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PubMed2004

Epidemiology of appendicectomy in primary sclerosing cholangitis and ulcerative colitis: its influence on the clinical behaviour of these diseases.

BACKGROUND AND AIMS: Appendicectomy and smoking are environmental factors that are known to influence ulcerative colitis (UC). The phenotype of UC is different in patients with coexistent primary sclerosing cholangitis (PSC). This study investigates the interaction of appendicectomy and PSC on the epidemiology and clinical behaviour of colitis. METHODS: Patients were from the Brisbane IBD Research Group database. Controls were from the Australian twin registry. Seventy eight PSC-inflammatory bowel disease (PSC-IBD) patients, 12 pure PSC, and 294 UC patients were matched with 1466 controls by sex and birth cohort that comprised randomly selected twins from each twin pair. The effects of appendicectomy, smoking, or PSC on the onset of disease, disease extent, disease severity (as identified by immunosuppression-colectomy or liver transplant), and disease related complications (high grade dysplasia, colorectal cancer, or cholangiocarcinoma) were investigated using univariate and multiple logistic regression analyses. RESULTS: PSC-IBD patients had a more extensive colitis than UC patients (p<0.0001) but required less immunosuppression (p = 0.007), which was independent of disease extent. They were more likely to have high grade dysplasia or colorectal cancer (p = 0.029) than UC patients. Appendicectomy rates in the PSC groups were not different from the control groups (p = 0.72, 0.76), which was in sharp contrast with UC where the rate was four times less (p = 0.0001). Prior appendicectomy appeared to be associated with an approximate five year delay in the onset of intestinal (PSC-IBD or UC) or hepatic (PSC) disease, which was independent of smoking. Appendicectomy did not independently alter the extent or severity of disease in PSC. In contrast, prior appendicectomy in UC was associated with more extensive disease but with a lesser requirement for immunosuppression or colectomy for the treatment of colitis (p = 0.004). There were trends for high grade dysplasia or colorectal cancer with appendicectomy in both PSC-IBD and UC. Although these trends were not statistically significant, colorectal cancer appeared more frequent with appendicectomy in a meta-analysis of the available UC data from this and another Australian study. CONCLUSIONS: In contradistinction to UC, appendicectomy did not significantly influence the prevalence of the PSC groups, or the extent of colitis in PSC-IBD, but as with UC, did appear to delay their onset. The extensive milder colitis, which is characteristic of PSC-IBD, relates to other poorly understood factors. Further prospective studies are required to determine any influence of appendicectomy on the extent of colitis in IBD and an associated dysplasia or colorectal cancer.

Adult↗

PubMed2005

The RANKL/OPG system is activated in inflammatory bowel disease and relates to the state of bone loss.

BACKGROUND AND AIMS: A substantial proportion of patients with inflammatory bowel disease (IBD) develops osteopenia and osteoporosis in the course of disease. Recent data from a mouse model of colitis suggest that the receptor activator of nuclear factor kappa B (RANKL)/osteoprotegerin (OPG) system may be responsible for bone loss. METHODS: We investigated the activation state of the RANKL/OPG system and its association with bone loss in human IBD. Plasma levels of OPG and RANKL were correlated with bone mineral density and current IBD therapy. Colonic secretion of OPG and RANKL and cell types responsible for such secretion were determined. RESULTS: OPG plasma levels were elevated 2.4-fold in Crohn's disease (CD) and 1.9-fold in ulcerative colitis (UC) whereas soluble RANKL (sRANKL) levels were not significantly different in IBD patients compared with healthy controls. High levels of OPG were released from colonic explant cultures (CEC) derived from inflamed IBD specimens, and colonic macrophages and dendritic cells costained for OPG. sRANKL levels from CEC were low both in IBD patients and healthy controls. Interestingly, increased expression of RANKL was mainly confined to cells in the lamina muscularis. A significant negative correlation was found between OPG plasma levels and femoral neck/lumbar spine bone mineral density. CONCLUSIONS: We have demonstrated that IBD is associated with alterations in the RANKL/OPG system. Applying results from a murine model of colitis associated bone loss, the constellation of OPG and sRANKL regulation observed in our study raises the possibility that RANKL/OPG may contribute to the development of bone loss in IBD.

