Journal of the American College of Cardiology

2020

DOI: 10.1016/j.jacc.2020.10.027

|View full text |Cite

|

Sign up to set email alerts

|

Inflammatory Bowel Disease and Atherosclerotic Cardiovascular Disease

Miguel Cainzos‐Achirica

¹

,

²

,

³

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Introduction2

Inflammatory Bowel Disease (Ibd)2

Trp Absorption and Catabolism1

Citation Types

Supporting

1

Mentioning

41

Contrasting

0

Unclassified

3

Year Published

2021

2021

2024

2024

Publication Types

Select...

Article7

Preprint1

Book1

Relationship

Self Cite0

Independent9

Authors

Journals

Cited by 62 publications

(52 citation statements)

References 63 publications

Supporting

1

Mentioning

41

Contrasting

0

Unclassified

3

Order By: Relevance

“…Recently, different chronic inflammatory diseases have been associated themselves with a higher cardiovascular risk: systemic lupus erythematosus [21], inflammatory bowel disease [22], rheumatoid arthritis [23], psoriasis [24][25][26], or hidradenitis suppurativa [27,28] are among them.…”

Section: Introductionmentioning

confidence: 99%

Cumulative Inflammation and HbA1c Levels Correlate with Increased Intima-Media Thickness in Patients with Severe Hidradenitis Suppurativa

Sánchez‐Díaz

¹

,

Salvador‐Rodríguez

²

,

Montero‐Vílchez

³

et al. 2021

View full text Add to dashboard Cite

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease that has been associated with a greater risk of metabolic and cardiovascular comorbidities. The aim of this study is to assess cardiovascular risk by means of intima-media thickness (IMT), metabolic syndrome, and other potential biomarkers in patients with severe hidradenitis suppurativa who are candidates for biologic therapy and to explore potentially associated factors. A cross-sectional study was performed. Body mass index (BMI), carotid intima-media thickness (IMT), and blood tests, including glycemic and lipid profile, insulin, vitamin D, and inflammation markers were performed. Fifty patients were included in the study; the male/female ratio was 3:2. The mean age was 38 years, and the mean disease duration was 21.8 years. The mean carotid IMT was 651.39 μm. A positive association of IMT with disease duration, tobacco consumption, and HbA1c levels was observed. HbA1c correlated with the age of onset, hypertension, metabolic syndrome, and glucose levels. Vitamin D levels inversely correlated with the number of areas affected. In conclusion, patients with severe HS present a higher cardiovascular risk, but it is not distributed equally within the patients: Tobacco consumption, inadequate glycemic control, and disease duration could be useful clinical and biochemical markers to identify patients at higher risk.

“…Recently, different chronic inflammatory diseases have been associated themselves with a higher cardiovascular risk: systemic lupus erythematosus [21], inflammatory bowel disease [22], rheumatoid arthritis [23], psoriasis [24][25][26], or hidradenitis suppurativa [27,28] are among them.…”

Section: Introductionmentioning

confidence: 99%

Cumulative Inflammation and HbA1c Levels Correlate with Increased Intima-Media Thickness in Patients with Severe Hidradenitis Suppurativa

Sánchez‐Díaz

¹

,

Salvador‐Rodríguez

²

,

Montero‐Vílchez

³

et al. 2021

View full text Add to dashboard Cite

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease that has been associated with a greater risk of metabolic and cardiovascular comorbidities. The aim of this study is to assess cardiovascular risk by means of intima-media thickness (IMT), metabolic syndrome, and other potential biomarkers in patients with severe hidradenitis suppurativa who are candidates for biologic therapy and to explore potentially associated factors. A cross-sectional study was performed. Body mass index (BMI), carotid intima-media thickness (IMT), and blood tests, including glycemic and lipid profile, insulin, vitamin D, and inflammation markers were performed. Fifty patients were included in the study; the male/female ratio was 3:2. The mean age was 38 years, and the mean disease duration was 21.8 years. The mean carotid IMT was 651.39 μm. A positive association of IMT with disease duration, tobacco consumption, and HbA1c levels was observed. HbA1c correlated with the age of onset, hypertension, metabolic syndrome, and glucose levels. Vitamin D levels inversely correlated with the number of areas affected. In conclusion, patients with severe HS present a higher cardiovascular risk, but it is not distributed equally within the patients: Tobacco consumption, inadequate glycemic control, and disease duration could be useful clinical and biochemical markers to identify patients at higher risk.

