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Background/Objective Although gout flares are featured by systemic signs of inflammation, cellular sources of inflammatory mediators are not yet properly characterized. Our objective was to evaluate serum levels and gene expression in peripheral blood mononuclear cells (PBMCs) of several molecules associated with the activation of NLRP3 inflammasome. Methods Fifteen patients with gout flare and 15 individuals with asymptomatic hyperuricemia were cross-sectionally studied. Serum levels of interleukin 1β (IL-1β), IL-18, monocyte chemoattractant protein 1/chemokine (C-C motif) ligand 2 (CCL2), and vascular cell adhesion molecule 1 were measured as a reflection of systemic inflammation, whereas the expression of NLRP3, CASP1, IL18, and CCL2 genes was measured to assess the inflammatory characteristics of PBMCs. Results Serum levels of IL-1β (1.27 [0.07–1.99] pg/mL vs. 0 [0–0.82] pg/mL, p = 0.032) and vascular cell adhesion molecule 1 (606 [435–748] pg/mL vs. 349 [305–422] pg/mL, p = 0.014) were significantly higher in patients with gout flare than in individuals with asymptomatic hyperuricemia, whereas differences in IL-18 and monocyte chemoattractant protein 1/CCL2 were not found. Notably, no differences were observed in the expression of NLRP3, CASP1, IL18, or CCL2 in PBMCs from individuals of one or another group. Conclusions Systemic inflammation during gout flares does not appear to be associated with NLRP3 inflammasome activation in PBMCs, suggesting that it may represent the systemic spread of local (synovial) inflammation to monosodium urate crystals, which provides a rationale for redirecting anti-inflammatory therapy from a systemic approach to one centered on the inflamed joint.

Objective:The aim of the study was to assess whether a recent SARS-CoV-2 infection could by itself be a risk or prognostic factor for ST-segment elevation myocardial infarction (STEMI). Method: An observational study in unvaccinated patients with STEMI confirmed by cardiac catheterization was conducted. A recent or concurrent SARS-CoV-2 infection was identified by the presence of serum IgG against the nucleocapsid protein, or a positive polymerase chain reaction test on nasopharyngeal swabs. Baseline cardiovascular risk factors, clinical STEMI severity, main catheterization findings, and occurrence of major adverse cardiovascular events (MACE) during hospitalization were compared between study subgroups. Results: Of a total of 89 patients recruited, 14 (16%) had a recent SARS-CoV-2 infection. Patients with STEMI and recent SARS-CoV-2 infection had a markedly lower frequency of high blood pressure (20% versus 55%; P = 0.03) as well as a tendency to have fewer comorbidities. Regarding the clinical presentation, there were no differences in the severity of the STEMI. Furthermore, the main findings during cardiac catheterization including the atherosclerotic burden and the number of vessels affected, as well as the occurrence of MACE during follow-up, were not significantly different between the groups. Conclusions: A recent SARS-CoV-2 infection appears to facilitate the triggering of STEMI, as these patients have fewer traditional cardiovascular risk factors than their uninfected counterparts. However, this does not seem to affect the clinical presentation or the in-hospital course of STEMI patients.