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PubMed1979

Biochemical studies with infectious bursal disease virus: comparison of some of its properties with infectious pancreatic necrosis virus.

Infectious bursal disease (IBD) virus was purified from the bursae of infected chickens. Two morphologically indistinguishable populations of virus particles were separated in sucrose gradients and possessed sedimentation coefficients of 295S and 460S. Both populations contained RNA and had identical polypeptide compositions. IBD virus banded at a density of 1.31 g/ml in CsCl and at 1.24 g/ml in sodium potassium tartrate. IBD virus contained two RNA segments with mol. wts. of 2.4X10(6) and 2.2X10(6) as estimated by polyacrylamide-agarose gel electrophoresis, but sedimented in sucrose gradients at 15S. Virus RNA was resistant to 0.1 micrograms/ml ribonuclease treatment under conditions in which ribosomal RNA was completely hydrolysed, but was sensitive to 1.0 and 10 micrograms/ml treatments. These results suggest that the RNA consists of either double-stranded or highly ordered single-stranded molecules. IBD virus contained seven polypeptides with mol. wts. in the range 97,000 to 24,000. Two polypeptides were absent in empty particles of IBD virus. IBD and infectious pancreatic necrosis (IPN) viruses were morphologically indistinguishable. IPN virus possessed a sedimentation coefficient of 440S and banded at a density of 1.32 g/ml in CsCl. In addition the electrophoretic mobilities of IBD and IPN virus RNAs were almost identical. Polyacrylamide slab gel electrophoresis showed that while the number and size of the polypeptides were different for each virus there were similarities in the overall pattern.

Animals↗
PubMed1993

Increased risk of early colorectal neoplasms after hepatic transplant in patients with inflammatory bowel disease.

UNLABELLED: Inflammatory bowel disease (IBD) is associated with an increase in colon and rectal carcinoma. Immunosuppression after transplantation increases the incidence of certain types of tumors. PURPOSE: We reviewed the postoperative course of IBD patients who had undergone hepatic transplantation for primary sclerosing cholangitis to see whether there was an increase in the rate of colorectal neoplasms. METHODS: The charts of 44 patients from two institutions who had undergone a hepatic transplant for primary sclerosing cholangitis were reviewed. Of these 44 patients, 33 had IBD (32 chronic ulcerative colitis, 1 Crohn's). Of these 33 patients, 2 had previously undergone total colectomy/proctectomy and 4 died in the perioperative period. The remaining 27 patients had all undergone colonoscopic evaluation just prior to transplant. Postoperatively all patients were given prednisone, cyclosporine, and azathioprine. Minimum follow-up was 12 months; mean follow-up was 39 months. RESULTS: Three of the 27 patients (11.1 percent) developed early colorectal neoplasms (2 cancers, 1 large villous adenoma with severe dysplasia) at 9, 12, and 13 months post-transplant. All three patients were successfully treated with a total colectomy/proctectomy or resection of any remaining colon. These 3 patients had a mean 19-year history of IBD (range, 9-27 years), while the 24 patients without tumors had a mean 18-year history of IBD (range, 6-39 years). CONCLUSION: There is a subset of transplant patients with primary sclerosing cholangitis and IBD who rapidly develop colorectal neoplasms. Frequent surveillance is recommended for IBD patients in the post-transplant period.

Adult↗
PubMed1997

Preliminary report on the Mount Sinai Hospital Inflammatory Bowel Disease Genetics Project.

