Variation in the Bombesin Staining of Pulmonary Neuroendocrine Cells in Pediatric Pulmonary Disorders - A Useful Marker for Airway Maturity.
- 作者列表："Emiralioğlu N","Orhan D","Cinel G","Tuğcu GD","Yalçın E","Doğru D","Özçelik U","Griese M","Kiper N
OBJECTIVES:Pulmonary neuroendocrine cells (NEC) increase with the age due to pulmonary maturity. The aim of this study was to determine whether open lung biopsies from patients with interstitial lung diseases have increased pulmonary NEC compared with NEHI. Our second aim was to assess pulmonary NECs in the lung autopsy of children without lung disease who died from different causes. METHODS:Lung tissue of 5 infants with neuroendocrine cell hyperplasia of infancy (NEHI); 21 patients with pediatric interstitial lung disease (chILD); 17 lung autopsies of infants at varying age without lung disease were included. The percentage of the airways containing neuroendocrine cells, the average percentage of NECs per airway and the number of neuroendocrine bodies (NEBs) in each case were analyzed. RESULTS:The mean percentage of the airways containing neuroendocrine cells were 95% in NEHI group, 30% in chILD group, 89% under intrauterine 37 weeks, 70% between intrauterine 37-40 weeks, 52% at postnatal 4 days-6 months of autopsy ages. In NEHI group, diffuse NE cell distribution and large NEBs were noticed in the lung biopsy. In chILD group, neuroendocrine cells were dispersed, did not form clusters and NE cells showed solitary distribution. In lung autopsy group, linear NE cells were detected at younger aged fetuses and solitary distribution of NE cells was detected with the older increasing age. CONCLUSIONS:Our findings confirm that NECs are seen in many other childhood ILDs; NE cell hyperplasia may be a marker of decreased pulmonary development and NE cells decrease with the increasing age of the fetus during intrauterine life. This article is protected by copyright. All rights reserved.
目的: 肺成熟使肺神经内分泌细胞 (NEC) 随年龄增长而增加。本研究的目的是确定与 NEHI 相比，间质性肺疾病患者的开放性肺活检是否增加了肺 NEC。我们的第二个目的是在不同原因死亡的无肺病儿童的肺尸检中评估肺 NECs。 方法: 5 例婴儿期神经内分泌细胞增生 (NEHI) 患儿; 21 例儿童间质性肺疾病 (chILD) 患儿; 纳入 17 例不同年龄无肺部疾病婴儿的肺部尸检。分析每个病例中含有神经内分泌细胞的气道百分比、每个气道中 NECs 的平均百分比和神经内分泌体 (NEBs) 的数量。 结果: NEHI 组气道内含有神经内分泌细胞的平均百分比为 95%，chILD 组为 30%，宫内 37 周时为 89%，宫内 37 ~ 40 周时为 70%,52% 出生后 4 天-6 个月尸检年龄。NEHI 组肺活检可见弥漫性 NE 细胞分布，NEBs 较大。ChILD 组神经内分泌细胞分散，不形成簇，NE 细胞呈孤立分布。在肺尸检组中，在年龄较小的胎儿中检测到线性 NE 细胞，并且随着年龄的增长，检测到 NE 细胞的孤立性分布。 结论: 我们的研究结果证实 NECs 见于许多其他儿童期 ILDs; 宫内胎龄增加，NE 细胞增生可能是肺发育下降的标志，NE 细胞减少。本文受版权保护。保留所有权利。
METHODS:OBJECTIVES:To asses the clinical course in RA-related interstitial lung disease (RA-ILD) patients with and without rituximab (RTX). The influence of other variables was also evaluated. METHODS:A longitudinal multicentre study was conducted in RA diagnosed with ILD from 2007 until 2018 in Madrid. Patients were included in a registry [pNEumology RhEumatology Autoinmune diseases (NEREA)] from the time of ILD diagnosis. The main endpoint was functional respiratory impairment (FI), when there was a decline ≥5% in the predicted forced vital capacity compared with the previous one. Pulmonary function was measured at baseline and in follow-up visits every 6-12 months. The independent variable was therapy with RTX. Covariables included sociodemographic, clinical, radiological and other therapies. Survival techniques were used to estimate the incidence rate (IR) and 95% CI of functional impairment, expressed per 100 patient-semesters. Cox multivariate regression models were run to examine the influence of RTX and other covariates on FI. Results were expressed