scholarly journals Uric Acid—An Emergent Risk Marker for Thrombosis?

2021 ◽  
Vol 10 (10) ◽  
pp. 2062
Author(s):  
Laura Țăpoi ◽  
Delia Lidia Șalaru ◽  
Radu Sascău ◽  
Cristian Stătescu
Keyword(s):  
Uric Acid ◽  
Elevated Serum ◽  
Experimental Studies ◽  
Risk Scores ◽  
Current Evidence ◽  
Prothrombotic State ◽  
Clinical Scenarios ◽  
Increased Risk ◽  
Established Cardiovascular Risk Factor

Hyperuricemia is nowadays an established cardiovascular risk factor. Experimental studies linked elevated serum uric acid (SUA) levels with endothelial dysfunction (ED), inflammation, and prothrombotic state. The purpose of this review is to summarize the current evidence that emphasizes the possible role of uric acid as a biomarker for a prothrombotic state. A large number of clinical trials correlated SUA levels with both incident and recurrent cases of venous thromboembolism (VTE), independent of other confounding risk factors. Moreover, increased SUA levels may be an important tool for the risk stratification of patients with pulmonary embolism (PE). Left atrial thrombosis was correlated with high SUA levels in several studies and its addition to classical risk scores improved their predictive abilities. In patients with acute myocardial infarction (MI), hyperuricemia was associated with increased mortality, and the idea that hyperuricemia may be able to act as a surrogate to unstable coronary plaques was advanced. Finally, SUA was correlated with an increased risk of thromboembolic events in different systemic diseases. In conclusion, uric acid has been considered a marker of a thrombotic milieu in several clinical scenarios. However, this causality is still controversial, and more experimental and clinical data is needed.

scholarly journals Uric Acid Mediated the Association between BMI and Postmenopausal Breast Cancer Incidence: A Bidirectional Mendelian Randomization Analysis and Prospective Cohort Study

2021 ◽  
Author(s):  
Yue Feng ◽  
Mengying Li ◽  
Yansen Bai ◽  
Guyanan Li ◽  
Xiulong Wu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Uric Acid ◽  
Postmenopausal Women ◽  
Mendelian Randomization ◽  
Breast Cancer Incidence ◽  
Elevated Serum ◽  
Postmenopausal Breast Cancer ◽  
Genome Wide Association Studies ◽  
Increased Risk

Abstract Background: The observational epidemiological studies have reported the associations of high body mass index (BMI) with elevated serum uric acid (UA) level and increased risk of postmenopausal breast cancer. However, whether UA is causally induced by BMI and functioned in the BMI-breast cancer relationship remains unclear. Methods: To elucidate the causality direction between BMI and serum UA, the bidirectional Mendelian randomization (MR) analyses were performed by using summarized data from the largest Asian genome-wide association studies (GWAS) of BMI and UA carried out in over 150,000 Japanese populations. Then, a total of 19,518 postmenopausal women from the Dongfeng-Tongji (DFTJ) cohort (with a mean 8.2-year follow-up) were included and analyzed on the associations of BMI and serum UA with incidence risk of postmenopausal breast cancer by using multivariable Cox proportional hazard regression models. Mediation analysis was further conducted among DFTJ cohort to assess the intermediate role of serum UA in the BMI-breast cancer association.Results: In the bidirectional MR analyses, we observed that genetically determined BMI was causally associated with elevated serum UA [β(95%CI)=0.225(0.111, 0.339), P<0.001], but not vice versa. In the DFTJ cohort, each standard deviation (SD) increment in BMI (3.5 kg/m2) and UA (75.4 μmol/L) was associated with a separate 24% and 22% increased risk of postmenopausal breast cancer [HR(95%CI)= 1.24(1.07, 1.44) and 1.22(1.05, 1.42), respectively]. More importantly, serum UA could mediate 16.9% of the association between BMI and incident postmenopausal breast cancer.Conclusions: The current findings revealed a causal effect of BMI on increasing serum UA and highlighted the mediating role of UA in BMI-breast cancer relationship. Controlling the serum level of UA among overweight postmenopausal women may help to decrease their incident risk of breast cancer.

