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Potassium bromate (KBrO3) present in consumed ozonised water was recently documented to exacerbate experimental gastric ulcer. Information, however, is vague as regards its effects in the colon where water reabsorption occurs. In this study, we observed the possible effects of KBrO3 on oxidative stress and inflammatory biomarkers in sodium hydroxide (NaOH) – induced Crohn’s colitis (CC). Wistar rats (180–200 g) were divided into six groups (n = 10): (i) control; (ii) untreated CC (induced by 1.4% NaOH; intra-rectal administration); and (iii–vi) CC treated with vitamin E, KBrO3, vitamin E+KBrO3, and sulphazalazine, respectively, for 7 days. Body weight and stool score were monitored daily. By day 3 and 7, excised colon was evaluated for ulcer scores and biochemical and histological analysis. Blood samples collected on days 3 and 7 were assayed for haematological indices using standard methods. Data were subjected to analysis of variance (ANOVA) and p ≤ 0.05 considered significant. Platelet/lymphocyte ratio, colonic ulcer score, malondialdehyde, and mast cells were significantly decreased while colonic sulfhydryl, and Ca2+- and Na+/K+-ATPase activities were increased following KBrO3 treatment compared with untreated CC. These findings suggest that KBrO3 may mitigate against NaOH-induced CC via inhibiting mast cell population and oxidative and inflammatory content but stimulating colonic sulfhydryl and Ca2+- and Na+/K+-ATPase activities.

Background and Aims The Self-assembling Peptide Hydrogel [SAPH, PuraMatrix], a fully synthetic peptide solution designed to replace collagen, has recently been used to promote mucosal regeneration in iatrogenic ulcers following endoscopic submucosal dissection. Herein, we evaluated its utility in ulcer repair using a rat model of topical trinitrobenzene sulphonic acid [TNBS]-induced colonic injuries. Methods Colonic injuries were generated in 7-week-old rats by injecting an ethanol solution [35%, 0.2 mL] containing 0.15 M TNBS into the colonic lumen. At 2 and 4 days post-injury, the rats were subjected to endoscopy, and SAPH [or vehicle] was topically applied to the ulcerative lesion. Time-of-flight secondary ion mass spectrometry [TOF-SIMS] was used to detect SAPH. Colonic expression of cytokines and wound healing-related factors were assessed using real-time polymerase chain reaction or immunohistochemistry. Results SAPH treatment significantly reduced ulcer length [p = 0.0014] and area [p = 0.045], while decreasing colonic weight [p = 0.0375] and histological score [p = 0.0005] 7 days after injury. SAPH treatment also decreased colonic expression of interleukin [IL]-1α [p = 0.0233] and IL-6[p = 0.0343] and increased that of claudin-1 [p = 0.0486] and villin [p = 0.0183], and β-catenin staining [p = 0.0237]. TOF-SIMS revealed lesional retention of SAPH on day 7 post-injury. Furthermore, SAPH significantly promoted healing in in vivo mechanical intestinal wound models. Conclusions SAPH application effectively suppressed colonic injury, downregulated inflammatory cytokine expression, and upregulated wound healing-related factor expression in the rat model; thus, it may represent a promising therapeutic strategy for IBD-related colonic ulcers.

We report two cases of histoplasmosis in orthotopic liver transplant (OLT) recipients to illustrate the variable presentations, complications encountered during treatment, the spectrum of diagnostic modalities, and case outcomes. Case 1 describes the insidious presentation of presumed gastrointestinal histoplasmosis 12 years after OLT, which was defined by months of intermittent diarrhea and focal colonic disease on colonoscopy. A diagnosis of Histoplasma capsulatum was ultimately made by broad range PCR performed on colonic tissue. Due to the patient’s inability to tolerate itraconazole, treatment consisted of two weeks of liposomal amphotericin B with resolution of colonic ulcers on follow-up colonoscopy. Case 2 illustrates a case of severe pulmonary histoplasmosis with dissemination in an OLT recipient one year after transplantation. Treatment was complicated by the development of acute respiratory distress syndrome requiring mechanical ventilation and hemodynamic shock requiring extracorporeal membrane oxygenation therapy. A review of the literature on histoplasmosis in OLT recipients accompanies our cases and emphasizes the epidemiology, clinical manifestations, diagnosis, treatment, and prevention.