Adolescent↗

PubMed2005

Anti-inflammatory effects of pancreatitis associated protein in inflammatory bowel disease.

BACKGROUND AND AIMS: Increased pancreatitis associated protein (PAP) mRNA has been reported in active inflammatory bowel disease (IBD). The aims of the current study were to characterise PAP production in IBD and the effects of PAP on inflammation. PATIENTS AND METHODS: Serum PAP levels were determined in healthy controls (n = 29), inflammatory controls (n = 14), and IBD patients (n = 171). Ex vivo PAP secretion in intestinal tissue was measured in 56 IBD patients and 13 healthy controls. Cellular origin of PAP was determined by immunohistochemistry. The effects of exogenous PAP on nuclear factor kappaB (NFkappaB) activation, proinflammatory cytokine production, and endothelial adhesion molecule expression were also analysed ex vivo. RESULTS: Patients with active IBD had increased serum PAP levels compared with controls, and these levels correlated with clinical and endoscopic disease severity. Ex vivo intestinal PAP synthesis was increased in active IBD and correlated with endoscopic and histological severity of inflammatory lesions. PAP localised to colonic Paneth cells. Incubation of mucosa from active Crohn's disease with PAP dose dependently reduced proinflammatory cytokines secretion. PAP prevented TNF-alpha induced NFkappaB activation in monocytic, epithelial, and endothelial cells and reduced proinflammatory cytokine mRNA levels and adhesion molecule expression. CONCLUSIONS: PAP is synthesised by Paneth cells and is overexpressed in colonic tissue of active IBD. PAP inhibits NFkappaB activation and downregulates cytokine production and adhesion molecule expression in inflamed tissue. It may represent an anti-inflammatory mechanism and new therapeutic strategy in IBD.

Analysis of Variance↗

PubMed1995

Respiratory burst of intestinal macrophages in inflammatory bowel disease is mainly caused by CD14+L1+ monocyte derived cells.

Macrophages play a crucial role in intestinal mucosal defence, forming dense subepithelial aggregates, particularly in the colon. One of their important bactericidal mechanisms is production of oxygen radicals but this may damage the intestinal epithelium, perhaps as an early step in inflammatory bowel disease (IBD). The potential for release of oxygen radicals from mucosal macrophages in IBD was measured and whether a difference exists between newly arrived (CD14+L1+) monocyte-like cells and resident macrophages (CD14(-)L1-), without or with additional priming in vitro, was investigated. Lamina propria mononuclear cells from six patients with IBD and five with a normal intestine were isolated with an ethylenediaminetetra acetic acid/collagenase/dispase technique and cultured for three days. The cells were tested with or without interferon gamma (200 U/ml) priming in the presence or absence of lipopolysaccharide (1 microgram/ml) for the last 48 hours in cultures. Samples from inflamed IBD mucosa depleted of CD14+ cells by immunomagnetic beads were compared with their undepleted counterparts and with samples from virtually normal mucosa from the same patients. The production of oxygen radicals was measured as the amount of reduced cytochrome C 2.5 hours after triggering with phorbol 12-myristate 13-acetate. The oxygen radical production in macrophages from moderately or severely inflamed mucosa was reduced by median 69% (range 22%-79%, p < 0.027) after depletion of CD14+ cells, reaching a level similar to that found for virtually normal samples from the same IBD patients. Furthermore, this production did not increase significantly in mucosal macrophages from normal reference mucosa and from virtually normal or inflamed IBD mucosa after priming with interferon gamma with or without addition of lipopolysaccharide. Upregulation of a respiratory burst in subepithelial resident macrophages os not a likely pathogenetic step in IBD. The increased oxygen radical production shown by macrophages from IBD lesions can, however, be ascribed to recently extravasated CD14+L1+ monocyte-like cells. Inhibition of extravasation of these reactive cells may form part of a therapeutic approach in the future.

Antigens, Surface↗

PubMed1998

Secretion imbalance between tumour necrosis factor and its inhibitor in inflammatory bowel disease.

