Prevention of malignant digestive system tumors should focus on the control of chronic inflammation

Chronic inflammation,through a variety of mechanisms,plays a key role in the occurrence and development of digestive system malignant tumors(DSMTs).In this study,we feature and provide a comprehensive understanding of DSMT prevention strategies based on preventing or controlling chronic inflammation.The development and evaluation of cancer prevention strategies is a longstanding process.Cancer prevention,especially in the early stage of life,should be emphasized throughout the whole life course.Issues such as the time interval for colon cancer screening,the development of direct-acting antiviral drugs for liver cancer,and the Helicobacter pylori vaccine all need to be explored in long-term,large-scale experiments in the future.

Hepatic steatosis,low-grade chronic inflammation and hormone/growth factor/adipokine imbalance

Non-alcoholic fatty liver disease (NAFLD), a further expression of metabolic syndrome, strictly linked to obesity and diabetes mellitus, is characterized by insulin resistance (IR), elevated serum levels of free fatty acids and fatty infi ltration of the liver, which is known as hepatic steatosis. Hepatocyte apoptosis is a key feature of this disease and correlates with its severity. Free-fatty-acidinduced toxicity represents one of mechanisms for the pathogenesis of NAFLD and hormones, growth factors and adipokines influence also play a key role. This review highlights the various pathways that contribute to the development of hepatic steatosis. Circulating concentrations of inflammatory cytokines are reckoned to be the most important factor in causing and maintaining IR. Low-grade chronic inflammation is fundamental in the progression of NAFLD toward higher risk cirrhotic states.

Prostate chronic inflammation type Ⅳ and prostate cancer risk in patients undergoing first biopsy set:Results of a large cohort study

Objective:In prostate specimens,chronic inflammatory infiltrate(CII)type Ⅳ has been detected,but its association with prostate cancer(PCa)is controversial.The aim of the present study is to investigate on associations of CII with PCa detection in patients undergoing prostate first biopsy set.Methods:Ultrasound transrectal-guided biopsies by the transperineal approach were retrospectively evaluated in 441 consecutive patients.The study excluded patients who were in active surveillance,prostate specific antigen(PSA)
30 ng/mL,re-biopsies,incidental PCa after transurethral resection of the prostate(TURP),less than 14 cores or metastatic.Analysis of population and subpopulations(with or without PCa)was performed by statistical methods which included ManneWhitney(U test),KruskaleWallis test,Chi-squared statistic,logistic regression.Multivariate logistic regression models predicting mean probability of PCa detection were established.Results:PCa detection rate was 46.03%.Age,PSA,prostate volume(PV),prostate intraepithelial neoplasia(PIN)and CII were the significant independent predictors of PCa detection.PV(OR Z 0.934)and CII(OR Z 0.192)were both negative independent predictors.CII was a significant negative independent predictor in multivariate logistic regression models predicting the mean probability of PCa detection by age,PSA and PV.The inverse association of CII with PCa does not necessary mean protection because of PSA confounding.Conclusion:In a population of patients undergoing prostate first biopsy set,CII was a strong negative independent predictor of PCa detection.CII type Ⅳ should be considered as an adjunctive parameter in re-biopsy or active surveillance protocols.

Atherosclerotic cardiovascular disease in inflammatory bowel disease:The role of chronic inflammation

Inflammatory bowel disease(IBD)causes systemic vascular inflammation.The increased risk of venous as well as arterial thromboembolic phenomena in IBD is well established.More recently,a relationship between IBD and atherosclerotic cardiovascular disease(ASCVD)has been postulated.Systemic inflammatory diseases,such as rheumatoid arthritis and systemic lupus erythematosus,have well characterized cardiac pathologies and treatments that focus on prevention of disease associated ASCVD.The impact of chronic inflammation on ASCVD in IBD remains poorly characterized.This manuscript aims to review and summarize the current literature pertaining to IBD and ASCVD with respect to its pathophysiology and impact of medications in order to encourage further research that can improve understanding and help develop clinical recommendations for prevention and management of ASCVD in patients with IBD.