Serum uric acid levels and risk of prehypertension: a meta-analysis

2017 ◽  
Vol 55 (3) ◽  
Author(s):  
Menglin Jiang ◽  
Dandan Gong ◽  
Yu Fan
Keyword(s):  
Uric Acid ◽  
Serum Uric Acid ◽  
Meta Analysis ◽  
Elevated Serum ◽  
China National Knowledge Infrastructure ◽  
Cross Sectional ◽  
Knowledge Infrastructure ◽  
Increased Risk ◽  
Cross Sectional Studies ◽  
The Relationship

AbstractElevated serum uric acid (SUA) levels may increase the risk of prehypertension. However, the findings from these studies remain conflicting. The objective of this study was to determine the relationship between SUA levels and risk of prehypertension by conducting a meta-analysis. We conducted a comprehensive literature search of PubMed, Embase, China National Knowledge Infrastructure, VIP, and the Wangfang database without language restrictions through May 2015. Observational studies assessing the relationship between SUA levels and prevalence of prehypertension were included. Pooled adjust odds ratio (OR) and corresponding 95% confidence intervals (CI) of prehypertension were calculated for the highest vs. lowest SUA levels. Prehypertension was defined as systolic blood pressure (BP) ranging from 120 to 139 mmHg or diastolic BP ranging from 80 to 89 mmHg. Eight cross-sectional studies with a total of 21,832 prehypertensive individuals were included. Meta-analysis showed that elevated SUA levels were associated with increased risk of prehypertension (OR: 1.84; 95% CI: 1.42–2.38) comparing the highest vs. lowest level of SUA levels. Subgroup analyses showed that elevated SUA levels significantly increased the risk of prehypertension among men (OR: 1.60; 95% CI: 1.12–2.21) and women (OR: 1.59; 95% CI: 1.17–2.16). Elevated SUA levels are positively associated with the risk of prehypertension in the general population. However, more well-designed longitudinal studies are needed before a definitive conclusion can be drawn due to the cross-sectional studies included are susceptible to bias.

scholarly journals Role of Bacterial Overgrowth in the Stomach as an Additional Risk Factor for Gastritis

2003 ◽  
Vol 17 (suppl b) ◽  
pp. 13B-17B ◽  
Author(s):  
Gregory Naylor ◽  
Anthony Axon
Keyword(s):  
Gastric Cancer ◽  
Cell Mass ◽  
Bacterial Overgrowth ◽  
Nitroso Compounds ◽  
Current Evidence ◽  
Additional Risk Factor ◽  
Proximal Small Bowel ◽  
Increased Risk ◽  
H Pylori

Gastric bacteria can either be ingested or ascend from the distal bowel; however, their survival is usually limited by gastric acidity and motility. A reduction in gastric acid can result in bacterial overgrowth in the stomach and proximal small bowel, and the number of organisms rises as the intragastric pH rises.The increased risk of noncardia gastric cancer seen in patients with hypochlorhydria may be explained by an excess of nitrites and N-nitroso compounds (NOCs). These compounds are found in the diet of populations with a high gastric cancer risk, but can also be produced by the organisms that exist in the hypochlorhydria stomach. It has long been hypothsized that nitrites and NOCs act as one of the triggers in the atrophy-metaplasia-dysplasia-carcinoma path. However, although indirect data have linked the premalignant changes of metaplasia and dysplasia to NOCs, direct measurement of gastric nitrites and NOCs has not confirmed such a link.The role ofHelicobacter pyloriin bacterial overgrowth is mainly as a cause of hypochlorhydria resulting from atrophic gastritis, leading to a reduction in the parietal cell mass.Acid-suppressing drugs can result in bacterial overgrowth and increased nitrites and NOCs, although there is no current evidence for an increased risk of gastric cancer in patients taking them. One explanation is that the stomach appears to be colonized by different organisms than those in patients with hypochlorhydria for other reasons. There is some evidence that bacterial overgrowth per se can cause gastric inflammation in mice; however, although in humans the degree of gastric inflammation is greater when overgrowth is more prominant this may simply reflect the greater degree of hypochlorhydria in patients with a more severe H pylori-induced inflammation.

scholarly journals Circulating Lysophosphatidylcholines, Phosphatidylcholines, Ceramides, and Sphingomyelins and Ovarian Cancer Risk: a 23-year Prospective Study