BACKGROUND: Although the etiology of inflammatory bowel disease (IBD) is unknown, there is increasing evidence that genetic predisposition plays a major etiologic role. To provide the framework for gene identification using a positional cloning approach, ascertainment of families with multiple affected members and careful documentation of pedigrees are essential. OBJECTIVE: To report the initial findings of the IBD Genetics Project of the Mount Sinai Hospital IBD Research Unit. METHODS: All records of patients with ulcerative colitis and Crohn's disease followed at the Mount Sinai Hospital IBD Unit were reviewed. A questionnaire was sent to all patients to ascertain those with a family history of IBD. Patients with a presumed family history were contacted by a research assistant, and after confirmation of diagnosis, relevant clinical information, pedigrees, and consent to contact family members were obtained. Blood for DNA and cell line preparation were collected from affected and nonaffected family members. RESULTS: Of 2,504 patients registered in the IBD database, 231 (9.2 percent) were found to have an affected family member: 96 of 964 (10 percent) with Crohn's disease (CD) and 135 of 1,540 (8.8 percent) with ulcerative colitis (UC). A mean of 2.4 family members were affected. In families in which the proband had CD, 82.3 percent had only two affected family members, 78.1 percent had only family members affected with CD, and 82.3 percent had only first-degree family members affected. In families in which the proband had UC, 70.4 percent had only two affected family members, 71.1 percent had only family members affected with UC, and 65.2 percent had only first-degree family members affected. In the 231 families, there were 103 sibling pairs: 46 percent with CD, 28 percent with UC, and 26 percent with CD/UC. CONCLUSION: These data suggest that approximately 10 percent of IBD patients have affected family members, with the rate being similar in UC and CD. Future research is directed to genome scanning and linkage analysis in this cohort of patients.

Colitis, Ulcerative↗
PubMed2000

Inflammatory bowel disease.

Till about 3 decades ago, inflammatory bowel disease (IBD) was considered as non-existent in our country. However, since that time several reports of IBD, mainly ulcerative colitis have been published. More recently, Crohn's disease is also being reported from the country. This trend of UC appearing first in a population followed by CD also appears to be true in other developing nations. A substantial increase in the rates of CD over UC in the last few decades is reported from developed nations as well. Of the other epidemiological factors, an increased risk of CD and lower risk of UC in smokers is established in adults. However, it appears that smoking increases the risk of IBD in children. The etiology of IBD remains elusive. Within the triad of genetics, immunity and antigen responsible for the development of IBD, maximum advances have been made in the field of immune aberrations and this is being exploited to treat the disease. It is well established that IBD results from a disordered immune system in the gut, in response to an unidentified antigen in a predisposed individual. The immune response is enhanced and revolves around antigen-presenting cells, CD 4 T-lymphocytes and tumor necrosis factor alpha. CD results from an enhanced Th1 activity. The pathogenesis of UC is less clear but appears to be humoral. Advances in diagnostics include the availability of serology, ultrasound and nuclear scans, none of which have been tried in our setting where infectious diseases and tuberculosis is rampant. Growth failure and the importance of nutrition in IBD, especially CD, cannot be underemphasized. In many situations nutritional interventions have been used solely as a form of therapy for CD. Newer steroid molecules with minimal systemic effects are also being considered. Other treatment options highlighted are the use of immunosuppressive agents, biologic agents and role of surgery.

Adult↗
PubMed1990

Lymphoid cell subsets in colonic mucosa and HLA-DR antigens on colonic epithelia in colitis excluding ulcerative colitis and Crohn's disease.

Lymphoid cell subsets, including T cells as well as Ig-containing cells in the colonic mucosa and HLA-DR antigens on colonic epithelia, were examined in non-IBD colitis (colitis excluding ulcerative colitis (UC) and Crohn's disease) by the indirect immunoperoxidase staining method. Mouse anti-CD5, CD8, CD4, IgG, IgA1, IgA2, IgM, IgD, IgE, HLA-DR, and NuIa monoclonal antibodies were used as the first antibody. The results were compared to those of the normal controls and UC. T cell subsets in non-IBD colitis were almost similar to those of the controls and UC. The number of Ig-containing cells of all classes, except for IgA, tended to be increased in non-IBD colitis. In particular, both IgG- and IgE-containing cells were significantly increased compared to those in the controls. Compared to UC, IgG-containing cells were decreased in non-IBD colitis. Namely, in non-IBD colitis, as well as in UC, the change of Ig-containing cells (B cell lineage) was more pronounced than that of T cells. The frequency of the expression of HLA-DR antigens on colonic epithelia in non-IBD colitis was 70%, which was significantly higher than that in controls (0%), but significantly lower than that in UC (100%). Whether the differences in the number of IgG-containing cells, and the frequency of epithelial HLA-DR expression between non-IBD colitis and UC was due to the differences of the degree of local inflammation or due to the differences of the nature of the two diseases was not elucidated in this study.