Background: Gisekia pharnaceoides Linn. (Aizoaceae), traditionally known as baluka saag or sareli is commonly found in the deep Cholistan region of Pakistan. It is used by native community for the mitigation of a range of diseases, including inflammatory disorders and gastric ulcers. Objective: This study is designed to evaluate the defensive impact of G. pharnaceoides in acetic acid-induced ulcerative colitis in mice and to discover the mechanism for anti-inflammatory action. Method: The ethanolic crude extract of G. pharnaceoides (Gp.Cr) was prepared and evaluated for phytochemical substances by preliminary screening and HPLC analysis. Anti-inflammatory activity of Gp.Cr (300 and 500 mg/kg) was examined by administration of 200 µl of 7.5% acetic acid intra-rectally to induce ulcerative colitis and colonic mucosal injury, while mucosal homeostasis was evaluated by disease activity index, colonic ulcer score and hematological parameters. Anti-inflammatory potential was quantified by assessing antioxidant enzymes (SOD, CAT, GPX-1), lipid peroxides, nitric oxide and cytokines (IL-1β, IL-6, TNF-α) immunoassays and further analyzed by histological analysis of colon tissues. Results: Phytochemical screening of Gp.Cr revealed the presence of alkaloids, phenols, flavonoids, steroids, tannins and saponins, while HPLC analysis confirmed the presence of quercetin, gallic acid, coumaric and sinapic acid. In acetic acid-induced ulcerative colitis model, Gp.Cr (300 and 500 mg/kg) along with sulphasalazine (500 mg/kg) decreased disease activity index, ulcer scores and hematological parameters. Gp.Cr showed a significant anti-inflammatory potential by increasing antioxidant enzymes and decreasing lipid peroxides, nitric oxide and cytokines levels. Histopathological examination showed significant decline in ulceration and tissue disruption. Conclusion: Hence, the findings confirmed the effectiveness of G. pharnaceoides crude extract in the treatment of ulcerative colitis and might be a promising remedy to manage inflammatory disorders.

Clinical characteristics of intestinal ulcers complicated with Epstein-Barr virus (EBV) infection remain poorly studied. This study is aimed at providing further insight into clinical features of this patient cohort. The presence of serum EBV DNA was assessed in 399 patients with colonic ulcers, of which 30 cases were positive. In EBV-positive patients, the EBV-encoded RNA (EBER) was detected in intestinal tissues of 13 patients (EBER-positive group). The test was negative in 17 patients (EBER-negative group). Acute EBV infection rate in patients with colonic ulcer was 7.52%. Age and sex differences between two groups were not statistically significant. Fever, abdominal lymph node enlargement, and crater-like gouged ulcer morphology were more common in the EBER-positive group ( P < 0.05 ). The albumin level in the EBER-positive group was significantly lower compared to that in the EBER-negative group ( P < 0.05 ). The copy count of EBV DNA in the blood of patients from the EBER-positive group was higher, and the prognosis was worse ( P < 0.05 ). Clinical manifestations were more severe in the EBER-positive group. Endoscopic, histopathological, and biochemical findings were also more serious in this group of patients. The findings point to the importance of assessing the EBER expression in patients with intestinal ulcers of various etiology. EBER positivity should be viewed as a diagnostic marker of more severe condition requiring more aggressive treatment.

Background We often meet colonic ulcer when we do colonoscopy for patients. The colonic ulcer is isolate or multiple. We can diagnose some colon ulcer at once. But sometimes we do not recognize what disease of these colon ulcers even if we do a biopsy. So, we tracked some patients with colon ulcer in order to know the etiology of these colon ulcers. Methods A total of 32 cases were enrolled. The mean age was (46.3 ± 14.8) years old (range, 21–70 years). The ratio of male to female was 9:7. The main reasons for patients. Undergoing colonoscopy were abdominal pain, diarrhea, and bloody purulent stool. The symptoms lasted for at least a month or more. The basic information, medical history, clinical manifestations, computed tomography (CT), endoscopy of the patients and pathological examination were analyzed. Results The 32 patients’ colonoscopy showed isolate or multiple colon ulcer. At the same time, we did a biopsy. The histopathology showed mucosal chronic inflammation. Combined with the detailed medical history, lab examination, abdominal CT and colonoscopy, we made the initial diagnosis. 8(25%) were NSAIDs-related colonic ulcer (figure 1). 6(18.8%) were ischemic bowel disease. 3(9.4%) were allergic purpura. 2(6.3%) were Behcet’ disease. 1(3.1%) was Wegener’s granulomatosis (figure 2). There are 12 cases, we did not find a clear etiology of colonic ulcer. We did colonoscopy and multi-slice biopsy for all the patients after 3 months. The 20 patients, who had an initial diagnosis, the colon ulcer changed small even disappear after treatment. The other 12 patients, who had no initial diagnosis without any treatment, 6 of them had no changes in the lesions. The histopathology showed 3 were tuberculosis, 2 developed typical ulcerative colitis, 1 was lymphoma. The ulcerations of the other 3 with no initial diagnosis changed small. But the histopathology showed nonspecific mucosal chronic inflammation. The remaining 3, the lesions had disappeared. The follow-up continues. Conclusions There are various manifestations of colonic ulcer with colonoscopy. A detailed medical history is helpful for our diagnosis. The follow-up is important for no reason colonic ulcer. We should not diagnose and use medicine blindly.