2019 ◽  
Author(s):  
Oana A. Zeleznik ◽  
Clary B. Clish ◽  
Peter Kraft ◽  
Julian Avila-Pancheco ◽  
A. Heather Eliassen ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Risk ◽  
Postmenopausal Women ◽  
Clear Cell ◽  
Statistical Significance ◽  
Experimental Studies ◽  
P Value ◽  
Ovarian Cancer Risk ◽  
Increased Risk

AbstractBackgroundExperimental evidence supports a role of lipid dysregulation in ovarian cancer progression and metastasis. We estimated associations with ovarian cancer risk for circulating levels of four lipid groups measured 3-23 years before diagnosis.MethodsAnalyses were conducted among cases (N = 252) and matched controls (N = 252) from the Nurses’ Health Studies. We used logistic regression adjusting for risk factors to investigate associations of lysophosphatidylcholines (LPC), phosphatidylcholines (PC), ceramides (CER), and sphingomyelins (SM) with ovarian cancer risk overall and by histotype. A Bonferroni adjusted p-value threshold of 0.0125 (0.05/4; 4 measured lipid groups) was used to evaluate statistical significance. Odds ratios (OR; 10thto the 90thpercentile) and 95% confidence intervals of ovarian cancer risk were estimated.ResultsC16:0 SM, C18:0 SM, C16:0 CER and SM sum were significantly positively associated with ovarian cancer risk, with ORs ranging from 1.95-2.10, with stronger ORs for postmenopausal women (2.02-3.22). ORs were generally similar for serous/poorly differentiated and endometrioid/clear cell tumors, although most did not meet the Bonferroni-adjusted p-value for significance. C18:1 LPC and the ratio of LPC to PC were significantly inversely, while C18:0 SM was significantly positively, associated with risk of endometrioid/clear cell tumors.ConclusionElevated levels of circulating SMs 3-23 years before diagnosis were associated with increased risk of ovarian cancer, regardless of histotype, with stronger associations among postmenopausal women. Prospective and experimental studies are required to validate our findings and understand the role of lipid dysregulation, SMs in particular, in ovarian carcinogenesis.

Profile study: Genetic prostate cancer risk stratification for targeted screening.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 5054-5054
Author(s):  
Elena Castro ◽  
Elizabeth Bancroft ◽  
Natalie Taylor ◽  
Tokhir Dadaev ◽  
Elizabeth Page ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Genetic Model ◽  
Genetic Risk Score ◽  
Prostate Cancer Risk ◽  
Screening Tools ◽  
Risk Scores ◽  
Severe Side Effect ◽  
Cancer Worry ◽  
Increased Risk

5054 Background: Prostate cancer (PC) screening is controversial and better approaches are needed, including a better assessment of individualized PC risk. Several studies have identified a number of common single nucleotide polymorphisms (SNPs) that confer a cumulative risk of PC. We have explored the potential role of genetic markers in identifying men who should be selectively targeted for screening in a population with increased risk of PC due to family history (FH) of the disease. Methods: PROFILE has been developed as a pilot study. The primary aim is to determine the feasibility of targeted PC screening using prostatic biopsy (PB) and its association with specific genetic profiles in men with FH. Secondary aims are to evaluate the role of PSA and Diffusion Weighted MRI (DW-MRI) as screening tools in this population. From December 2010 men aged 40-69 with FH of PC were invited into the study until 100 men were enrolled. Blood samples were provided for PSA and DNA extraction. The cumulative SNP risk scores for each patient were calculated by summing 59 risk alleles for each locus using the weighted effect as estimated in previous studies (log-additive model). DW-MRI was performed in 50 patients. All participants were asked to undergo a 10 core PB regardless of baseline PSA. Those who declined PB have been excluded from this analysis. Data on side effects and cancer worry were also collected. Results: 35% of invited men entered the study. Median age was 53 yrs (40-69) and median PSA was 1.15. Ninety men accepted to undergo a PB as primary PC screening. Twenty-two tumours were found and 45% of them were clinically significant [Median age 64yrs (47-69), median PSA 5.4 (0.91-9.3)]. The predictive performance of DW-MRI, PSA, genetic model and genetic model plus PSA measured by AUC were: 0.85, 0.73, 0.57 and 0.74, respectively. The genetic model performed better in men with PSA<3(AUC 0.63). No severe side effect or adverse psychosocial variables were noted. Conclusions: Our results indicate that PB is acceptable as a means of PC screening in men with FH of PC. Overall, DW-MRI and PSA were more predictive of PC than the genetic risk score. As more SNPs are found, a larger study is warranted to evaluate their role in the PC screening algorithm.

