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Adherence to therapy, defined as the extent to which a patient follows prescribed therapeutic recommendations, is a pivotal factor in the effective management of chronic diseases such as diabetes, hypertension, and cardiovascular conditions. This review highlights the profound influence of adherence on clinical outcomes, healthcare costs, and patient quality of life. Despite its critical importance, non-adherence remains a pervasive challenge globally, contributing to suboptimal treatment results, higher rates of complications, increased hospitalizations, and substantial healthcare expenditures. This narrative review examines the multifaceted impact of adherence, focusing on its role in achieving clinical efficacy, mitigating economic burdens, and enhancing patient well-being. The findings reveal that poor adherence exacerbates the risk of disease progression, complications, and higher healthcare costs. Conversely, improved adherence promotes better disease control, fewer complications, and enhanced patient quality of life. Interventions such as patient education, streamlined treatment regimens, and the integration of digital health tools have shown promise in addressing adherence barriers. Furthermore, the role of healthcare professionals is underscored as fundamental, with their continuous support, effective communication, and efforts to build patient trust being essential to fostering better adherence. In conclusion, adherence significantly affects clinical outcomes, healthcare costs, and patient quality of life. Addressing barriers to adherence requires a comprehensive and personalized approach, considering individual patient needs and circumstances. Future research should prioritize the long-term evaluation of emerging technologies and the development of tailored strategies to improve adherence across diverse patient populations. Strengthening adherence is not only crucial for individual patient outcomes, but also for enhancing the sustainability and efficiency of healthcare systems.

Despite the high efficacy of the anti-coronavirus disease 2019 (COVID-19) BNT162b2 vaccine (Comirnaty , Pfizer-BioNTech), variability in the antibody titers following vaccination has been described. However, little is known about the risk factors that are associated with a poorer antibody response to the BNT162b2 vaccine. We studied the determinants of the humoral response to the anti-COVID-19 vaccine BNT162b2 in 200 healthcare workers followed up for 2 years. Serum samples were tested for the anti-spike immunoglobulin G (IgG) levels and neutralizing antibody titers against selected severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants at different time points after primary and booster vaccinations. Anthropometric data and clinical and lifestyle information were also collected. Statistical analyses consisted of linear and logistical regressions for point estimations and the Mann-Whitney, Friedman, and generalized estimating equations for repeated measures. After the primary vaccination, the antibody titers and the percentage of seroconverted individuals peaked at 5 weeks but declined after 1 year; however, they remained high after the booster administration. After the first dose of the vaccine, negative associations of the anti-spike IgG levels with age ( = -0.01, 95%CI = -0.03 to -0.003), smoking habit ( = -1.08, 95%CI = -1.70 to -0.46), and alcohol consumption ( = -1.43, 95%CI = -2.20 to -0.65) were found. With regard to the booster vaccine, the following associations were retained in the stepwise multivariate model: anti-Delta neutralizing antibodies with hip circumference (OR = 1.07, 95%CI = 1.01-1.12, = 0.008), anti-Delta-K antibodies with hip circumference (OR = 1.06, 95%CI = 1.01-1.11, = 0.007), and anti-Omicron antibodies with the Mediterranean diet score (OR = 0.74, 95%CI = 0.58-0.96, = 0.023). Lifestyle habits and age had an association with the humoral response to the BNT162b2 vaccine.