The inhalation of carbon monoxide (CO) gas and the administration of CO-releasing molecules were shown to inhibit the development of intestinal inflammation in a murine colitis model. However, it remains unclear whether CO promotes intestinal wound healing. Herein, we aimed to evaluate the therapeutic effects of the topical application of CO-saturated saline enemas on intestinal inflammation and elucidate the underlying mechanism. Acute colitis was induced with trinitrobenzene sulfonic acid (TNBS) in male Wistar rats. A CO-saturated solution was prepared via bubbling 50% CO gas into saline and was rectally administrated twice a day after colitis induction; rats were sacrificed 3 or 7 days after induction for the study of the acute or healing phases, respectively. The distal colon was isolated, and ulcerated lesions were measured. In vitro wound healing assays were also employed to determine the mechanism underlying rat intestinal epithelial cell restitution after CO treatment. CO solution rectal administration ameliorated acute TNBS-induced colonic ulceration and accelerated ulcer healing without elevating serum CO levels. The increase in thiobarbituric acid-reactive substances and myeloperoxidase activity after induction of acute TNBS colitis was also significantly inhibited after CO treatment. Moreover, the wound healing assays revealed that the CO-saturated medium enhanced rat intestinal epithelial cell migration via the activation of Rho-kinase. In addition, the activation of Rho-kinase in response to CO treatment was confirmed in the inflamed colonic tissue. Therefore, the rectal administration of a CO-saturated solution protects the intestinal mucosa from inflammation and accelerates colonic ulcer healing through enhanced epithelial cell restitution. CO may thus represent a novel therapeutic agent for the treatment of inflammatory bowel disease.

Amebiasis is a frequently occurring parasitic infection in South East Asia. We present a case of a 54-year-old man with right lower quadrant abdominal pain that persisted for longer than 1 year. He had been diagnosed with inflammatory bowel disease in Indonesia. His abdominal pain persisted, despite therapy, and he visited Malaysia for transnational medical advice. Abdominal ultrasound showed fatty liver, gallbladder polyps, and a small left renal stone. Colonoscopy showed multiple ulcers in the cecum and a histopathological examination confirmed amebic infection of the cecum. The colonic ulcers subsided after anti-amebic treatment. This case highlights the need to consider the differential diagnosis of amebic colitis in patients presenting with manifestations of inflammatory bowel disease, especially in patients who live in or have traveled to endemic areas.

Background: The clinical significance of gastrointestinal wall thickening (GWT) on abdominal computed tomography (CT) is not certain, yet. Despite the need for clinical guidelines describing the importance and evaluation of GWT on a CT scan, there have been few studies evaluating these incidental imaging abnormalities. The aim of this study is to endoscopically evaluate certain etiologies that cause incidental GWT found on CT. Methods: This retrospective cohort study was carried out with patients who had incidentally detected GWT on a CT scan at the Kanuni Sultan Suleyman Training and Research Hospital between February 2016 and December 2018. Results: A total of 129 patients (62 males and 67 females; mean age 57.5 years, range: 26-87 years) were included in the study. Abnormalities observed during endoscopy at the exact site of the GWT noted on a CT image were found in 114 patients (99%): upper endoscopy revealed malignancy in 33 (29%), gastritis in 63 (52%), hiatal hernia in 19 (16%), a gastric ulcer in 7 (6%), and alkaline gastritis in 3 (2%). Colonoscopy revealed malignancy in 4 (33%), benign polyps in 5 (35%), colonic ulcer in 2 (16%), and 2 patients (16%) had normal findings. Malignancy was detected more frequently in the cardioesophageal region compared with the antrum (P=0.020). Conclusion: In this study, detection of GWT on CT often indicated pathologies which were subsequently confirmed endoscopically. Pathological findings were detected in 83% of these patients, with approximately 30% determined to be malignant. Endoscopic evaluation is recommended when GWT is reported on a CT scan.

Background Conventional colonoscopy is gold standard for the diagnosis and monitoring of patients with suspected or known inflammatory bowel disease (IBD). Nevertheless, it is a potentially painful procedure with risk of complications, including bleeding and perforation. Colon capsule endoscopy (CCE) is a minimally invasive alternative for patients unwilling to undergo colonoscopy or when it is contraindicated or unfeasible. However, CCE produces thousands of frames and their revision is a time-consuming and monotonous task. The detection of ulcers and erosions is paramount for the diagnosis and assessment of the activity of IBD. However, these lesions may appear in a very small number of frames, thus increasing the risk of overlooking significant lesions. Our aim was to develop an Artificial Intelligence (AI) algorithm, based on a multilayer Convolutional Neural Network (CNN) for automatic detection of ulcers and erosions in CCE exams. Methods A total of 24 CCE exams (PillCam COLON 2®) performed at a single centre between 2010–2020 were analysed. From these exams, 3 635 frames of the colonic mucosa were extracted, 770 containing colonic ulcers or erosions and 2 865 showing normal colonic mucosa. These images were used for construction of training (80% of the frames) and validation (20% of the frames) datasets. For automatic identification of these lesions, these images were inputted in a CNN model with transfer learning. The output provided by the CNN (Figure 1) was compared to the classification provided by a consensus of specialists. Performance marks included sensitivity, specificity, positive and negative predictive values, accuracy and area under the receiving operator characteristics curve (AUROC). Results After the optimization of the neural architecture of the CNN, our model automatically detected colonic ulcers and erosions with a sensitivity of 90.3%, specificity of 98.8% and an accuracy of 97.0% (Figure 2). The AUROC was 0.99 (Figure 3). The mean processing time for the validation dataset was 11s (approximately 66 frames/s). Conclusion We developed a CNN model which demonstrated high levels of efficiency for the automatic detection of ulcers and erosions in CCE images. Our study lays the foundations for the development of effective AI tools for application to CCE exams. These systems may enhance the diagnostic accuracy and reading efficiency of CCE, thus expanding the role of minimally-invasive colonic exploration in the management of IBD patients.

