRNA-let7c were upregulated, and levels of TEAC and TGF-beta increased compared to the controls. Correlations were found between clinical and biological variables. A differential expression profile of microRNAs was detected in patients with LC. Moreover, in LC patients with COPD, plasma oxidative stress levels increased, whereas those of GSH declined. Systemic oxidative and antioxidant markers are differentially expressed in LC patients with respiratory diseases, thus implying its contribution to the pathogenesis of tumorigenesis in these patients.

Human tonsils from the nasopharyngeal mucosa mount frontline antibody responses, including IgD secretion by IgD+IgM– plasma cells (IgD-PCs). The developmental origins and functional significance of these IgD responses remain poorly understood. Here, we show that most IgD-PCs clonally emerge from a heterogeneous population of IgD class-switched IgD+IgM– memory (IgD-ME) B cells that reside within the epithelial, subepithelial, and interfollicular areas of the nasopharyngeal mucosa and share transcriptional and phenotypic properties with atypical B cells. These IgD-ME B cells arise from a mutation-intensive pathway that involves integrated innate and adaptive signals and engenders reactivities to respiratory commensal bacteria, common environmental antigens, and allergens. Such reactivities weaken in germline IgD revertants. Thus, the secreted IgD response heavily relies on nasopharyngeal mucosal IgD-ME B cells via a germinal center–imprinted mutational program that presumably enhances mucosal homeostasis and environmental tolerance.