scholarly journals Recent Advances in Diagnosis and Management of Crohn’s Disease

2021 ◽  
Author(s):  
Anjana Bali ◽  
Monika Rani
Keyword(s):  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Intestinal Inflammation ◽  
Inflammatory Cascade ◽  
Recent Advances ◽  
Mucosal Edema ◽  
Inflammatory Bowel ◽  
Assessment Of Disease Activity

The initiation of Crohn’s disease, an inflammatory bowel disease, has been primarily associated with crypt inflammation and abscesses, which further progresses towards the development of mucosal lesion and ulcers followed by mucosal edema. Despite many years of research for the confirmatory role of inflammation in this disease, various pathways and diagnosis for this inflammatory cascade is still unrevealed, which in fact is of utmost importance in the assessment of disease activity and for tailoring the therapy. Till now, various histopathological as well as endoscopic examinations has been found to be effectively and accurately assess inflammatory activity, but they are invasive, time consuming and expensive and therefore are unsuitable for routine use. Consequently, the latest research is focusing on various biomarkers of intestinal inflammation and the corresponding biological therapy. So, this chapter will cover the recent advances in diagnosis and pharmacological therapies for the same.

Physiological Basis for Novel Drug Therapies Used to Treat the Inflammatory Bowel Diseases I. Immunology and therapeutic potential of antiadhesion molecule therapy in inflammatory bowel disease

2005 ◽  
Vol 288 (2) ◽  
pp. G169-G174 ◽  
Author(s):  
Gert Van Assche ◽  
Paul Rutgeerts
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Adhesion Molecules ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Therapeutic Potential ◽  
Physiological Basis ◽  
Inflammatory Bowel

Adhesion molecules regulate the influx of leukocytes in normal and inflamed gut. They are also involved in local lymphocyte stimulation and antigen presentation within the intestinal mucosa. In intestinal inflammation, many adhesion molecules are upregulated, but α4-integrins most likely hold a key position in directing leukocytes into the inflamed bowel wall. Therapeutic compounds directed against trafficking of leukocytes have been designed and are being developed as a novel class of drugs in the treatment of Crohn's disease and ulcerative colitis. This review deals with the immunological aspects of leukocyte trafficking focused on gut homing of T cells. Second, the changes in adhesion molecules and T cell trafficking during intestinal inflammation are discussed. Finally, we review the clinical data that have been gathered with respect to the therapeutic potential and the safety of antiadhesion molecule treatment. Antegren, or natalizumab, a humanized anti-α4 integrin IgG4 antibody, has been most extensively evaluated and may be close to registration. A more specific humanized α4β7-integrin MLN-02 has shown preliminary clinical efficacy in ulcerative colitis, and both antergren and MLN-02 appear to be very safe. Trials with the anti-ICAM-1 antisense oligonucleotide ISIS-2302 in steroid refractory Crohn's disease have provided conflicting efficacy data. In the near future, some of these novel biological agents may prove valuable therapeutic tools in the management of refractory inflammatory bowel disease, although it is too early to define the patient population that will benefit most from these agents.

scholarly journals Comorbid Inflammatory Diseases of Digestive System and Eye

2021 ◽  
Vol 18 (1) ◽  
pp. 20-29
Author(s):  
S. A. Bulgakov ◽  
G. M. Chernakova ◽  
E. A. Kleshcheva ◽  
S. V. Simonova
Keyword(s):  
Ulcerative Colitis ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Inflammatory Bowel Diseases ◽  
Intestinal Inflammation ◽  
Ophthalmological Examination ◽  
Extraintestinal Manifestations ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Crohn’s disease and ulcerative colitis are chronic inflammatory bowel diseases, which are often accompanied by inflammation of other organs. This article presents modern data on etiology, pathogenesis and clinical course of inflammatory bowel diseases, as well as information on extraintestinal eye manifestations of nonspecific ulcerative colitis and Crohn’s disease. The role of microbiota, genetic factors, immune system defects in pathogenesis of intestinal inflammation and extraintestinal eye manifestations is considered. The possibility the development of ophthalmopathology not only against the background of intestinal inflammation, but also as a consequence of therapeutic and surgical methods of treatment of ulcerative colitis and Crohn’s disease is noted. The peculiarities of the course of episcleritis/scleritis, keratitis, uveitis, chorioretinitis, optical neuritis for patients with inflammatory bowel diseases are considered. The presence of these complications may reflect the activity of the underlying disease, which in some cases requires correction of therapy. Anterior uveitis and episcleritis/scleritis are the most common extraintestinal manifestations of inflammatory bowel disease. Inflammation of tissues of the posterior segment of the eye and optic nerve against the background of ulcerative colitis and Crohn’s disease are less common, but are of clinical importance, as they can catastrophically damage the structures of the eye and, as a consequence, lead to complete blindness. Considering the possibility of mild clinical symptoms and asymptomatic course of inflammation in the eye envelopes, the importance of ophthalmological examination of all patients with ulcerative colitis and Crohn’s disease is emphasized. Aspects of modern therapy of ophthalmopathology and background intestinal inflammation are highlighted. Biological preparations — antagonists of pro-inflammatory cytokines — have been identified as the most promising in the treatment of inflammatory intestinal diseases and extraintestinal manifestations. The important role of proper nutrition and biologically active supplements containing omega-3 fatty acids, vitamin D, microelements, was noted as auxiliary therapy of both intestinal and extraintestinal inflammation.

