Colonic Ulceration Research Articles

Glasgow coma scale score and albumin level are associated with patient survival after emergent colonoscopy in the intensive care unit

AbstractDue to poor patient condition and the high risk associated with the procedure, colonoscopy is rarely performed in the intensive care unit (ICU). It is indicated for ICU patients with suspected ischemic colitis, decompression of colonic distension, or lower gastrointestinal hemorrhage. ICU patients usually have more co‐morbidities and higher mortality rates than other inpatient patients. Data in the literature regarding the outcomes of ICU patients after colonoscopy are limited. The aim of this study was to identify factors that are predictive of outcomes following colonoscopy in ICU patients. We retrospectively analyzed the medical records and imaging findings of patients who underwent colonoscopy in an ICU setting between January 2018 and June 2020. A total of 79 patients were identified and enrolled for analysis. The median age of the patients was 78 years. The colonoscopy findings included angiodysplasia (n = 3, 3.8%), colitis (n = 17, 21.5%), colonic ulcer (n = 2, 2.5%), diverticulosis (n = 3, 3.8%), hemorrhoid (n = 10, 12.7%), rectal ulcer (n = 16, 20.3%), tumor (n = 10, 12.7%), volvulus (n = 1, 1.3%), bleeding of unknown origin (n = 4, 5.1%), and no diagnosis (n = 13, 16.5%). A total of 46 patients (58%) survived to discharge. Patients who survived had statistically significantly higher Glasgow coma scale (GCS) scores (P = .009) and albumin levels (P = .002) than patients who did not survive. Patient survival is associated with GCS score and albumin level, but not with colonoscopy findings.

THE EFFECT OF SALVIA FRUTICOSA WATER EXTRACT IN ACETIC-ACID-INDUCED COLITIS IN MICE

Inflammatory bowel disease (IBD) including Ulcerative colitis (UC) and Crohn’s disease, is a chronic condition of the intestine characterized by an uncontrolled inflammatory response. Current biologic treatments developed to treat IBD are expensive and associated with significant side effects; thus, alternative approaches are required. Recently, herbal concoctions have emerged as promising intervention. This study investigates the protective effects of Salvia fruticosa (SF) against acetic acid-induced colitis in mice, a model of human inflammatory bowel disease (IBD). Mice were divided into four groups (n=3). IBD was induced with acetic acid (6%). SF was administered by gavage at 1.5ug/kg mimicking folk medicine. SF treatment was given for 2, 4 & 6 days. After treatment, colons were collected for colonic biochemical markers, and histopathological evaluation. SF treatment induced enhancement in the colon’s structure and decreased ulcerations and inflammation. It significantly decreased pro-inflammatory cytokines TNF-α, IL-17 by 2.1-fold and 0.9-fold respectively at day2 and 6 and IL-6 by 2.8-fold at day 2 & 1.7-fold at day 6. Also, pro-inflammatory cytokine INF-γ showed a significant 22-fold decrease at day2 in SF-treated colitic group. Moreover, Myeloperoxidase (MPO) and Malondialdehyde (MDA) levels decreased showing the anti-oxidant property of the extract. Anti-oxidant Glutathione (GSH) level and anti-inflammatory cytokine IL-10, remained at normal levels while an increase by 0.9-fold at day 2 and 0.5-fold at day 6 in anti-inflammatory cytokine TGF-β in healthy SF-treated groups was significant. Hence, Salvia fruticosa exerts an anti-inflammatory and anti-oxidant effects against IBD as well as it help healing colon ulcers and maintain its architecture.

Mucus-Penetrating Alginate-Chitosan Nanoparticles Loaded with Berberine Hydrochloride for Oral Delivery to the Inflammation Site of Ulcerative Colitis.

