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Ulcerative colitis is the most common form of inflammatory bowel disease. Its course is often mild, with few complications, and it can be cured by colectomy. Our current understanding of its pathophysiology, diagnosis, and treatment is reviewed. Ulcerative colitis was first described in the mid-1800s, 1 whereas Crohn's disease was first reported later, in 1932, as “regional ileitis.” 2 Because Crohn's disease can involve the colon and shares clinical manifestations with ulcerative colitis, these entities have often been conflated and diagnosed as inflammatory bowel disease, although they are clearly distinct pathophysiological entities. Ulcerative colitis is the most common form of inflammatory bowel disease worldwide. In contrast to Crohn's disease, ulcerative colitis is a disease of the mucosa that is less prone to complications and can be cured by means of colectomy, and in many patients, its course is mild. . . .

Intestinal fibrosis, which is usually the consequence of chronic inflammation, is a common complication of inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis. In the past few years, substantial advances have been made in the areas of pathogenesis, diagnosis and management of intestinal fibrosis. Of particular interest have been inflammation-independent mechanisms behind the gut fibrotic process, genetic and environmental risk factors (such as the role of the microbiota), and the generation of new in vitro and in vivo systems to study fibrogenesis in the gut. A huge amount of work has also been done in the area of biomarkers to predict or detect intestinal fibrosis, including novel cross-sectional imaging techniques. In parallel, researchers are embarking on developing and validating clinical trial end points and protocols to test novel antifibrotic agents, although no antifibrotic therapies are currently available. This Review presents the state of the art on the most recently identified pathogenic mechanisms of this serious IBD-related complication, focusing on possible targets of antifibrotic therapies, management strategies, and factors that might predict fibrosis progression or response to treatment.Intestinal fibrosis is an important feature of inflammatory bowel disease (IBD) that remains poorly understood. Here, D’Alessio and Ungaro et al. review the cellular and molecular mechanisms contributing to intestinal fibrosis and discuss future therapeutic strategies for IBD-related fibrosis.

The coronavirus disease (COVID-19) worldwide outbreak has led to a dramatic challenge for all healthcare systems, including inflammatory bowel disease (IBD) centres. Here, we describe the fast changes and clinical issues that IBD specialists could face during this SARS-CoV-2 infection pandemic, highlighting the potential rearrangements of care and resetting of clinical priorities.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease of unknown aetiology affecting the colon and rectum. Multiple factors, such as genetic background, environmental and luminal factors, and mucosal immune dysregulation, have been suggested to contribute to UC pathogenesis. UC has evolved into a global burden given its high incidence in developed countries and the substantial increase in incidence in developing countries. An improved understanding of the mechanisms underlying UC has led to the emergence of new treatments. Since the early 2000s, anti-tumour necrosis factor (TNF) treatment has significantly improved treatment outcomes. Advances in medical treatments have enabled a paradigm shift in treatment goals from symptomatic relief to endoscopic and histological healing to achieve better long-term outcomes and, consequently, diagnostic modalities have also been improved to monitor disease activity more tightly. Despite these improvements in patient care, a substantial proportion of patients, for example, those who are refractory to medical treatment or those who develop colitis-associated colorectal dysplasia or cancer, still require restorative proctocolectomy. The development of novel drugs and improvement of the treatment strategy by implementing personalized medicine are warranted to achieve optimal disease control. However, delineating the aetiology of UC is necessary to ultimately achieve disease cure. Ulcerative colitis is a chronic inflammatory bowel disease affecting the rectum and the colon. This Primer describes the epidemiology, the current understanding of ulcerative colitis pathophysiology and its diagnosis. In addition, Hibi and colleagues highlight the current and emerging therapeutic strategies and discuss the most pressing questions in the field.

Key Points Six biologic agents are currently approved for the treatment of IBD refractory to standard medications: four anti-TNF agents, infliximab, adalimumab, golimumab, certolizumab pegol; and two anti-integrin agents, natalizumab and vedolizumab When choosing a first-line biologic agent, several parameters should be taken into account, including specific country availability and labelling, efficacy and safety profile, route of administration, patient preferences and cost-effectiveness The sequence of prescribing anti-TNF therapies relative to vedolizumab will be assessed in further head-to-head trials; currently, labelling is similar for both drug classes No switch between anti-TNF agents should be proposed in instances of adequate primary response to a first-line anti-TNF therapy For secondary loss of response to a first-line anti-TNF agent, a second-line anti-TNF therapy could be proposed; primary nonresponders should be swaped to biologic agents with a different mechanism of action In the next few years, results of head-to-head trials will be available to help decision-making between therapeutic options for IBD and treatment algorithms will evolve with the launch of biosimilars and new drugs The landscape of treatment for IBD changed dramatically with the introduction of biologic agents, of which several are now in use for this condition. Here, the authors provide practical insights into the use of biologic agents in IBD, discussing issues such as comparative effectiveness, safety, immunogenicity, cost and patient preference. Six biologic agents are currently approved for the treatment of IBD: four anti-TNF agents (infliximab, adalimumab, golimumab and certolizumab pegol) and two anti-integrin agents (natalizumab and vedolizumab). In Crohn's disease and ulcerative colitis refractory to standard medications, treatment choice among available biologic agents can be challenging. Several parameters should be taken into account to help physicians through the decision-making process, including the comparative effectiveness and long-term safety profile, availability and labelling in the prescriber's country, international guidelines, and cost, as well as patient preferences (such as the route of administration). Herein, we provide practical insights on the use of biologic agents in IBD. The results of head-to-head trials between biologic agents are eagerly awaited to guide decision-making regarding the choice of first-line biologic agents and to determine whether switching within the same drug class or swapping (switching out of the drug class) is preferable after primary or secondary loss of response to the first biologic agent. In the near future, treatment algorithms might evolve with the launch of new drugs (such as ustekinumab, tofacitinib and etrolizumab) and the increased use of biosimilars.