scholarly journals Treatment of Inflammatory Bowel Disease in Children

1990 ◽  
Vol 4 (7) ◽  
pp. 404-406 ◽  
Author(s):  
D Grant Gall
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Enteral Nutrition ◽  
Bowel Disease ◽  
Growth Failure ◽  
Nutritional Therapy ◽  
Inflammatory Bowel

As no curative therapy exists, supportive measures play an important role in the management of patients with inflammatory bowel disease (IBO). Aminosalicylic acid (ASA) compounds and corticosteroids remain the mainstay of medical therapy. Aminosalicylates are recommended for therapy of mild to moderate active ulcerative colitis and for the maintenance of remission in ulcerative colitis. The role of 5-ASA preparations in Crohn's disease is less clear. In granulomatous colitis, 5-ASA therapy is recommended. With the development of new delivery systems, the role for 5-ASA in the treatment of small bowel Crohn's disease is under investigation. Prednisone remains the drug of choice in severe ulcerative colitis and active Crohn's disease. The role of immunosuppressive drugs in pediatric patients is unclear. Nutritional therapy has been an important advance in the treatment of children with Crohn's disease, especially those with growth failure. Nutritional therapy can consist of combined total parenteral and enteral nutrition or enteral nutrition alone. An initial period of total parenteral nutrition followed by a six to eight week course of enteral therapy with a semisynthetic diet has been shown to be effective in the management of patients with severe active disease and growth failure.

scholarly journals Genome-Wide Analysis of the DNA Methylation Profile Identifies the Fragile Histidine Triad (FHIT) Gene as a New Promising Biomarker of Crohn’s Disease

2020 ◽  
Vol 9 (5) ◽  
pp. 1338 ◽  
Author(s):  
Tae-Oh Kim ◽  
Dong-Il Park ◽  
Yu Kyeong Han ◽  
Keunsoo Kang ◽  
Sae-Gwang Park ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Methylation Profile ◽  
Fhit Gene ◽  
Genome Wide ◽  
Dna Methylation Profile ◽  
Inflammatory Bowel

Inflammatory bowel disease is known to be associated with a genetic predisposition involving multiple genes; however, there is growing evidence that abnormal interactions with environmental factors, particularly epigenetic factors, can also significantly contribute to the development of inflammatory bowel disease (IBD). Although many genome-wide association studies have been performed to identify the genetic changes underlying the pathogenesis of Crohn’s disease, the role of epigenetic alterations based on molecular complications arising from Crohn’s disease (CD) is poorly understood. We employed an unbiased approach to define DNA methylation alterations in colonoscopy samples from patients with CD using the HumanMethylation450K BeadChip platform. Technical and functional validation was performed by methylation-specific PCR (MSP) and bisulfite sequencing of a validation set of 207 patients with CD samples. Immunohistochemistry (IHC) analysis was performed in the representative sample sets. DNA methylation profile in CD revealed that 135 probes (24 hypermethylated and 111 hypomethylated probes) were differentially methylated. We validated the methylation levels of 19 genes that showed hypermethylation in patients with CD compared with normal controls. We uniquely identified that the fragile histidine triad (FHIT) gene was hypermethylated in a disease-specific manner and its protein level was downregulated in patients with CD. Pathway analysis of the hypermethylated candidates further suggested putative molecular interactions relevant to IBD pathology. Our data provide information on the biological and clinical implications of DNA hypermethylated genes in CD, identifying FHIT methylation as a promising new biomarker for CD. Further study of the role of FHIT in IBD pathogenesis may lead to the development of new therapeutic targets.