The rectal enemas of berberine hydrochloride (BH) have emerged as one of the most effective strategies in the clinical treatment of ulcerative colitis (UC). However, oral dosages of BH exhibit a poor anti-inflammatory effect of UC, which may attribute to premature absorption of BH by the upper gastrointestinal tract. Moreover, the thick colonic mucus layer obstructs the penetration of the drug, resulting in low bioavailability to the inflammatory site of the colon. The aim of this study was to develop the mucus-penetrating sodium alginate-chitosan nanoparticles (SA-CS NPs) for oral delivery of BH to the site of colonic ulcer lesions. BH-loaded SA-CS NPs were developed through the ionic gelation method and analyzed for physicochemical characteristics, release performance, penetrability, site retention, and therapeutic efficacy. The results showed that the NPs have a particle size of 257 nm with a negative charge, presenting desired pH-dependent release behavior. The permeation studies elucidated that negatively charged SA-CS NPs had 2.9 times higher mucus penetration ability than positively charged CS NPs. An ex vivo retention study indicated the high retention of BH-SA-CS NPs at the colon site for more than 16 h. In vivo therapeutic effectiveness demonstrated that the prepared NPs could not only alleviate colonic injury by decreasing the disease activity index and colon mucosa damage index, but also improve the immunologic function by decreasing the spleen index. In conclusion, the BH-SA-CS NPs could enhance the mucus permeability and deliver drugs to the colonic inflammation site, providing new insights into improving the therapeutic effect of UC.

Symptoms compatible with Rome IV functional bowel disorder in patients with ankylosing spondylitis.

To determine the frequency of symptoms meeting Rome IV functional bowel disorder (FBD) in patients with ankylosing spondylitis (AS), investigate factors associated with FBD symptoms, and assess whether having FBD symptoms might influence AS disease activity. In this cross-sectional study, we enrolled 153 AS patients without known colonic ulcers and 56 sex- and age-matched controls to evaluate FBD (or its subtypes) symptoms. Disease characteristics were also evaluated in the AS group. Sixty (39.2%) of 153 AS patients had FBD symptoms, which were more prevalent than controls (23.2%). Besides, symptoms compatible with irritable bowel syndrome (IBS) and chronic diarrhoea were detected in 18 and 43 AS patients, respectively. For the AS group, multivariable logistic regression analyses showed that symptoms of FBD, IBS, and chronic diarrhoea were negatively associated with using non-steroidal anti-inflammatory drugs and positively associated with comorbid fibromyalgia, respectively. In exploration about the effects of FBD (or its subtypes) symptoms on AS disease activity by multivariable linear regression analyses, FBD symptoms and chronic diarrhoea had universal positive associations with assessments of AS disease characteristics, respectively. Patients with AS had frequent symptoms compatible with FBD, IBS, and chronic diarrhoea, proportions of which were lower in those with non-steroidal anti-inflammatory drug use. The improvement of FBD symptoms and chronic diarrhoea might be conducive to the disease status of AS patients.

Recurrent Abdominal Distension: Colonic Ulcer is a Cause or a Consequence?

Question: A 48-year-old woman presented with a 5-month history of recurrent abdominal distension and constipation. She had a history of pulmonary tuberculosis in childhood and breast cancer treated with surgery and chemotherapy (adriamycin/cyclophosphamide [AC] regimen) 1 year ago followed by long-term endocrine therapy with toremifene. Additionally, she took 3 months of Chinese herbs including high-dose aconite postoperatively. Physical examination revealed the distended abdomen with diffuse tenderness. Laboratory investigations indicated anemia and hypoalbuminemia. Indicators of inflammation were normal. Plain abdominal radiographs and computed tomography showed massive dilation of the small intestine and colon, and thickening of the wall of the transverse and descending colon (Figure A). Subsequently, colonoscopy was performed and revealed 2 large irregular ulcers in the transverse and descending colon (Figure B). Biopsies of lesions showed nonspecific inflammation. Based on the history of pulmonary tuberculosis, she was empirically started on antituberculosis therapy. Five months later, unfortunately, her abdominal distension was worsening (Figure C). Transverse colostomy was subsequently performed to alleviate the symptoms. Furthermore, a repeated colonoscopy showed no improvement of the ulcer lesions after a standard course of antituberculosis treatment (1 year). Thereafter, the patient received a 3-month therapy of prednisone and thalidomide. None of these therapies seemed to improve the patient’s intestinal symptoms and ulcer lesions, nor did they halt progression. What is the diagnosis? What shall we do? See the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI. Finally, segmental colon resection was performed and the pathology showed thickening of muscularis mucosae, muscularis propria atrophy and fibrosis, aberrant muscularization in serosa (Figure D), and reduction of ganglion cells accompanied by inflammatory cells infiltration, consistent with obstructive enteritidis. Additionally, histopathology demonstrated some bluish-purple crystallin-like substances engulfed by multinucleated giant cells (Figure E). Based on these findings, the patient was diagnosed with chronic intestinal pseudo-obstruction (CIPO), which may be secondary to drug-induced gut injury. Unfortunately, 1 month later, her abdominal distension recurred. Subsequently, radiopaque marker test for colonic transit was performed and revealed impaired motility of the entire colon (24 of 24 radiopaque markers diffusely distributed throughout the colon after 72 hours; Figure F). Pseudo-obstruction is characterized by signs and symptoms of a mechanical obstruction of the small or large bowel in the absence of an anatomic lesion.1De Giorgio R. Sarnelli G. Corinaldesi R. et al.Advances in our understanding of the pathology of chronic intestinal pseudo-obstruction.Gut. 2004; 53: 1549-1552Crossref PubMed Scopus (196) Google Scholar Because the symptoms of CIPO are nonspecific, it is a challenge to make precise diagnosis, especially for patients with colonic ulcers as in our case, and it may be misdiagnosed with intestinal tuberculosis and Crohn’s disease, which might be mistaken for the cause of the intestinal symptoms. Many patients undergo futile and potentially harmful surgical procedures2De Giorgio Roberto Cogliandro Rosanna F. Barbara Giovanni et al.Chronic intestinal pseudo-obstruction: clinical features, diagnosis, and therapy.Gastroenterol Clin North Am. 2011; 40: 787-807Abstract Full Text Full Text PDF PubMed Scopus (101) Google Scholar as in our case. In fact, in our patient, CIPO, which may be secondary to drug-induced gut injury, is the cause of the colonic ulcers and intestinal symptoms. Unfortunately, the patient may need total colectomy to alleviate the symptoms.