“…Gut dysbiosis could contribute to inflammation and immune responses leading to IBD and this inflammatory environment could in turn promote dysbiosis (Sartor and Wu 2017). Results of several prospective observational studies suggested that patients with IBD may be at increased risk of multiple chronic diseases such as cardiovascular disease (Cainzos-Achirica et al 2020), respiratory disease, arthritis, liver conditions, kidney failure (Xu 2018), osteoporosis and depression (Bernstein et al 2019), consistent with the view that dysbiosis exerts systemic negative effects promoting human diseases.…”

Section: Introductionmentioning

confidence: 63%

A multidimensional Mendelian randomization study on the impact of gut dysbiosis on chronic diseases and human longevity

¹

,

²

,

³

et al. 2021

Preprint

View full text Add to dashboard Cite

Alterations of the gut microbiota, often referred to as gut dysbiosis, have been associated with several chronic diseases and longevity in pre-clinical models as well as in observational studies. Whether these relationships underlie causal associations in humans remains to be established. We aimed to determine whether gut dysbiosis influences the risk of chronic diseases and longevity using a comprehensive 2-Sample Mendelian randomization (2SMR) approach. We included as exposures inflammatory bowel disease (IBD) as a human model of gut dysbiosis, 11 gut-associated metabolites and pathways and 48 microbial taxa. Study outcomes included eight chronic diseases previously linked with gut dysbiosis using observational studies (Alzheimer's disease, depression, type 2 diabetes, non-alcoholic fatty liver disease, coronary artery disease (CAD), stroke, osteoporosis and chronic kidney disease) as well as parental longevity and life expectancy. Neither IBD, nor gut-associated metabolites were causally associated with chronic disease or lifespan. After multiple testing correction for 582 tests, no microbial taxa-chronic disease associations remained significant. After robustness analyses and multivariate MR to correct for body mass index and alcohol intake on all 42 nominally significant causal relationships, four associations remained. Altogether, results of this multidimensional Mendelian randomization study suggest that gut dysbiosis has little impact on chronic diseases and human longevity and that previous documented associations may not underly causal relationships. Studies with larger sample sizes and more optimal taxonomic discrimination may ultimately be required to determine whether the human gut microbiota plays a causal role in the etiology of chronic diseases and longevity.

“…Increasing evidence has suggested a strong relationship between gut microbiota and its derived metabolites with CVD [ 40 ]. In this regard, patients with inflammatory bowel disease (IBD) have an increased risk of atherothrombotic complications [ 41 ], suggesting a link between the intestine and the cardiovascular system. Given the importance of Trp metabolites in gastrointestinal homeostasis, they may play a significant role in CVD.…”

Section: Trp Absorption and Catabolismmentioning

confidence: 99%

Tryptophan: From Diet to Cardiovascular Diseases

¹

,

²

2021

View full text Add to dashboard Cite

Cardiovascular disease (CVD) is one of the major causes of mortality worldwide. Inflammation is the underlying common mechanism involved in CVD. It has been recently related to amino acid metabolism, which acts as a critical regulator of innate and adaptive immune responses. Among different metabolites that have emerged as important regulators of immune and inflammatory responses, tryptophan (Trp) metabolites have been shown to play a pivotal role in CVD. Here, we provide an overview of the fundamental aspects of Trp metabolism and the interplay between the dysregulation of the main actors involved in Trp metabolism such as indoleamine 2, 3-dioxygenase 1 (IDO) and CVD, including atherosclerosis and myocardial infarction. IDO has a prominent and complex role. Its activity, impacting on several biological pathways, complicates our understanding of its function, particularly in CVD, where it is still under debate. The discrepancy of the observed IDO effects could be potentially explained by its specific cell and tissue contribution, encouraging further investigations regarding the role of this enzyme. Thus, improving our understanding of the function of Trp as well as its derived metabolites will help to move one step closer towards tailored therapies aiming to treat CVD.

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

hi@scite.ai

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

Product

Browser Extension Assistant by scite Citation Statement Search Reference Check Visualizations Dashboards Explore Journals Explore Organizations Explore Funders Embedding Badge Embedding Citation Search Pricing

Resources

Blog Help & FAQ Accessibility Statement API Terms For Universities & Governments For Researchers For Publishers For Corporate, Pharma & Enterprise Author Marketing Become an Affiliate Get an organization trial or quote scite Data & Services

About

News & Press Careers Read our Paper Coverage

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Copyright © 2024 scite LLC. All rights reserved.

Made with 💙 for researchers

Part of the Research Solutions Family.