Cases Of Ulcerative Colitis Research Articles

Gastric-like (pseudopyloric and pseudofoveolar) metaplasia and Paneth cell hyperplasia-neglected histological features of chronic ileal inflammation.

Architectural distortion and basal plasmacytosis are the most widely recognized histologic features of chronic ileal inflammation. However, these features might be difficult to assess in small, poorly oriented, or superficial biopsies. Additional features of chronic mucosal damage, including pseudopyloric or pseudofoveolar metaplasia and Paneth cell hyperplasia, have been less commonly reported, and their broader appreciation could facilitate the diagnosis of chronic ileal inflammatory conditions. The prevalence of gastric-like (pseudopyloric and pseudofoveolar) metaplasia and Paneth cell hyperplasia was evaluated in 102 ileal biopsies obtained from patients with Crohn's disease (n = 47), ulcerative colitis with endoscopically normal ileum (n = 20) or with backwash ileitis (n = 20), and nonsteroidal anti-inflammatory drugs- (NSAIDs-) induced ileitis (n = 15). Gastric-like metaplasia was identified in 23% of CD and 13% of NSAID-induced ileitis cases, whereas it was absent among all ulcerative colitis cases. Pseudopyloric metaplasia, pseudofoveolar metaplasia, or a combination of both was documented in 13%, 2%, and 9% of Crohn's disease cases, respectively. NSAID-associated cases showed only pseudopyloric metaplasia. Paneth cell hyperplasia was detected in 43% of Crohn's disease cases, 13% of NSAID-induced ileitis cases, and 5% of backwash ileitis cases. Accordingly, pseudofoveolar metaplasia, pseudopyloric metaplasia, and Paneth cell hyperplasia are not uncommon in conditions causing chronic ileal inflammation. They are most frequently detected in Crohn's disease, but may also be present in NSAID-induced ileitis, whereas they are significantly less common in backwash ileitis and absent in normal ileum. Given the surface localization of pseudofoveolar metaplasia, its identification can be particularly helpful when dealing with poorly oriented or superficial samples.

Association of Childhood Abuse with Incident Inflammatory Bowel Disease.

A link between inflammatory bowel disease (IBD), stressful life events and psychological factors has previously been reported. Our objective was to examine the relationship between childhood emotional, physical, and sexual abuse and risk of IBD using a large cohort of female health professionals. We included participants in the Nurses' Health Study II who completed the Physical and Emotional Abuse Subscale of the Childhood Trauma Questionnaire and the Sexual Maltreatment Scale of the Parent-Child Conflict Tactics Scale in 2001. Diagnosis of IBD was determined by self-report and confirmed independently by two physicians through review of medical records. We used Cox proportional hazard modeling to estimate the risk of Crohn's disease (CD) and ulcerative colitis (UC) while adjusting for covariates. Among 68,167 women followed from 1989 until 2017, there were 146 incident cases of CD and 215 incident cases of UC. Compared to women with no history of abuse, the adjusted hazard ratios of CD were 1.16 (95% CI 0.67 - 2.02) for mild, 1.58 (95% CI 0.92 - 2.69) for moderate, and 1.95 (95% CI 1.22 - 3.10) for severe abuse (Ptrend = 0.002). We did not observe an association between childhood abuse and risk of UC. Women who reported early life severe abuse had an increased risk of CD. These data add to the growing body of evidence on the critical role of early life stressors in development of CD.

The impact of achieving remission in inflammatory bowel disease on plasma matrix -carboxyglutamate protein levels