Introduction Solitary ulcers in the colon are rare and infrequent; little over 200 cases have been reported in medical literature. We present a case of a patient presenting with a solitary colonic ulcer associated with NSAIDs intake, mimicking a malignant lesion. A review of the literature is also revised. Presentation of case 68- year-old female patient with past history of nonsteroidal anti-inflammatory drugs (NSAID) intake for chronic pain, complaining of severe abdominal pain was admitted to our teaching hospital. The diagnosis of a low-grade dysplasia was made with colonoscopy and biopsy, a malignant lesion could not be ruled out. A laparoscopy right colectomy was performed without complications. The final diagnosis resulted in a solitary cecal ulcer. Discussion The majority of the cases of solitary colonic ulcers occur in the ascending colon, at the cecum, which has been attributed mostly to the intake of NSAIDs. There could be solitary colonic ulcers in other portions of the large intestine, caused by different etiologies: ischemia, inflammatory disease, sterocoraceus ulcers, ulcers caused by infections, among other more uncommon causes. The diagnosis is often made through a biopsy of the tissue during a colonoscopy, with either surgical or conservative care. Conclusion The diagnosis of solitary cecal ulcer should be considered in patients presenting with RLQ abdominal pain and with history of NSAIDs consumption. Recognition of this diagnosis by surgeons, ruling out malignancies, understanding the morphologic features, and carefully taking the patient's history are essential for the diagnosis and treatment of this uncommon disease., Highlights • We present a case report of a 68- year-old female patient with a solitary cecum ulcer, mimicking a carcinoma. • Little over 200 cases have been reported in medical literature. • The most common cause of this ethology is: NSAIDs consumption. • The gold standard for diagnostic is colonoscopy, taking a biopsy in order to rule out malignancies.

We present a rare case of fecaloma, 7 cm in size, in the setting of systemic scleroderma. A colonoscopy revealed a giant brown fecaloma occupying the lumen of the colon and a colonic ulcer that was caused by the fecaloma. The surface of the fecaloma was hard, large and slippery, and fragmentation was not possible despite the use of various devices, including standard biopsy forceps, an injection needle, and a snare. However, jumbo forceps were able to shave the surface of the fecaloma and break it successfully by repeated biting for 6 h over 2 d. The ability of the jumbo forceps to collect large mucosal samples was also appropriate for achieving fragmentation of the giant fecaloma.

Simple, isolated nonspecific colonic ulcer (NSCU) is a rare pathological entity which has not been adequately explored in the past literature. It is predominant between the ages of 40 and 60 years, and the most common complication is perforation which can be life threatening. Here we present a case of a young female who presented with a perforated NSCU and was successfully managed surgically.

Cytomegalovirus infection, which can occur as a result of reactivation due to immunosuppressive treatment in patients with granulomatosis with polyangiitis, is a serious condition that should be kept in mind because of its fatal course. In this article, we report a 49-year-old male patient with a diagnosis of granulomatosis with polyangiitis who developed a life-threatening colonic ulcer due to cytomegalovirus colitis and a shrunken spleen with irregular contours that was detected on abdominal computed tomography. This is a rare case of cytomegalovirus disease in a patient with granulomatosis with polyangiitis and splenic necrosis.

We report a 54-year-old female patient with myelodysplastic syndrome (MDS) associated with trisomy 8, who had multiple colonic ulcers. The patient had been diagnosed as having MDS of refractory cytopenia with trisomy 8 10 years previously. She underwent colonoscopy for abdominal pain, which revealed severe circumferential stenosis with multiple ulcers in the ileocecal region and a discrete excavating ulcer in the transverse colon. The patient had been free from any dermatological, oral, genital or ocular symptoms suggestive of Behçet's disease (BD). A diagnosis of multiple colonic ulcers associated with MDS with trisomy 8 was thus suggested. Follow-up colonoscopies 5 and 6 years later revealed progression of the ileocecal stenosis to a circumferential ulcer, while the ulcer in the transverse colon had not changed. Because our patient lacked extraintestinal symptoms of BD, trisomy 8 was presumed to be responsible for her colonic ulcers.