scholarly journals Monozygotic twins with Crohn’s disease and ulcerative colitis: a unique case report

Gut ◽  
1997 ◽  
Vol 41 (4) ◽  
pp. 557-560 ◽  
Author(s):  
N P Breslin ◽  
A Todd ◽  
C Kilgallen ◽  
C O’Morain
Keyword(s):  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Case Report ◽  
Crohn's Disease ◽  
Bowel Disease ◽  
Monozygotic Twins ◽  
Antineutrophil Cytoplasmic Antibody ◽  
Environmental Agents ◽  
Inflammatory Bowel

Background—A large number of monozygotic and dizygotic twin pairs with inflammatory bowel disease have been reported. To date no twin pair has developed phenotypically discordant inflammatory bowel disease. This case report is the first documented occurrence of discordant inflammatory bowel disease occurring in monozygotic twins.Case report—Twenty two year old identical male twins presented within three months of each other with inflammatory bowel disease that proved to be discordant in overall disease type, disease distribution, clinical course, and histopathological findings. Twin 1 developed a severe pancolitis necessitating total colectomy while twin 2 developed a predominantly distal patchy colitis with frequent granulomas, controlled by aminosalicylates. Twin 1 was antineutrophil cytoplasmic antibody (ANCA) negative at the time of testing while twin 2 (Crohn’s disease) was ANCA positive. Significantly, the twins possessed the HLA type DR3-DR52-DQ2 previously associated with extensive colitis.Conclusion—This case report confirms the important role played by genetic factors in the development of inflammatory bowel disease. It also highlights the crucial role of undetermined environmental agents in dictating disease expression and phenotype.

scholarly journals Intestinal Ultrasound in Inflammatory Bowel Disease: A Valuable and Increasingly Important Tool

2021 ◽  
pp. 1-17
Author(s):  
Catarina Frias-Gomes ◽  
Joana Torres ◽  
Carolina Palmela
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Disease Activity ◽  
Bowel Disease ◽  
Response To Therapy ◽  
Inflammatory Bowel

<b><i>Background:</i></b> Intestinal ultrasound is emerging as a non-invasive tool for monitoring disease activity in inflammatory bowel disease patients due to its low cost, excellent safety profile, and availability. Herein, we comprehensively review the role of intestinal ultrasound in the management of these patients. <b><i>Summary:</i></b> Intestinal ultrasound has a good accuracy in the diagnosis of Crohn’s disease, as well as in the assessment of disease activity, extent, and evaluating disease-related complications, namely strictures, fistulae, and abscesses. Even though not fully validated, several scores have been developed to assess disease activity using ultrasound. Importantly, intestinal ultrasound can also be used to assess response to treatment. Changes in ultrasonographic parameters are observed as early as 4 weeks after treatment initiation and persist during short- and long-term follow-up. Additionally, Crohn’s disease patients with no ultrasound improvement seem to be at a higher risk of therapy intensification, need for steroids, hospitalisation, or even surgery. Similarly to Crohn’s disease, intestinal ultrasound has a good performance in the diagnosis, activity, and disease extent assessment in ulcerative colitis patients. In fact, in patients with severe acute colitis, higher bowel wall thickness at admission is associated with the need for salvage therapy and the absence of a significant decrease in this parameter may predict the need for colectomy. Short-term data also evidence the role of intestinal ultrasound in evaluating therapy response, with ultrasound changes observed after 2 weeks of treatment and significant improvement after 12 weeks of follow-up in ulcerative colitis. <b><i>Key Messages:</i></b> Intestinal ultrasound is a valuable tool to assess disease activity and complications, and to monitor response to therapy. Even though longer prospective data are warranted, intestinal ultrasound may lead to a change in the paradigm of inflammatory bowel disease management as it can be used in a point-of-care setting, enabling earlier intervention if needed.

scholarly journals On the Pathogenesis Trail: What Marker B Cell Clones Tell Us about Inflammatory Bowel Disease

1996 ◽  
Vol 10 (2) ◽  
pp. 115-119
Author(s):  
Jonathan Braun ◽  
Yadrira Valles-Ayoub ◽  
Linda Berberian ◽  
Mark Eggena ◽  
Lynn K Gordon ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
B Cell ◽  
Bowel Disease ◽  
Practical Importance ◽  
Cell Clones ◽  
Inflammatory Bowel

