scholarly journals What Links an Increased Cardiovascular Risk and Inflammatory Bowel Disease? A Narrative Review

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2661
Author(s):  
Liliana Łykowska-Szuber ◽  
Anna Maria Rychter ◽  
Magdalena Dudek ◽  
Alicja Ewa Ratajczak ◽  
Aleksandra Szymczak-Tomczak ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Normal Weight ◽  
Reactive Protein ◽  
Intestinal Dysbiosis ◽  
Increased Risk ◽  
Inflammatory Bowel ◽  
Endothelial Dysfunctions

Several studies have shown increased rates of cardiovascular disease (CVD) in patients suffering from inflammatory bowel disease (IBD), particularly in cases of early atherosclerosis and myocardial infarction. IBD most frequently begins at an early age, patients usually present normal weight and remain under constant care of a physician, as well as of a nutritionist. Therefore, the classical risk factors of CVD are not reflected in the higher prevalence of CVD in the IBD population. Still, both groups are characterised by chronic inflammation and display similar physiopathological mechanisms. In the course of IBD, increased concentrations of pro-inflammatory cytokines, such as C-reactive protein (CRP) and homocysteine, may lead to endothelial dysfunctions and the development of CVD. Furthermore, gut microbiota dysbiosis in patients with IBD also constitutes a risk factor for an increased susceptibility to cardiovascular disease and atherosclerosis. Additionally, diet is an essential factor affecting both positively and negatively the course of the aforementioned diseases, whereas several dietary patterns may also influence the association between IBD and CVD. Thus, it is essential to investigate the factors responsible for the increased cardiovascular (CV) risk in this group of patients. Our paper attempts to review the role of potential inflammatory and nutritional factors, as well as intestinal dysbiosis and pharmacotherapy, in the increased risk of CVD in IBD patients.

Ethnic Differences in the Smoking-Related Risk of Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis

2021 ◽  
Author(s):  
Daniele Piovani ◽  
Claudia Pansieri ◽  
Soumya R R Kotha ◽  
Amanda C Piazza ◽  
Celia-Louise Comberg ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Latin American ◽  
Bowel Disease ◽  
Meta Analysis ◽  
Study Data ◽  
Future Research ◽  
Related Risk ◽  
Increased Risk ◽  
Inflammatory Bowel

Abstract Background and aims The association between smoking and inflammatory bowel disease (IBD) relies on old meta-analyses including exclusively non-Jewish White populations. Uncertainty persists regarding the role of smoking in other ethnicities. Methods We systematically searched Medline/PubMed, Embase and Scopus for studies examining tobacco smoking and the risk of developing IBD, i.e., Crohn’s disease (CD) or ulcerative colitis (UC). Two authors independently extracted study data and assessed each study’s risk-of-bias. We examined heterogeneity and small-study effect, and calculated summary estimates using random-effects models. Stratified analyses and meta-regression were employed to study the association between study-level characteristics and effect estimates. The strength of epidemiological evidence was assessed through prespecified criteria. Results We synthesized 57 studies examining the smoking-related risk of developing CD and UC. Non-Jewish White smokers were at increased risk of CD (29 studies; RR: 1.95, 95% CI: 1.69‒2.24; moderate evidence). No association was observed in Asian, Jewish and Latin-American populations (11 studies; RR: 0.97; 95% CI: 0.83–1.13), with no evidence of heterogeneity across these ethnicities. Smokers were at reduced risk of UC (51 studies; RR: 0.55, 95% CI: 0.48–0.64; weak evidence) irrespectively of ethnicity; however, cohort studies, large studies and those recently published showed attenuated associations. Conclusions This meta-analysis did not identify any increased risk of CD in smokers in ethnicities other than non-Jewish Whites, and confirmed the protective effect of smoking on UC occurrence. Future research should characterize the genetic background of CD patients across different ethnicities to improve our understanding on the role of smoking in CD pathogenesis.