Sevelamer Induced Colitis Causing Deep Cratered Ulcer in an End-Stage Renal Disease Patient

Sevelamer is phosphate lowering oral agent used in chronic kidney disease (CKD) to decrease oral phosphate absorption. Sevelamer has been shown to cause crystalline induced colitis. This can manifest as abdominal pain or gastrointestinal bleeding. We present a case with chronic kidney disease and Moyamoya syndrome that presented with abdominal pain and anemia. Colonoscopy revealed a single circumferential cratered ulcer in the transverse colon. Pathology showed crystalline induced colitis. Sevelamer was discontinued and the patient`s symptoms improved.

Short-Term High-Fat Diet Fuels Colitis Progression in Mice Associated With Changes in Blood Metabolome and Intestinal Gene Expression.

Clinical cases and animal experiments show that high-fat (HF) diet is involved in inflammatory bowel disease (IBD), but the specific mechanism is not fully clear. A close association between long-term HF-induced obesity and IBD has been well-documented. However, there has been limited evaluation of the impact of short-term HF feeding on the risk of intestinal inflammation, particularly on the risk of disrupted metabolic homeostasis. In this study, we analyzed the metabolic profile and tested the vulnerability of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis after short-term HF feeding in mice. The results showed that compared with the control diet (CD), the fatty acid (FA), amino acid (AA), and bile acid (BA) metabolisms of mice in the HF group were significantly changed. HF-fed mice showed an increase in the content of saturated and unsaturated FAs and a decrease in the content of tryptophan (Trp). Furthermore, the disturbed spatial distribution of taurocholic acid (TCA) in the ileum and colon was identified in the HF group using matrix-assisted laser desorption/ionization-mass spectrometry imaging (MALDI-MSI). After HF priming, mice on TNBS induction were subjected to more severe colonic ulceration and histological damage compared with their CD counterparts. In addition, TNBS enema induced higher gene expressions of mucosal pro-inflammatory cytokines under HF priming conditions. Overall, our results show that HF may promote colitis by disturbing lipid, AA, and BA metabolic homeostasis and inflammatory gene expressions.

Mechanism of Fructus Mume Pills Underlying Their Protective Effects in Rats with Acetic Acid-Inducedulcerative Colitis via the Regulation of Inflammatory Cytokines and the VEGF-PI3K/Akt-eNOS Signaling Pathway.