Matrix -carboxyglutamic acid (MGLA) protein is a vitamin K dependent peptide which contributes to the immunomodulatory activity of mesenchymal stromal cells. There is a possible association between MGLA protein and inflammatory bowel disease (IBD) which is divided into Crohn’s disease (CD) and ulcerative colitis (UC). However, little is known about the clinical utility of MGLA protein in IBD patients. This study aimed to assess the impact of achieving remission on the serum MGLA protein levels in IBD patients. This prospective observational study included 60 newly diagnosed IBD patients. All patients were subjected to full clinical, laboratory, radiological, and histopathological assessment of IBD at baseline and six months after initiating treatment. Serum MGLA protein level was assessed using an enzyme-linked immunosorbent assay. There were 29 (48.3%) UC cases and 31 (51.67%) CD cases. We observed a significant decrease in serum MGLA protein levels after 6 months of treatment compared to pretreatment values in UC patients (120.490 ± 26.273 vs. 26.320 ± 17.378 nmol/L, p<0.001) and CD patients (125.576 ± 28.208 vs. 28.520 ± 18.443 nmol/L, p<0.001). Serum MGLA protein levels were significantly higher in non-remittent patients compared to remittent UC patients before treatment (142.556 ± 17.096 vs. 110.560 ± 23.659 nmol/L, p<0.001) and after six months of treatment (51.222 ± 4.410 vs. 15.114 ± 3.302 nmol/L, p<0.001). Serum MGLA protein levels were significantly higher in non-remittent patients compared to remittent CD patients before treatment (150.727 ± 7.198 vs. 111.743 ± 25.718 nmol/L, p<0.001) and after six months of treatment (52.182 ± 5.269 vs. 15.506 ± 4.475 nmol/L, p<0.001). This response was irrespective of the therapeutic modality. In conclusion, achievement of remission in IBD patients resulted in a significant decrease in serum MGLA protein levels.

Concurrent occurrence of ulcerative duodenitis and ulcerative colitis displaying unique responses to golimumab and ustekinumab.

Recent studies have reported the occurrence of upper gastrointestinal (UGI) inflammation in patients with ulcerative colitis (UC). However, whether UC-associated UGI and colorectal lesions share pathogenic cytokine profiles and responses to biologics remains unknown. Herein, we report a case of concurrent UC and ulcerative duodenitis (UD) that displayed unique responses to biologic treatment. Although treatment with prednisolone (PSL) failed to induce remission in both disorders, golimumab (GLM) and ustekinumab (UST) were effective against UD and UC, respectively, and remission of both disorders was achieved using UST. Immunofluorescence analyses revealed that numbers of immune cells expressing TNF-α were comparable in both duodenal and rectal mucosa before the treatment. GLM or UST treatment markedly decreased numbers of TNF-α-expressing duodenal immune cells, suggesting the presence of correlation between TNF-α expression and disease activity of UD. In contrast, TNF-α expression was not parallel to disease activity of UC because GLM or PSL failed to induce remission despite a marked reduction in TNF-α expression. Responsiveness to GLM or UST together with immunofluorescence studies suggests that TNF-α and IL-12/23p40 are pathogenic cytokines causing UD and UC, respectively, in the present case.

Early life exposures and risk of inflammatory bowel disease: A nested case-control study in Quebec, Canada

BackgroundEarly life factors for inflammatory bowel disease are likely to impact the gut microbiota. AimWe investigated the associations between early exposures and inflammatory bowel disease. MethodsThis case-control study was nested within the CO·MMUNITY cohort. Cases of Crohn's disease (CD) and ulcerative colitis (UC) were identified using validated algorithms. All cases and randomly selected controls were invited to complete a questionnaire including early life exposures. Analyses were conducted by logistic regression and causal mediation (direct/indirect effects for passive/active smoking). ResultsEarly introduction of solid foods at 3–6 months tended to increase CD risk compared to later introduction (>6 months): OR = 1.23; 95 % CI: 0.96–1.56, but not of UC. Exclusive breastfeeding tended to decrease the risk of CD (OR = 0.77; 95 % CI: 0.55–1.08), less so for UC. Antibiotics tended to decrease CD (OR = 0.89; 95 % CI: 0.74–1.07) and UC (OR = 0.88; 95 % CI: 0.71–1.09). No association was found between pets and CD or UC. Passive smoking increased CD risk (OR = 1.23; 95 % CI: 1.00–1.51), 20 % of which was mediated by active smoking, but not UC. ConclusionDifferences were noticed in early risk factors for CD and UC. The impact of passive smoking was largely independent of active smoking, highlighting its importance for prevention.

Challenges in Managing Cytomegalovirus Colitis in a Complex Case of Ulcerative Colitis With Hyposplenism and Ustekinumab Therapy

ABSTRACT Colitis secondary to cytomegalovirus (CMV) infection is a recognized complication in patients with ulcerative colitis. This case report details a patient with a background of ulcerative colitis with resultant hyposplenism on ustekinumab therapy who presented with CMV colitis. The presence of hyposplenism with the use of ustekinumab resulted in challenges when treating the CMV infection due to the absence of immune response and required individual tailoring of therapy with higher doses of ganciclovir and valganciclovir according to trough level measurement.