Colitis↗
PubMed2000

Expression of platelet P-selectin and detection of soluble P-selectin, NPY and RANTES in patients with inflammatory bowel disease.

OBJECTIVE AND DESIGN: P-selectin, a membrane glycoprotein which is expressed on activated platelets and endothelial cells, plays a crucial role in the inflammatory response. The main action is adhesion of leukocytes, facilitation of diapedesis and induction of cytokine production from monocytes (MCP-1 and IL-8), mediated via RANTES released from activated platelets. An abnormal platelet activity has been reported in patients with ulcerative colitis (UC) and Crohn's disease (CD), jointly referred to as inflammatory bowel disease (IBD), which could have an aggravating influence on the inflammatory response. In addition, an up-regulation of platelet IL-8 receptors among patients with IBD has been reported. To reveal a presumptuous platelet dysfunction we analysed the expression of platelet surface P-selectin at resting state and after stimulation with thrombin, collagen, epinephrine and interleukin 8 (IL-8), and plasma levels of soluble P-selectin, neuropeptide Y (NPY) and RANTES in patients with IBD. SUBJECTS: Blood from twelve healthy subjects (control group) and twenty-one patients with IBD who had not taken any anti-platelet drugs or steroids were analysed. METHODS: Patients were sub-grouped according to disease entity, disease activity and 5ASA medication. Surface P-selectin expression on isolated human platelets and plasma P-selectin, NPY and RANTES were analysed with ELISA. All values are presented as mean +/- standard error of the mean (SEM). Mann-Whitney U test and Wilcoxon matched rank test were used for statistical analyses. RESULTS: Patients with IBD in remission (n = 9) had higher basal P-selectin expression, 0.38+/-0.04, compared to the control group (n = 12), 0.22+/-0.03,p < 0.01. UC patients (n = 16) showed down-regulation of P-selectin expression after stimulation with IL-8, 0.26+/-0.03 to 0.22+/-0.02, p < 0.05. No significant differences could be observed concerning soluble P-selectin and NPY in plasma. Patients with 5ASA (n = 12) had lower levels of plasma RANTES, 2.39+/-0.06 microg/l, compared to the control group (n = 12), 3.29+/-0.19 microg/l, p < 0.01, and patients without 5ASA (n = 9), 2.90+/-0.17 microg/l, p < 0.05. CONCLUSIONS: Patients with IBD in remission have higher basal platelet surface P-selectin expression. An exaggerated platelet activity with increased expression of platelet P-selectin and release of inflammatory mediators such as RANTES, which is chemotactic and induce chemokine production, could have a reinforcing and aggravating influence on the inflammatory response and increase the susceptibility to IBD. In addition IL-8 has a down-regulating effect on platelet surface P-selectin expression and 5ASA medication seems to lower plasma RANTES. If 5ASA is responsible for lowering the concentration of RANTES this could be one of the beneficial outcomes of 5ASA medication.

Adult↗
PubMed2003

Association of inflammatory bowel disease with indicators for childhood antigen and infection exposure.