BACKGROUND: Tumour necrosis factor (TNF) alpha and TNF-beta are soluble ligands binding to TNF receptors with similar activities; soluble TNF receptors neutralise TNF activity by acting as inhibitors. Little is known about the cytokine/soluble receptor role in inflammatory bowel disease (IBD). AIMS: To test the hypothesis that an imbalance in secretion between TNF and TNF inhibitors plays a role in gut inflammation in patients with IBD. METHODS: The secretion of TNF-alpha, TNF-beta, and soluble TNF receptors was compared in the culture supernatants of colonic biopsy specimens and isolated lamina propria mononuclear cells from patients with active colonic IBD. RESULTS: Spontaneous secretion of TNF-alpha in involved IBD mucosa was higher than in normal control and self limited colitis mucosa. Secretion of TNF-beta was higher in patients with Crohn's disease than in those with ulcerative colitis. Soluble TNF receptor in IBD mucosa inhibited TNF activity. Type 2 soluble receptor release from IBD mucosa was increased in active inflammation; release from lamina propria cells was not increased. Mucosal TNF-alpha production correlated with severity of disease. CONCLUSIONS: Results showed enhanced secretion of TNF-alpha but failure to release enhanced amounts of soluble TNF receptor in lamina propria mononuclear cells of patients with IBD. An imbalance in secretion between TNF and TNF inhibitor may be implicated in the pathogenesis of IBD.

Adolescent↗

PubMed2000

Neurokinin-1 receptor expression in inflammatory bowel disease: molecular quantitation and localisation.

BACKGROUND: Substantial evidence implicates the neuropeptide substance P (SP) in mucosal immunoinflammatory responses. Autoradiographic studies have suggested a disturbance in SP receptor expression in inflammatory bowel disease (IBD). AIMS: Because of technical limitations such as poor cellular resolution with autoradiography, we used molecular methods to specifically localise the cellular expression of the neurokinin-1 receptor (NK-1R) in IBD colon, and to quantitate NK-1R mRNA expression levels therein. METHODS: In situ hybridisation and immunohistochemistry were used to localise NK-1R mRNA and protein, respectively, in normal, ulcerative colitis (UC), and Crohn's disease (CD) colonic resections. NK-1R mRNA expression levels of normal, UC, and CD mucosal biopsies were quantitated by competitive reverse transcription-polymerase chain reaction. RESULTS: NK-1R expression was localised to lamina propria mononuclear cells, epithelium, submucosal vasculature, smooth muscle, and myenteric plexus of normal and IBD colon. No ectopic NK-1R expression was observed in IBD. However, we found increased numbers of NK-1R expressing lymphoid cells in IBD tissue, aberrant negative epithelial expression of NK-1R in UC, and increased expression of NK-1R in CD myenteric plexus. Quantitation of NK-1R mRNA expression in IBD colonic mucosal biopsies revealed marked upregulation of NK-1R mRNA levels compared with non-inflamed mucosal expression levels (p<0.01). CONCLUSIONS: This report demonstrates the strategic localisation and upregulation of NK-1R expression in IBD colon, and thereby suggests the involvement of substance P in the pathophysiological symptoms of IBD.

Adult↗

PubMed2000

Increased incidence of non-Hodgkin's lymphoma in inflammatory bowel disease patients on immunosuppressive therapy but overall risk is low.

BACKGROUND: There is concern that the incidence of non-Hodgkin's lymphoma (NHL) will rise with increasing use of immunosuppressive therapy. AIMS: Our aim was to determine the risk of NHL in a large cohort of patients with inflammatory bowel disease (IBD), and to study the association between IBD, NHL, and immunosuppressive therapy. METHODS: We studied 782 IBD patients (238 of whom received immunosuppressive therapy) who attended our medical centre between 1990 and 1999 (median follow up 8.0 years). Standardised incidence ratios (SIRs) and 95% confidence intervals (CI) were calculated. Expected cases were derived from 1995 age and sex specific incidence rates recorded by the National Cancer Registry of Ireland. RESULTS: There were four cases of NHL in our IBD cohort (SIR 31.2; 95% CI 2.0-85; p=0.0001), all of whom had received immunosuppressive therapy: azathioprine (n=2), methotrexate (n=1), and methotrexate and cyclosporin (n=1). Our immunosuppressive group had a significantly (59 times) higher risk of NHL compared with that expected in the general population (p=0.0001). Three cases were intestinal NHL and one was mesenteric. Mean age at NHL diagnosis was 49 years, mean duration of IBD at the time of NHL diagnosis was 3.1 years, and mean duration between initiation of immunosuppressive therapy and diagnosis of NHL was 20 months. CONCLUSIONS: Although underlying IBD may be a causal factor in the development of intestinal NHL, our experience suggests that immunosuppressive drugs can significantly increase the risk of NHL in IBD. This must be weighed against the improved quality of life and clinical benefit immunosuppressive therapy provides for IBD patients.