Role of myeloid cells in mediating the effects of lipids on ulcerative colitis.

To evaluate the causal relationship between lipids and ulcerative colitis (UC) through Mendelian Randomization (MR), and to further investigate the involvement of immune cells in mediating this process. Utilizing summary statistics from genome-wide association studies (GWAS) of individuals with European ancestry, we analyzed the causal link between 179 lipid types and UC (2,569 UC cases and 453,779 controls) through Two-sample Mendelian randomization (2SMR) and Bayesian-weighted MR (BWMR). Based on this, a mediation screening of 731 immune cell phenotypes was conducted to identify exposure and mediator factors. Lastly, the role and proportion of immune cells in mediating the causal effects of lipids on UC were assessed via reverse MR (RMR) and two-step MR. The results of MR showed that there was a causal relationship between the six genetically predicted lipid types and UC (P <0.05), and the four immune cell phenotypes were identified as mediators of the association between lipids and UC. Notably, Phosphatidylcholine (PC) (16:0_0:0) served as the exposure factor, and myeloid cells CD11b on CD33+ HLA DR+ CD14dim acted as the mediator. Mediation analysis showed that CD11b on CD33+ HLA DR+ CD14dim had a mediation effect of -0.0205 between PC (16:0_0:0) and UC, with the mediation effect ratio at 15.38%. Our findings elucidate the causal effect of lipids on UC and identify the significant mediating role of myeloid cells CD11b on CD33+ HLA DR+ CD14dim in regulating UC through PC (16:0_0:0), offering new pathways and strategies for UC clinical treatment.

Combination of granulocyte–monocyte apheresis and tofacitinib: Multicentre and retrospective study

ObjectiveGranulocyte–monocyte apheresis (GMA) has shown to be safe and effective in treating ulcerative colitis (UC), also in combination with biologics. The objective of this study is to evaluate the efficacy and safety of combining GMA after primary non-response (PNR) or loss of response (LOR) to tofacitinib (TOFA) in patients with UC. Patients and methodsRetrospective study including all patients with refractory UC who received GMA plus TOFA. Efficacy was assessed 1 and 6 months after finishing GMA by partial Mayo score, C-reactive protein (CRP) and fecal calprotectin (FC). Descriptive statistics and non-parametric tests were used in the statistical analysis. ResultsTwelve patients were included (median 46 years [IQR, 37–58]; 67% female; 67% E3). Patients were mostly receiving TOFA 10mg bid (75%), and 33% also concomitant steroids at baseline. Median partial Mayo score at baseline was 7 (IQR, 5–7), and it decreased to a median of 2 (IQR, 0–3) and 0 (IQR, 0–3) after 1 and 6 months (p=0.027 and 0.020, respectively), while no differences were found in CRP and FC. Clinical remission was achieved by 6 patients both at 1 (50%) and 6 months (67%). CF values<250mg/kg were achieved by 2 and 4 patients at 1 and 6 months (data available in 5 and 7 patients, respectively). No patient required dose-escalation of TOFA, and one patient was able to de-escalate the drug. No patient required colectomy and all patients under steroids were able to stop them. ConclusionThe combination of GMA and TOFA can be effective in selected cases of UC after PNR or LOR to this drug.

Causes of Colectomy in Patients with Ulcerative Colitis: Findings from an Iranian National Registry.

Ulcerative colitis (UC) is a form of inflammatory bowel disease (IBD) marked by rectal and colon inflammation, leading to relapsing symptoms. Its prevalence is increasing, particularly in developed nations, impacting patients' health. While its exact cause remains unclear, genetic and environmental factors are implicated, elevating the risk of colorectal cancer (CRC). Colectomy, though declining, is still performed in select UC cases, necessitating further study. We analyzed data from the Iranian Registry of Crohn's and Colitis (IRCC) to examine UC patients undergoing colectomy. We collected demographic and clinical data from 91 patients, focusing on dysplasia. Statistical analyses assessed dysplasia risk factors. Patients with dysplasia were older at diagnosis and surgery compared to those without dysplasia. Age emerged as a significant risk factor for dysplasia in UC patients undergoing colectomy. No significant associations were found between dysplasia and other factors. Age plays a crucial role in dysplasia risk among UC patients undergoing colectomy. Older age at diagnosis and surgery may indicate a higher risk of dysplasia and CRC. Clinicians should consider age when managing UC patients and implementing screening protocols. Further research with larger samples is needed to confirm these findings.