The risk of atrial fibrillation associated with hyperuricemia

2021 ◽  
Author(s):  
V. A. Chernyshov
Keyword(s):  
Oxidative Stress ◽  
Atrial Fibrillation ◽  
Elevated Serum ◽  
Renin Angiotensin System ◽  
Oxidase Inhibitor ◽  
Important Place ◽  
Xanthine Oxidase Inhibitor ◽  
Increased Risk ◽  
The Relationship

The article summarizes mechanisms, linking hyperuricemia, the elevated serum levels of uric acid (UA), and atrial fibrillation (AF), the most frequent cardiac arrhythmia. The actuality of the problem is explained by the fact that UA is considered as an independent risk marker of AF closely associated with the onset and subsequent persistence of AF as well as by the AF increased risk in males and females with hyperuricemia. It has been shown how hyperuricemia, combined with other AF risk factors, contributeы to the development of arrhythmia, as well as the role of hyperuricemia, oxidative stress and renin‑angiotensin system (RAS) activation in the AF pathogenesis. The consideration have been given to the hyperuricemia association with a prevalence of AF among the patients with carbohydrate exchange disorders such as metabolic syndrome and type 2 diabetes mellitus as well as to the relationship between hyperuricemia and endothelial vascular dysfunction, oxidative stress, high blood concentration of systemic inflammatory markers and insulin resistance (IR). Some mechanisms of hyperuricemia participation in cardiac remodeling as a risk factor of AF are adduced. In particular, the relationship between hyperuricemia and left atrial (LA) size that could be mediated through systemic inflammation and IR is discussed. A significance of a direct impaired action of UA on LA cardiomyocytes resulted in their structural and ionic remodeling is shown. The role of xanthinoxidase (XO) activation in initiation of oxidative stress and inflammation in cardiomyocytes and endothelial cells is discussed. All these mechanisms are emphasized to be able to shorten a potential of action of atrial cardiomyocytes as well as to reduce a threshold of re‑entry mechanism initiation and to promote an appearance of the first and the following AF episodes. An important place in the review is taken for an intracellular UA and its cellular transporters in the context of their participation in pathogenesis of AF. The possibilities of drug hyperuricemia correction have been described in regards the reduction of AF risk, in particular, the role of reducing of the oxidative stress intensity with the use of xanthine oxidase inhibitor allopurinol, the inhibitor of NADPH oxidase apocynin, the antioxidant N‑acetylcysteine in the reduction of the risk of onset and subsequent recurrences of AF episodes, and transition of arrhythmia in the persistent form. Some perspectives of probenecid (an inhibitor of UA intracellular transporter activity) usage in the reduction of AF risk due to such of its mechanisms as a reduction of intracellular UA accumulation and antiapoptotic action as well as an ability of this agent to inhibit a locally activated oxidative stress and locally activated tissue RAS are discussed. A significance of the further detailed study of pathophysiological mechanisms of AF in hyperuricemia is emphasized for elaboration of the most effective practical recommendations in prevention of this arrhythmia in persons with UA exchange disorders.

scholarly journals Role of Testosterone in the Treatment of Cardiovascular Disease

2017 ◽  
Vol 12 (02) ◽  
pp. 1 ◽  
Author(s):  
Carolyn M Webb ◽  
Peter Collins ◽  
◽  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Cardiovascular System ◽  
Serum Testosterone ◽  
Current Evidence ◽  
Premature Coronary Artery Disease ◽  
Cvd Risk ◽  
Testosterone Levels ◽  
Increased Risk

Cardiovascular disease (CVD) is the most prevalent non-communicable cause of death worldwide. Testosterone is a sex hormone that is predominant in males but also occurs in lower concentrations in females. It has effects directly on the blood vessels of the cardiovascular system and on the heart, as well as effects on risk factors for CVD. Serum testosterone concentrations are known to decrease with age and reduced testosterone levels are linked to premature coronary artery disease, unfavourable effects on CVD risk factors and increased risk of cardiovascular mortality independent of age. A significant number of men with heart failure demonstrate reduced serum testosterone concentrations and there is early evidence suggesting that low testosterone levels affect cardiac repolarisation. Any association between endogenous testosterone concentrations and CVD in women has yet to be established. Testosterone replacement is used to treat men with hypogonadism but also has cardiovascular effects. This review will present the current evidence, expert opinion and controversies around the role of testosterone in the pathophysiology of CVD and surrounding the use of testosterone treatment and its effects on the cardiovascular system and CVD.