Adult↗

PubMed2001

Helicobacter-induced inflammatory bowel disease in IL-10- and T cell-deficient mice.

Inflammatory bowel disease (IBD) is thought to result from a dysregulated mucosal immune response to luminal microbial antigens, with T lymphocytes mediating the colonic pathology. Infection with Helicobacter spp has been reported to cause IBD in immunodeficient mice, some of which lack T lymphocytes. To further understand the role of T cells and microbial antigens in triggering IBD, we infected interleukin (IL)-10(-/-), recombinase-activating gene (Rag)1(-/-), T-cell receptor (TCR)-alpha(-/-), TCR-beta(-/-), and wild-type mice with Helicobacter hepaticus or Helicobacter bilis and compared the histopathological IBD phenotype. IL-10(-/-) mice developed severe diffuse IBD with either H. bilis or H. hepaticus, whereas Rag1(-/-), TCR-alpha(-/-), TCR-beta(-/-), and wild-type mice showed different susceptibilities to Helicobacter spp infection. Proinflammatory cytokine mRNA expression was increased in the colons of Helicobacter-infected IL-10(-/-) and TCR-alpha(-/-) mice with IBD. These results confirm and extend the role of Helicobacter as a useful tool for investigating microbial-induced IBD and show the importance, but not strict dependence, of T cells in the development of bacterial-induced IBD.

Animals↗

PubMed2007

Meta-analysis of risk of malignancy with immunosuppressive drugs in inflammatory bowel disease.

BACKGROUND: There is a concern as to whether long-term administration of immunosuppressants in patients with inflammatory bowel disease (IBD) would increase the risk of malignancy. OBJECTIVE: To compare the risks of developing malignancy between patients with IBD treated with immunosuppressive agents and patients with IBD not receiving these agents. METHODS: A systematic literature review was conducted, and a meta-analysis was performed on data retrieved from cohort studies that followed patients with IBD who received immunosuppressive agents for more than a year and documented the incidence of newly developed malignancy. An electronic search was conducted using MEDLINE (1966-September 2006), the Cochrane Library (issue 3, 2006), and Japana Centra Revuo Medicina (1981-September 2006). Medical subject headings used in the searches were azathioprine, 6-mercaptopurine, cyclosporine, methotrexate, tacrolimus, inflammatory bowel disease, and neoplasms. We imposed no language limitation in the searches. Additionally, a manual search of reference listings from all articles retrieved from the electronic databases was performed. Using data obtained from control groups or population-based studies, the incidence of newly developed malignancy in patients with IBD treated with immunosuppressive agents was compared with that of patients with IBD who were not receiving immunosuppressive agents. Statistical analysis for the change in risk of developing malignancy was performed using the weighted mean difference (WMD) normalized to per person-year and its 95% confidence interval. RESULTS: Nine cohort studies met the inclusion criteria for this meta-analysis. Analysis of these studies showed no discernible difference (WMD -0.3 x 10(-3)/person-year; 95% CI -1.2 x 10(-3) to 0.7 x 10(-3)) in the incidence of any kind of malignancy in patients with IBD who received immunosuppressants compared with those who did not receive immunosuppressants. No significant difference in WMD was observed when the data from patients with either Crohn's disease (CD) or ulcerative colitis (UC) were analyzed separately. CONCLUSIONS: Our findings suggest that the administration of immunosuppressive agents in patients with either CD or UC probably does not confer a significantly increased risk of malignancy compared with patients with IBD who are not receiving these agents.

Cohort Studies↗

PubMed1999

Current pharmacotherapy for inflammatory bowel disease.