Possible role of intestinal fungal dysbiosis in dectin-1 and cytokines expression in patients with ulcerative colitis.

Dysregulation of cytokines and intestinal mycobiome has been surveyed in the progression of inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn's disease (CD). On the other hand, the intestinal fungal flora and its main receptor, Dectin-1, induce immune-derived cytokines. Total 64 individuals comprising 32 patients with UC (case group) and 32 healthy subjects (HS group) were assessed. The type and prevalence of fecal yeast species were determined by deoxyribonucleic acid (DNA) sequencing through polymerase chain reaction (PCR) amplification usingITS4 and ITS5 primers. Furthermore, the ribonucleic acid (RNAs) of IL-4, IL-10, IL-17, IL-22 and IFN-γ were extracted. The expression of Dectin-1 gene was then measured in the excised tissue samples. A higher global fungal load in UC-affectedpatients (75%) was found in comparison with the HS group (25%), especially Candida albicans. Saccharomyces cerevisiae was significantly reduced in the fecal samples of UC-affected patients compared to HS (15.04% vs. 1.93% UC). The expression level of Dectin-1 was significantly elevated in patients with active UC (7.37 ± 0.81) than in patients with non-active UC (5.01 ± 77.25) and healthy controls (0.97 ± 0.24) (p < 0.05). The expression levels of IL-4, IL-10, especially both IL-17 and IL-22, were higher in the active UC group compared to the HS group (p = 0.0101, p = 0.0155, p < 0.0001, p < 0.0001, respectively). Similar expression level of IL-4, IL-10, IL-17, IL-22 (p > 0.999) and lower expression of interferongamma (IFN-γ) (p = 0.0021) were found in the non-active UC group compared to the HS group. A significant weak to moderate correlation was detected between Dectin-1 and IL-17 (r = 0.339, p = 0.019), as well as Dectin-1 and IL-22 (r = 0.373, p = 0.015). Furthermore, the expression levels of Dectin-1, IL-17 and IL-22 displayed significant associations with disease activity (p < 0.001, p = 0.029 and p = 0.003, respectively), regardless of the participant group. The current study revealed a possible role for intestinal fungi to promote colonic inflammation and increase UC activity through Dectin-1 stimulation. A positive correlation was detected between intestinal fungal richness with UC susceptibility and activity. IL-4 and IL-10 were associated with disease activity. Besides, the expression levels of Dectin-1, IL-17 and IL-22 were independently associated with disease activity.

Gastrointestinal: A case of ulcerative colitis complicated by Tolosa-hunt syndrome and pyoderma gangrenosum and featuring rare extraintestinal manifestations.

Gastrointestinal: A case of ulcerative colitis complicated by Tolosa-hunt syndrome and pyoderma gangrenosum and featuring rare extraintestinal manifestations.

Safety and efficacy of osimertinib plus bevacizumab as first-line treatment in EGFR-mutant NSCLC with brain metastases: A dynamic ctDNA-guided study.