Background Fructus mume pills (FMPs) have been clinically proven to be effective for treating ulcerative colitis (UC). However, the therapeutic and protective mechanisms have not been fully studied. Aim We aimed to explore the mechanism of FMPs in an acetic acid (AA)-induced ulcerative colitis rat model. Methods The targets, GO terms, and KEGG pathways for the FMPs and UC were screened and constructed using network pharmacology. A possible mechanism was verified in a 4% AA-induced colitis rat model. Colitis activity and state were evaluated using the disease activity index, and colon ulceration and intestinal mucosal damage were determined by histopathological observation through HE, AB-PAS, and Masson pathological staining. The concentrations of TNF-α, IL-6, IL-8, IL-10, MPO, MMP9, CXCR1, eNOS, and VEGF were measured to evaluate vascular permeability effects. Results The network pharmacology results showed 108 active compounds, and 139 FMP-related targets were identified. Twenty-nine targets were identified for FMPs against UC, which included MMP9, MMP3, ESR1, PTGS1, PPARA, MPO, and NOS2. A total of 1,536 GO terms and 41 pathways were associated with FMP treatment of UC. The pharmacological evaluation showed that FMPs attenuated inflammation in AA-induced colitis by reducing the serum concentrations of TNF-α, IL-6, IL-8, and IL-10 and the colonic concentrations of MPO, MMP9, and CXCR1. FMPs ameliorated hyperpermeability by reducing the colonic VEGF and eNOS concentrations. FMPs also significantly decreased the VEGFA, VEGFR2, Src, and eNOS protein expressions in colon tissue through the VEGF-PI3K/Akt-eNOS signaling pathway. Conclusion These results suggest that FMPs control UC inflammation by regulating inflammatory cytokine concentrations. FMPs alleviate AA-induced UC by regulating microvascular permeability through the VEGF-PI3K/Akt-eNOS signaling pathway.

Niche‐specific transcriptional reprogramming leads to pro‐angiogenic neutrophil specialization in colon cancer

Robust neutrophil (PMN) tissue accumulation is an important clinical feature in active Ulcerative Colitis (UC) lesions and in colorectal cancer (CRC). Using murine colitis‐associated CRC model, we observed prominent and persistent PMN accumulation as the inflamed colon tissue progressed from colonic ulceration to CRC. Given the emerging evidence of PMN phenotypic and functional heterogeneity in homeostatic and pathologic conditions, we analyzed the transcriptomic landscape of these immune cells in blood and tissue during the transition from inflammatory ulceration to CRC. Principal component analysis effectively stratified neutrophils across different conditions into three discrete clusters that marked distinct spatial compartments of peripheral blood, inflamed colon tissue and the CRC tumor niche. Importantly, combinatory analyses of pathway overrepresentation, protein‐network mapping, and gene‐ontology scoring revealed a robust enrichment of biological pathways involved in vasculature development and angiogenesis uniquely in PMNs associated with the advanced CRC niche. These findings were validated in vivo as we found that temporary PMN depletion profoundly reduced tumor vascularity, vessel branching, and penetration depth of the tumor vessels. Moreover, we identified Spp1 (OPN) and Mmp14(MT1‐MMP) to be highly induced transcriptionally in PMNs as they left the circulation and entered the tumor niche, where Spp1 and Mmp14 directly promoted tumor angiogenesis. TCGA data mining and validation in UC/CRC patient cohorts further confirmed significant upregulation of Spp1 and Mmp14in high‐grade CRC, but not in UC patients. In conclusion, the current study identified a niche‐specific compartmentalization of PMN transcriptional programing, highlighting the novel PMN plasticity. Our findings further established the contribution of CRC‐associated PMNs via Spp1/Mmp14 activity to the formation of a complex tumor vasculature and subsequent neoplastic progression from inflammatory colitis to advanced CRC.

Colonic cryptococcosis presenting with chronic diarrhea in a person with advanced human immunodeficiency virus disease: a case report

Cryptococcus neoformans infection usually occurs in patients with advanced human immunodeficiency virus (HIV) infection or with a CD4 T lymphocyte count of <100 cells/μL. Pulmonary and central nervous system infections are the most frequently encountered forms of cryptococcosis; however, colonic cryptococcosis is uncommon. We describe the case of a 41-year-old antiretroviral-naïve man with HIV infection diagnosed eight years prior and intermittent diarrhea for 4 months who presented to the emergency department with a 1-day history of low-grade fever and confusion. Brain magnetic resonance imaging and cerebrospinal fluid analysis revealed normal results; however, he was diagnosed with Pneumocystis jirovecii pneumonia based on chest computed tomography and bronchoalveolar lavage analysis. Trimethoprim-sulfamethoxazole administration was initiated followed by antiretroviral treatment. Although his condition gradually improved, he developed fever and abdominal discomfort, and the diarrhea worsened. Endoscopy revealed a small ulcer in the distal transverse colon. Histopathological examination of a colon tissue sample revealed cryptococcal infection. He improved substantially during liposomal amphotericin B and fluconazole treatment. We encountered a rare case of colonic cryptococcosis that caused chronic diarrhea in a patient with advanced HIV infection. Colonic cryptococcosis should be considered when patients with acquired immune deficiency syndrome present with gastrointestinal symptoms.

