Search Results for: Urgenza intestinale nella colite ulcerosa. Revisione delle LL.GG.

Circulation, Volume 150, Issue Suppl_1, Page A4144803-A4144803, November 12, 2024. Background:ST elevation myocardial infarction (STEMI) patients are at increased risk for secondary cardiovascular events. Modulation of purinergic signaling is the mainstay of post-MI antithrombotic therapy. CD39, encoded by theENTPD1gene, is a key modulator of vascular homeostasis that hydrolyzes prothrombotic and proinflammatory extracellular nucleotides. The goal of this study was to determine if theENTPD1promoter polymorphism rs3814159 genotype associates with inflammatory cell expression of CD39 and with secondary cardiovascular events in patients following STEMI.Approach and Results:FACS analysis of circulating inflammatory cells from volunteers and STEMI patients was conducted. We found that 1) the ENTPD1 promoter polymorphism rs3814159 genotype associates with the level of CD39 expression on T cells, 2) Integrated immunophenotype analysis depicts a temporal expression pattern of increased CD39 on Tregs following myocardial infarction, and 3) Treg phenotype differs by rs3814159 genotype early following STEMI. Next to determine if the rs3814159 genotype associates with STEMI outcomes we analyzed data from the POPular Genetics study. A total of 1964 patients from the original POPular Genetics study cohort had rs3814159 genotype assignment (Treg CD39highAA: 517 (24.3%);CD39intAG: 982 (46.2%);CD39lowGG: 625 (29.4%) consistent with expected frequencies. There were no differences in baseline characteristics by rs3814159 genotype. The primary endpoint of ischemic outcomes (all-cause death, myocardial infarction, target vessel revascularization, and/or stent thrombosis) was significantly higher in those patients homozygous for GG (Treg CD39low) versus AA (Treg CD39high) at rs3814159 by both univariate (HR:1.44; 95% CI:1.04-2.00, p=0.029) and multivariate (HR:1.43; 95% CI:1.03-1.98, p=0.034) analysis using an additive model. No significant differences in bleeding outcomes were observed by genotype using BARC criteria. Kaplan-Meier analysis revealed a significant increase in primary ischemic events in patient homozygous GG (Treg CD39low) versus homozygous AA (Treg CD39high) at rs3814159 (Figure).Conclusions:These data suggest for the first time thatENTPD1rs3814159 genotype associates with the level of CD39 expression on T-cells and with the incidence of the primary ischemic endpoint of all-cause death, myocardial infarction, target vessel revascularization, and/or stent thrombosis after ST elevation myocardial infarction.

Circulation, Volume 150, Issue Suppl_1, Page A4142629-A4142629, November 12, 2024. Introduction:Over 9 million people are estimated to die annually due to Ischemic Heart Disease (IHD). It also serves as an inviolable risk factor for diabetes mellitus type II-related mortality. However, trends in IHD-related mortality tend to show disparities, which if addressed, can improve outcomes.Research Question:What are the trends in IHD-associated mortality in individuals with diabetes mellitus type II in the USA?Goal:Determining trends stratified by age, gender, race, geographical location, and metropolitan status in IHD-associated mortality in diabetic individuals.Methodology:The CDC Wonder database was used to extract crude mortality rates (CMRs) and age-adjusted mortality rates (AAMRs) per 100,000 population from 1999 to 2020. Annual percentage change (APC) was determined using Joinpoint regression analysis to identify temporal trends.Results:The overall AAMR doubled from 1999 (AAMR: 6.61) to 2020 (AAMR: 12.50). It increased from 1999-2005 (APC: 3.67), followed by a decrease during 2005-2014 (APC: -1.09), and finally a steep incline till 2020; 2014-2018 (APC: 5.53) and 2018-2020 (APC: 12.70). Men had a higher AAMR than women, 11.57 versus 6.19. Older adults aged 85+ had the highest CMR (137). NH American Indians or Alaska Natives had the highest AAMR (12.01), followed by Hispanic or Latino (9.73), NH Black or African American (8.81), NH White (8.44), and NH Asian or Pacific Islander (6.69) populations. Stratified by census regions, the highest death rate was in the Midwestern region (AAMR: 10.07), followed by the Western, Southern, and Northeastern regions; AAMR: 9.74, 7.81, and 6.29, respectively. Among the states, West Virginia had the highest AAMR of 16.61, while Nevada had the lowest AAMR of 3.47. Non-metropolitan areas consistently showed higher rates (AAMR: 10.87).Conclusions:Rising trends were observed in IHD-related fatalities in type ll diabetes patients between 1999 and 2020. Amongst various groups, the highest AAMRs were found in those over 85 years, men, American Indians or Alaska Natives, and residents of the Midwest, West Virginia, and non-metropolitan areas. These findings can aid in developing targeted interventions and strategies to counter the alarming rise in mortality rates.