BACKGROUND AND AIMS: Genetic susceptibility plays an important role in the predisposition to inflammatory bowel disease (IBD), but genetics alone cannot explain the six- to eightfold rise in incidence accompanying postwar socioeconomic changes in developed countries. It is presently unclear how environmental factors either trigger or modify the risk for and course of IBD in the presence of genetic susceptibility. PATIENTS AND METHODS: We evaluated 2,351 consecutive responses from IBD patients and from 3,364 of their unaffected first-degree relatives (parents/siblings) who completed a multi-item questionnaire with their physicians as part of a study of IBD genetics. All single-patient families were excluded from the analysis to avoid ascertainment bias, resulting in 120-133 independent cases for the analysis of environmental factors and 1,685 patients to be included in the analysis of birth rank. RESULTS: No statistically significant association was observed between the presence of IBD and the availability of either (warm) tap water, water toilets, or central heating during childhood. However, higher birth rank (> or =3) was significantly associated with a lower risk of IBD (odds ratio 0.68). CONCLUSION: Lower birth rank as a possible indicator of increased childhood infection exposure was associated with a higher risk for IBD. Future studies need to address the interaction of known genetic variations (e.g., in the NOD2 gene) with environmental factors potentially mediating this effect.

Birth Order↗
PubMed2006

What is the impact of resistance to activated protein C (Leiden mutation to factor V) in inflammatory bowel disease?

BACKGROUND AND AIMS: Resistance to activated protein C (APCR) caused by the Leiden mutation to factor V is the most common cause of inherited thrombosis. Patients with inflammatory bowel disease (IBD) are considered to have an increased risk of thromboembolic complications, and the role of APCR as a cause has previously been investigated. In this study, we investigated if APCR was associated with non-thrombotic morbidities in IBD. PATIENTS/METHODS: Of 951 patients asked to participate, 389 agreed by returning a signed informed consent and filled questionnaire and took the blood test for APCR. Self-reported IBD-related surgery was used as a rough indicator for increased morbidity. RESULTS: APCR was present in 6.6% of patients with Crohn's disease (CD; 10/152) and in 12.7% of ulcerative colitis (UC) patients (30/237). The difference of 6.1% is significant (p=0.039). Among patients with CD and APCR, 9 out of 10 had had surgery, significantly more than among those without APCR (81/142). In patients with UC and APCR, 10 out of 30 had had surgery, still significantly more than in those without APCR (36/207). For the whole group of IBD patients, APCR is associated with a significantly increased risk for thrombosis (p=0.0018), and for the UC group (8/28) p=0.0029, but not for the CD patients alone (2/9), p=0.2323. No other significant differences could be shown for parameters normally related to increased morbidity. CONCLUSIONS: APCR in IBD was associated with an increased frequency of IBD-related surgery, which may warrant screening for APCR in therapy-resistant IBD. In patients with APCR, it may be more difficult and/or important to control inflammation.

Activated Protein C Resistance↗
PubMed1996

Life insurance and inflammatory bowel disease: is there discrimination against patients?

The aims of this study were to compare and contrast the attitude of major insurance companies to patients with inflammatory bowel disease (IBD) and to a Consultant Gastroenterologist (JFM) requesting guidelines for patients with IBD. The experience of patients in Leicester with insurance companies was also investigated. A standard letter requesting information regarding the likelihood of loading on life assurance in connection with a mortgage was sent to 50 major insurance companies from a typical patient. A similar letter was constructed from a consultant gastroenterologist (JFM) to the same 50 insurance companies requesting simple guidelines for patients with IBD when applying for various types of insurance. A questionnaire investigating the experience of patients with IBD when applying for insurance was also sent to 100 patients with IBD selected at random from the Leicestershire data base of patients with Crohn's disease and ulcerative colitis, 39 insurance companies responded to the request for information by a typical patient, (response rate = 78%). 24 were split between those who thought the patient would be accepted at normal rates (n = 7) and those who would request an increased premium (n = 17). Only 27 companies replied to the letter by a consultant gastroenterologist requesting general guidelines, (response rate = 54%). There were only 17 overlapping replies to the two letters. Of these 17 overlapping replies, five companies (30%) informed the patient to expect increased premiums whilst advising the consultant a similar patient could expect normal rates. Six companies conferred (35%), telling both the patient and the consultant to expect normal rates. Either one or both of the remaining six companies (35%) felt unable to comment without either specific details of the patient or a medical examination. 69% of patients responded to the questionnaire. Over half (54%) had applied for an insurance policy. More than a third of patients had required either a medical examination (36%) or a report from their GP (41%) before being accepted for a policy. 39% of patients had received an additional loading on their policies because of IBD including two patients who had been turned down altogether. In conclusion patients with IBD are clearly discriminated against by insurance companies. Life tables should be amended to take account of the low mortality recognised in recent years. Patients should be aware of the difficulties that currently exist.