e20606 Background: Non-small cell lung cancer (NSCLC) patients with positive driver genes had a higher incidence of brain metastasis. This study evaluates the efficacy and safety of Osimertinib combined with Bevacizumab as first line treatment in EGFR-mutant NSCLC with brain metastases, utilizing liquid biopsy and dynamic molecular detection to guide treatment strategies. This approach is anticipated to bring progression-free survival (PFS) benefits and shows different resistant mechanisms. Methods: We enrolled EGFR-mutant NSCLC patients with brain metastases receiving Osimertinib and Bevacizumab as first-line therapy. Paired plasma and cerebrospinal fluid (CSF) samples were collected at baseline, during stable disease, and at disease progression for Next-Generation Sequencing (NGS) analysis. The study's primary endpoints were central nervous system (CNS) PFS and objective response rate (ORR). Secondary endpoints included overall PFS, ORR, disease control rate (DCR), and safety. We also investigated resistance mechanisms to the combination therapy. Results: A total of 28 patients from Beijing TianTan Hospital (May 2020 - July 2023) were retrospectively enrolled. The average Bevacizumab treatment duration was 8.21 months (range: 1-27 months). CNS PFS was 26.73 months (95% CI, not reached), and overall PFS was 21.93 months (95% CI, 18.84-25.02 months). The CNS PFS for patients with 19del and L858R mutations were not reached and 26.73 months (95% CI, 15.11-38.35 months), respectively (p = 0.25). Patients undergoing intracranial local treatment showed a CNS PFS not reached, compared to 23.33 months (95% CI, 16.21-30.45 months) for those who did not (p = 0.417). The CNS ORR was 88%, ORR was 76%, and DCR was 100%. At the time of data cutoff (Dec 15th, 2023), 1 patient progressed in both lung and CNS metastases, 8 patients only progressed in lung, 8 patients only progressed in CNS metastases .EGFR C797S mutation was detected in 2 plasma sample, Met amplification in 1 tumor tissue, EGFR C719S mutation in 1 paired plasma-tumor tissue and PIK3CA in 2 plasma sample. Increasing abundance in TP53 and CDKN2A were detected in 2 paired plasma-tumor tissue. Adverse events of grade 3 or higher included one case (3.6%) of severe ulcerative colitis leading to Osimertinib discontinuation and two cases (7.1%) of bevacizumab discontinuation due to bleeding events. Conclusions: Osimertinib combined with Bevacizumab as a first-line treatment significantly prolonged CNS PFS in EGFR-mutant NSCLC patients with brain metastases, offering superior control over intracranial lesions compared to Osimertinib monotherapy (15.2 months, FLAURA study). This study underscores the potential of dynamic ctDNA monitoring in guiding effective treatment strategies for this patient population. Further research is warranted to explore the broader clinical implications of these findings.

A Polygenic Risk Analysis for Identifying Ulcerative Colitis Patients with European Ancestry.

The incidence of ulcerative colitis (UC) has increased globally. As a complex disease, the genetic predisposition for UC could be estimated by the polygenic risk score (PRS), which aggregates the effects of a large number of genetic variants in a single quantity and shows promise in identifying individuals at higher lifetime risk of UC. Here, based on a cohort of 2869 UC cases and 2900 controls with genotype array datasets, we used PRSice-2 to calculate PRS, and systematically analyzed factors that could affect the power of PRS, including GWAS summary statistics, population stratification, and impact of variants. After leveraging a stepwise condition analysis, we eventually established the best PRS model, achieving an AUC of 0.713. Meanwhile, samples in the top 20% of the PRS distribution had a risk of UC more than ten times higher than samples in the lowest 20% (OR = 10.435, 95% CI 8.571-12.703). Our analyses demonstrated that including population-enriched, more disease-associated SNPs and using GWAS summary statistics from similar ethnic background can improve the power of PRS. Strictly following the principle of focusing on one population in all aspects of generating PRS can be a cost-effective way to apply genotype-array-derived PRS to practical risk estimation.

Difficulties in diagnosis of non-conventional dysplasia in inflammatory bowel disease

Purpose: To provide a morphological characterization of dysplasia occurring against the background of inflammatory bowel disease (IBD), considering the new classification of dysplasia. Materials and methods. A retrospective analysis was conducted, and biopsies were reviewed from 257 patients with IBD treated at Sechenov University clinics from 2018 to 2023. Patients' ages ranged from 19 to 63 years. Diagnosis was based on a combination of clinical, laboratory, and instrumental methods. Multiple biopsies were taken during colonoscopy, processed using standard metods. Results. Non-traditional dysplasia was diagnosed in 5 patients, accounting for 1.95% of cases over a 6-year period. Two cases involved hypermucinous dysplasia in patients aged 35 and 43 with ulcerative colitis, with disease durations of 12 and 9 years, respectively. crypt cell atypia/dysplasia was diagnosed in two patients aged 40 and 30, with ulcerative colitis durations of 5 and 10 years, respectively. In a 51- year-old patient with Crohn's disease for over 15 years, dysplasia resembling a dentate lesion was found in the ascending intestine. Dysplasia diagnosis was confirmed using immunohistochemical (IHC) staining with TP53 antibodies (clone DO-7 Leica RTU, Germany), showing positive staining of tumor cell nuclei, indicating TP53 gene mutation. Two out of five cases exhibited total colon involvement in inflammatory process, and one ulcerative colitis case was combined with primary sclerosing cholangitis. Conclusion. Before the appearance of the latest classifications of dysplasia in IBD, we rarely diagnosed dysplasia in biopsies from IBD patients. We now understand that the spectrum of potential neoplastic precursor lesions of colorectal cancer in IBD patients is much wider and this understanding can ensure that clinically important but rare lesions will not be undiagnosed. Future studies of their natural course may eventually determine that some lesions are more clinically important than others.