Utility of colonoscopy in detection of early lower gastrointestinal bleeding at a tertiary care hospital.

Objective: To determine the prevalence of the common causes of lower gastrointestinal bleeding by Colonoscopy as a diagnostic modality in patients with gastrointestinal bleeding. Study Design: Cross Sectional Descriptive study. Setting: Department of Gastroenterology, Liaquat University of Medical and Health Sciences, Jamshoro. Period: March 2021 to August 2021. Material & Methods: This study was performed in Liaquat University of Medical and Health Sciences, Jamshoro in patients presenting with lower gastrointestinal bleeding. History, examination and investigations were carried out. After stabilizing the patient lower gastrointestinal endoscopy was performed. Results: Total 139 patients were included in this study. Intermittent bleeding per rectum was the main presenting complaint followed by continuous bleeding per rectum. The average age of the patients was 45.61 ±16.40 years. Out of 139 patients, 94(67.6%) males and 45(32.4%) females. Bleeding related to internal hemorrhoids was present in 40(28.8 %) patients 30(21.6%) male and 10(7.2%) females as the most common cause of lower GI bleed followed by rectal ulcers 14(10.1%) and polyps in 9(6.5%) patients. infective colitis, proctitis and colonic ulcers were noted in 8(5.8%), 6(4.3%) and 5(3.6%) patients respectively. Malignant lesions in colon and rectum were noted in 8(5.8%) and 3(2.2%) patients while ulcerative colitis, crhon’s and diverticular disease were noted in 5(3.6%), 1(1.4%), 2(0.7%) patients respectively. 29(%) had normal clonoscopic examination. Conclusion: In our population hemorrhoid bleed is the leading cause of lower gastrointestinal bleeding followed by bleeding due to rectal ulcer and polyps.

Dual-targeted colon-based integrated micelle drug delivery system for treatment of ulcerative colitis

Emodin (EMO) is an active ingredient of Chinese traditional medicine with the potential to reportedly treat ulcerative colitis (UC). However, the solubility of EMO in water is poor coupled with low oral bioavailability, whilst existing conventional oral preparations of the drug lack targeting ability. Thus, this work sought to design and fabricate a mannose modified colon targeted micelle drug delivery system comprising quantum dots (QDs) and EMO to obtain Eu-CS-Man-Ps-P(HEMA-DMAM)/EMO-QDs, which exhibited stable physicochemical properties, smaller average sized droplets (226.22 ± 1.83 nm), better polydispersity (PDI = 0.060 ± 0.005), negative ζ-potential (−19.19 ± 0.89 mV) and high efficiency of encapsulation (95.14 ± 0.23%). We observed Eu-CS-Man-Ps-P(HEMA-DMAM)/EMO-QDs to be an effective approach for the improvement of EMO solubility in an aqueous medium with an increased oral bioavailability (3.23 times higher than native drug) of the drug. Besides, the micelle could increase the retention and release of EMO in colonic ulcers through multi-stage targeting, improve oral bioavailability, regulate the expression of inflammatory factors and repair damaged tissues, which helped us to achieve the design goal of integrated diagnosis and treatment of UC. Conclusively, the therapeutic effect of EMO was enhanced through an integrated micelle, which exhibited good prospects in improving solubility and oral biological availability.

Clinical Spectrum of Monogenic Infantile-Onset Inflammatory Bowel Disease.

Very-early-onset IBD and infantile-onset IBD is extremely rare in children. There is paucity of data with regards to clinical profile and outcome of children with infantile-onset IBD from India. The clinicolaboratory profile, molecular genetic testing and treatment details of 8 children diagnosed with monogenic infantile-onset IBD during 2015-2020 is described here. The median age at onset of symptoms was 3 mo. Sibling death and consanguinity were noted in 4 (50%) each respectively. Diarrhea was the presentation in all (100%) and hematochezia in 5 (62%). Colonic ulcers on colonosopy was seen in 7 infants. The common mutation identified was IL-10R gene in 3 (42%) and LRBA gene mutation in 2 (25%). HSCT was done in 4 children and the rest were managed conservatively. Although there was no mortality in this series, two children (25%) were lost for follow-up.

