Hyperuricemia is commonly associated with traditional risk factors such as dysglicemia, dyslipidemia, central obesity and abnormal blood pressure, i.e. the metabolic syndrome. Concordantly, recent studies have revived the controversy over the role of circulating uric acid, hyperuricemia, and gout as an independent prognostic factor for cardiovascular morbidity and mortality. In this regard, different studies also evaluated the possible role of xanthine inhibitors in inducing blood pressure reduction, increment in flow-mediated dilation, and improved cardiovascular prognosis in various patient settings. The vast majority of these studies have been conducted with either allopurinol or its active metabolite oxypurinol, i.e. two purine-like non-selective inhibitors of xanthine oxidase. More recently, the role of uric acid as a risk factor for cardiovascular disease and the possible protective role exerted by reduction of hyperuricemia to normal level have been evaluated by the use of febuxostat, a selective, non purine-like xanthine oxidase inhibitor. In this review, we will report current evidence on hyperuricemia in cardiovascular disease. The value of uric acid as a biomarker and as a potential therapeutic target for tailored old and novel “cardiometabolic” treatments will be also discussed.
Background Vitamin D plays a role in several immune-mediated diseases, but its association with inflammatory bowel disease (IBD) is unclear. We conducted a systematic review and meta-analysis to assess the association between IBD and vitamin D deficiency. Methods We searched electronic databases from inception to December 2014 for observational studies reporting the presence of vitamin D deficiency (defined as serum 25-hydroxycholecalciferol [25(OH)D] level of ≤20 ng/ml) in IBD patients and having a control group without IBD. Odds ratios (OR) were combined using a random effects model. Meta-regression was performed using latitude as a moderator. Study quality was assessed using the Newcastle-Ottawa scale. Results Out of 816 citations, 14 eligible studies were identified, comprising 1891 participants (938 IBD cases and 953 controls). Meta-analysis showed that patients with IBD had 64% higher odds of vitamin D deficiency when compared to controls (OR = 1.64; 95% CI: 1.30, 2.08; I2 = 7%; p < 0.0001). UC patients had more than double the odds of vitamin D deficiency when compared to normal controls (OR = 2.28; 1.18, 4.41; I2 = 41%; p=0.01). Latitude did not influence the association between IBD and vitamin D deficiency (p = 0.34). Generalizability of our results might be limited as we summarized unadjusted ORs, due to non-availability of adjusted ORs in individual studies. Conclusions IBD is significantly associated with having higher odds of vitamin D deficiency. Well-designed RCTs and longitudinal studies are needed to further clarify the role of vitamin D in IBD pathogenesis and its therapy.
Aim Periodontitis is a relapsing–remitting disease. Compared with bleeding on probing (BoP), expression of disease activity, periodontal inflamed surface area (PISA), incorporates chronic disease parameters. We tested the association of PISA and BoP with blood pressure (BP) in NHANES III. Materials and methods A total of 8,614 subjects (≥30 years) with complete periodontal and BP examinations were enrolled. PISA was derived from periodontal probing depth and BoP. The association of PISA and BoP with high/uncontrolled BP was examined by multiple‐adjusted models. Inflammatory markers were tested as possible mediators. A machine learning (ML) approach was used to define the relative importance of PISA and BoP and estimate the power of BP status prediction. Results Compared to no inflammation, severe PISA and BoP were associated with 43% (p < .001) and 32% (p = .006) higher odds of high/uncontrolled BP (≥130/80 mmHg), and with higher systolic BP by ≈4 (p < .001) and 5 (p < .001) mmHg, respectively. Inflammatory markers appeared to mediate this association with various extents, without threshold effect. BoP predicted high/uncontrolled BP more efficiently than PISA using ML. Conclusion PISA and BoP describe the association of periodontal inflammation and hypertension with subtle differences. The contribution of local inflammation to the global inflammatory burden might explain the observed findings.
Orthostatic changes in systolic blood pressure (SBP) impact cardiovascular outcomes. In this study, we aimed to determine the pattern of orthostatic systolic pressure changes in participants enrolled in the SBP Intervention Trial (SPRINT) at their baseline visit before randomization and sought to understand clinical factors predictive of these changes. Of the 9323 participants enrolled in SPRINT, 8662 had complete data for these analyses. The SBP after 1 minute of standing was subtracted from the mean value of the three preceding seated SBP values. At the baseline visit, medical history, medications, anthropometric measures, and standard laboratory testing were undertaken. The mean age of SPRINT participants was 68 years, two-thirds were male, with 30% black, 11% Hispanic, and 55% Caucasian. The spectrum of SBP changes on standing demonstrated that increases in SBP were as common as declines, and about 5% of participants had an increase, and 5% had a decrease of >20 mm Hg in SBP upon standing. Female sex, taller height, more advanced kidney disease, current smoking, and several drug classes were associated with larger declines in BP upon standing, while black race, higher blood levels of glucose and sodium, and heavier weight were associated with more positive values of the change in BP upon standing. Our cross-sectional results show a significant spectrum of orthostatic SBP changes, reflecting known (eg, age) and less well-known (eg, kidney function) relationships that may be important considerations in determining the optimal target blood pressure in long-term outcomes of older hypertensive patients.
High blood pressure (BP) and periodontitis are two highly prevalent conditions worldwide with a significant impact on cardiovascular disease (CVD) complications. Poor periodontal health is associated with increased prevalence of hypertension and may have an influence on blood pressure control. Risk factors such as older age, male gender, non-Caucasian ethnicity, smoking, overweight/obesity, diabetes, low socioeconomic status, and poor education have been considered the common denominators underpinning this relationship. However, recent evidence indicates that the association between periodontitis and hypertension is independent of common risk factors and may in fact be causal in nature. Low-grade systemic inflammation and redox imbalance, in particular, represent the major underlying mechanisms in this relationship. Neutrophil dysfunction, imbalance in T cell subtypes, oral-gut dysbiosis, hyperexpression of proinflammatory genes, and increased sympathetic outflow are some of the pathogenetic events involved. In addition, novel findings indicate that common genetic bases might shape the immune profile towards this clinical phenotype, offering a rationale for potential therapeutic and prevention strategies of public health interest. This review summarizes recent advances, knowledge gaps and possible future directions in the field.
Highlights COVID-19 poses an additional burden on pre-existing cardiovascular diseases. Inflammation-related hypercoagulability can be dramatic. Monitor electrocardiograms, electrolytes, coagulation, and congestion in severe COVID-19. Discontinuing renin-angiotensin-aldosterone system inhibitors is not supported by evidence and could be detrimental.
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