Oral mucosal findings in ambulatory patients with inflammatory bowel disease

Does Consuming the Recommend Daily Level of Fiber Prevent Crohn's Disease?

Anti–Integrin αvβ6 Antibody as a Diagnostic Marker for Pediatric Patients With Ulcerative Colitis

There is evidence that, in Crohn's disease (CD), lamina propria T lymphocytes (LPLs) are resistant to FAS-mediated apoptosis and that this defect contributes to the mucosal T-cell accumulation. In this study we examined the functional role of Flip, a Flice inhibitor protein, in the resistance of CD LPL to FAS-mediated apoptosis. Biopsy specimens and LPLs were taken from CD and ulcerative colitis (UC) patients and normal controls and analyzed for Flip by Western blotting. We also examined whether inhibition of Flip by antisense oligonucleotide restored the susceptibility of CD LPLs to FAS-induced apoptosis. LPL apoptosis was assessed by flow cytometry. After FAS stimulation, the rate of apoptosis of CD3+ LPLs was higher in normal controls and patients with UC than in patients with CD. Enhanced expression of both long and short Flip isoforms was seen in biopsy specimens and purified CD3+ and CD45RO+ LPLs of CD patients in comparison with UC patients and normal controls. No increase in Flip was documented in untreated celiac disease mucosa, thus suggesting the possibility that induction of Flip in the gut does not simply rely on the ongoing inflammation. Finally, we showed that inhibition of Flip by antisense oligonucleotide reverted the resistance of CD LPLs to FAS-induced apoptosis. Data suggest a role for Flip in the resistance of CD LPLs to FAS-mediated apoptosis.

P-049: Reproducibility of serologic antibody activity at diagnosis and after treatment in pediatric ulcerative colitis and Crohn’s disease

Interleukin-21 enhances T-helper cell type I signaling and interferon-γ production in Crohn’s disease

P-056: Buccal epithelial cell chemokine release as a biomarker for clinical response to therapy in inflammatory bowel disease

Neither Hide Nor Hair: The Difficulty of Identifying Useful Disease Biomarkers

Ulcerative Colitis and Crohn's Disease Genetics: More Similar Than We Thought?

East Meets West: The Increasing Incidence of Inflammatory Bowel Disease in Asia as a Paradigm for Environmental Effects on the Pathogenesis of Immune-Mediated Disease

Social and demographic characteristics, features of disease course and treatment options of inflammatory bowel disease in Russia: results of two multicenter studies

The aims of this study were to assess bone metabolism in inflammatory bowel disease (IBD) patients and to evaluate potential differences between Crohn's disease (CD) and ulcerative colitis (UC) with respect to the mechanisms underlying bone loss in this group of diseases. This was a cross-sectional study which started in 1992. Patients were randomly selected for invitation to participate and were examined during the years 1992-95 in one research clinic in Milan. Fifty-one patients suffering from CD (30 women and 21 men, mean age 38.7 +/- 13.2 years) and 40 with UC (15 women and 25 men, mean age 34.4. +/- 12.5 years) entered the study. Thirty healthy subjects were selected as sex- and age-matched controls (C). Spine and femoral neck bone mineral density (expressed as T score), calciotropic hormones (parathyroid hormone, PTH; 25-hydroxycholecalciferol, 25(OH)D3; 1,25-hydroxycholecalciferol, 1, 25(OH)D3) and biochemical markers of bone turnover (ostecalcin, OC; total alkaline phosphatase, ALP; type I collagen C-terminal telopeptide, ICTP) were evaluated. Spine and femur T scores were similar in the two groups (spine: CD = -1.49 +/- 1.46; UC = -1. 67 +/- 1.13; femur: CD = -1.80 +/- 1.36; UC = -1.60 +/- 1.03). Based upon the WHO guidelines, only 8% of CD patients and 15% of UC patients had a normal bone mineral density (BMD), 55% (CD) and 67% (UC) were osteopenic, and 37% (CD) and 18% (UC) were osteoporotic. The distribution amongst the three different diagnostic groups was not significantly different between CD and UC groups (P = 0.11). PTH and 25(OH)D3 concentrations were not significantly different between CD and UC patients and controls, whilst 1,25(OH)D3 concentrations were significantly lower in both CD and UC patients compared with controls (P < 0.05). Bone turnover was increased in UC but not in CD patients, as shown by significantly increased concentrations in UC patients of both OC (CD = 7.77 +/- 5.06, UC = 10.03 +/- 6.24, C = 6. 58 +/- 2.87, P < 0.05 vs. C) and ICTP (CD = 5.74 +/- 3.94, UC = 10.2 +/- 8.47, C = 3.48 +/- 0.95, P < 0.05 vs. CD and C). In a stepwise regression that included age, sex, disease duration and cumulative prednisolone dose as independent variables, the femur T score was significantly inversely related to disease duration (r2 = 0.125, F = 6.06) in CD patients. In UC patients, the spine T score was inversely related to age (r2 = 0.107, F = 5.49) and significantly related to sex (more negative in males: r2 = 0.3, F = 16.1); the femur T score was significantly related to sex (more negative in males) and inversely related to the cumulative prednisolone dose (r2 = 0.283, F = 7.3). These data show that IBD patients have a diffuse osteopenia, the degree of which is not different in CD and UC; however, bone turnover is significantly higher in UC. Finally, osteopenia is related to disease duration in CD, whilst it is related to the male sex and glucocorticoid treatment in UC.