Pectic polysaccharides ameliorate the pathology of ulcerative colitis in mice by reducing pyroptosis.

BackgroundUlcerative colitis (UC) is an inflammatory bowel disease which seriously affects the quality of life of patients. There has been an increasing amount of research related to the therapeutic effects and mechanisms of natural plant substances in the treatment of recurrent UC. Rauwolfia verticillata var. Hainanensis is a medicinal plant that is native to Hainan Island, China. Some studies have documented that pectic polysaccharides (PPs) from Rauvolfia inhibited the progression of colon ulcers. However, their mechanisms of action have not been established. Studies have revealed that suppressing pyroptosis can attenuate the damage of experimental colitis. However, it is unclear whether PPs from Rauvolfia verticillata inhibit inflammation through pyroptosis. This study investigated the effects and potential mechanisms of PPs extracted from Rauvolfia verticillata on experimental UC in mice.MethodsMale C57 mice (6–8 weeks old) were allocated into the control group, the dextran sulfate sodium (DSS)-induced UC model group (DSS group), or the DSS with pectic polysaccharides treatment group (DSS + PP group). The body weights, rectal bleeding, and stool consistencies in the mice were observed, and the disease activity index (DAI) score was calculated. Colon tissues were collected for pathological analysis by histological hematoxylin and eosin (H&E) staining. The levels of caspase-1 and interleukin (IL)-1β were detected by immunohistochemistry. Pyroptosis was assessed by transmission electron microscopy.ResultsUC in mice induced by DSS resulted in decreased general physical activity and body weight, increased DAI score, significant histological changes, inhibited caspase-1 and IL-1β expression, and promoted pyroptosis. These DSS-induced changes could be partially ameliorated by administration of PP.ConclusionsPPs exerted an ameliorative effect on DSS-induced UC in mice by reducing pyroptosis.

A196 DIARRHEA AS A PRESENTING SYMPTOM OF RELAPSED GRANULOMATOSIS WITH POLYANGIITIS

Abstract Background Granulomatosis with polyangiitis (GPA) is a rare, small-to-medium sized-vessel vasculitis that typically involves the sinus, respiratory, and renal systems. The gastrointestinal (GI) tract is rarely involved, but its exact frequency is poorly characterized. GI symptoms have been reported to occur in up to 10% of acute presentations, and a historic series of 56 autopsies of GPA patients found 24% to have focal necrotizing arteriolitis of the intestine (Storesund, 1998). There are few case reports of colitis associated with GPA. They commonly describe abdominal pain, rectal bleeding, and less frequently, perforation, early in the disease course in conjunction with other classic systems involvement which aid in the diagnosis of GPA. Aims We present the case of a 77 year-old woman with lung biopsy-proven cANCA-positive GPA who was found to have colonic vasculitis after she had been in remission for several years. Methods Case report and literature review Results The patient presented with a 1-month history of progressive back pain, followed by 1 week of severe abdominal pain and watery diarrhea. She was afebrile, with a leukocyte count of 13.8x109/L, C-reactive protein of 213 mg/L, and fecal calprotectin of 669mg/kg. cANCA was strongly positive at 5.4 AI. Computed tomography scan revealed focal inflammatory change at the cecum and terminal ileum. Stool cultures were negative. Colonoscopy showed a polypoid, inflammatory-appearing hard mass at the ileocecal valve with surrounding fragile mucosa. Ileocecal valve biopsies described fibropurulent material and granulation tissue consistent with ulcer bed with surrounding mucosa showing chronic ischemic colitis with various degrees of acute cryptitis. The most likely etiology was speculated by the pathologist to be involvement of the colon by vasculitis, as other etiologies appeared to be ruled out. The patient had mild kidney injury, but no additional lung findings, in contrast to her initial presentation of GPA. She was started on prednisone 50mg/day. Her back pain, abdominal pain, and diarrhea resolved within 1 week, and renal function improved. Currently, there is a plan to start Rituximab for chronic treatment. Conclusions Our case of GPA-associated colitis is unique for several reasons. First, most case reports describe rectal bleeding as the presenting symptom of GPA colitis, whereas our patient presented with non-hemorrhagic diarrhea. Second, where available, reports of colitis correlated endoscopically with colonic ulcerations, whereas our patient had an ileocecal mass. Third, most reports present colitis associated with a new diagnosis of GPA, whereas our patient presented with colitis as new GI system involvement with likely inflammatory back pain as the presenting feature of GPA relapse. While a rare feature, colitis secondary to GPA can be considered in the appropriate context. Funding Agencies None