Hypoganglionosis is a rare form of intestinal neuronal malformation, which is characterized by reduced number and size of ganglion cells of parasympathetic nerves in the intestinal wall. Pathophysiology is not well known, however intestinal ischemia, inflammation, autoimmune process or neurotoxin may play a role. Here, we report the case of a 56-year-old man with colonic pseudoobstruction and ulcerations in marked dilatedcolon above transitional zone who was later diagnosed with colonic hypoganglionosis.

Aims To review the clinical and pathological factors associated with fulminant amoebic colitis (FAC) requiring colonic resection and its outcome. Methods We retrospectively identified adult patients admitted to our centre between June 2007 and December 2011 with FAC who underwent colonic resection and were diagnosed with amoebic colitis based on the presence of trophozoites on histological examination. The clinical details were extracted from the medical notes and correlated with the pathological findings. Results Thirty patients (18 men and 12 women) met the inclusion criteria. Their mean age was 50.1 years (range 21–89). The most frequent symptoms were abdominal pain, vomiting and fever. More than half the patients (16/30) had underlying conditions associated with immunosuppression including diabetes mellitus and tuberculosis. Pathological investigation of colonic resections showed predominantly right-sided involvement with geographic colonic ulcers covered with a creamy-white pseudomembrane, perforations, gangrenous changes, amoeboma and lesions mimicking inflammatory bowel disease. All showed basophilic dirty necrosis with abundant nuclear debris and amoebic trophozoites on histological examination. 21/30 patients (70%) had involvement beyond the caecum. 17/30 patients (57%) died. Those with involvement beyond the caecum were more likely to die (15/21, 71.4%) than those with less extensive disease. Conclusions FAC presents as acute abdomen and can mimic appendicitis, ischaemic bowel disease, tuberculosis and malignancy. Comorbidities causing immunosuppression frequently associated. Mortality remains high despite surgery, so FAC should be suspected in every case of acute abdomen with colonic perforation if associated with typical gross and microscopic findings and a history of stay in an endemic area.

Background Colitis is associated with functional abnormalities in proximal non-inflamed gut areas, but animal models to study small bowel dysfunction in colitis have limitations. This study aims to determine small intestinal alanine absorption and cytokine expression in a novel model of colonic ulceration induced by electro-cautery. Methods A descending colon ulcer was induced in rats by a bipolar electro-cautery probe. Ulcer score was determined using Satoh’s criteria. Jejunal alanine absorption was measured immediately and at different time intervals post ulcer induction. Levels of interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) protein and m-RNA were determined in mucosal scrapings obtained from the colon, duodenum, jejunum and ileum at various time intervals after colonic ulcer induction. Results The mean ulcer score was 3 up to 48 h, followed by healing by 96 h post ulcer induction. Small bowel histology was normal throughout. Jejunal alanine absorption was reduced by 12–34% immediately and up to 72 h after cautery and returned to normal at 96 h. IL-1 and TNF-α mRNA increased significantly in the colon, duodenum, jejunum and ileum 3 h post electro-cautery and returned to normal at 48 h, while that of IL-6 increased significantly at 48 h post ulcer induction. Similarly, IL-1, IL-6 and TNF-α protein levels increased in the duodenum, jejunum, ileum and colon up to 48 h post ulcer induction. Conclusions Electrically induced localized colonic injury increased production of pro-inflammatory cytokines in non-inflamed segments of the small intestine and was associated with derangements of jejunal absorptive function.

Background Detection of human herpesviruses (HHVs) other than cytomegalovirus (CMV) in colonic mucosa of individuals with inflammatory bowel disease (IBD) remains unknown. This study identified eight HHVs in the colonic mucosa of individuals with IBD and compared the results with immunocompetent and human immunodeficiency virus (HIV)-infected individuals. Methods A total of 89 individuals who had colorectal ulcer on colonoscopy were enrolled: 26 with immunocompetency (n = 26), 41 with IBD, and 22 with HIV infection. We examined the colonic ulcers for the presence of eight HHVs—herpes simplex virus (HSV)-1/2, varicella zoster virus (VZV), CMV, Epstein–Barr virus (EBV), HHV-6, HHV-7, and HHV-8—using mucosal PCR. Results The IBD group had positivity rates of 0%, 0%, 0%, 53.7%, 24.4%, 39%, 39%, and 0% for HSV-1, HSV-2, VZV, EBV, CMV, HHV-6, HHV-7, and HHV-8, respectively. The positivity rates of EBV and CMV in colonic mucosa increased significantly in the order of the immunocompetent, IBD, and HIV groups (EBV: 23.1%, 53.7%, 72.7%, P for trend = 0.0005; CMV, 7.7%, 24.4%, 54.5%, P for trend = 0.0003, respectively), but no increase was found in the other HHVs. Median mucosal EBV DNA values in the immunocompetent, IBD, and HIV groups were 0, 76, and 287 copies/μg DNA, respectively (P for trend = 0.002). Corresponding median mucosal CMV DNA values were 0, 0, and 17 copies/μg DNA (P for trend = 0.0001). There was no significant difference in the positivity rates of the eight HHVs between ulcerative colitis and Crohn’s disease. Conclusion The HHVs of EBV, CMV, HHV-6, and HHV-7, but not of HSV-1, HSV-2, VZV, or HHV-8, were identified in the colonic mucosa of IBD individuals. EBV and CMV in colonic mucosa was correlated with host immune status in increasing order of immunocompetent, IBD, and HIV-infected individuals.