Novel Approach to Microbiological Study of Chronic Inflammations at Upper Respiratory Tract: Research of Blood L-Form Microbiota

Background: The recognition of human blood microbiota, consisting of cell wall-deficient microbes (L-forms), is a major challenge today in the field of microbiology. There are accumulating data confirming the concept of “internal” blood L-form microbiota and its significance for health and diseases. Finding out whether the blood microbiota can be of diagnostic and prognostic importance for detection and evaluation of chronic infections anywhere in the body is a major objective. In the context of chronically infected upper respiratory tract (URT), the aim of the current study was to understand whether a local infection can be a source for entry of bacteria and fungi in the blood. Methods: Blood samples from six persons with chronic inflammations in URT diagnosed with hypertrophied adenoids, chronic sinusitis, nasal polyps, chronic naso-pharyngitis and one control healthy person were studied. Blood microbiota assessment methodology that be used, included three phases: 1) isolation of L-form cultures from blood-development and propagation;2) cultivation directed to conversion of L-forms into bacterial and fungal cultures;3) isolation of pure classical bacterial and fungal cultures and their identification by MALDI-TOF method. Results: From the patients were isolated L-forms of opportunistic bacteria (Streptococcus mitis, Roseomonas mucosa, Dermacoccus nishinomiyaensis, Enterococcus faecalis, Acinetobacter johnsonii, Pseudomonas putida, Staphylococcus aureus, Pseudomonas luteola, Enterobacter cloacae) and fungi such as Rhodotorula mucilaginosa, Aspergillus niger, Aspergillus fumigatus and Mucorales. Conclusion: The novel innovative methodology for assessment of blood L-form microbiota was successfully applied for detection of microbes responsible for chronic infections at URT.

Sudden cardiac arrest in a patient with epilepsy induced by chronic inflammation on the cerebral surface

The present study analyzed a patient with epilepsy due to chronic inflammation on the cerebral surface underwent sudden cardiac arrest. Paradoxical brain discharge, which occurred prior to epileptic seizures, induced a sudden cardiac arrest. However, when the focal brain pressure was relieved, cardiac arrest disappeared. A 27-year-old male patient underwent pre-surgical ram monitoring for 160 hours. During monitoring, secondary tonic-clonic seizures occurred five times. A burst of paradoxical brain discharges occurred at 2-19 seconds （mean 8 seconds） prior to epileptic seizures. After 2-3 seconds, sudden cardiac arrest occurred and lasted for 12-22 seconds （average 16 seconds）. The heart rate subsequently returned to a normal rate. Results revealed arachnoid pachymenia and adhesions, as well as mucus on the focal cerebral surface, combined with poor circulation and increased pressure, lntracranial electrodes were placed using surgical methods. Following removal of the arachnoid adhesions and mucus on the local cerebral surface, paradoxical brain discharge and epileptic seizures occurred three times, but sudden cardiac arrest was not recorded during 150-hour monitoring. Post-surgical histological examination indicated meningitis. Experimental findings suggested that paradoxical brain discharge led to cardiac arrest instead of epileptic seizures; the insult was associated with chronic inflammation on the cerebral surface, which subsequently led to hypertension and poor blood circulation in focal cerebral areas.

Synchronous gastric and colon cancers:Important to consider hereditary syndromes and chronic inflammatory disease associations

In this editorial we comment on the manuscript,describing management and surveillance strategies in synchronous and metachronous,gastric and colon cancers.Synchronous or metachronous primary malignancies at different sites of the gastrointestinal tract pose a unique diagnostic and therapeutic challenge.Multidisciplinary services and strategies are required for the management of multiple site primary malignancies,to provide the best oncological outcomes.Although this study highlights the dual cancers in 76 sporadic cases,the authors excluded 55 patients due to combination of factors which includes;incomplete clinical data,genetic syndrome,gastric stump cancers.In addition,the authors did not elaborate if any patients presented with signet ring cell morphology,E-cadherin mutations or presence of inflammatory bowel disease.Genetic and mutational errors and epithelial field defects from chronic inflammatory diseases of the gastrointestinal tract are important when considering synchronous gastric and colonic cancers.We will briefly discuss these in this editorial.

Therapeutic potential of exosome-based personalized delivery platform in chronic inflammatory diseases

In the inflammatory microenvironment,there are numerous exosomes secreted by immune cells(Macrophages,neutrophils,dendritic cells),mesenchymal stem cells(MSCs)and platelets as intercellular communicators,which participate in the regulation of inflammation by modulating gene expression and releasing anti-inflammatory factors.Due to their good biocompatibility,accurate targeting,low toxicity and immunogenicity,these exosomes are able to selectively deliver therapeutic drugs to the site of inflammation through interactions between their surface-antibody or modified ligand with cell surface receptors.Therefore,the role of exosome-based biomimetic delivery strategies in inflammatory diseases has attracted increasing attention.Here we review current knowledge and techniques for exosome identification,isolation,modification and drug loading.More importantly,we highlight progress in using exosomes to treat chronic inflammatory diseases such as rheumatoid arthritis(RA),osteoarthritis(OA),atherosclerosis(AS),and inflammatory bowel disease(IBD).Finally,we also discuss their potential and challenges as anti-inflammatory drug carriers.