Ulcerative colitis (UC) and Crohn's disease (CD), collectively termed inflammatory bowel disease (IBD), are chronic spontaneously relapsing enteropathies of unknown aetiology. Pharmacotherapy for IBD has essentially been unchanged for over twenty years, with therapy based around 5-aminosalicylic acid (5-ASA) preparations, corticosteroids, antibiotics and immunosuppression. Much of the controversy surrounding optimal use of these drugs in IBD arises as a consequence of methodological deficiencies in many of the early trials combined with the difficulty in consistent patient selection due to the heterogeneous nature of both UC and CD. More recently, well-designed clinical trials have attempted to provide an 'evidence based' approach to managing IBD which, in time, will allow optimisation of current therapies and accurate evaluation of novel agents. Over the past two decades, improved research methodology has considerably increased our molecular understanding of the aetiopathogenesis of IBD which has ultimately lead to the development of specific mediator directed or 'designer' drug therapy for IBD. This review evaluates the literature on current IBD therapy, summarises the important recent studies which have made an impact on clinical practice, and examines the risks and benefits of the novel agents which are currently under investigation in clinical trials of IBD therapy.

Clinical Trials as Topic↗

PubMed2003

Emerging biotherapies for inflammatory bowel disease.

The immunological and genetic pathogeneses of inflammatory bowel disease (IBD) have been well studied, but not well elucidated in recent years. Accordingly, the pharmacological treatment of IBD is focusing upon the individual pathologic step (targeting therapy). It has recently become apparent that new drugs such as biological immunomodulating agents and anti-inflammatory cytokines have better short-term effects in some respects than conventional drugs, and they could change the treatment strategy of IBDs in the near future. Many options are now available to treat IBD. The choice depends on the type of IBD, the location of inflammation and the severity of symptoms. Many key processes in the inflammatory cascade have been targeted by cytokine and anticytokine therapies ranging from antigen presentation, T cell activation, overproduction of pro-inflammatory cytokines and migration of inflammatory cells to blockade of effector signals. TNF-alpha plays an important role in the induction of other cytokines as well as in the upregulation of adhesion molecules in chronic IBDs, Crohn's disease (CD) and ulcerative colitis. In fact, the most successful approaches so far in the treatment of IBD have been anti-TNF strategies. In contrast, the use of antiadhesion molecules strategies has been demonstrated to be ineffective in IBD.

Clinical Trials as Topic↗

PubMedDate not supplied

Perinuclear antineutrophilic cytoplasmic antibody and response to treatment in diarrheic dogs with food responsive disease or inflammatory bowel disease.

The goal of this study was to investigate the correlation between perinuclear antineutrophilic cytoplasmic antibody (pANCA) and clinical scores before and after treatment in diarrheic dogs with food-responsive disease (FRD) or inflammatory bowel disease (IBD). pANCA serology was evaluated prospectively by indirect immunofluorescence in 65 dogs with signs of gastrointestinal disease, and if positive, pANCA antibody titers were determined. Thirty-nine dogs with FRD responded to a novel diet, and 26 dogs with IBD were treated with corticosteroids. The severity of clinical signs was scored by means of a canine IBD activity index (CIBDAI). At initial examination, a significantly (P = .002) higher percentage of dogs were pANCA-positive in the FRD group (62%) compared with the IBD group (23%). pANCA titers were significantly higher (P = .003) before treatment in the FRD group (median titer 100) compared with the IBD group (median titer 1). However, there was no difference in pANCA titers between the groups after respective treatments because dogs in the IBD group had a significant increase in pANCA titer after treatment. The CIBDAI score decreased significantly (P < .001) after treatment in both groups (74% moderate to severe in FRD dogs before versus 8% after treatment; 85% moderate to severe in IBD dogs before versus 32% after treatment). There was no correlation between pANCA status in FRD or IBD dogs before treatment and scores for CIBDAI, endoscopy, or histopathology before or after treatment, except for the endoscopic duodenal score in dogs with FRD after treatment (P = .03). A positive pANCA test before therapy may aid in the diagnosis of FRD.

Animals↗

PubMed1996

Primary sclerosing cholangitis in Japanese patients: association with inflammatory bowel disease.