Clonal patterns of B cell activity have been recognized in inflammatory bowel disease, most notably in the immunogenetic relationship of perinuclear-antineutrophil cytoplasmic antibodies to ulcerative colitis. Conceptually, this most likely reflects the B cell response to antigens predominating at these sites of mucosal inflammation. Identification of these B cell clones and their antigenic targets may be of pathogenetic and practical importance to diagnosis and treatment. The authors describe strategies to identify such clones, based on recent advances in the characterization and detection of antibody gene products. As an example of this strategy, a clonal detection system was used to identify new marker antibodies potentially useful in the laboratory diagnosis of Crohn’s disease and ulcerative colitis. One surprising outcome of such studies is the unexpected and specific association of the B cell clonal response inCampylobacter jejunienterocolitis and inflammatory bowel disease. By analogy to the pathogenetic role ofHelicobacter pylori-induced mucositis in peptic ulcer disease, this evidence renews attention to the role of Cjejuniin the initiation of ulcerative colitis and Crohn’s disease.

scholarly journals Role of Intestinal Microflora in Initiation and Perpetuation of Inflammatory Bowel Disease

1990 ◽  
Vol 4 (7) ◽  
pp. 271-277 ◽  
Author(s):  
RB Sartor
Keyword(s):  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Bowel Disease ◽  
Autoimmune Response ◽  
Parasitic Infections ◽  
Viral Agent ◽  
Septic Complications ◽  
Inflammatory Bowel

Ulcerative colitis and Crohn's disease occur in regions of the intestine colonized by the highest concentrations of normal flora bacteria and resemble certain chronic bacterial, viral or parasitic infections. However, the role of endogenous and pathogenic bacteria in the induction and perpetuation of chronic idiopathic intestinal inflammation remains controversial. No convincing evidence incriminates a single bacterial, mycobacterial or viral agent as the cause of a high percentage of cases of idiopathic inflammatory bowel disease (IBD). Subtle alterations of luminal microbial flora are nearly impossible to detect, but concentrations of certain anaerobic bacteria, including Bacteroides vulgatus, are increased in active Crohn's disease and correlate with disease activity. Recent investigations suggest mechanisms which bacteria may induce an autoimmune response through molecular mimicry or alterations in host antigens or immunoregulation. Intestinal bacteria contain formylated peptides and cell wall polymers ( endotoxin and peptidoglycan-polysaccharide complexes) which have potent and well characterized inflammatory and immunoregulatory properties and can produce acute and chronic intestinal and systemic inflammation in experimental animals. These proinflammatory molecules are probably absorbed more readily in IBO due ro increased mucosa! permeability during active and perhaps quiescent phases of disease. While the primary mechanisms of intestinal injury remain unknown, it is likely that commensal bacteria and their products amplify and perpetuate the inflammatory response of IBO and may be responsible for extraintestinal manifestations in addition to the frequent septic complications of these diseases.

scholarly journals Vitamin D and Inflammatory Bowel Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-16 ◽  
Author(s):  
Marco Ardesia ◽  
Guido Ferlazzo ◽  
Walter Fries
Keyword(s):  
Inflammatory Bowel Disease ◽  
Vitamin D ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Vitamin D Receptor ◽  
Bowel Disease ◽  
Vitamin D Levels ◽  
Inflammatory Bowel ◽  
Low Serum

Vitamin D deficiency has been recognized as an environmental risk factor for Crohn’s disease since the early 80s. Initially, this finding was correlated with metabolic bone disease. Low serum 25-hydroxyvitamin D levels have been repeatedly reported in inflammatory bowel diseases together with a relationship between vitamin D status and disease activity. Subsequently, low serum vitamin D levels have been reported in various immune-related diseases pointing to an immunoregulatory role. Indeed, vitamin D and its receptor (VDR) are known to interact with different players of the immune homeostasis by controlling cell proliferation, antigen receptor signalling, and intestinal barrier function. Moreover, 1,25-dihydroxyvitamin D is implicated in NOD2-mediated expression of defensin-β2, the latter known to play a crucial role in the pathogenesis of Crohn’s disease (IBD1 gene), and several genetic variants of the vitamin D receptor have been identified as Crohn’s disease candidate susceptibility genes. From animal models we have learned that deletion of the VDR gene was associated with a more severe disease. There is a growing body of evidence concerning the therapeutic role of vitamin D/synthetic vitamin D receptor agonists in clinical and experimental models of inflammatory bowel disease far beyond the role of calcium homeostasis and bone metabolism.

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