In three phase 3 trials involving patients with ulcerative colitis, tofacitinib (an oral, small-molecule Janus kinase inhibitor) was more effective as induction and maintenance therapy than placebo. Infections were more common with tofacitinib. Ulcerative colitis is characterized by an increased frequency of bowel movements and bloody diarrhea, which has a negative effect on quality of life. 1 Current therapies for ulcerative colitis include mesalamine, glucocorticoids, thiopurines, and antagonists to tumor necrosis factor (TNF) and α4β7 integrin. 1 – 5 Many patients do not have a response to these therapies or have a response that is not sustained. Additional treatment options with new mechanisms of action are needed to increase efficacy rates. The Janus kinase (JAK) family comprises four intracellular tyrosine kinases — JAK1, JAK2, JAK3, and nonreceptor tyrosine-protein kinase 2 — that activate signal transducers and . . .

Gut inflammation is strongly associated with spondyloarthritis (SpA), as exemplified by the high prevalence of inflammatory bowel disease (IBD) and the even higher occurrence of subclinical gut inflammation in patients with SpA. The gut–joint axis of inflammation in SpA is further reinforced by similarities in immunopathogenesis at both anatomical sites and by the clinical success of therapies blocking TNF and IL-23 in IBD and in some forms of SpA. Many genetic risk factors are shared between SpA and IBD, and changes in the composition of gut microbiota are seen in both diseases. Current dogma is that inflammation in SpA initiates in the gut and leads to joint inflammation; however, although conceptually attractive, some research does not support this causal relationship. For example, therapies targeting IL-17A are efficacious in the joint but not the gut, and interfering with gut trafficking by targeting molecules such as α4β7 in IBD can lead to onset or flares of SpA. Several important knowledge gaps remain that must be addressed in future studies. Determining the true nature of the gut–joint axis has real-world implications for the treatment of patients with co-incident IBD and SpA and for the repurposing of therapeutics from one disease to the other.In this article, the authors summarize the latest clinical and basic research on gut inflammation in spondyloarthritis and highlight important questions to address in future research.

Big data methodologies, made possible with the increasing generation and availability of digital data and enhanced analytical capabilities, have produced new insights to improve outcomes in many disciplines. Application of big data in the health-care sector is in its early stages, although the potential for leveraging underutilized data to gain a better understanding of disease and improve quality of care is enormous. Owing to the intrinsic characteristics of inflammatory bowel disease (IBD) and the management dilemmas that it imposes, the implementation of big data research strategies not only can complement current research efforts but also could represent the only way to disentangle the complexity of the disease. In this Review, we explore important potential applications of big data in IBD research, including predictive models of disease course and response to therapy, characterization of disease heterogeneity, drug safety and development, precision medicine and cost-effectiveness of care. We also discuss the strengths and limitations of potential data sources that big data analytics could draw from in the field of IBD, including electronic health records, clinical trial data, e-health applications and genomic, transcriptomic, proteomic, metabolomic and microbiomic data.In this Review, the authors explore potential applications of big data in IBD research, including predictive models of disease course and response to therapy, characterization of disease heterogeneity, drug safety and development, precision medicine and cost-effectiveness of care.

In this 52-week randomized trial, the α 4 β 7 integrin antibody vedolizumab was effective in treating ulcerative colitis. There were not significantly more adverse events with vedolizumab than with placebo, but the trial was not large or long enough to fully assess safety. Ulcerative colitis is a chronic inflammatory bowel disease characterized by symptoms of bloody diarrhea, abdominal cramps, and fatigue. 1 Current medical therapy has important limitations. Aminosalicylates 2 – 4 are only modestly effective; glucocorticoids can cause unacceptable adverse events and do not provide a benefit as maintenance therapy. Tumor necrosis factor (TNF) antagonists, although efficacious, 5 , 6 predispose patients to serious infection. 7 Thus, new treatment strategies are needed. The migration of leukocytes into inflamed intestinal tissue is highly regulated by specific molecular mechanisms. The α 4 β 7 integrin, 8 a cell-surface glycoprotein variably expressed on circulating B and T lymphocytes, interacts with mucosal addressin-cell . . .