Background Eotaxin-1 concentrations in plasma have been inversely associated with malaria exposure, malaria infection and pregnancy, but the effect of these conditions on the levels of the related chemokines eotaxin-2 and eotaxin-3 remains unknown. Methods Eotaxin-2 and -3 concentrations were measured in 310 peripheral or placental plasma samples from pregnant and non-pregnant individuals from Papua New Guinea (malaria-endemic country) and Spain (malaria-naïve individuals) with previous data on eotaxin-1 concentrations. Correlations between eotaxin concentrations were examined with the Spearman’s test. Differences in eotaxin concentrations among groups were evaluated with the Kruskal–Wallis or Mann Whitney tests. The pairwise Wilcoxon test was performed to compare eotaxin-2 concentration between peripheral and placental matched plasmas. Univariable and multivariable linear regression models were estimated to assess the association between eotaxins and Plasmodium infection or gestational age. Results Eotaxin-2 concentrations in plasma showed a weak positive correlation with eotaxin-3 (rho = 0.35, p < 0.05) concentrations. Eotaxin-2 concentrations in the malaria-exposed non-pregnant group were significantly lower than the in the malaria-naive non-pregnant and the malaria-exposed pregnant groups. Eotaxin-3 plasma concentrations were lower in malaria-exposed than in non-exposed groups (p < 0.05), but no differences were found associated to pregnancy. Eotaxin-2 and eotaxin-3 plasma concentrations were negatively correlated with anti- Plasmodium IgG levels: PfDBL5ε-IgG (rho Eo2  = − 0.35, p = 0.005; rho Eo3  =− 0.37, p = 0.011), and eotaxin-3 was negatively correlated with PfDBL3x-IgG levels (rho Eo3  =− 0.36; p = 0.011). Negative correlations of eotaxin-2 and 3 in plasma were also observed with atypical memory B cells (rho Eo2  = − 0.37, p < 0.001; rho Eo3= − 0.28, p = 0.006), a B cell subset expanded in malaria-exposed individuals. In addition, a borderline negative association was observed between eotaxin-3 concentrations and Plasmodium infection (adjusted effect estimate, β = − 0.279, 95% CI − 0.605; 0.047, p = 0.091). Moreover, eotaxin-2 placental concentrations were significantly increased compared to peripheral concentrations in the malaria-exposed pregnant group whereas the contrary was observed in the non-exposed pregnant group (p < 0.005). Conclusion Although a clear epidemiological negative association is observed between eotaxins concentrations and malaria exposure and/or infection, pregnancy may alter this association for eotaxin-2. Further research is required to understand the role of these chemokines in this disease and in combination with pregnancy.

Vaccine-induced immunity against COVID-19 generates antibody and lymphocyte responses. However, variability in antibody titers has been observed after vaccination, and the determinants of a better response should be studied. The main objective of this investigation was to analyze the inflammatory biomarker response induced in healthcare workers vaccinated with BNT162b2, and its association with anti-Spike (a SARS-CoV-2 antigen) antibodies measured throughout a 1-year follow-up. Anti-spike antibodies and 92 biomarkers were analyzed in serum, along with socio-demographic and clinical variables collected by interview or exploration. In our study, four biomarkers (ADA, IL-17C, CCL25 and CD8α) increased their expression after the first vaccine dose; and 8 others (uPA, IL-18R1, EN-RAGE, CASP-8, MCP-2, TNFβ, CD5 and CXCL10) decreased their expression. Age, body mass index (BMI), smoking, alcohol consumption, and prevalent diseases were associated with some of these biomarkers. Furthermore, higher baseline levels of T-cell surface glycoprotein CD6 and hepatocyte growth factor (HGF) were associated with lower mean antibody titers at follow-up, while levels of monocyte chemotactic protein 2 (MCP-2) had a positive association with antibody levels. Age and BMI were positively related to baseline levels of MCP-2 (β=0.02, 95%CI 0.00-0.04, p=0.036) and HGF (β=0.03, 95%CI 0.00-0.06, p=0.039), respectively. Our findings indicate that primary BNT162b2 vaccination had a positive effect on the levels of several biomarkers related to T cell function, and a negative one on some others related to cancer or inflammatory processes. In addition, a higher level of MCP-2 and lower levels of HGF and CD6 were found to be associated with higher anti-Spike antibody titer following vaccination.