Adult↗
PubMed2005

Sensorineural hearing loss in patients with inflammatory bowel disease: a subclinical extraintestinal manifestation.

Isolated case reports in which symptomatic hearing loss develops suddenly during the course of inflammatory bowel disease (IBD) have been reported, but the presence of subclinical sensorineural hearing loss (SNHL) associated with IBD has been investigated in only two preliminary studies. In order to research this further, we aimed to investigate the presence of subclinical SNHL in IBD by comparison with a control group and to examine possible relations between the bowel disease parameters and hearing loss.Otoscopy, tympanometry, and pure tone audiometry were carried out in 39 patients with IBD (21 Crohn's disease [CD], 18 ulcerative colitis [UC]) and 25 healthy age- and sex-matched controls. All patients and control subjects had normal otoscopy findings and tympanometry was unremarkable, excluding middle ear disease and conductive hearing loss. Analysis of each frequency examined showed that the average hearing thresholds were increased significantly in the study group compared to those of the control group at higher frequencies (2, 4, and 8 kHz). When these parameters were compared with the control group according to subgroups of IBD, a significant difference was determined for the UC group at frequencies of 2, 4, and 8 kHz and for the CD group only at the frequency of 4 kHz. Although there was a trend of increment in SNHL as the age of the patient and duration and extent of UC increased, no significant correlation was observed between SNHL and these parameters or sex, activity, involvement site, medication history of IBD, and coexistence of other extraintestinal manifestations. In conclusion, it was demonstrated that a subclinical SNHL may be associated with UC and somewhat with CD, affecting mainly the high frequencies. In light of this finding, it may be advisable to investigate labyrinth functions as well as other extraintestinal manifestations in patients with IBD.

Adolescent↗
PubMed2006

Colonic ornithine decarboxylase in inflammatory bowel disease: ileorectal activity gradient, guanosine triphosphate stimulation, and association with epithelial regeneration but not the degree of inflammation and clinical features.

The role of colonic mucosal ornithine decarboxylase (ODC) in inflammatory bowel disease (IBD) remains controversial. This study assessed mucosal ODC activity in IBD patients segment by segment with regard to patient characteristics, disease activity/duration, medication, degree of mucosal inflammation, and presence/absence of epithelial regeneration and guanosine triphosphate (GTP) stimulation. Mucosal ODC activity was determined in biopsy specimens from the terminal ileum, cecum/ascending, transverse, and descending colon, and the sigmoid/rectum of 35 patients with IBD (18 with Crohn's disease, 17 with ulcerative colitis) and 29 controls, using the amount of 14CO2 liberated from (carboxyl-14C)ornithine hydrochloride. GTP-stimulatable activity was expressed as the ratio of ODC activity in the presence and absence of GTP (70 micromol/L). Mucosal inflammation was assessed endoscopically/microscopically with previously described criteria. Presence/absence of mucosal regeneration also was determined by predefined criteria. Mucosal ODC-activity did not significantly differ in IBD patients and controls. There was a 4.4-fold activity gradient from the ileum to the rectum. Mucosal ODC activity was significantly higher in areas with epithelial regeneration compared to those without regeneration, and was stimulated by GTP by a factor of 1.42 in Crohn's disease and 1.19 in ulcerative colitis patients compared to controls (p < 0.004). On the other hand, there was no significant association/relationship of mucosal ODC activity with disease activity/duration and the endoscopic/histologic degree of mucosal inflammation. The observation of unchanged mucosal ODC activity in patients with IBD and the absence of a significant relationship with clinical and endoscopic/histologic disease characteristics speaks against a major role of ODC in IBD as a major disease marker. The role of the ileorectal gradient, the enhanced activity in areas with epithelial regeneration, and the GTP-stimulatable form, however, need further investigation with regard to a possible involvement in carcinogenesis in IBD.

