The annual economic burden among patients hospitalized for community-acquired pneumonia (CAP): a retrospective US cohort study.
社区获得性肺炎 (CAP) 住院患者的年度经济负担: 一项回顾性美国队列研究。
- 作者列表："Divino V","Schranz J","Early M","Shah H","Jiang M","DeKoven M
:Objective: To assess the 1-year economic burden among patients hospitalized for community-acquired pneumonia (CAP) in the US.Methods: Adult patients hospitalized for CAP between 1/2012 and 12/2016 were identified from the IQVIA hospital charge data master (CDM) linked to the IQVIA Real-World Data Adjudicated Claims - US Database (date of admission = index date). Patients had continuous enrollment 180-days pre- and 360-days post-index, and empiric antimicrobial treatment (monotherapy [EM] or combination therapy [EC]) and chest x-ray on the index date or day after. All-cause and CAP-related healthcare resource utilization and cost were assessed over the 1-year follow-up. Generalized linear models (GLM) examined adjusted total cost.Results: The cohort comprised 1624 patients hospitalized for CAP (mean age 50.3; 52.8% female). The majority (78.2%) initiated EC, most frequently with beta-lactams + macrolides (30.4%). The index hospitalization was associated with a mean length of stay (LOS) of 5.7 days and mean cost of $17,736; 22.7% had a transfer to the intensive care unit (ICU). All-cause readmission rates at 30- and 180-days were 8.8% and 20.1%, respectively. Mean annual all-cause total cost was $61,928; one-third (33.8%, $20,954) was related to CAP. The primary cost driver was inpatient care, which accounted for more than half (56.0%) of total all-cause cost and 94.3% of total CAP-related cost. Mean total inpatient cost was significantly higher among EC versus EM patients ($37,106 versus $25,999, p = .0399). Adjusted mean total all-cause cost was $55,391.Conclusions: Patients hospitalized for CAP incurred a significant annual economic burden, driven substantially by the high cost of hospitalizations.
目的: 评估美国社区获得性肺炎 (CAP) 住院患者 1 年的经济负担。方法: 从 IQVIA hospital charge data master (CDM) 中识别出 1/2012-12/2016 因 CAP 住院的成人患者链接到 IQVIA 真实世界数据裁定索赔-美国数据库 (批准日期 = 索引日期)。患者连续入组前 180 天和后 360 天，以及经验性抗菌治疗 (单药治疗 [EM] 或联合治疗 [EC]) 和胸片在索引日期或后一天。在 1 年的随访中评估了全因和 CAP 相关的医疗资源利用和成本。广义线性模型 (GLM) 检查了调整后的总成本。结果: 该队列包括 1624 例因 CAP 住院的患者 (平均年龄 50.3 岁; 52.8% 为女性)。大多数 (78.2%) 启动 EC，最常见的是 β-内酰胺酶 + 大环内酯类 (30.4%)。指数住院与平均住院时间 (LOS) 5.7 天、平均费用 17,736 美元相关; 22.7% 的患者转入重症监护病房 (ICU)。30 天和 180 天的全因再入院率分别为 8.8% 和 20.1%。平均年全因总成本为 61,928 美元; 3分之1 (33.8%，20,954 美元) 与 CAP 相关。主要成本动因为住院治疗，占总全因成本的一半以上 (56.0%)，占总 CAP 相关成本的 94.3%。EC 与 EM 患者的平均总住院费用显著高于 EM 患者 ($37,106 vs $25,999，p = 0399)。调整后的平均全因总费用为 55,391 美元。结论: 因 CAP 住院的患者每年承受重大经济负担，这主要是由高住院费用驱动的。
METHODS:BACKGROUND AND PURPOSE:A critical role for sphingosine kinase/sphingosine-1-phosphate (S1P) pathway in the control of airway function has been demonstrated in respiratory diseases. Here, we address S1P contribution in a mouse model of mild chronic obstructive pulmonary disease (COPD). EXPERIMENTAL APPROACH:C57BL/6J mice have been exposed to room air or cigarette smoke up to 11 months and killed at different time points. Functional and molecular studies have been performed. KEY RESULTS:Cigarette smoke caused emphysematous changes throughout the lung parenchyma coupled to a progressive collagen deposition in both peribronchiolar and peribronchial areas. The high and low airways showed an increased reactivity to cholinergic stimulation and α-smooth muscle actin overexpression. Similarly, an increase in airway reactivity and lung resistances following S1P challenge occurred in smoking mice. A high expression of S1P, Sph-K2 , and S1P receptors (S1P2 and S1P3 ) has been detected in the lung of smoking mice. Sphingosine kinases inhibition reversed the increased cholinergic response in airways of smoking mice. CONCLUSIONS AND IMPLICATIONS:S1P signalling up-regulation follows the disease progression in smoking mice and is involved in the development of airway hyperresponsiveness. Our study defines a therapeutic potential for S1P inhibitors in management of airways hyperresponsiveness associated to emphysema in smokers with both asthma and COPD.