Leukemia in hospitalized patients with inflammatory bowel disease: An analysis of the National Inpatient Sample (NIS) database.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. 10576-10576
Author(s):  
Colin Wikholm ◽  
Shiva Shankar Vangimalla ◽  
Ehab Abaza ◽  
Akram Ahmad ◽  
Ioannis Pothoulakis ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Age Groups ◽  
Black Patients ◽  
Increased Risk ◽  
Leukemia Diagnosis ◽  
Inflammatory Bowel ◽  
Over Time ◽  
White Patients

10576 Background: Inflammatory bowel disease (IBD) and use of immunosuppressive therapy in IBD is linked with increased risk of leukemia. We studied the NIS database from 2003-2017 to analyze trends in any type of leukemia in IBD hospitalizations over time and examined the role of age, sex, and race. Methods: We analyzed NIS data of all adult hospitalizations for ulcerative colitis (UC) or Crohn’s disease (CD) with any type of leukemia as a primary or secondary diagnosis using validated ICD 9/10 codes. Age, sex, and racial demographics were collected. Trend analysis of leukemia was performed with Cochran-Armitage and Jonckheere-Terpstra tests. Results: Overall Trends: From 2003-2017, a total of 11,385 of 2,235,413 (0.51%) CD hospitalizations and 8,105 of 1,324,746 (0.61%) UC hospitalizations contained diagnosis of leukemia. An increase in leukemia was seen in both CD and UC group from 0.24% to 0.79% (pTrend < 0.0001) and 0.28% to 0.81% (pTrend < 0.0001) respectively. Sex: In both UC and CD patients, leukemia diagnoses were predominantly male in 2003 but approximated a near 1:1 ratio by 2017 (Table). In CD, the proportion of female (FEM) leukemia diagnoses grew from 31.33% to 45.05% from 2003 to 2017 (pTrend = 0.1898). In UC, the proportion of female leukemia diagnoses grew from 27.49% to 45.79% from 2003 to 2017 (pTrend = 0.0030). Age: Leukemia was more common with increasing age, with no significant changes in proportion of cases between age groups over time (pTrend >.05). Ethnicity: White patients composed 87.80% and 84.24% of leukemia diagnoses in CD and UC, respectively. In CD, an increasing proportion of leukemia diagnoses occurred in black (BK) patients, and a decreasing proportion occurred in white patients (pTrends <.0001; Table 1) during the study time. No trends in race were observed in the UC group (pTrend = 0.4229). Conclusions: Our study showed an increased prevalence of leukemia in CD and UC hospitalizations from 2003-2017 which may be related to increasing use of immunosuppressants such as anti-TNF medications. In both CD and UC, leukemia was male-predominant, but increasingly female by 2017. Rate of leukemia diagnosis increased with age. In the CD group but not the UC group, leukemia was increasingly prevalent in black patients.[Table: see text]

Cardiovascular Risk Assessment and Impact of Medications on Cardiovascular Disease in Inflammatory Bowel Disease

2020 ◽  
Author(s):  
Preetika Sinh ◽  
Raymond Cross
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Inflammatory Bowel Disease ◽  
Cardiovascular Risk ◽  
Lupus Erythematosus ◽  
Bowel Disease ◽  
Severe Heart Failure ◽  
Janus Kinase ◽  
Increased Risk ◽  
Inflammatory Bowel

Abstract There is increased risk of cardiovascular disease in patients with chronic inflammatory disorders such as rheumatoid arthritis, psoriatic arthritis, and systemic lupus erythematosus. Studies have shown association between cardiovascular disease (eg, myocardial infarction, heart failure, stroke) and inflammatory bowel disease. Medications such as infliximab and adalimumab (monoclonal antibodies to tumor necrosis factor α) may help decrease the inflammatory burden and cardiovascular risk; however, there have been reports of hypertriglyceridemia and worsening of moderate to severe heart failure with these medications. Janus kinase inhibitors, such as tofacitinib, have been associated with hyperlipidemia and thromboembolism. We aim to discuss clinical and imaging modalities to assess cardiovascular risk in inflammatory bowel disease patients and review the role of various medications with respect to cardiovascular disease in this population.

scholarly journals Predictors and Management of Loss of Response to Vedolizumab in Inflammatory Bowel Disease

2018 ◽  
Vol 24 (11) ◽  
pp. 2461-2467 ◽  
Author(s):  
Eugenia Shmidt ◽  
Gursimran Kochhar ◽  
Justin Hartke ◽  
Prianka Chilukuri ◽  
Joseph Meserve ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Bowel Disease ◽  
C Reactive Protein ◽  
Dose Intensification ◽  
Reactive Protein ◽  
Loss Of Response ◽  
Increased Risk ◽  
Tnf Antagonist ◽  
Inflammatory Bowel