A Clinical Study on the Treat ment of Chronic Pelvic Inflammation of Qi-stagnation with Blood Stasis Syndrome by Penyanqing Capsule (盆炎清胶囊)

Objective： To observe the clinical efficacy of Penyanqing Capsule （盆炎清胶囊, PYQC） in treating pelvic inflammation of Qi-stagnation with blood stasis syndrome. Methods： The randomized, single blinded, parallel positive drug controlled method was adopted, with 82 patients assigned into two groups by envelop method. The 42 patients in the treated group received PYQC 3 times a day, 4 capsules each time taken orally; the 40 patients in the control group were given orally Fuyankang tablets （妇炎康片, FYKT） 3 times a day, 6 tablets each time. The therapeutic course for both groups was 2 months, and 2 courses of treatment were given successively to observe the comprehensive effect, changes of symptoms and signs before and after treatment. The effects of PYQC on hemorrheological character in part of the patients and on the pathogenetic chlamydia and mycoplasma were also observed. Results： The total effective rate in the treated group was 83.3%, which was insignificantly different from that in the control group （77.5%, P〉0.05）. However, PYQC could significantly lower the hemorrheologic indexes in patients and showed definite influence on the pathogenetic chlamydia and mycoplasma. Conclusion： PYQC has good therapeutic effect in treating chronic pelvic inflammation of Qi-stagnation with blood stasis syndrome, and showed definite effect on chlamydia and mycoplasma.

Chronic intermittent hypoxia induces cardiac inflammation and dysfunction in a rat obstructive sleep apnea model

Chronic intermittent hypoxia is considered to play an important role in cardiovascular pathogenesis during the development of obstructive sleep apnea（OSA）.We used a well-described OSA rat model induced with simultaneous intermittent hypoxia.Male Sprague Dawley rats were individually placed into plexiglass chambers with air pressure and components were electronically controlled.The rats were exposed to intermittent hypoxia 8 hours daily for 5weeks.The changes of cardiac structure and function were examined by ultrasound.The cardiac pathology,apoptosis,and fibrosis were analyzed by H＆E staining,TUNNEL assay,and picosirius staining,respectively.The expression of inflammation and fibrosis marker genes was analyzed by quantitative real-time PCR and Western blot.Chronic intermittent hypoxia/low pressure resulted in significant increase of left ventricular internal diameters（LVIDs）,endsystolic volume（ESV）,end-diastolic volume（EDV）,and blood lactate level and marked reduction in ejection fraction and fractional shortening.Chronic intermittent hypoxia increased TUNNEL-positive myocytes,disrupted normal arrangement of cardiac fibers,and increased Sirius stained collagen fibers.The expression levels of hypoxia induced factor（HIF）-l α,NF-κB,IL-6,and matrix metallopeptidase 2（MMP-2） were significantly increased in the heart of rats exposed to chronic intermittent hypoxia.In conclusion,the left ventricular function was adversely affected by chronic intermittent hypoxia,which is associated with increased expression of HIF-lα and NF-κB signaling molecules and development of cardiac inflammation,apoptosis and fibrosis.

Systematic Review and Meta-Analysis of Fuke Qianjin Tablets(妇科千金片)in the Treatment of Chronic Pelvic Inflammation