In persistent infections that are accompanied by chronic immune activation, such as human immunodeficiency virus, hepatitis C virus, and malaria, there is an increased frequency of a phenotypically distinct subset of memory B cells lacking the classic memory marker CD27 and showing a reduced capacity to produce antibodies. However, critical knowledge gaps remain on specific B cell changes and immune adaptation in chronic infections. We hypothesized that expansion of atypical memory B cells (aMBCs) and reduction of activated peripheral marginal zone (MZ)-like B cells in constantly exposed individuals might be accompanied by phenotypic changes that would confer a tolerogenic profile, helping to establish tolerance to infections. To better understand malaria-associated phenotypic abnormalities on B cells, we analyzed peripheral blood mononuclear cells from 55 pregnant women living in a malaria-endemic area of Papua Nueva Guinea and 9 Spanish malaria-naïve individuals using four 11-color flow cytometry panels. We assessed the expression of markers of B cell specificity (IgG and IgM), activation (CD40, CD80, CD86, b220, TACI, and CD150), inhibition (PD1, CD95, and CD71), and migration (CCR3, CXCR3, and CD62l). We found higher frequencies of active and resting aMBC and marked reduction of MZ-like B cells, although changes in absolute cell counts could not be assessed. Highly exposed women had higher PD1 -, CD95 -, CD40 -, CD71 -, and CD80 -activated aMBC frequencies than non-exposed subjects. Malaria exposure increased frequencies of b220 and proapoptotic markers PD1 and CD95, and decreased expression of the activation marker TACI on MZ-like B cells. The increased frequencies of inhibitory and apoptotic markers on activated aMBCs and MZ-like B cells in malaria-exposed adults suggest an immune-homeostatic mechanism for maintaining B cell development and function while simultaneously downregulating hyperreactive B cells. This mechanism would keep the B cell activation threshold high enough to control infection but impaired enough to tolerate it, preventing systemic inflammation.

Plasmodium vivax malaria is a neglected disease, particularly during pregnancy. Severe vivax malaria is associated with inflammatory responses but in pregnancy immune alterations make it uncertain as to what cytokine signatures predominate, and how the type and quantity of blood immune mediators influence delivery outcomes. We measured the plasma concentrations of a set of thirty-one biomarkers, comprising cytokines, chemokines and growth factors, in 987 plasma samples from a cohort of 572 pregnant women from five malaria-endemic tropical countries and related these concentrations to delivery outcomes (birth weight and hemoglobin levels) and malaria infection. Samples were collected at recruitment (first antenatal visit) and at delivery (periphery, cord and placenta). At recruitment, we found that P. vivax-infected pregnant women had higher plasma concentrations of proinflammatory (IL-6, IL-1β, CCL4, CCL2, CXCL10) and TH1-related cytokines (mainly IL-12) than uninfected women. This biomarker signature was essentially lost at delivery and was not associated with birth weight nor hemoglobin levels. Antiinflammatory cytokines (IL-10) were positively associated with infection and poor delivery outcomes. CCL11 was the only biomarker to show a negative association with P. vivax infection and its concentration at recruitment was positively associated with hemoglobin levels at delivery. Birth weight was negatively associated with peripheral IL-4 levels at delivery. Our multi-biomarker multicenter study is the first comprehensive one to characterize the immunological signature of P. vivax infection in pregnancy thus far. In conclusion, data show that while TH1 and pro-inflammatory responses are dominant during P. vivax infection in pregnancy, antiinflammatory cytokines may compensate excessive inflammation avoiding poor delivery outcomes, and skewness toward a TH2 response may trigger worse delivery outcomes. CCL11, a chemokine largely neglected in the field of malaria, emerges as an important marker of exposure or mediator in this condition.

Tocilizumab (TCZ) has been administered in SARS-CoV-2 pneumonia but the factors associated with mortality before and after treatment remain unclear. Cox regression models were used to estimate the predictors of time to death in a cohort of hospitalized patients with COVID-19 receiving TCZ. In addition, the mean differences between discharged and deceased patients in laboratory parameters measured before and 3, 6 and 9 days after TCZ administration were estimated with weighted generalized estimation equations. The variables associated with time to death were immunosuppression (Hazard Ratio-HR 3.15; 95% confidence interval-CI 1.17, 8.51), diabetes mellitus (HR 2.63; 95% CI 1.23–5.64), age (HR 1.05; 95% CI 1.02–1.09), days since diagnosis until TCZ administration (HR 1.05, 95% CI 1.00–1.09), and platelets (HR 0.27; 95% CI: 0.11, 0.69). In the post-TCZ analysis and compared to discharged patients, deceased patients had more lactate dehydrogenase ( p = 0.013), troponin I ( p = 0.013), C-reactive protein ( p = 0.013), neutrophils ( p = 0.024), and fewer platelets ( p = 0.013) and lymphocytes ( p = 0.013) as well as a lower average PaO 2 /FiO 2 ratio. In conclusion, in COVID-19 diagnosed patients receiving TCZ, early treatment decreased the risk of death, while age, some comorbidities and baseline lower platelet counts increased that risk. After TCZ administration, lower platelet levels were again associated with mortality, together with other laboratory parameters.