The relationship between elevated serum uric acid and arterial stiffness in a healthy population

Vascular ◽  
2020 ◽  
Vol 28 (4) ◽  
pp. 494-501 ◽  
Author(s):  
Ye Jiang ◽  
Ji-Yong Ge ◽  
Yu-Yan Zhang ◽  
Fang-Fang Wang ◽  
Yuan Ji ◽  
...  
Keyword(s):  
Uric Acid ◽  
Arterial Stiffness ◽  
Serum Uric Acid ◽  
Elevated Serum ◽  
Healthy Population ◽  
Diabetic Mellitus ◽  
The Relationship ◽  
Circulating Levels ◽  
Randomization Method

Objective This study aims to investigate the relationship between serum uric acid and arterial stiffness in a healthy population. Methods Among the 979 participants, baPWV was non-invasively measured, the circulating levels of uric acid were tested, and the uric acid polymorphisms (rs2231142 and rs11722228) were genotyped. Then, the Mendelian randomization method was employed to test the relationship between serum uric acid and arterial stiffness in a healthy population. Results After adjusting for age, gender, antihypertensive medication, body mass index, waist-to-hip ratio, urea nitrogen, creatinine and diabetic mellitus, there was a significant allelic difference in uric acid levels for each genotype ( P <  0.0001 for rs2231142; P =  0.007 for rs11722228). However, there were no differences on the potential confounders between the genotypes of rs2231142 and rs11722228 ( P >  0.05). The baPWV was significantly associated with circulating levels of uric acid after adjusting for cardiovascular risk factors and other potential confounders ( P =  0.002). However, neither the single polymorphism, nor the accumulation of culprit alleles was associated with baPWV ( P =  0.92 for rs2231142; P =  0.60 for rs11722228; P for trend = 0.77 for the combined analysis of culprit alleles). Conclusion These results do not support the causal role of circulating levels of uric acid in the development of arterial stiffness.

scholarly journals Hyperuricemia and Hypertension, Coronary Artery Disease, Kidney Disease: From Concept to Practice

2020 ◽  
Vol 21 (11) ◽  
pp. 4066 ◽  
Author(s):  
Mélanie Gaubert ◽  
Thomas Bardin ◽  
Alain Cohen-Solal ◽  
François Diévart ◽  
Jean-Pierre Fauvel ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Renal Function ◽  
Uric Acid ◽  
Coronary Artery ◽  
Kidney Disease ◽  
Serum Uric Acid ◽  
Elevated Serum ◽  
Renal Diseases ◽  
Increased Risk ◽  
Artery Disease

Since the publication of the Framingham Heart Study, which suggested that uric acid should no longer be associated with coronary heart disease after additional adjustment for cardiovascular disease risk factors, the number of publications challenging this statement has dramatically increased. The aim of this paper was to review and discuss the most recent studies addressing the possible relation between sustained elevated serum uric acid levels and the onset or worsening of cardiovascular and renal diseases. Original studies involving American teenagers clearly showed that serum uric acid levels were directly correlated with systolic and diastolic pressures, which has been confirmed in adult cohorts revealing a 2.21-fold increased risk of hypertension. Several studies involving patients with coronary artery disease support a role for serum uric acid level as a marker and/or predictor for future cardiovascular mortality and long-term adverse events in patients with coronary artery disease. Retrospective analyses have shown an inverse relationship between serum uric acid levels and renal function, and even a mild hyperuricemia has been shown to be associated with chronic kidney disease in patients with type 2 diabetes. Interventional studies, although of small size, showed that uric acid (UA)-lowering therapies induced a reduction of blood pressure in teenagers and a protective effect on renal function. Taken together, these studies support a role for high serum uric acid levels (>6 mg/dL or 60 mg/L) in hypertension-associated morbidities and should bring awareness to physicians with regards to patients with chronic hyperuricemia.

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