Background: Nowadays, capsule endoscopy is the first-line procedure to assess the small bowel. During small bowel procedures, other segments of the gastrointestinal tract may be visualized. The aim of the current study was to evaluate the incidence of colonic abnormalities in patients undergoing small bowel capsule and its impact on patient management. Patients and methods: This study is a retrospective analysis of data from 526 consecutive capsule endoscopy procedures performed at a single tertiary-care centre between 2008 and 2011. Patients with incomplete procedures were excluded from the analysis. Patient baseline characteristics, colonic lesions, diagnosis and management before and after capsule endoscopy were recorded and a descriptive analysis was performed. Results: Four hundred and sixty four patients were finally included in the analysis. Two hundred and ninety three patients were male (57.3%) and the mean age was 61.3 ± 20.03 years (18-86). Obscure gastrointestinal bleeding (59%) and inflammatory bowel disease (19%) were the main indications for the procedure. Colonic abnormalities were detected by capsule endoscopy in 47 (9%) of 464 patients. The most common types of missed lesions were vascular lesions (34%) and colonic ulcers (32%). This information had a clinical or diagnostic impact of 7.55% and a therapeutic impact of 6.03%. Conclusion: All images of the colon should be evaluated during small bowel capsule endoscopy as they may provide relevant information that may result in changes in patient management.

Although endoscopy is the definitive diagnostic method for the detection of colonic ulcers, the equipment required for performing the test is costly and difficult to use. Therefore, a simple cost-effective and reliable screening test for intestinal tract bleeding is needed. To this end, we measured carbonic anhydrase isozymes (CA-I and CA-II) originating from erythrocytes by ELISA in order to determine if they could be used as markers of occult blood in feces. For fecal extract preparation, 2 g of feces were mixed with 4 ml of 0.01 M Tris-HCl (pH 8.0) containing 0.01% thimerosal. The concentrations of CA-I and CA-II in the fecal samples of 13 clinically normal racehorses were found to be 30.0 ± 10.0 and 34.0 ± 13.0 ng/ml, respectively. Increased concentrations of CA-I were detected in the fecal samples of 5 horses after blood administration; however, no increase was observed in CA-II. The concentrations of CA-I and CA-II in the fecal samples of 88 racehorses with clinical signs of equine gastric ulcer syndrome (EGUS) were 115.3 ± 79.0 and 41.0 ± 42.0 ng/ml, respectively. Thus, our results indicate that CA isozymes can be useful as markers of occult blood in the fecal samples of horses with intestinal tract bleeding.

We present a case of massive lower gastrointestinal hemorrhage secondary to Salmonella enterica subtype Typhi (S. Typhi) colitis, in a 29 year-old female treated for S. Typhi bacteremia. One week post-treatment, she unexpectedly developed a large volume of rectal bleeding. Endoscopy showed colonic ulcers and ileitis, but no endoscopic hemostasis was required. Treatment was supportive with transfusions and a prolonged course of antimicrobials, with the bleeding stopping spontaneously. This case illustrates the phenomenon of delayed lower gastrointestinal hemorrhage, as a rare complication of S. Typhi infection.

AIM To investigate management of patients who develop ipilimumab-mediated enterocolitis, including association of endoscopic findings with steroid-refractory symptoms and utility of infliximab as second-line therapy. METHODS We retrospectively reviewed all patients at our center with metastatic melanoma who were treated with ipilimumab between March 2011 and May 2014. All patients received a standard regimen of intravenous ipilimumab 3 mg/kg every 3 wk for four doses or until therapy was stopped due to toxicity or disease progression. Basic demographic and clinical data were collected on all patients. For patients who developed grade 2 or worse diarrhea (increase of 4 bowel movements per day), additional data were collected regarding details of gastrointestinal symptoms, endoscopic findings and treatment course. Descriptive statistics were used. RESULTS A total of 114 patients were treated with ipilimumab during the study period and all were included. Sixteen patients (14%) developed ≥ grade 2 diarrhea. All patients were treated with high-dose corticosteroids (1-2 mg/kg prednisone daily or equivalent). Nine of 16 patients (56%) had ongoing diarrhea despite high-dose steroids. Steroid-refractory patients received one dose of intravenous infliximab at 5 mg/kg, and all but one had brisk resolution of diarrhea. Fourteen of the patients underwent either colonoscopy or sigmoidoscopy with variable endoscopic findings, ranging from mild erythema to colonic ulcers. Among 8 patients with ulcers demonstrated by sigmoidoscopy or colonoscopy, 7 patients (88%) developed steroid-refractory symptoms requiring infliximab. With a median follow-up of 264 d, no major adverse events associated with prednisone or infliximab were reported. CONCLUSION In patients with ipilimumab-mediated enterocolitis, the presence of colonic ulcers on endoscopy was associated with a steroid-refractory course.