A189 INFLAMMATORY BOWEL DISEASE IN PEDIATRIC PATIENTS POST RENAL TRANSPLANT:A CASE SERIES

BackgroundDiarrhea in renal transplant recipients may be due to infection, medication induced colitis and post-transplant lymphoproliferative disease. Uncommonly a subset of these children develop denovo inflammatory bowel disease (IBD), despite being already immunosuppressed. Paucity of literature in the pediatric population has been noted.AimsTo describe the clinical presentation, investigations and response to treatment in a cohort of children diagnosed with IBD post renal transplantMethodsPatients diagnosed with IBD post renal transplant between January 1 - October 1, 2021 at BC Children’s Hospital were identified. Medical history, symptoms at presentation, histological characteristics, results of investigations and response to treatment were reviewedResultsData of 3 children were collected. Ages of the children were 11, 16 and 17 years (2 female). All patients had bloody diarrhea, abdominal pain and weight loss for 1 to 2 months. IBD diagnosis was made 8, 7 and 4 years respectively post renal transplant. All children were on maintenance immunosuppression with prednisone, MMF and tacrolimus. Bacterial, viral and parasitic causes were ruled out by relevant studies. All patients had negative anti-tissue transglutaminase.Patient 1 (transplanted for renal dysplasia) was diagnosed with Crohn disease involving the antrum, ileum, and colon with rectal sparing. Fecal calprotectin (FC) was 1742 ug/g, CRP elevated at 56mg/L. Histology showed focally active chronic gastritis and changes in ileum with cryptitis and crypt dropout. The colon had features of moderate chronic active colitis with focal severe ulceration in the rectum. The patient achieved clinical remission on treatment with methylprednisolone, then started on vedolizumab in context of rising BK virus titre.Patient 2 (transplanted for focal segmental glomerulosclerosis) was diagnosed with indeterminate colitis involving the IC valve and scattered colonic ulcers. FC was 674 ug/g and CRP and ESR were normal. Histology showed normal ileum, moderate active chronic changes in colon and rectal sparing. Clinical remission was achieved with oral mesalamine.Patient 3 (transplanted for Bardet-Biedl syndrome) was diagnosed with indeterminate colitis with a colonoscopy that showed patchy colonic erythema and normal ileum. FC was 966 ug/g, and CRP and ESR were normal. Histology showed patchy chronic active colitis and mild active ileitis. Clinical remission was achieved with oral and rectal mesalamine.ConclusionsDenovo IBD occurs in children post renal transplant and must be considered in the differential for ongoing diarrhea in these patients. It can be a challenge to distinguish between IBD and other causes of diarrhea. The patients in this series entered clinical remission in a short period of time. Further exploration of the pathogenesis of IBD in these immunosuppressed patients would be valuableFunding AgenciesNone

Atezolizumab‐associated colitis mimic inflammatory bowel disease: A case report

AbstractImmune checkpoint inhibitors (ICIs) are monoclonal antibodies that target downregulators of the anticancer immune response. ICIs have revolutionized the treatment of various malignancies. However, many immune‐related adverse events have also been described, which mainly occurs when the immune system becomes less suppressed, and affects various organs, including the gastrointestinal tract. We report a case of atezolizumab‐associated colitis with clinical and endoscopic follow‐ups. The patient was a 72‐year‐old male diagnosed with advanced squamous cell lung cancer treated with atezolizumab and combination chemotherapy. Two months after atezolizumab therapy, bloody diarrhea and abdominal pain were reported. Initial colonoscopy revealed colonic ulcers with diffuse erythema and loss of vascularity. Histology demonstrated ulcerated mucosa with acute inflammation. Steroids were promptly indicated due to suspicion of immune‐related colitis caused by atezolizumab. Follow‐up sigmoidoscopy performed 6 weeks after initiating steroid therapy showed improvement of inflammation. Histological findings revealed eroded colonic mucosa with abortive crypts, lymphoplasma, and eosinophil cell infiltration, which mimicked inflammatory bowel disease (IBD). However, there was no colitis relapse after steroid discontinuation. The case demonstrated endoscopic and histological presentations of immune‐mediated colitis that mimicked IBD.

