Low patient engagement is associated with reduced health-related quality of life in adults with cyclic vomiting syndrome.

INTRODUCTION: Patient engagement, adaptation and self-management play a critical role in improving Health Related Quality of Life (HRQOL) and reducing health care utilization in chronic disorders. There is no data on the level of patient engagement in patients with cyclic vomiting syndrome (CVS); we thus sought to determine their level of engagement and its association with clinical covariates. METHODS: The Patient Activation Measure (PAM-13), a validated tool that measures the degree of patient engagement in their health was administered prospectively to patients with CVS. Data on demographics, health care utilization, and HRQOL (using the NIH PROMIS 10) were obtained. Patients were stratified into low engagement (PAM 1 & 2) and high engagement (PAM 3 & 4). The Fisher's exact test and Wilcoxon rank-sum tests were used to identifying significant differences between the groups. RESULTS: Of 96 patients, 45% of patients had low levels of patient engagement. On multivariate analysis, low patient engagement was significantly associated with an increased number of CVS hospitalizations in the past year (aOR 1.26 [1.07, 1.54] p = .010), lower mental HRQOL scores (aOR 0.88 [0.78, 0.97] p = .022), current tobacco use (aOR 4.85 [1.24, 22.74] p = .031), and patients who were newly established in a specialized CVS clinic (aOR 44.40 [5.38, 70.02] p = .002). CONCLUSION: Almost half of CVS patients demonstrate poor patient engagement, which is associated with poor outcomes. Identifying these patients and treatment in a specialized CVS center can potentially improve HRQOL, reduce health care utilization and improve overall healthcare outcomes.

Triggering Receptor Expressed on Myeloid Cells-2 Expression Tracks With M2-Like Macrophage Activity and Disease Severity in COPD.

BACKGROUND: Cell and animal models show a key role for Triggering Receptor Expressed on Myeloid Cells (TREM)-2 in chronic airway disease after viral infection, but comparable evidence in humans still needs to be established. METHODS: Lung tissue samples were obtained from lung transplant recipients with Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage IV COPD (n = 16), nontransplantable donor lung tissues (n = 7), and resected lung tissues from patients at risk or with GOLD stage I through IV (n = 55) and were assessed for TREM-2 and TREM-1 messenger RNA (mRNA), protein expression, and other markers of a type 2 immune response. RESULTS: TREM2 (but not TREM1) mRNA levels were increased in GOLD stage IV COPD lung tissues compared with non-COPD lung tissues. TREM2 mRNA was coexpressed with its signaling molecule DAP12 and the macrophage marker CD68 and M2-macrophage markers CD206 and CHIT1. TREM-2 protein was also increased in COPD lung tissues and was localized to CD14+ macrophages by flow cytometry and CD68+ and CCR2+ macrophages by tissue immunostaining. In lung samples from patients at risk and with GOLD stage I through IV COPD, TREM2 but not TREM1 mRNA levels were also increased, and the ratio of TREM2/TREM1 mRNA levels was associated with increases in CHIT1 mRNA and decreases in FEV1 and FEV1/FVC. CONCLUSIONS: TREM-2 expression is increased in lung macrophages in COPD, particularly in comparison with TREM-1. Therefore, TREM-2 levels and the ratio of TREM-2/TREM-1 signifies M2 activation in COPD lung tissues and may help to guide therapeutics directed against the type 2 immune response in patients with this disease.

Long-term IL-33-producing epithelial progenitor cells in chronic obstructive lung disease.

Chronic obstructive lung disease is characterized by persistent abnormalities in epithelial and immune cell function that are driven, at least in part, by infection. Analysis of parainfluenza virus infection in mice revealed an unexpected role for innate immune cells in IL-13-dependent chronic lung disease, but the upstream driver for the immune axis in this model and in humans with similar disease was undefined. We demonstrate here that lung levels of IL-33 are selectively increased in postviral mice with chronic obstructive lung disease and in humans with very severe chronic obstructive pulmonary disease (COPD). In the mouse model, IL-33/IL-33 receptor signaling was required for Il13 and mucin gene expression, and Il33 gene expression was localized to a virus-induced subset of airway serous cells and a constitutive subset of alveolar type 2 cells that are both linked conventionally to progenitor function. In humans with COPD, IL33 gene expression was also associated with IL13 and mucin gene expression, and IL33 induction was traceable to a subset of airway basal cells with increased capacities for pluripotency and ATP-regulated release of IL-33. Together, these findings provide a paradigm for the role of the innate immune system in chronic disease based on the influence of long-term epithelial progenitor cells programmed for excess IL-33 production.