Circulation, Volume 150, Issue Suppl_1, Page A4143606-A4143606, November 12, 2024. Background:Chagas disease (CD) is an infectious disease caused by the protozoaTrypanosoma cruzi, affecting around 6-7 million people in Latin America. Although most infected individuals remain asymptomatic throughout their lives, annually 2-5% of them progress to chronic chagasic cardiomyopathy (CCC), digestive megasyndromes, or both. Ficolins are innate immunity proteins that play a crucial role in the lectin pathway (LP) of complement activation. They recognize pathogen-associated molecular patterns and mediate the clearance of apoptotic cells and cellular debris. Genetic polymorphisms of components of LP have been associated with clinical forms of CD; however, the relationship between Ficolin-1 (FCN1) gene polymorphisms and CD remains unclear.Hypothesis:We hypothesize that polymorphisms in theFCN1gene, previously related to its expression, are associated with clinical forms of CD, possibly impacting LP activation.Goals:To investigate the association of genetic variants of theFCN1gene with the clinical forms of chronic CD.Methods:We evaluated three single-nucleotide polymorphisms (SNPs): rs2989727G >A (c.-1981G >A), rs17039495 (-399G >A) and rs10858293 (+33G >T) by sequence-specific amplification in 200 patients with chronic CD (23.5% asymptomatic, 52% CCC, 10% digestive form, and 14.5% cardiodigestive form) from Southern Brazil, and 210T. cruziseronegative controls. Logistic regression models were adjusted for sex, age, and self-identified ethnicity, followed by Bonferroni correction.Results:The haplotypes GGG, AGT, AGG, GAT, and AAT were more frequently found in patients, while GGG, AGT, AGG, and AAT were more common in controls. We observed a higher frequency of the G allele (p=0.004; OR 1.49; 95% CI 1.14, 1.99) of SNP rs2989727 and the GG genotype (p=0.010; OR 1.82; 95% CI 1.10, 3.03) in CD patients, particularly those with symptomatic forms (p=0.008; OR 1.51; 95% CI 1.11, 2.03; and p=0.012; OR 2.05; 95% CI 1.17, 3.59) and CCC (p=0.013; OR 1.54; 95% CI 1.10, 2.16, and p=0.013; OR 2.16; 95% CI 1.18, 3.97), compared to the control group.Conclusion:TheFCN1rs2989727 variant is associated with chronic CD and CCC, likely due to its impact onFCN1gene expression.

Pazienti, “raccontarsi è la chiave per una vita migliore”

Ok da Aifa, riduce i sintomi intestinali senza l’uso di steroidi

Ok da Aifa, riduce i sintomi intestinali senza l’uso di steroidi

Garantire l’apertura h24 dei Centri assistenza e urgenza

The sun had moved an hour through the sky, unknown to me, because I was asleep, awash in dark so deep, perhaps I’ll die. My body lies prepared to take the leap, a throw tucked tight, two pillows for support. I sleep at night, I sleep in day, I take a breath, I rise and walk, my life cut short. Dreamless, I sleep. I try to tame the snake with tiny prayers, as if a beast could hear, and still the squeeze. If I could be a leaf falling this fall, if I could disappear, the wind would steal me like a gentle thief. But I am waiting for another spring, and so I sleep and tend my broken wing.

C’è l’urgenza di vaccinarne oltre 640.000

In due sono nel reparto Medicina d’urgenza

Annals of Internal Medicine, Ahead of Print.