[This corrects the article DOI: 10.3389/fimmu.2017.00966.].[This corrects the article DOI: 10.3389/fimmu.2017.00966.].

P. vivax infection during pregnancy has been associated with poor outcomes such as anemia, low birth weight and congenital malaria, thus representing an important global health problem. However, no vaccine is currently available for its prevention. Vir genes were the first putative virulent factors associated with P. vivax infections, yet very few studies have examined their potential role as targets of immunity. We investigated the immunogenic properties of five VIR proteins and two long synthetic peptides containing conserved VIR sequences (PvLP1 and PvLP2) in the context of the PregVax cohort study including women from five malaria endemic countries: Brazil, Colombia, Guatemala, India and Papua New Guinea (PNG) at different timepoints during and after pregnancy. Antibody responses against all antigens were detected in all populations, with PNG women presenting the highest levels overall. P. vivax infection at sample collection time was positively associated with antibody levels against PvLP1 (fold-increase: 1.60 at recruitment -first antenatal visit-) and PvLP2 (fold-increase: 1.63 at delivery), and P. falciparum co-infection was found to increase those responses (for PvLP1 at recruitment, fold-increase: 2.25). Levels of IgG against two VIR proteins at delivery were associated with higher birth weight (27 g increase per duplicating antibody levels, p<0.05). Peripheral blood mononuclear cells from PNG uninfected pregnant women had significantly higher antigen-specific IFN-γ TH1 responses (p=0.006) and secreted less pro-inflammatory cytokines TNF and IL-6 after PvLP2 stimulation than P. vivax-infected women (p<0.05). These data demonstrate that VIR antigens induce the natural acquisition of antibody and T cell memory responses that might be important in immunity to P. vivax during pregnancy in very diverse geographical settings.

PTH 7: Health Policy and Health Services 2, B308 (FCSH), September 5, 2025, 11:30 - 12:24 Aim We aimed to adapt screening recommendations for infectious diseases(ID)?and female genital mutilation(FGM) for migrants in?primary?care settings of two Spanish regions, Catalonia and Almería. Methods We followed a modified version of the ADAPTE framework. A literature review of clinical guidelines on ID and FGM screening at national and international levels was conducted. Two multidisciplinary teams of experts participated in independent consensus workshops, one at each site, where they agreed on the conditions and the criteria for the adapted screening recommendations. A questionnaire sent to the experts evaluated their level of agreement. Results Participants at both sites defined a target migrant population, including Africans, Latin Americans, Asians, and Eastern Europeans. They agreed to include human immunodeficiency virus(HIV), hepatitis B(HBV) and C virus(HCV), active tuberculosis(TB), schistosomiasis, strongyloidiasis, Chagas disease(CD) and FGM in the recommendations. In Almería, participants also included syphilis, latent TB, and intestinal parasites. Participants in both regions agreed to test for HBV in migrants from countries with an HBV-prevalence >2%, active TB in newly-arrived migrants (<5years) from countries with a TB-incidence >50 cases/100,000population, and schistosomiasis, strongyloidiasis and FGM in migrants from endemic areas. In Catalonia, participants agreed to test for HIV and HCV if the prevalence was >1% and >2%, respectively, and for CD in migrants from endemic countries. In contrast, participants in Almería agreed to test all migrants for HIV, HCV, and syphilis, and women of child-bearing age from endemic countries for CD. The recommendation for latent TB targeted migrants aged 16-35 years from countries with a TB-incidence >50 cases/100,000population, and the intestinal parasites’ recommendation targeted migrants from sub-tropical and tropical countries. Conclusions We developed screening recommendations adapted to the targeted migrant populations’ profiles and the local context of each health system, considering the available resources at the primary care level, which will lead to better healthcare provision for migrants.