Adult↗
PubMed2004

Inflammatory bowel disease in Ashkenazi Jews: implications for familial colorectal cancer.

Inflammatory bowel disease (IBD) has a multifactorial etiology and includes ulcerative colitis (UC) and Crohn's disease (CD). Powerful epidemiologic and genetic studies have provided ample evidence that a subset of both CD and UC are attributable to a likely primary genetic etiology. This is evidenced by the recent identification of the IBD1 gene ( NOD2 ) mutations which show an association with susceptibility to CD. The IBD complex shows a significant increased frequency in Jews when compared to non-Jews. While there is an increased incidence of colorectal cancer (CRC) in patients with IBD, it nevertheless is important to realize that IBD likely accounts for no more than 1-3% of all cases of CRC in Ashkenazi Jews. Importantly, however, awareness of the increased CRC risk in IBD may aid immeasurably in preventive interventions. The molecular pathway leading to CRC in IBD appears to differ from the well-known adenoma-to-CRC sequence, given the fact that these cancers appear to arise from either flat, dysplastic tissue or dysplasia-associated lesions or masses (DALMs). An important model, but by no means an absolute one, for colon carcinogenesis in IBD follows progression from an absence of dysplasia, to indefinite dysplasia, to low-grade dysplasia, on to high-grade dysplasia, and ultimately to invasive CRC. This carcinogenic process relates to the disease duration with respect to the extent of colonic involvement and may also involve primary sclerosing cholangitis. Given this knowledge of an increased risk for CRC in UC and CD, surveillance colonoscopy should initially be performed 8-10 years after onset of symptoms as opposed to diagnosis, and it should be performed 1-2 years after 8 years of disease in patients with pancolitis or after 15 years in those with left-sided colitis. A search for dysplasia of colonic mucosa with biopsies performed in all four quadrants every 10 cm throughout the colon is exceedingly important. Additional biopsies should be taken of any flat lesions, masses, or strictures. Prophylactic colectomy may then be indicated when severe dysplasia is confirmed by knowledgeable pathologists.

Adult↗
PubMed1995

Immunoregulatory role of interleukin 10 in patients with inflammatory bowel disease.

BACKGROUND/AIMS: Active inflammatory bowel disease (IBD) is associated with increased proinflammatory cytokines. Deficiency of interleukin (IL) 10, a contrainflammatory cytokine, leads to the development of colitis in IL-10 knockout mice. We characterized IL-10 regulation of proinflammatory cytokine (tumor necrosis factor [TNF] alpha and IL-1 beta) expression in IBD in vitro and in vivo. METHODS: IL-10 regulation of IL-1 beta, TNF-alpha, and IL-1 receptor antagonist expression by peripheral monocytes or isolated lamina propria mononuclear cells (LPMNC), respectively, was studied by enzyme-linked immunosorbent assay (cytokine secretion) and by semiquantitative reverse-transcription polymerase chain reaction. RESULTS: IL-10 down-regulates IL-1 beta and TNF-alpha secretion as well as messenger RNA levels in IBD peripheral monocytes and LPMNC in a dose-dependent manner. In parallel, IL-1 receptor antagonist secretion is induced, and IL-10 can restore diminished in vitro IL-1 receptor antagonist/IL-1 beta ratios in IBD to normal levels. Equal concentrations of IL-10 are detectable in both normal and IBD intestinal lamina propria biopsy homogenates. After topical IL-10 enema treatment of three steroid therapy-refractory patients with ulcerative colitis, in vitro release of proinflammatory cytokines from IBD peripheral monocytes as well as LPMNC is dramatically down-regulated. CONCLUSIONS: IL-10 down-regulates the enhanced secretion as well as messenger RNA levels of proinflammatory cytokines by IBD mononuclear phagocytes in vitro. In vivo topical application of IL-10 induces down-regulation of proinflammatory cytokine secretion both systemically and locally.