Langerhans cell histiocytosis of the colon: A case report

Langerhans cell histiocytosis (LCH) is a neoplastic proliferation of myeloid dendritic cells that can be confined to a single organ system (usually bone) or multisystemic. We present a rare case of LCH encountered as a solitary ulcer in the transverse colon of a 45-year-old woman. Histological examination revealed expansion of the submucosa by a mixed infiltrate, including sheets of histiocytoid ‘LCH’ cells and numerous eosinophils. The LCH cells had abundant pale cytoplasm, folded nuclear contours, open chromatin and inconspicuous nucleoli.

P156 A multicentric study on the development and application of a deep learning algorithm for automatic detection of ulcers and erosions in the novel PillCam™ Crohn’s capsule

Abstract Background Crohn’s disease has the potential to involve all segments of the gastrointestinal tract, requiring frequent and judicious clinical and endoscopic surveillance. Capsule endoscopy (CE) has revolutionized the management of these patients, playing a role in diagnosis, classification, and assessment of response to treatment. In 2017, PillCam™ Crohn’s Capsule (PCC) was introduced to provide a panenteric assessment to this panenteric disease. However, reviewing each PCC exam is time-consuming and prone to errors as it implies examining thousands of images while significant lesions may only be represented in a small number of frames. Recently, the development of artificial intelligence (AI) algorithms for automatic interpretation of endoscopic images has generated a large interest. The performance of these tools, particularly convolutional neural networks have shown potential to overcome some of the main drawbacks of CE. This multicentric study aims to assess the performance of a deep learning algorithm for the automatic detection of small intestinal and colonic ulcers and erosions in PCC images. Methods We included a total of 59 PCC exams from two centres (ManopH Gastroenterology Clinic and Centro Hospitalar Universitário de São João) performed between 2017 and 2021. A total of 78415 frames were extracted. This pool of images was constituted by 14124 images depicting ulcers and erosions and 64291 with normal enteric and colonic mucosa. For the automatic identification of these findings, this image pool was split into training and validation datasets in a patient-based manner. Therefore, images from the same patient were restricted to a single dataset. A CNN model with transfer learning was developed using tensorflow and keras tools. Results The neural architecture of our CNN was optimized for the detection of enteric and colonic ulcers and erosions. An example of the output provided by the CNN is shown in Figure 1. The deep learning model had a sensitivity of 86.7%, a specificity of 98.6%, a positive predictive value of 92.3% and a negative predictive value of 97.4%. The overall accuracy of our network was 96.6% (Figure 2). At a threshold value of 50%, our CNN had an area under the curve of 0.98 for the detection of ulcers and erosions (Figure 3). Conclusion In this multicentric study, our group has developed a CNN and assessed its performance in a patient-based design, which provides significant robustness to our results. Patient-split analyses are the first step towards real-life application of AI solutions which, allied to the high-performance results of our model, may significantly improve the diagnostic yield of this panendoscopic tool.

Anti-ulcerative effects of wogonin on ulcerative colitis induced by dextran sulfate sodium via Nrf2/TLR4/NF-κB signaling pathway in BALB/c mice.

Ulcerative colitis (UC) is an inflammatory disease on the deepest lining of the colon and rectum. Wogonin is an antitumor flavonoid, which possesses various therapeutic properties. Even if the anti-colitis effect of wogonin was documented earlier, but the wogonin effect on inflammation underlying mechanism is not fully elucidated. In this present study, we hypothesized to study the oxidative damage, anti-inflammatory, and molecular action of wogonin on dextran sulfate sodium (DSS)-induced UC mice model. In methods, mice were categorized into four groups: that is, normal control, DSS alone, DSS + wogonin (30 mg/kg/day), and DSS + sulfasalazine (50 mg/kg/day). We determined the biochemical markers, inflammatory cytokines, histopathology of colon tissue, and western blot analysis. DSS significantly reduced body weight, colon length, and increased inflammation in the colon. Wogonin treatment prevented colonic ulceration, neutrophil infiltration, oxidative stress, pro-inflammatory cytokines, and histological changes. Oxidative damage and inflammatory mediators' elevation were also dramatically diminished by wogonin. Wogonin activates apoptosis via inhibiting Bcl-2 and augmenting Bax, caspase-3, and -9 expressions. Wogonin downregulated the COX-2 and iNOS, thereby repressing NF-κB. Wogonin regulated the Nrf2 signaling pathway and decreased TLR-4/NF-κB triggering. Taken together our study exposed that wogonin has a promising anti-ulcerative agent and recommended for good anti-inflammatory drug in the colon.