METHODS::The interim results from this 90-day multi-dose, inhalation toxicology study with life-time post-exposure observation has shown an important fundamental difference in persistence and pathological response in the lung between brake dust derived from brake-pads manufactured with chrysotile, TiO2 or chrysotile alone in comparison to the amphiboles, crocidolite and amosite asbestos. In the brake dust exposure groups no significant pathological response was observed at any time. Slight macrophage accumulation of particles was noted. Wagner-scores, were from 1 to 2 (1 = air-control group) and were similar to the TiO2 group. Chrysotile being biodegradable, shows a weakening of its matrix and breaking into short fibers & particles that can be cleared by alveolar macrophages and continued dissolution. In the chrysotile exposure groups, particle laden macrophage accumulation was noted leading to a slight interstitial inflammatory response (Wagner-score 1-3). There was no peribronchiolar inflammation and occasional very slight interstitial fibrosis. The histopathology and the confocal analyses clearly differentiate the pathological response from amphibole asbestos, crocidolite and amosite, compared to that from the brake dust and chrysotile. Both crocidolite and amosite induced persistent inflammation, microgranulomas, and fibrosis (Wagner-scores 4), which persisted through the post exposure period. The confocal microscopy of the lung and snap-frozen chestwalls quantified the extensive inflammatory response and collagen development in the lung and on the visceral and parietal surfaces. The interim results reported here, provide a clear basis for differentiating the effects from brake dust exposure from those following amphibole asbestos exposure. The subsequent results through life-time post-exposure will follow.
METHODS::The respiratory tract is lined by a pseudo-stratified epithelium from the nose to terminal bronchioles. This first line of defense of the lung against external stress includes five main cell types: basal, suprabasal, club, goblet and multiciliated cells, as well as rare cells such as ionocytes, neuroendocrine and tuft/brush cells. At homeostasis, this epithelium self-renews at low rate but is able of fast regeneration upon damage. Airway epithelial cell lineages during regeneration have been investigated in the mouse by genetic labeling, mainly after injuring the epithelium with noxious agents. From these approaches, basal cells have been identified as progenitors of club, goblet and multiciliated cells, but also of ionocytes and neuroendocrine cells. Single-cell RNA sequencing, coupled to lineage inference algorithms, has independently allowed the establishment of comprehensive pictures of cell lineage relationships in both mouse and human. In line with genetic tracing experiments in mouse trachea, studies using single-cell RNA sequencing (RNAseq) have shown that basal cells first differentiate into club cells, which in turn mature into goblet cells or differentiate into multiciliated cells. In the human airway epithelium, single-cell RNAseq has identified novel intermediate populations such as deuterosomal cells, 'hybrid' mucous-multiciliated cells and progenitors of rare cells. Novel differentiation dynamics, such as a transition from goblet to multiciliated cells have also been discovered. The future of cell lineage relationships in the respiratory tract now resides in the combination of genetic labeling approaches with single-cell RNAseq to establish, in a definitive manner, the hallmarks of cellular lineages in normal and pathological situations.