Adult↗
PubMed2006

Alterations in intestinal fatty acid metabolism in inflammatory bowel disease.

Inflammatory bowel disease (IBD) constitutes a severe intestinal disorder in developed countries with increasing incidence worldwide. Upcoming evidence indicates an important role of intestinal epithelial barrier function in the development of IBD. Fatty acids exert nutritional and protective effects on enterocytes, serve as activators of transcription and constitute precursors of inflammatory mediators. The aim of this study was to investigate differential regulation of genes involved in fatty acid uptake and endogenous fatty acid biosynthesis in IBD. Mucosal biopsy specimens from non-affected regions of the intestine were subjected to DNA microarray analysis. Gene array analysis revealed a variety of genes involved in fatty acid uptake and synthesis to be differentially expressed in ileum and colon of selected IBD patients. To verify these results, real-time RT-PCR was performed for selected regulated candidate genes in larger IBD sample numbers. In single biopsy analysis long chain acyl-CoA synthetase (ACSL) 1 and 4 were upregulated in IBD (P<0.05), while a significant decrease in fatty acid synthase expression was found in ileum and colon of ulcerative colitis patients (P<0.001). Expression of the transcription factor liver X receptor (LXR) which was previously shown to induce fatty acid synthase gene expression was not altered on mRNA level in IBD. However, in cell culture experiments using the human intestinal cell line LS174T induction of fatty acid synthase by the LXR ligand T0901317 was inhibited by TNFalpha. Moreover, these experiments indicated a decrease of LXR protein levels by TNFalpha treatment. These data suggest that the decrease of fatty acid synthase expression in ulcerative colitis patients could be at least partially due to a loss of LXR expression and function in the presence of pro-inflammatory cytokines. Observed alterations in expression of genes of fatty acid metabolism may contribute to the pathophysiology of ulcerative colitis.

Animals↗
PubMed2005

Inflammatory bowel disease-related dysplasia and cancer: A referral center study in northwestern Greece.

BACKGROUND: An increased risk of colorectal cancer in ulcerative colitis (UC) and Crohn's disease (CD) has been reported. No data on inflammatory bowel disease (IBD)-related dysplasia and cancer is available in Greece, where the disease profile seems to be milder than that of northern Europe. METHODS: A study was conducted of 215 IBD patients (182 with UC, 33 with CD) from a referral center. Patients were followed up for 3-18 years. The prevalence of cancer and dysplasia among the IBD patients who were diagnosed in northwestern Greece was analyzed and registered. Statistical analysis was performed assuming that this IBD cohort had the same risk of developing malignancies as the general population in Greece. RESULTS: Six of the 215 patients in this IBD cohort had cancer, and 20 of 126 patients for whom bowel biopsies were available had dysplasia. Three of these cases were high-grade dysplasia. There was no significant difference in the numbers of calculated and expected cases of IBD-related cancer at any sites except for the skin [2.7 vs. 2.0]. CONCLUSIONS: This IBD cohort did not appear to have an increased risk of cancer during the time period studied. It would be interesting to re-assess the risk after the second and third decades of follow-up.

Journal Article↗
PubMed2006

Surgical approaches to cancer in patients who have inflammatory bowel disease.