A 94-year-old female with end-stage renal disease presents with fever, fatigue, and hematochezia. She had previously resided in Hunan Province, China, and Myanmar, and she immigrated to Taiwan 30 years ago. Colonoscopy revealed a colonic ulcer. Biopsy of the colonic ulcer showed ulceration of the colonic mucosa, and many Paragonimus westermani-like eggs were noted. Serum IgG antibody levels showed strong reactivity with P. westermani excretory-secretory antigens by ELISA. Intestinal paragonimiasis was thus diagnosed according to the morphology of the eggs and serologic finding. After treatment with praziquantel, hematochezia resolved. The present case illustrates the extreme manifestations encountered in severe intestinal paragonimiasis.

Nicorandil is widely accepted in the therapeutic armamentarium of ischemic heart disease and, although nicorandil-induced oral and anal ulcerations have been established in the literature, only five cases have reported the possibility of nicorandil-induced ulceration elsewhere in the gastrointestinal tract. There have been recent case reports which have suggested the possible causative association between nicorandil and colonic ulceration, either in isolation or in combination with anal ulceration. We report a case series of eight patients prescribed with nicorandil therapy presenting with gastrointestinal symptoms and subsequently diagnosed with colonic ulceration on colonoscopy. Eight patients were identified (five female, three male). Colonoscopic findings varied from solitary to multiple colonic ulcers. No concomitant oral or anal ulcerations were noted in these patients. Biopsies from the ulcers showed only non-specific inflammation. Cessation of nicorandil therapy resulted in resolution of symptoms and complete healing of colonic ulcers. Nicorandil therapy appears to be an emerging etiology in the development of idiopathic colonic ulceration and therefore should be considered as a differential diagnosis in a selected group of patients.

Experimental colitis induced by chemical agents leads to upregulation of inflammatory cytokines in distant unaffected small intestine and to a decrease in nutrient absorption. To preclude any possible proximal diffusion of these chemicals, we designed a novel method for ulcer induction in the colon by electrocautery.Under light anesthesia, a colonic ulcer was induced in rats by a special electrocautery probe introduced in the descending colon through the rectum allowing the injection of a controlled electrolytic current. A direct current (3-7 mA) was delivered through the electrodes for 30s and then for another 30s after reversing the polarity of the electrodes. Then, the probe was moved for a distance of +/-0.5 cm and the current injection was repeated. Rats were sacrificed at various time intervals after ulcer induction (3-96 h). Samples from colon and jejunum were taken for histological assessment and determination, by ELISA, of the levels of interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). In other groups of animals, jejunal amino acid absorption was determined in vivo at 24 and 48 h post electrocautery.A colonic ulcer persisted for 72 h after cauterization. A significant upregulation of the levels of different cytokines was observed in the colon and jejunum post cauterization and persisted for at least 48 h. In the jejunum, IL-1beta increased from 81+/-9 to 652+/-110 (p0.01) and 243+/-47 (p0.05) pg/mg protein at 24 and 48 h, respectively. Similarly, jejunal TNF-alpha levels increased by approximately 2 folds at 24 and 48 h post ulcer induction (p0.05). A similar but higher increase in cytokines was observed in the colon. Jejunal alanine absorption (0.2+/-0.02 micromol/20 min/cm) decreased significantly at 24 and 48 h after colitis induction (0.12+/-0.01 and 0.14+/-0.02, respectively; p0.01).This model may be used as an alternative or a complement to chemical models of colitis.