Objective:To systematically evaluate the efficacy and safety of Fuke Qianjin Tablets(妇科千金片)in the treatment of chronic pelvic inflammation.Methods:A systematically and comprehensively search was conducted in 4 Chinese databases of CNKI,VIP,Wan Fang and CBM and the foreign language databases of Pubmed,EMbase and The Cochrane Library.The retrieval time was from database establishment to March 2019.The randomized controlled trials of Fuke Qianjin Tablets(妇科千金片)in the treatment of chronic pelvic inflammation were selected according to the predetermined criteria.The quality of the included study was evaluated by Cochrane collaborative network bias risk evaluation tool,and the meta-analysis was performed by Rev Man5.3 software.Results:A total of 1009 related literatures were searched.After initial screening and strict evaluation,55 studies were included,with a total sample size of 6826 cases,including 3416 cases in the experiment group and 3410 cases in the control group.The results of meta-analysis showed that the total effective rate of Fuke Qianjin Tablets(妇科千金片)combined with antibiotics in the treatment of chronic pelvic inflammation was better than that of antibiotics alone(RR=1.20,95%CI[1.17,1.22],P<0.00001).Fuke Qianjin Tablets(妇科千金片)combined with antibiotics was better than that of antibiotics alone in the improvement of abdominal pain symptoms(RR=1.40,95%CI[1.04,1.88],P<0.00001),leukorrhea abnormality(RR=1.38,95%CI[1.16,1.65],P<0.0004).In terms of safety,Fuke Qianjin Tablets(妇科千金片)combined with antibiotics could reduce the incidence of adverse reactions(RR=0.67,95%CI[0.48,0.93],P<0.02).The main adverse reactions were nausea and vomiting,bitterness and astringency in the mouth,rash and so on.All of them could be tolerated and the symptoms could disappear in the short term,and had no effect on the treatment.Conclusion:Fuke Qianjin Tablets(妇科千金片)combined with antibiotics in the treatment of chronic pelvic inflammation can improve the total effective rate,relieve abdominal pain and abnormal leukorrhea and other clinical discomfort symptoms,improve the quality of life of patients to a certain extent,and no serious adverse reactions are found.Due to the limitation of the quality and quantity of the included literature,the above conclusions need to be further studied and verified by high-quality research.

Alcohol,inflammation,and gut-liver-brain interactions in tissue damage and disease development

Chronic inflammation is often associated with alcoholrelated medical conditions. The key inducer of such inflammation, and also the best understood, is gut microflora-derived lipopolysaccharide (LPS). Alcohol can significantly increase the translocation of LPS from the gut. In healthy individuals, the adverse effects of LPS are kept in check by the actions and interactions of multiple organs. The liver plays a central role in detoxifying LPS and producing a balanced cytokine milieu. The central nervous system contributes to anti-inflammatory regulation through neuroimmunoendocrine actions. Chronic alcohol use impairs not only gut and liver functions, but also multi-organ interactions, leading to persistent systemic inflammation and ultimately, to organ damage. The study of these interactions may provide potential new targets for therapeutic intervention.

Pathological,immunohistochemical and microbiologicalal analysis of lacrimal sac biopsies in patients with chronic dacrocystitis

AIM:To analyze cases of obstruction of the nasolacrimal duct which creates a fertile environment for secondary bacterial Infection and can result in dacryocystitis,which is a constant threat to cornea and orbital soft tissue and a potential source of endophthalmitis following intraocular surgery.The majority of obstructions of the lacrimal excretory outflow system are acquired ones occurring in adulthood and involving the distal parts of the system.Acquired obstruction may be primary/idiopathic or secondary to a wide variety of infectious,inflammatory,traumatic,mechanical,toxic or neoplastic causes mimicking idiopathic inflammation.These cases are treated by dacryocystorhinostomy(DCR).METHODS:The present study was conducted to determine the histopathologic,immunohistochemical and current microbiologic characteristics of lacrimal sac specimens in patients undergoing external dacryocystorhinostomy.RESULTS:Non-specific lacrimal sac pathology was present in all 33 cases and 81.8%of the cases showed moderate chronic inflammation with a chronic inflammatory score(CIS)ranging between 4 and 6,whereas 12.12%showed severe inflammatory changes with a CIS of 7.Mild degree of inflammation was seen in6.06%with a CIS of 3.The total prevalence of grampositive,gram-negative,and culture-negative samples were 59.4%,37.5%,and 3%respectively.CONCLUSION:Non-specific chronic inflammation withfibrosis is indeed the most commonly reported histopathological finding in lacrimal sac wall biopsy specimens.