To characterize primary sclerosing cholangitis (PSC) in Japanese patients and its association with inflammatory bowel disease (IBD), 155 reported cases of PSC, including 6 cases of our own, were reviewed. The prevalence of IBD was less in Japanese PSC patients than in Western patients (23% versus 62-100%). Japanese PSC patients with IBD were younger (mean age, 33.1 versus 51.8 years) and were more often women (51% versus 36%) than those without IBD. Seventy-four percent of PSC patients with IBD had extensive colonic lesions, and 89% of those developed IBD simultaneously, with or prior to PSC. There were 3 cases of neutrophilic cholangitis among the PSC patients with IBD but none in those without IBD. Based on these observations, we speculate that there may be subtypes of PSC which differ pathophysiologically.

Adolescent↗

PubMed1982

An analysis of peripheral blood and salivary polymorphonuclear leukocyte function, circulating immune complex levels and oral status in patients with inflammatory bowel disease.

In an earlier case report, we described a 28-year-old man with active Crohn's disease and rapidly progressive alveolar bone loss, who presented with enhanced peripheral blood polymorphonuclear leukocyte activity as assessed by phagocytosis and lysis of a target bacterium. To assess the significance of this finding, peripheral blood polymorphonuclear leukocytes (PMN) from thirty patients with active or inactive inflammatory bowel disease (IBD) were examined for spontaneous and stimulated hexose monophosphate shunt (HMS) activity. Analysis revealed the PMN from active IBD patients displayed greater metabolic activity than PMN from inactive IBD patients, which in turn were more active than PMN from normal subjects. Since circulating immune complex (CIC) levels might be of importance in the in vivo activation of PMN, analysis of serum CIC levels via polyethylene glycol 6000 precipitation was carried out. This indicated that active IBD patients had higher levels of CIC activity then inactive IBD patients. Ten of these patients were evaluated for spontaneous HMS activity by salivary PMN. As compared to controls, comparable numbers of salivary PMN from IBD patients displayed an average of 45% less activity than control salivary PMN. Analysis of the oral status of 10 IBD patients referred to the Peter Bent Brigham Dental Clinic indicated that two patients had overt oral pathoses apparently attributable to IBD. These two patients also had the highest CIC levels observed in the 30 serum samples tested.

Adult↗

PubMed2006

Angiographic diagnosis of inflammatory bowel disease in patients presenting with gastrointestinal bleeding.

OBJECTIVE: The objective of our study was to review the final diagnosis and outcome in patients undergoing visceral angiography for gastrointestinal hemorrhage in whom a diagnosis of inflammatory bowel disease (IBD) had been suspected on the basis of angiographic findings. MATERIALS AND METHODS: A retrospective review was performed of all visceral angiography referrals over a 10-year period. During that time, 522 visceral angiograms were obtained for the investigation of acute or chronic gastrointestinal bleeding. IBD was reported as a possible or probable diagnosis based on the angiographic findings in 43 patients (8.2%) (male-to-female ratio, 23:20; age range, 11-79 years; mean age, 48.6 years). RESULTS: Active IBD was confirmed in 25 (58%) of these 43 individuals (male-to-female ratio, 15:10; mean age, 46.5 years), representing 4.8% of all patients referred for the investigation of gastrointestinal bleeding. In 14 of these individuals, a diagnosis of IBD had not been suspected previously. A diagnosis other than IBD was found to be the cause of the angiographic findings in seven subjects. In the 32 patients in whom a cause for the angiographic findings was identified, IBD was the diagnosis in 25 (78%). CONCLUSION: In a group of patients referred for angiography to investigate acute or chronic gastrointestinal bleeding, IBD can be expected to be the cause in approximately 5%. Radiologists should be aware of the angiographic abnormalities seen in patients with IBD and be prepared to consider this diagnosis even if the results of other previous investigations have been reported as normal.

Adult↗

PubMed1994

A prospective study of first attacks of inflammatory bowel disease and infectious colitis. Clinical findings and early diagnosis.

