PROSPERO no. 143178.

In the absence of perinatal anxiety screening, clinically significant symptoms of anxiety remain under-detected and undertreated during perinatal period. Perinatal anxiety has a significant and far reaching impact on mothers and their children. There are well established recommendations for routine mental health screening during the perinatal period, yet less than one in five of providers routinely screen and one in seven women receive the mental health intervention they need. The validity of anxiety screening scales needs to be ascertained by criterion validity parameters such as sensitivity, specificity, and predictive values. Criterion validity, which is assessed against a reference standard, allows clear interpretation of screening results, supporting their integration with clinical care pathways. However, few existing validation studies of anxiety scales in perinatal populations examined criterion validity. Construct validity of anxiety scales, the focus of existing validation studies, does not use reference standard; thus, it lacks clear clinical interpretability for screening application. Future validation studies should focus on assessing the criterion validity of anxiety scales in perinatal populations. This will help nurses, midwives, and other members of interdisciplinary teams to clarify scale validity, interpretation, and utility for screening women for anxiety in the perinatal period.

<b><i>Background:</i></b> Screening for major depression with the Patient Health Questionnaire-9 (PHQ-9) can be done using a cutoff or the PHQ-9 diagnostic algorithm. Many primary studies publish results for only one approach, and previous meta-analyses of the algorithm approach included only a subset of primary studies that collected data and could have published results. <b><i>Objective:</i></b> To use an individual participant data meta-analysis to evaluate the accuracy of two PHQ-9 diagnostic algorithms for detecting major depression and compare accuracy between the algorithms and the standard PHQ-9 cutoff score of ≥10. <b><i>Methods:</i></b> Medline, Medline In-Process and Other Non-Indexed Citations, PsycINFO, Web of Science (January 1, 2000, to February 7, 2015). Eligible studies that classified current major depression status using a validated diagnostic interview. <b><i>Results:</i></b> Data were included for 54 of 72 identified eligible studies (<i>n</i> participants = 16,688, <i>n</i> cases = 2,091). Among studies that used a semi-structured interview, pooled sensitivity and specificity (95% confidence interval) were 0.57 (0.49, 0.64) and 0.95 (0.94, 0.97) for the original algorithm and 0.61 (0.54, 0.68) and 0.95 (0.93, 0.96) for a modified algorithm. Algorithm sensitivity was 0.22–0.24 lower compared to fully structured interviews and 0.06–0.07 lower compared to the Mini International Neuropsychiatric Interview. Specificity was similar across reference standards. For PHQ-9 cutoff of ≥10 compared to semi-structured interviews, sensitivity and specificity (95% confidence interval) were 0.88 (0.82–0.92) and 0.86 (0.82–0.88). <b><i>Conclusions:</i></b> The cutoff score approach appears to be a better option than a PHQ-9 algorithm for detecting major depression.

Glucocorticoid administration before cardiopulmonary bypass (CPB) can reduce the systemic inflammatory response and improve clinical outcome. Long pentraxin PTX3 is a novel inflammatory parameter that could play a protective cardiovascular role by regulating inflammation. Twenty-nine children undergoing open heart surgery were enrolled in the study. Fourteen received dexamethasone (1st dose 1.5 mg/Kg i.v. or i.m. the evening before surgery; 2nd dose 1.5 mg/kg i.v. before starting bypass) and fifteen children served as control. Blood PTX3, short pentraxin C-reactive protein (CRP), interleukin-1 receptor II (IL-1RII), fibrinogen and partial thromboplastin time (PTT) were assayed at different times. PTX3 levels significantly increased during CPB in dexamethasone-treated (+D) and dexamethasone-untreated (-D) subjects, but were significantly higher in +D than -D patients. CRP levels significantly increased both in +D and -D patients in the postoperative days, with values significantly higher in -D than +D patients. Fibrinogen and PTT values were significantly higher in -D than +D patients in the 1st postoperative day. IL-1RII plasma levels increased in the postoperative period in both groups. Dexamethasone prophylaxis in pediatric patients undergoing CPB for cardiac surgery is associated with a significant increase of blood PTX3 that could contribute to decreasing inflammatory parameters and improving patient clinical outcome.

Timely diagnosis of lung infection in critically ill patients is key to guide therapy and avoid futile antibiotic prescription. The gold standard for diagnosis is microbiological culture of bronchoalveolar lavage fluid (BALf). However, it takes up to 48 hours to disclose results. Pentraxin 3 (PTX3) is an acute phase mediator of infection that can be assayed in a few hours. We described a relationship between BALf PTX3 presence and lung infection in acute respiratory distress syndrome patients. The aim of this study was to validate BALf PTX3 as an early marker of lung infection in critically ill patients.

An intrinsic (oncogene-driven) pathway and an extrinsic (microenvironment-driven) pathway connect inflammatory reactions and cancer. M2-polarized tumor-associated macrophages and the related myeloid-derived suppressor cells are key prototypic components of smoldering inflammation driving neoplastic progression. However, mononuclear phagocytes can exert anti-tumor activity by killing tumor cells and eliciting tissue disruptive reactions (M1), a likely scenario in the early phases of carcinogenesis of immunogenic tumors and following therapeutic intervention. Shifting the macrophage balance represents a viable therapeutic target. Herein, the 'macrophage balance' is discussed in the context of the apparent paradox of tumor promotion by innate immunity-driven inflammation and the seemingly opposed tumor surveillance by adaptive immune responses.

Tumor-associated macrophages (TAMs) and other myeloid cells that infiltrate neoplastic lesions promote tumor progression and are associated with poor patient prognosis. We have recently demonstrated that trabectedin, a licensed and commercially available anticancer agent, is selectively cytotoxic for TAMs and their circulating precursors (monocytes). The macrophage-depleting effect of trabectedin is a key component of its antitumor activity.

The long pentraxin PTX3 has multiple roles in innate immunity. For example, PTX3 regulates C1q binding to pathogens and dead cells and regulates their uptake by phagocytes. It also inhibits P-selectin-mediated recruitment of leukocytes. Both of these mechanisms are known to be involved in autoimmunity and autoimmune tissue injury, e.g. in systemic lupus erythematosus, but a contribution of PTX3 is hypothetical. To evaluate a potential immunoregulatory role of PTX3 in autoimmunity we crossed Ptx3-deficient mice with Fas-deficient (lpr) C57BL/6 (B6) mice with mild lupus-like autoimmunity. PTX3 was found to be increasingly expressed in kidneys and lungs of B6lpr along disease progression. Lack of PTX3 impaired the phagocytic uptake of apoptotic T cells into peritoneal macrophages and selectively expanded CD4/CD8 double negative T cells while other immune cell subsets and lupus autoantibody production remained unaffected. Lack of PTX3 also aggravated autoimmune lung disease, i.e. peribronchial and perivascular CD3+ T cell and macrophage infiltrates of B6lpr mice. In contrast, histomorphological and functional parameters of lupus nephritis remained unaffected by the Ptx3 genotype. Together, PTX3 specifically suppresses autoimmune lung disease that is associated with systemic lupus erythematosus. Vice versa, loss-of-function mutations in the Ptx3 gene might represent a genetic risk factor for pulmonary (but not renal) manifestations of systemic lupus or other autoimmune diseases.