Abstract Background We quantified loss of response (LOR) to vedolizumab (VDZ) in clinical practice and assessed the effectiveness of VDZ dose intensification for managing LOR. Methods Retrospective review (May 2014–December 2016) of a prospectively maintained inflammatory bowel disease (IBD) registry. Kaplan-Meier estimates were used to determine rates of LOR to VDZ . Independent predictors of LOR were identified using univariate and multivariable Cox proportional hazard regression. Success of recapturing response (>50% reduction in symptoms from baseline) and remission (complete resolution of symptoms) after dose intensification was quantified. Results Cumulative rates for VDZ LOR were 20% at 6 months and 35% at 12 months, with slightly lower rates in Crohn’s disease than in ulcerative colitis (6 months 15% vs 18% and 12 months 30% vs 39%, P = 0.03). On multivariable analysis, LOR to a tumor necrosis factor (TNF) antagonist before VDZ use was associated with an increased risk for LOR to VDZ [hazard ratio (HR) 1.93; 95% confidence interval (CI) 1.25–2.97] in all patients. For Crohn’s disease patients specifically, higher baseline C-reactive protein concentration was associated with increased risk for LOR to VDZ (HR 1.01 per mg/dL increase, 95% CI 1.01–1.02). Shortening of VDZ infusion interval from 8 to every 4 or 6 weeks recaptured response in 49% and remission in 18% of patients. Conclusions LOR to a TNF antagonist before VDZ use and higher baseline C-reactive protein are important predictors of VDZ LOR. Treatment response can be recaptured in almost half of these patients with VDZ infusion interval shortening.

Inflammation and Cancer IV. Colorectal cancer in inflammatory bowel disease: the role of inflammation

2004 ◽  
Vol 287 (1) ◽  
pp. G7-G17 ◽  
Author(s):  
Steven H. Itzkowitz ◽  
Xianyang Yio
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Colonic Mucosa ◽  
Normal Colonic Mucosa ◽  
Sporadic Colorectal Cancer ◽  
Increased Risk ◽  
Inflammatory Bowel ◽  
Repair Genes

Patients with ulcerative colitis and Crohn's disease are at increased risk for developing colorectal cancer. To date, no known genetic basis has been identified to explain colorectal cancer predisposition in these inflammatory bowel diseases. Instead, it is assumed that chronic inflammation is what causes cancer. This is supported by the fact that colon cancer risk increases with longer duration of colitis, greater anatomic extent of colitis, the concomitant presence of other inflammatory manifestations such as primary sclerosing cholangitis, and the fact that certain drugs used to treat inflammation, such as 5-aminosalicylates and steroids, may prevent the development of colorectal cancer. The major carcinogenic pathways that lead to sporadic colorectal cancer, namely chromosomal instability, microsatellite instability, and hypermethylation, also occur in colitis-associated colorectal cancers. Unlike normal colonic mucosa, however, inflamed colonic mucosa demonstrates abnormalities in these molecular pathways even before any histological evidence of dysplasia or cancer. Whereas the reasons for this are unknown, oxidative stress likely plays a role. Reactive oxygen and nitrogen species produced by inflammatory cells can interact with key genes involved in carcinogenic pathways such as p53, DNA mismatch repair genes, and even DNA base excision-repair genes. Other factors such as NF-κB and cyclooxygenases may also contribute. Administering agents that cause colitis in healthy rodents or genetically engineered cancer-prone mice accelerates the development of colorectal cancer. Mice genetically prone to inflammatory bowel disease also develop colorectal cancer especially in the presence of bacterial colonization. These observations offer compelling support for the role of inflammation in colon carcinogenesis.

Role of perivascular nerve and sensory neurotransmitter dysfunction in inflammatory bowel disease

2021 ◽  
Author(s):  
Charles E. Norton ◽  
Elizabeth A. Grunz-Borgmann ◽  
Marcia L. Hart ◽  
Benjamin W. Jones ◽  
Craig L. Franklin ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Blood Flow ◽  
Substance P ◽  
Bowel Disease ◽  
Vascular Dysfunction ◽  
Receptor Expression ◽  
Mesenteric Arteries ◽  
Increased Risk ◽  
Inflammatory Bowel

Inflammatory Bowel Disease (IBD) is associated with both impaired intestinal blood flow and increased risk of cardiovascular disease, but the functional role of perivascular nerves that control vasomotor function of mesenteric arteries (MAs) perfusing the intestine during IBD is unknown. Because perivascular sensory nerves and their transmitters calcitonin gene-related peptide (CGRP) and substance P (SP) are important mediators of both vasodilation and inflammatory responses, our objective was to identify IBD-related deficits in perivascular sensory nerve function and vascular neurotransmitter signaling. In MAs from an IL-10-/- mouse model, IBD significantly impairs electrical field stimulation (EFS)-mediated sensory vasodilation and inhibition of sympathetic vasoconstriction, despite decreased sympathetic nerve density and vasoconstriction. The MA content and EFS-mediated release of both CGRP and SP are decreased with IBD, but IBD has unique effects on each transmitter. CGRP nerve density, receptor expression, hyperpolarization and vasodilation are preserved with IBD. In contrast, SP nerve density and receptor expression are increased, and SP hyperpolarization and vasodilation are impaired with IBD. A key finding is that blockade of SP receptors restores EFS-mediated sensory vasodilation and enhanced CGRP-mediated vasodilation in MAs from IBD but not Control mice. Together, these data suggest that an aberrant role for the perivascular sensory neurotransmitter SP and its downstream signaling in MAs underlies vascular dysfunction with IBD. We propose that with IBD, SP signaling impedes CGRP-mediated sensory vasodilation, contributing to impaired blood flow. Thus, substance P and NK1 receptors may represent an important target for treating vascular dysfunction in IBD.