Treatment of benign rectal stricture caused by repeated anal insertion by endoscopy and balloon dilation:A case report

BACKGROUND Benign rectal strictures can be categorized as primary(disease-related)and secondary(surgical anastomosis-related).Secondary strictures arise from surgical complications,whereas primary strictures have diverse etiologies,including various inflammatory conditions.Benign strictures are usually managed by surgery and endoscopy.We present an unusual etiology of benign rectal stricture caused by the repeated insertion of foreign objects into the rectum for sexual purposes,resulting in rectal injury and subsequent chronic inflammation.CASE SUMMARY A 53-year-old man presented to the outpatient clinic of the Colorectal Surgery Department with symptoms of chronic constipation and bloody stools.The patient previously experienced rectal injury due to foreign object insertion for sexual purposes.Colonoscopy revealed benign circumferential narrowing of the rectum.He underwent treatment by endoscopic argon plasma coagulation and balloon dilation and follow-up as an outpatient for 4 months.A colonoscopy at the end of the follow-up period revealed no evidence of rectal stricture relapse.CONCLUSION A history of rectal injury,followed by chronic inflammation,should be considered in patients with benign rectal strictures.Management with endoscopic argon plasma coagulation and balloon dilation can prevent the need for surgical resection of benign rectal strictures.

Decoy receptor 3: Its role as biomarker for chronic inflammatory diseases

Members of the tumor-necrosis factor-α(TNF-α) and TNF-α receptor(TNFR) superfamilies of proteins(TNFSF and TNFRSF, respectively) play important roles in the function of the immune system. Decoy receptor 3(Dc R3, TNFRSF6b) is a decoy receptor that binds to three TNFSF ligands, Fas L, LIGHT and TL1 A. Association to these ligands competes with the corresponding functional receptors and blocks downstream signaling, leading to immunomodulatory effects, including the prevention of apoptosis. Dc R3 lacks a transmembrane region and exists only as a secreted protein, which is detectable in biological fluids. Recent studies have shown that Dc R3 is upregulated and may be pathogenetically implicated in several and diverse chronic inflammatory diseases. The strongest associations have been described for rheumatological diseases, mainly systemic lupus erythematosus and rheumatoid arthritis, inflammatory bowel disease, and serious infectious conditions, including systemic inflammatory response syndrome. In the majority of these conditions, Dc R3 m RNA and protein expression is elevated both at the target tissues as well as in the systemic circulation. Dc R3 concentration in the serum is untraceable in the majority of healthy individuals but can be detected in patients with various inflammatory diseases. In mostsuch cases, soluble Dc R3 correlates with disease severity, as patients with severe forms of disease have significantly higher levels than patients with milder or no activity. In addition, effective anti-inflammatory treatment leads to the disappearance of soluble Dc R3 from the circulation. Taken together, current evidence suggests that serum Dc R3 may become a useful biomarker for chronic inflammatory disorders, as it is upregulated in response to inflammatory stimuli, and may serve both as a prognostic marker for disease severity and as a surrogate indicator of response to treatment.

Excellent response of severe aplastic anemia to treatment of gut inflammation: A case report and review of the literature

BACKGROUND Cumulative evidence suggests that the aberrant immune responses in acquired aplastic anemia(AA) are sustained by active chronic infections in genetically susceptible individuals. Recently, the constant source to trigger and sustain the pathophysiology has been proposed to come from the altered gut microbiota and chronic intestinal inflammation. In this case, our serendipitous finding provides convincing evidence that the persistently dysregulated autoimmunity may be generated, at least in a significant proposition of AA patients, by the altered gut microbiota and compromised intestinal epithelium.CASE SUMMARY A 30-year-old Chinese male patient with refractory severe AA experienced a 3-month-long febrile episode, and his fever was refractory to many kinds of injected broad-spectrum antibiotics. When presenting with abdominal cramps, he was prescribed oral mannitol and gentamycin to get rid of the gut infection. This treatment resulted in a quick resolution of the fever. Unanticipatedly, it also produced an excellent hematological response. He had undergone three episodes of recurrence within the one-year treatment, with each recurrence occurring 7-8 wk from the gastrointestinal inflammation eliminating preparations. However,subsequent treatments were able to produce subsequent remissions and consecutive treatments were successful in achieving durative hematological improvements, strongly indicating an etiological association between chronic gut inflammation and the development of AA. Interestingly, comorbid diseases superimposed on this patient(namely, psychiatric disorders, hypertension,insulin resistance, and renal dysfunction) were ameliorated together with the hematological improvements.CONCLUSION Chronic gut inflammation may be responsible for AA pathogenesis. The comorbidities and AA may share a common etiological association.