The relationship between weight change and inflammatory bowel disease. A population-based cohort study, the HUNT study

Background The incidence of inflammatory bowel disease (IBD) is increasing. The prevalence of overweight and obesity is increasing in parallel with IBD and could contribute to IBD development. The aim of this study was to assess the relationship between weight change and the risk for IBD. Methods Data gathered from 55,896 adult participants in the three first population-based Trøndelag Health Studies (HUNT1-3), Norway, performed in 1984–2008 was used. The exposure was change in body mass index between two HUNT studies. The outcome was a new IBD diagnosis recorded during a ten-year follow-up period after the exposure assessment. The risk of IBD by weight change was assessed by Cox regression analyses reporting hazard ratios (HRs) and 95% confidence intervals (CIs), adjusted for sex, age, and smoking status. Results There were 334 new cases of ulcerative colitis (UC) and 54 of Crohn’s disease (CD). Weight loss decreased the risk of a new UC diagnosis by 38% (adjusted HR 0.62, 95% CI 0.39–0.97) and seemed to double the risk of getting a new CD diagnosis (adjusted HR 2.01, 95% CI 0.91–4.46). Weight gain was not associated with a new diagnosis of neither UC (adjusted HR 1.00, 95% CI 0.78–1.26) nor CD (adjusted HR 1.08, 95% CI 0.56–2.08). Conclusion In this study, weight loss was associated with decreased risk of UC. However, no associations were seen between weight gain and the risk of UC or CD, suggesting that the increasing weight in the general population cannot explain the increasing incidence of IBD.

Bacterial dysbiosis in newly diagnosed treatment naïve pediatric ulcerative colitis in Saudi Arabia.

The role of microbiota in the pathogenesis of ulcerative colitis (UC) has been increasingly recognized. However, most of the reports are from Western populations. In Middle Eastern countries, including Saudi Arabia, little is known about the role of microbiota. Therefore, our aim was to describe the bacterial microbiota profile and signature in pediatric UC in Saudi Arabia. Twenty children with UC and 20 healthy controls enrolled in the study gave stool samples. Twenty rectal mucosal samples were taken from UC and 20 from non-UC controls. Inclusion criteria included newly diagnosed and untreated children and lack of antibiotic exposure for at least 6 months before stool collection was required for children with UC and controls. Bacterial deoxyribonucleic acid was extracted and sequenced using shotgun metagenomic analysis. Statistical analysis included Shannon alpha diversity metrics, Bray-Curtis dissimilarity, DESeq2, and biomarker discovery. The demographic characteristics were similar in children with UC and controls. There was a significant reduction in alpha diversity (P = 0.037) and beta diversity in samples from children with UC (P = 0.001). Many taxa were identified with log2 abundance analysis, revealing 110 and 102 species significantly depleted and enriched in UC, respectively. Eleven bacterial species' signatures were identified. In Saudi Arabian children with UC, we demonstrate a dysbiosis similar to reports from Western populations, possibly related to changes of lifestyle. Microbial signature discovery in this report is an important contribution to research, leading to the development of adjunctive non-invasive diagnostic options in unusual cases of UC.

The GIPP Never Lies: A Case of Refractory Ulcerative Colitis

The GIPP Never Lies: A Case of Refractory Ulcerative Colitis

Combination of granulocyte–monocyte apheresis and ustekinumab: Multicentre and retrospective study

ObjectiveGranulocyte–monocyte apheresis (GMA) has shown to be safe and effective in ulcerative colitis (UC), also in combination with biologics, mainly with anti-TNF. The aim of this study was to evaluate the efficacy and safety of combining GMA after primary non-response (PNR) or loss of response (LOR) to ustekinumab (UST) in patients with UC. Patients and methodsA retrospective study was performed in 12 IBD Units, including all patients with refractory UC or unclassified IBD (IBD-U) who received combined GMA plus UST. The number and frequency of GMA sessions, filtered blood volume and time of each session were registered. Efficacy was assessed 1 and 6 months after finishing GMA by partial Mayo score, C-reactive protein (CRP) and fecal calprotectin (FC). Descriptive statistics and non-parametric tests were used in the statistical analysis. ResultsSeventeen patients were included (15 UC, 2 IBD-U; median age 47 years [IQR, 35–61]; 59% male; 53% E3). Most patients (89%) had prior exposure to anti-TNF agents and 53% to vedolizumab; 65% were also receiving steroids at baseline. Median partial Mayo score at baseline was 6 (IQR, 5–7) and it significantly decreased after 1 and 6 months (p=0.042 and 0.007, respectively). Baseline FC significantly decreased after 6 months (p=0.028) while no differences were found in CRP. During follow-up, 18% patients started a new biologic therapy and 12% required surgery; 64% of patients under steroids were able to discontinue them. Adverse events were reported in one patient. ConclusionGMA can recapture the response to UST in selected cases of UC after PNR or LOR to this drug.