scholarly journals Inflammatory Bowel Disease and Risk of Colorectal Cancer: An Overview From Pathophysiology to Pharmacological Prevention

2021 ◽  
Vol 12 ◽  
Author(s):  
Marianna Lucafò ◽  
Debora Curci ◽  
Martina Franzin ◽  
Giuliana Decorti ◽  
Gabriele Stocco
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Inflammatory Process ◽  
Current Knowledge ◽  
Genetic Alterations ◽  
Pharmacological Prevention ◽  
Increased Risk ◽  
Inflammatory Bowel

Increased risk of colorectal cancer (CRC) in inflammatory bowel disease (IBD) patients has been attributed to long-standing chronic inflammation, with the contribution of genetic alterations and environmental factors such as the microbiota. Moreover, accumulating data indicate that IBD-associated CRC (IBD-CRC) may initiate and develop through a pathway of tumorigenesis distinct from that of sporadic CRC. This mini-review summarizes the current knowledge of IBD-CRC, focusing on the main mechanisms underlying its pathogenesis, and on the important role of immunomodulators and biologics used to treat IBD patients in interfering with the inflammatory process involved in carcinogenesis.

Abstract 8: The Membrane-associated Guanylate Kinase Ww and Pdz Domain-containing Protein 1 magi1 is Required for Disturbed Flow-induced Endothelial Inflammation and Atherosclerotic Plaque Formation

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Ikjae Shin ◽  
Jong Hak Won ◽  
Kyung Ae Ko ◽  
Ji-Hyun Shin ◽  
Elena McBeath ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Genome Wide Association Study ◽  
Nuclear Translocation ◽  
Pdz Domain ◽  
Post Translational Modification ◽  
Disturbed Flow ◽  
Increased Risk ◽  
Inflammatory Bowel

Rationale: Major chronic inflammatory diseases including inflammatory bowel disease and psoriasis are clinically associated with accelerated atherosclerosis and increased risk of cardiovascular diseases (CVD). Atherosclerosis has long been recognized as an inflammatory process, which is initiated by the inflammation and dysfunction of endothelial cells (ECs). Genome-wide association study (GWAS) has identified a significant association between the deletion in ADAMTS9-MAGI1 locus with inflammatory bowel disease and psoriasis, suggesting a potential involvement of MAGI1 in EC inflammation and its associated events. Objective: To investigate the role and regulatory mechanism of MAGI1 as well as MAGI1 post-translational modification in EC inflammation, after various pro-atherogenic stimuli. Methods and Results: MAGI1 depletion significantly inhibits NF-κB activation and adhesion molecule expression induced by various pro-atherogenic stimuli in both in vitro and in vivo . We show that p90RSK associates with MAGI1 WW and PDZ2 domain, which is a crucial step for EC inflammation. In addition, p90RSK activation independently regulates MAGI1 S741 phosphorylation and K931 de-SUMOylation. While MAGI1 S741 phosphorylation is vital for Rap1 and subsequent NF-kB activation via increasing MAGI1-RAPGEF2 interaction, MAGI1 de-SUMOylation induces p90RSK-MAGI1 nuclear translocation as well as nuclear SENP2 T368 and ERK5 S496 phosphorylation. Those events are critical for EC inflammation. In addition, in partial carotid ligation mouse model, we observed a reduction in size of disturbed flow-induced carotid plaque lesion in Magi1 +/- / Ldlr -/- mice compared to that in Magi1 +/+ / Ldlr -/- mice fed with high fat diet, indicating the crucial role of MAGI1 in regulating EC inflammation and atherosclerosis formation. Conclusion: These data show the essential role of MAGI1 in regulating EC inflammation, and suggest that phosphorylation and de-SUMOylation of MAGI1 induced by p90RSK activation have distinctive mechanisms, leading to EC inflammation.

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