Genetics and Environmental Interactions Shape the Intestinal Microbiome to Promote Inflammatory Bowel Disease Versus Mucosal Homeostasis

INTRODUCTION: Acute pancreatitis (AP) can occur in patients with inflammatory bowel disease (IBD) and can be either due to the underlying inflammatory disease itself or as a side effect of treatment. We aimed to is to estimate the risk of AP in patients with IBD using a national population-based cohort compared to a control population without IBD and to estimate the impact of anti-inflammatory and biologic agents on this risk. METHODS: Patients with crohn’s disease (CD), ulcerative colitis (UC) and a control cohort without CD or UC were identified using a national population-based database, Explorys from 2015 to 2020. After excluding tobacco users, patients with alcohol abuse, and those with cholelithiasis from all three cohorts (to minimize the risk of confounders) the rates and odds ratios (OR) of CD and UC patients with de-novo AP were calculated with 95% confidence intervals (CI). The rates of AP diagnosed within 6 months, 1 year, 2 years, and 3 years of a CD or UC diagnosis were also recorded ORs of CD or UC patients with de-novo AP after exposure to different classes of medications were noted. RESULTS: A total of 168,950 cases of CD were identified and 1.8% of them subsequently diagnosed with AP. While, 133,980 patients with UC were identified and 1.6% of them subsequently developed AP. Patients with CD were 6.03 times more likely to develop AP than the general population (OR 6.03; 95% CI 5.81–6.26; P < 0.05) and those with UC were 4.09 times more likely to develop AP than the general population (OR 4.09; 95% CI 3.92–4.27; P < 0.05). Only the use of glucocorticosteroids [CD: (OR: 1.38; 95% CI 1.30–1.48; P < 0.05), UC: (OR: 1.34; 95% CI 1.23–1.44; P < 0.05)] decreased the risk of AP when compared to the overall CD and UC cohorts. Interestingly, treatment with 5-aminosalicylic acid medications (OR: 1.23, 95% CI 1.14–1.32; P < 0.05) and immunomodulators [CD: (OR: 1.21; 95% CI 1.11–1.31; P < 0.05) decreased the risk of AP only in the CD group. CONCLUSION: Patients with CD or UC are at a greater risk of developing AP than the general population. The majority are likely to be diagnosed with AP within the first 6 months of their inflammatory disease diagnosis. 5-aminosalicylic acid drugs, and immunomodulators decreased only CD patients’ AP risk, while glucocorticosteroids significantly decreased both CD and UC patients’ risk of developing AP.Figure 1.: Flow chart of the 3 study population.Table 1.: Demographics of crohn's disease and ulcerative colitis patientsTable 2.: Odds ratios for crohn's disease and ulcerative colitis patients developing denovo acute pancreatitis

Background: Bone loss and osteoporosis are commonly reported in inflammatory bowel disease (IBD), especially Crohn disease (CD). The aims of the present study were to evaluate changes in bone mineral density (BMD) in IBD patients during a 2‐year follow‐up period, and to investigate the role played by possible contributing factors in bone loss. Methods: Sixty patients with CD and 60 with ulcerative colitis (UC) were studied initially. Fifty‐five CD and 43 UC patients were re‐examined after 1 year, and 50 CD and 44 UC patients after 2 years. Lumbar spine, femoral neck and total body BMD were measured by dual X‐ray absorptiometry (DXA), and Z scores were obtained by comparison with age‐matched and sex‐matched healthy subjects. Biochemical variables were assessed at inclusion and at the 1‐year follow‐up visit. Results: Mean BMD values were unchanged in both CD and UC patients. In patients with repeated measurements, significant differences in Z scores (Δ Z score) were found for femoral neck and total body in CD and for total body in UC. Significant bone loss occurred in 11 CD (22%) and 12 UC (27%) patients. A significant increase in BMD was found in 21 CD (42%) and 20 UC (46%) patients. In CD patients the initial BMD values for lumbar spine and femoral neck were inversely correlated to BMD changes at the same sites and the change in body mass index (BMI) was positively correlated to change in the total body BMD. C‐reactive protein was significantly higher in CD patients with bone loss. Biochemical markers of bone metabolism could not be used to predict BMD changes. Although it was not significant, there was a relationship between corticosteroid therapy and bone loss in CD. Conclusions: Only minor changes in BMD were observed in both CD and UC patients during a 2‐year period. The multifactorial pathogenesis of bone loss in IBD makes it difficult to assess the importance of each single contributing factor. However, our results indicate that disease activity and corticosteriod therapy are involved in bone loss in CD patients.

Differential expression of serum miR-486 and miR-25 in ulcerative colitis and Crohn’s disease: Correlations with disease activity, extent, and location