Celiac Disease and Inflammatory Bowel Disease Are Associated With Increased Risk of Eating Disorders: An Ontario Health Administrative Database Study.

Previous national registry studies have reported an increased risk of eating disorders in immune-mediated conditions (inflammatory bowel disease and celiac disease). Our objective was to examine the association between immune-mediated gastrointestinal (GI) diseases and incident eating disorders in Ontario. This was a retrospective matched cohort study of individuals <50 years of age with a diagnosis of an immune-mediated GI disease between 2002 and 2020 ("cases"). Those with a pre-existing eating disorder were excluded. Cases (n = 83,920) were matched with controls (n = 167,776) based on birth year, sex, and region of residence. Incidence rate ratio and hazard ratio were estimated using Poisson regression model and adjusted Cox proportional models, respectively. Over the follow-up period (up to January 31, 2022), 161 cases and 160 controls were identified with eating disorders. The overall incidence rate ratio (95% confidence interval, P -value) of eating disorders in immune-mediated GI disease was 1.99 (1.6-2.5, P < 0.001). The adjusted hazard ratio for eating disorder in cases with immune-mediated GI diseases was 1.98 (1.6-2.5, P < 0.001). In the pediatric group of incident cases (≤18 years of age), overall adjusted hazard ratio was 2.62 (1.9-3.7, P < 0.001) compared with 1.56 (1.02-2.4, P = 0.041) for adults (>18 years of age). The largest hazard ratio of 4.11 (1.6-10.3, P = 0.003) was observed for pediatric incident cases of ulcerative colitis. Inflammatory bowel disease and celiac disease are associated with the development of eating disorders. The magnitude of the association was stronger in the pediatric age group, underscoring the need for early screening and detection.

Clinical characteristics and north-south differences of inflammatory bowel disease in China: A cross-sectional study and meta-analysis

Abstract Objective This study aimed to estimate the incidence rate and clinical characteristics of inflammatory bowel disease (IBD) in the Chinese population, specially comparing the North and South regions. Methods We designed a questionnaire survey for patients diagnosed with IBD and conducted a systematic literature search in PubMed, China National Knowledge Internet, and Wanfang digital database, covering studies published between 2012 and 2022. Meta-analysis was performed to determine the overall incidence rate and prevalence of clinical manifestations of Crohn’s disease (CD) and ulcerative colitis (UC) in mainland China. Clinical phenotypes and demographic characteristics were calculated with 95% confidence intervals (CI). A comparison between the northern and southern regions was also conducted. Results The questionnaire survey included 440 patients, and 64 publications were included for Meta-analysis. The overall incidence rates of IBD, CD, and UC were 1.36 (95% CI: 0.79-2.33) per 100,000 person-years, 0.23 (95% CI: 0.09-0.58) per 100,000 person-years, and 1.12 (95% CI: 0.69-1.80) per 100,000 person-years, respectively. The incidence rates of IBD, CD, and UC were all higher in southern China compared to the North. Clinical characteristics of 440 IBD patients from the questionnaire and 2,821 CD patients and 12,809 UC patients from the literature were analyzed. There were more male patients compared to female patients. CD cases in the North exhibited earlier disease diagnosis (P &lt; 0.01), more upper gastrointestinal lesions (P &lt; 0.01), and higher hospitalizations rates (P &lt; 0.01) compared to the South. UC cases in the North had higher severity (P &lt; 0.01), anemia rates (P &lt; 0.01), and weight loss (P &lt; 0.01) compared to the South. Conclusions The incidence rates of IBD, CD, and UC were higher in southern China than in the North. Northern patients exhibited more severe symptoms compared to their southern counterparts.