Acute-on-chronic liver failure：recent update

Acute on chronic liver failure（ACLF） was first described in 1995 as a clinical syndrome distinct to classic acute decompensation.Characterized by complications of decompensation,ACLF occurs on a background of chronic liver dysfunction and is associated with high rates of organ failure and significant short-term mortality estimated between45%and 90%.Despite the clinical relevance of the condition,it still remains largely undefined with continued disagreement regarding its precise etiological factors,clinical course,prognostic criteria and management pathways.It is concerning that,despite our relative lack of understanding of the condition,the burden of ACLF among cirrhotic patients remains significant with an estimated prevalence of 30.9%.This paper highlights our current understanding of ACLF,including its etiology,diagnostic and prognostic criteria and pathophysiology.It is evident that further refinement of the ACLF classification system is required in order to detect high-risk patients and improve short-term mortality rates.The field of metabolomics certainly warrants investigation to enhance diagnostic and prognostic parameters,while the use of granulocyte-colony stimulating factor is a promising future therapeutic intervention for patients with ACLF.

Contributions of the receptor for advanced glycation end products axis activation in gastric cancer

Compelling shreds of evidence derived from both clinical and experimental research have demonstrated the crucial contribution of receptor for advanced glycation end products(RAGE)axis activation in the development of neoplasms,including gastric cancer(GC).This new actor in tumor biology plays an important role in the onset of a crucial and long-lasting inflammatory milieu,not only by supporting phenotypic changes favoring growth and dissemination of tumor cells,but also by functioning as a pattern-recognition receptor in the inflammatory response to Helicobacter pylori infection.In the present review,we aim to highlight how the overexpression and activation of the RAGE axis contributes to the proliferation and survival of GC cells as and their acquisition of more invasive phenotypes that promote dissemination and metastasis.Finally,the contribution of some single nucleotide polymorphisms in the RAGE gene as susceptibility or poor prognosis factors is also discussed.

Future applications of exosomes delivering resolvins and cytokines in facilitating diabetic foot ulcer healing

Type 2 diabetes mellitus(T2DM)increases the risk of many lethal and debilitating conditions.Among them,foot ulceration due to neuropathy,vascular disease,or trauma affects the quality of life of millions in the United States and around the world.Physiological wound healing is stalled in the inflammatory phase by the chronicity of inflammation without proceeding to the resolution phase.Despite advanced treatment,diabetic foot ulcers(DFUs)are associated with a risk of amputation.Thus,there is a need for novel therapies to address chronic inflammation,decreased angiogenesis,and impaired granulation tissue formation contributing to the non-healing of DFUs.Studies have shown promising results with resolvins(Rv)and anti-inflammatory therapies that resolve inflammation and enhance tissue healing.But many of these studies have encountered difficulty in the delivery of Rv in terms of efficiency,tissue targetability,and immunogenicity.This review summarized the perspective of optimizing the therapeutic application of Rv and cytokines by pairing them with exosomes as a novel strategy for targeted tissue delivery to treat non-healing chronic DFUs.The articles discussing the T2DM disease state,current research on Rv for treating inflammation,the role of Rv in enhancing wound healing,and exosomes as a delivery vehicle were critically reviewed to find support for the proposition of using Rv and exosomes in combination for DFUs therapy.The literature reviewed suggests the beneficial role of Rv and exosomes and exosomes loaded with antiinflammatory agents as promising therapeutic agents in ulcer healing.

Cardiovascular implications of inflammatory bowel disease: An updated review

Emerging data highlights the heightened risk of atherosclerotic cardiovascular diseases(ASCVD)in patients with chronic inflammatory disorders,particularly those afflicted with inflammatory bowel disease(IBD).This review delves into the epidemiological connections between IBD and ASCVD,elucidating potential underlying mechanisms.Furthermore,it discusses the impact of current IBD treatments on cardiovascular risk.Additionally,the cardiovascular adverse effects of novel small molecule drugs used in moderate-to-severe IBD are investigated,drawing parallels with observations in patients with rheumatoid arthritis.This article aims to comprehensively evaluate the existing evidence supporting these associations.To achieve this,we conducted a meticulous search of PubMed,spanning from inception to August 2023,using a carefully selected set of keywords.The search encompassed topics related to IBD,such as Crohn’s disease and ulcerative colitis,as well as ASCVD,including coronary artery disease,cardiovascular disease,atrial fibrillation,heart failure,conduction abnormalities,heart blocks,and premature coronary artery disease.This review encompasses various types of literature,including retrospective and prospective cohort studies,clinical trials,meta-analyses,and relevant guidelines,with the objective of providing a comprehensive overview of this critical intersection of inflammatory bowel disease and cardiovascular health.