Glycemic control and FEV1 recovery during pulmonary exacerbations in pediatric cystic fibrosis-related diabetes.
小儿囊性纤维化相关糖尿病肺部加重期间的血糖控制和 FEV1 恢复。
- 作者列表："Okoniewski W","Hughan KS","Weiner GA","Weiner DJ","Forno E
RATIONALE:Whether short-term glucose control in cystic fibrosis-related diabetes (CFRD) is associated with FEV1 recovery during acute pulmonary exacerbations is unclear. METHODS:Data from all patients with CFRD ages 6-21 years hospitalized in 2010-2016 for pulmonary exacerbations at our CF Center were analyzed, including CFRD status at each encounter, all FEV1 recorded during each exacerbation, and relevant clinical covariates. Glucose control was analyzed using meter blood glucose area under the curve (AUC) indices. The primary outcome was FEV1 recovery. RESULTS:Patients with CFRD who finished IV antibiotics at home were treated for longer than those fully treated in the hospital (22.2 vs. 13.8 days). In those who finished treatment at home, poor inpatient glycemic control was associated with lower lung function improvement: when comparing the 75th to the 25th percentile of each glycemic index (i.e., "poorer" vs. "better" glycemic control), FEV1 recovery at discharge was 20.1% lower for glucose AUC (95%CI -0.4%, -39.9%); 20.9% lower for 48-h AUC (95%CI -2.7%, -39.1%); and 28.2% lower for AUC/day (95%CI -7.1%, -49.3%). Similar results were found at the end of IV antibiotics and at clinic follow-up. Likewise, patients with poor glycemic control had a lower slope of inpatient FEV1 recovery. Analysis in patients with normal glucose tolerance was largely non-significant. No associations were found between hemoglobin A1c and FEV1 recovery. CONCLUSIONS:In patients with CFRD who complete IV antibiotic treatment at home, poor inpatient glycemic control is associated with worse FEV1 recovery despite longer duration of treatment.
原理: 囊性纤维化相关糖尿病 (CFRD) 的短期血糖控制是否与急性肺加重期 FEV1 恢复相关尚不清楚。 方法: 分析我们 CF 中心 2010-2016 例因肺部加重住院的所有 6-21 岁 CFRD 患者的数据，包括每次就诊时的 CFRD 状态, 每次加重期间记录的所有 FEV1，以及相关的临床协变量。使用血糖仪血糖曲线下面积 (AUC) 指数分析血糖控制。主要结局为 FEV1 恢复。 结果: 在家完成静脉抗生素治疗的 CFRD 患者的治疗时间比在医院完全治疗的患者长 (22.2 vs.13.8 天)。在家中完成治疗的患者中，住院患者血糖控制不佳与肺功能改善较低相关: 当比较每个血糖指数的第 75 至第 25 百分位数时 (i。 e., “更差” vs.“更好” 血糖控制)，出院时 FEV1 恢复为葡萄糖 AUC 低 20.1% (95% CI-0.4%,-39.9%); 48 h AUC 低 20.9% (95% CI-2.7%，-39.1%); AUC/天低 28.2% (95% CI-7.1%，-49.3%)。在 IV 抗生素结束时和临床随访时也发现了类似的结果。同样，血糖控制不佳的患者住院 FEV1 恢复的斜率较低。正常糖耐量患者的分析在很大程度上是不显著的。未发现血红蛋白 A1c 与 FEV1 恢复之间存在关联。 结论: 在在家中完成 IV 抗生素治疗的 CFRD 患者中，尽管治疗持续时间较长，但住院患者血糖控制不佳与 FEV1 恢复较差相关。
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.