IBD clearly increases the risk for GI malignancies, especially CRC. The absolute number of patients that develops such malignancies is low compared with the overall cancer rate; however, younger age of onset, higher relative risk, unique clinical presentations, and problems with early diagnosis make this a serious complication of IBD. With the exception of patients with comorbid complications, such as primary sclerosing cholangitis, the prognosis is no worse for CRCs that arise as the result of IBD compared with those that arise sporadically. The prognosis remains poor for small bowel adenocarcinomas in patients who have CD, primarily because of their advanced stage at detection. Diligent surveillance is essential for early detection and treatment of IBD-related CRCs in patients with unresected colons, long-standing or extensive disease, and in those who have early-onset CD, although pundits still question whether it significantly affects prognosis and survival. Better surveillance techniques for small bowel dysplasia or malignancy in patients who have CD is needed, especially given the poor prognosis of these patients when advanced cancers are detected. Depending on the presentation and disease diagnosis, patients have several surgical treatment options and can expect good outcomes for all. When the appropriate surgical technique is used in patients who have colon or rectal cancer, along with adjuvant chemotherapy when appropriate, prognosis and function is good; however, the experience of the surgeon can affect the prognosis for IBD-related GI cancers. Surgical therapy is based not only on general oncologic principles, but also on the surgery that is appropriate for the IBD diagnosis. Resection of the mesentery and lymphadenectomy should be performed according to oncologic principles. Postoperative survival for IBD-related CRC is good, and diligent surveillance and follow-up are critical to the patient's overall prognosis.

Clinical Trials as Topic↗
PubMed2026

Global gut microbiome atlas identifies epidemiologic-stage-specific signatures in inflammatory bowel disease.

The global rise of inflammatory bowel disease (IBD) reflects environmental shifts, yet how these changes are embedded in the gut microbial ecology remains unclear. We construct a microbiome atlas comprising 245,627 profiles. By classifying countries into three epidemiologic stages, we establish a framework. As the IBD burden increases, the gut microbial alpha diversity declines, and community structures form distinct clusters. This transition is characterized by a gradient of core genera. Integrating six shotgun metagenomic cohorts, we identify the depletion of anabolic pathways in IBD patients. Strain-level analysis reveals that epidemiologic staging shapes genetic architecture within species, identifying an IBD-enriched subclade of Eisenbergiella associated with elevated fecal cholic acid. We develop a microbial inflammatory risk score (MIRS), based on 19 genera, that discriminates IBD from controls (area under the curve [AUC] = 0.92). MIRS correlates with IBD prevalence. Our study provides an atlas linking epidemiology to microbiome ecology and strain evolution, offering a foundation for population-level surveillance and interventions in IBD.

Humans↗
PubMed2003

Advances in clinical laboratory tests for inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a generic term that refers to Crohn's disease and chronic ulcerative colitis (UC). The CD and UC are considered to be distinct forms of IBD; but there is a subgroup of CD with a UC-like presentation. The genetic factors play a significant role in IBD. IBD is associated with a strong familial pattern. Recent studies support the hypothesis that IBD patients have a dysregulated immune response to endogenous bacteria in the gastrointestinal tract. The serologic responses seen in Crohn's disease include antibodies to Saccharomyces cerevisiae, mycobacteria, bacteroides and E. coli. The pANCA antibody seen in UC and CD has been demonstrated to react with epitopes of H1 histone, Bacteroides caccae (Ton-B linked outer membrane protein), Pseudomonas fluorescens-associated bacterial protein I-2, mycobacterial histone 1 homologue called Hup B. In recent years, several serologic markers have been found to be useful for the diagnosis and differentiation of CD and UC. These markers include the following antibodies: (a) pANCA, (b) ASCA, (c) anti-pancreatic antibody, (d) OmpC antibody and (e) I-2 antibody and antibodies to anaerobic coccoid rods. The application of a panel of markers with the use of an algorithm (i.e. IBD First Step) can identify specific subtypes of IBD that have different clinical courses and progression of the diseases. The serologic markers are useful for the diagnosis and management of CD and UC patients.

Antibodies↗