as the hazard ratio (HR) and CI. RESULTS:A total of 68 patients were included. FI occurred in 42 patients [IR 23.5 (95% CI 19, 29.1)] and 50% of them had FI within 1.75 years of an ILD diagnosis. A multivariate analysis showed that RTX exposure resulted in a lower risk of FI compared with non-exposure [HR 0.51 (95% CI 0.31, 0.85)]. Interstitial pneumonia, glucocorticoids, disease activity and duration also influenced FI. CONCLUSION:RA-ILD patients deteriorate over time, with the median time free of impairment being <2 years. Patients exposed to RTX had a higher probability of remaining free of FI compared with other therapies. Other factors have also been identified. Key words: rheumatoid arthritis, interstitial lung disease, observational study, rituximab and prognosis
METHODS:The safety of anti-programmed cell death 1 (PD-1) antibody for patients with preexisting interstitial lung disease (ILD) remains unknown. The aim of this study was to evaluate the dependence of preexisting ILD on anti-PD-1 antibody-induced pneumonitis in non-small cell lung cancer (NSCLC) patients. We retrospectively reviewed the association of preexisting ILD with the incidence, radiographic pattern, and outcome of pneumonitis in NSCLC patients receiving anti-PD-1 antibody. A total of 331 patients were included in this study. Of these patients, 17 had preexisting ILD. The incidence of pneumonitis was higher among the patients with preexisting ILD than among those without preexisting ILD (29% vs. 10%, P = 0.027). The distributions of the CT appearances at the onset of anti-PD-1 antibody-induced pneumonitis were as follows: for the patients with preexisting ILD, two patients (40%) had diffuse alveolar damage (DAD), one patient each with organizing pneumonia-like (OP), hypersensitivity pneumonitis (HP), and other patterns (20% each); for the patients without preexisting ILD, 19 patients (61%) had OP, 8 (26%) had HP, 3 (10%) had DAD, and 1 (3.2%) had other patterns. The median onset time from the initiation of anti-PD-1 antibody treatment until the development of pneumonitis was 1.3 months (range 0.3–2.1 months) for the patients with preexisting ILD and 2.3 months (range 0.2–14.6 months) for the patients without preexisting ILD. Careful attention to the development of pneumonitis is needed, especially within the first 3 months after the start of anti-PD-1 antibody treatment, when using anti-PD-1 antibody to treat patients with preexisting ILD.
METHODS::Bacteria of the Burkholderia cepacia complex (Bcc) are ubiquitous multidrug resistant organisms and opportunistic pathogens capable of causing life threatening lung infections among cystic fibrosis (CF) patients. No effective therapies are currently available to eradicate Bcc bacteria from CF patients, as these organisms are inherently resistant to the majority of clinically available antimicrobials. An immunoproteomics approach was used to identify Bcc proteins that stimulate the humoral immune response of the CF host, using bacterial cells grown under conditions mimicking the CF lung environment and serum samples from CF patients with a clinical record of Bcc infection. 24 proteins of the Bcc strain B. cenocepacia J2315 were identified as immunoreactive, 19 here reported as immunogenic for the first time. Ten proteins were predicted as extracytoplasmic, 9 of them being conserved in Bcc genomes. The immunogenic Bcc extracytoplasmic proteins are potential targets for development of novel therapeutic strategies and diagnostic tools to protect patients against the onset of chronic Bcc lung infections.