Risultati per: AGA: linee guida sulla de-prescrizione degli inibitori della pompa protonica
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AGA Living Clinical Practice Guideline on Pharmacological Management of Moderate-to-Severe Ulcerative Colitis
This American Gastroenterological Association (AGA) living guideline is intended to support practitioners in the pharmacological management of moderate-to-severe ulcerative colitis (UC).
Elsewhere in The AGA Journals (Preview Section)
AGA Living Clinical Practice Guideline on Pharmacological Management of Moderate-to-Severe Ulcerative Colitis
This American Gastroenterological Association (AGA) living guideline is intended to support practitioners in the pharmacological management of moderate-to-severe ulcerative colitis (UC).
Linee guida italiane su diagnosi e gestione del malato di celiachia: cosa cambia?
LE RECENTI LINEE GUIDA ESC – (A ∙ Scompenso cardiaco, B ∙ Management della malattia cardiovascolare nei pazienti diabetici)
Linee Guida per la prevenzione, diagnosi e gestione della BPCO
De Poli, in manovra incremento di 10 milioni per cure palliative
‘È un primo passo, ma da solo non basta’
AGA Clinical Practice Update on Nonampullary Duodenal Lesions: Expert Review
Nonampullary duodenal polyps are found in up to 5% of all upper endoscopies; the vast majority are identified incidentally in asymptomatic patients. Although most are benign, adenomas are estimated to account for 10%–20% of these lesions. Most international guidelines recommend that all duodenal adenomas should be considered for endoscopic resection; this may be associated with a near 15% adverse event rate (predominantly bleeding and perforation) in prospective studies, with substantial local recurrence on surveillance.
Linea guida sulla diagnosi e gestione dell’endometriosi
AGA Clinical Practice Update on Endoscopic Enteral Access: Commentary
The purpose of this American Gastroenterological Association (AGA) Clinical Practice Update is to facilitate understanding and improve the clinical practice of endoscopic enteral access.
Abstract 4144620: Outcomes with Drug-Coated Balloon Versus Drug-Eluting Stents for De-Novo Coronary Artery Disease: A Meta-Analysis
Circulation, Volume 150, Issue Suppl_1, Page A4144620-A4144620, November 12, 2024. Background:Drug-eluting balloons (DEB) are promising alternatives to drug-eluting stents (DES) for managing de novo coronary artery disease (CAD). Given the scarcity of available data, our objective was to evaluate the outcomes of DES versus DEB in CAD patients.Methods:Databases such as PubMed, Embase, Cochrane Library, and Google Scholar were searched to identify studies comparing clinical outcomes between DCB and DES in de novo CAD patients. Using a random-effects model, pooled estimates of the mean difference (MD) and odds ratio (OR) were calculated along the 95% confidence intervals (CI), with statistical significance set at p
Abstract 4136210: Meta-Analysis of Efficacy and Safety in DAPT De-escalation: Transitioning from Ticagrelor to Clopidogrel in Acute Myocardial Infarction Following Percutaneous Coronary Intervention at twelve-Month Follow-Up
Circulation, Volume 150, Issue Suppl_1, Page A4136210-A4136210, November 12, 2024. Background:In the management of acute myocardial infarction (AMI) following percutaneous coronary intervention (PCI), dual antiplatelet therapy (DAPT) plays a crucial role in preventing recurrent ischemic events. Recent studies have explored the feasibility and safety of de-escalating DAPT from ticagrelor to clopidogrel.Methods:We conducted a systematic review and meta-analysis by searching several databases, including Cochrane Central Register of Controlled Trials (CENTRAL), PubMed, MEDLINE (including MEDLINE InProcess) (OvidSP), Web of Science, Embase (OvidSP), and Scopus. We assessed the risk of bias using the ROB2 Cochrane tools for randomized controlled trials (RCTs). The analysis was performed using RevMan Cochrane software.Results:A total of ten studies including observational and clinical studies involving N=18,001patients (11,458 de-escalated from ticagrelor to clopidogrel after 12 months and 6,543 remained on ticagrelor after 12 months post-PCI) were included. There was no difference in the risk of all-cause death (RR 0.98; 95% CI 0.69 to 1.38; p=0.90), cardiovascular death (RR 1.09; 95% CI 0.68 to 1.74; p=0.73), myocardial infarction (RR 0.90; 95% CI 0.71 to 1.14; p=0.37) and stroke (RR 0.81; 95% CI 0.50 to 1.32; p=0.41) between the two groups.Conclusion:In conclusion, transitioning from ticagrelor to clopidogrel in acute myocardial infarction following percutaneous coronary intervention appears to be a feasible strategy for de-escalating dual antiplatelet therapy (DAPT). While maintaining efficacy in preventing adverse cardiovascular events, such as stent thrombosis, this approach may mitigate bleeding risks associated with prolonged ticagrelor use.