In 105 patients with a first attack of colitis, clinical, microbiologic, laboratory, and histologic features were studied prospectively with the aim of differentiating inflammatory bowel disease (IBD) from infectious colitis as early as possible. Of the patients who proved to have IBD the mode of onset of diarrhoeal symptoms was insidious in 56% and non-insidious in 44%, whereas in 81% of those who proved to have infectious colitis the onset was acute. Most patients with infectious colitis presented within 1 week, had early fever, and did not show histologic features characteristic of IBD. Most IBD patients with a more acute onset had clinical warning signs of IBD such as slight previous bowel symptoms, a late presentation time (> 1 week), and absence of early fever or had histologic features characteristic of IBD. These features were basal plasmacytosis, crypt distortion, more than two vertical crypt branches, villous mucosa, mucosal atrophy, epithelioid granuloma, and Paneth cell metaplasia. Moreover, 61% of the IBD patients with a non-insidious onset fell ill in connection with travelling abroad, gastrointestinal infection, or treatment with antibiotics. Knowledge of the above clinical and histologic factors will facilitate differentiation of IBD from infectious-type colitis.

Adolescent↗

PubMed2025

Cardiovascular Complications Are Increased in Inflammatory Bowel Disease: A Path Toward Achievement of a Personalized Risk Estimation.

Background/Objectives: The global burden of inflammatory bowel diseases (IBDs) continues to rise, with up to 50% of patients experiencing extraintestinal manifestations. Cardiovascular diseases (CVDs) are of particular concern, ranking as the second leading cause of mortality in this population. Despite a comparatively lower prevalence of traditional cardiovascular (CV) risk factors, the persistent inflammatory milieu and immune dysregulation inherent to IBD may contribute to heightened CVD risk. In this study, following a review of the current literature, an ongoing prospective trial designed to clarify CV risk profiles in IBD patients is detailed. Methods: A cohort of patients with IBD is being enrolled for comprehensive baseline evaluation of CV risk factors, lifestyle metrics, and disease characteristics. The incidence of major adverse cardiovascular events (MACEs) will be tracked and contrasted with a gender- and age-matched non-IBD cohort over a 2-year follow-up period. In cases of MACE occurrence, a multi-omics analysis-including genomic, proteomic, transcriptomic, and microbiome profiling-will be performed, along with a parallel evaluation in matched IBD controls without MACE. An artificial intelligence (AI) framework will support the analysis of this complex dataset. Results: To date, over 150 patients with IBD have been enrolled, and detailed phenotypic data and biological samples have been collected. Conclusions: We aim to introduce an IBD-specific correction factor for existing CV risk scores upon study completion. This is particularly relevant for individuals under 40 years of age, who are often inadequately assessed by current risk stratification models.

Crohn’s disease↗

PubMed2006

Novel strategies for the treatment of inflammatory bowel disease: Selective inhibition of cytokines and adhesion molecules.

The etiology of inflammatory bowel disease (IBD) has not yet been clarified and immunosuppressive agents which non-specifically reduce inflammation and immunity have been used in the conventional therapies for IBD. Evidence indicates that a dysregulation of mucosal immunity in the gut of IBD causes an overproduction of inflammatory cytokines and trafficking of effector leukocytes into the bowel, thus leading to an uncontrolled intestinal inflammation. Such recent advances in the understanding of the pathogenesis of IBD created a recent trend of novel biological therapies which specifically inhibit the molecules involved in the inflammatory cascade. Major targets for such treatment are inflammatory cytokines and their receptors, and adhesion molecules. A chimeric anti-TNF-alpha monoclonal antibody, infliximab, has become a standard therapy for CD and it is also likely to be beneficial for UC. Several anti-TNF reagents have been developed but most of them seem to not be as efficacious as infliximab. A humanized anti-TNF monoclonal antibody, adalimumab may be useful for the treatment of patients who lost responsiveness or developed intolerance to infliximab. Antibodies against IL-12 p40 and IL-6 receptor could be alternative new anti-cytokine therapies for IBD. Anti-interferon-gamma and anti-CD25 therapies were developed, but the benefit of these agents has not yet been established. The selective blocking of migration of leukocytes into intestine seems to be a nice approach. Antibodies against alpha4 integrin and alpha4beta7 integrin showed benefit for IBD. Antisense oligonucleotide of intercellular adhesion molecule 1 (ICAM-1) may be efficacious for IBD. Clinical trials of such compounds have been either recently reported or are currently underway. In this article, we review the efficacy and safety of such novel biological therapies for IBD.

Animals↗