Abstract 4141371: Comparing predictors of atrial fibrillation recurrence following de novo versus repeat catheter ablation
Circulation, Volume 150, Issue Suppl_1, Page A4141371-A4141371, November 12, 2024. Background:Approximately 1 of 5 catheter ablations for atrial fibrillation (AF) are repeat procedures. Despite this, little is known about risk factors for recurrence in patients undergoingrepeatablation compared with those undergoingde novoablation.Objective:To compare predictors of AF recurrence followingde novoandrepeatcatheter ablation.Methods:To compare AF recurrence between those with and without prior ablation, we conducted a retrospective cohort study of patients undergoing catheter ablation for treatment of symptomatic and drug-refractory AF. In this analysis, early recurrence was defined as 30 seconds of AF, atrial flutter, or atrial tachycardia within a 3-month blanking period, while late recurrence was defined as recurrent arrhythmia at >3 months. Multivariable Cox proportional hazard regression analysis was used to identify independent factors associated with recurrence.Results:Among 659 patients, 487 (mean age 63.3 +/- 10.1 years, 33% female, CHA2DS2-VASc 2.8 +/- 1.8, 62% paroxysmal) underwentde novoablation and 172 (mean age 65.1 +/- 10.0 years, 34% female, CHA2DS2-VASc 3.1 +/- 1.9, 60% paroxysmal) underwentrepeatablation with average follow up of 24.4+/-18.4 months. Multivariable modeling revealed that left atrial volume index (LAVi) [HR 1.015, p2 years follow-up. The left atrial volume index and early recurrence are the strongest predictors of late recurrence.
Abstract 4136584: The Association of De Novo Niacin Use with Long-Term Mortality
Circulation, Volume 150, Issue Suppl_1, Page A4136584-A4136584, November 12, 2024. Introduction:Niacin is a non-statin lipid-lowering therapy that has been shown to lower triglycerides and improve other risk factors for cardiovascular diseases. However, previous studies have reported inconsistent effects of niacin on mortality, and its effect on long-term prognosis has not been well studied.Goals:The aim of this study is to examine the association of niacin therapy with long-term all-cause mortality.Methods:In a nationwide historical cohort of 1,139,630 US Veterans with normal baseline kidney function, we examined the association of de novo niacin prescription from 2004 to 2006 with all-cause mortality during a 14-year follow-up. Associations were examined in Cox proportional hazard models adjusted for demographics, major comorbidities, and laboratory measurements. Prescription time-distribution matching was used to control for survival bias.Results:We identified 133,450 new users of niacin. Overall, patients had a mean (standard deviation) age of 60 (13) years, with 6% female, 78% White, 16% Black, and 6% Hispanic. Niacin users were more likely to be male, White, current, or former smokers and had higher frequencies of comorbidities. Niacin use (vs. non-use) was associated with a lower risk of death (Hazard ratio: 0.89, 95% confidential interval: 0.88-0.90) in the fully adjusted model (Model 4, Figure).Conclusion:In a large national cohort of US Veterans, niacin use was associated with a lower risk of death. Further studies are needed to corroborate the potential benefits of niacin on survival.
Abstract 4134148: Reduced BMPR2 in Monocytes De-represses HERV-K and Sustains Inflammation in Pulmonary Arterial Hypertension
Circulation, Volume 150, Issue Suppl_1, Page A4134148-A4134148, November 12, 2024. Background&Rationale:Human endogenous retroviral (HERV) elements are embedded in 8% of our genome. They remain quiescent but can be transiently activated by viral infection to induce an interferon (IFN) response. In pulmonary arterial hypertension (PAH), HERV-K expression is elevated in myeloid cells, and thus can promote inflammation observed in pulmonary arteries (PAs) with progressive obstructive remodeling. PAH is linked to a mutation or a decrease in BMPR2 expression which our laboratory has recently shown in monocytes (MONO). HERVs are silenced by SUMOylated (S) TRIM28 (KAP1, a methylase) and SPEN (a histone deacetylase) factors that are also sequestered by the lnc RNAXISTwhich is increased in females to inactivate the extra X-chromosome. When TRIM28 is phosphorylated (P) by DNA-PK, it loses methylase activity and can act as a transcription factor.Hypothesis:ReducedBMPR2in MONO results in DNA-PK mediated P-TRIM28 causing demethylation ofXISTtargets (X-related genes) andHERV-Kthus increasing their expression. Competitive SPEN binding to the increasedXISTalso de-repressesHERV-K.Approach:We used THP-1 MONOs withBMPR2shRNA and induced pluripotent stem cell (i) MONOs derived fromBMPR2mutant PAH patients and assessedHERV-K,XIST, IFNs and related our findings to DNA-PK–P-TRIM28 and sequestration of SPEN.Results:XISTandHERV-KmRNA were significantly elevated in THP-1 MONOs with shBMPR2 vs. shControl and in PAH-iMONO vs. control iMONO based on gender. ReducedBMPR2also increased IFN genes. These findings were consistent with nuclear DNA-PK and P-TRIM28 shown to bind in affinity purification mass spectrometry analysis. Bisulfite conversion assay demonstrated decreased methylation of HERV-K inBMPR2-deficient MONOs attributed to a reduction in the methylase S-TRIM28. RNA-IP in THP-1 MONOs with shBMPR2 vs. shControl indicated increased binding ofXISTwith TRIM28 and SPEN, suggesting a competitive reduction in binding to HERV-K.Conclusions:Loss of BMPR2 increasesXISTandHERV-Kin MONO related to DNA-PK induced P-TRIM28 and reduced methylase S-TRIM28. IncreasedHERV-Kmay also be a function of the increase inXISTsequestering its deacetylase SPEN. These molecular features underlie a chronicHERV-K-IFN inflammatory response in PAH. They may explain the female predisposition to PAH, because the increase inXISTin females heightens the propensity to activateHERV-K-IFN signaling and chronic inflammation in PAs infiltrated by MONO.