Aim The effects of short- or long-term administration of nonsteroidal anti-inflammatory drugs (NSAIDs) on the colon have not been well characterized. We assessed the risk of developing colonic mucosal lesions according to the duration of exposure to NSAIDs: short-term and/or long-term use. Method A case-controlled study was performed by reviewing medical records for endoscopic findings, underlying disease, pre-endoscopic symptoms, category of NSAIDs used and duration of use. The patients underwent colonoscopy between January and October 2004, and 75 colitis cases and 1801 non-colitis controls were identified. The prevalence of NSAID use was compared between the cases and controls. The age- and sex- adjusted odds ratios (OR) were estimated using multiple logistic regression models. Results NSAIDs had been used in colitis cases and non-colitis controls for over six months in 20.0% and 12.7%, and for one week in 4.0% and 2.1%. Overall 76.0% and 85.2% had not received NSAIDs. The adjusted OR (95% confidence interval) for colonic mucosal lesions with short- and long term NSAID administration combined vs. non-use was 2.04 (1.16–3.61). When determined separately for short- and long-term NSAID users, the adjusted ORs were 1.48 (0.42–5.25) and 2.21 (1.19–4.11), compared to non-users. These values signify a trend toward an increased frequency of colonic mucosal lesions with longer use of NSAIDs (P=0.011 for trend). Conclusion Long-term use of NSAIDs increased the risk of colonic mucosal lesions, suggesting that NSAIDs may contribute to the pathogenesis of colonic ulcer or colitis.

The aetiology of ulcerative colitis is inadequately understood, and drug therapy has been empirical rather than based on sound understanding of disease aetiology. This has been a major factor for refractoriness and adverse drug effects as additional complications. However, ulcerative colitis by its very nature is exacerbated and perpetuated by inflammatory cytokines, which are released by peripheral granulocytes and monocytes as well. Additionally, active ulcerative colitis is often associated with elevated peripheral granulocytes and monocytes with activation behaviour and are found in vast numbers within the colonic mucosa. Hence, from the clinicopathologic viewpoint, granulocytes and monocytes are appropriate targets for therapy in ulcerative colitis. Based on this thinking, an Adacolumn has been developed for depleting excess granulocytes and monocytes by adsorption.By colonoscopy, biopsy and histology, we investigated the impact of granulocyte and monocyte adsorption (GMA) on the mucosal level of granulocytes and monocytes in patients with active ulcerative colitis. Forty-five patients (26 steroid naïve and 19 steroid-dependent), mean age 44.7 yr, were included. Twenty patients had total colitis and 25 had left-sided colitis. Each patient was given up to 11 GMA sessions over 12 weeks. No patient received additional medications within 4 weeks (steroid) to 8 weeks (other immunosuppressants) prior to entry or during the GMA course. Colonoscopy together with biopsy was done at entry and within 2 weeks after the last GMA session.At entry, the mean clinical activity index was 12.6; range 10-16. A total of 400 colonic biopsies were examined, which revealed massive infiltration of the colonic mucosa by granulocytes, and GMA was associated with striking reduction of granulocytes in the mucosa. At week 12, 33 of 45 patients (73.3%, P0.01) had achieved clinical remission (the mean clinical activity indexor= 4). Colonoscopy revealed that most non-responders had deep colonic ulcers and extensive loss of the mucosal tissue. The response rate in steroid naïve subgroup was 22 of 26 patients (84.6%, P0.005) and in steroid-dependent was 11 of 19 (57.9%, P0.05 and P=0.02154 for steroid naïve vs. steroid-dependent). Patients who achieved remission could continue with their salicylates. On average, remission was sustained for 7.8 months in all 33 responders.This is the first report showing a striking difference in clinical response to GMA between steroid naïve and steroid-dependent patients. Further, patients with deep colonic ulcers together with extensive loss of the mucosal tissue are not like to respond to GMA.

Clostridium difficile-associated diarrhea (CDAD) is a well-known iatrogenic infection with typical endoscopic features including pseudomembranes and intervening normal mucosa. Clinically, diarrhea frequently occurs, but occurrence of hematochezia is rare. The objective of this study was to investigate the background and endoscopic features of CDAD patients with hematochezia.The endoscopic and clinical findings in 12 patients who showed evidence of C. difficile toxin A and who underwent colonoscopy between April 2002 and July 2007 were investigated retrospectively.Eight patients were diagnosed as having CDAD and 4 patients had a diagnosis of ulcerative colitis. Six of the patients with CDAD presented with hematochezia, and 4 of them were diagnosed with hematological malignancies and received anticancer chemotherapy. Colonic ulcer was demonstrated in all CDAD patients with hematochezia, and bleeding from the ulcer was endoscopically confirmed in all of them.CDAD accompanied by hematochezia is closely associated with ulcer formation. Ulcers are thought to occur during recovery from nadir after anticancer treatment, and white blood cells appear to be essential for their formation. Physicians should therefore pay close attention to the occurrence of colonic ulcer, especially in patients with CDAD during recovery from nadir.

Isolated ulcers of the large intestine are not associated with an underlying colitis and may be an incidental finding on screening colonoscopy or present with abdominal pain, hematochezia, chronic gastrointestinal bleeding, and rarely, perforation. A common cause of isolated colonic ulcers is the use of nonsteroidal anti-inflammatory drugs (NSAIDs), with ulcers in the cecum and right colon. Isolated rectal ulcers are caused by ischemia, solitary rectal ulcer syndrome (SRUS), radiation, or fecal impaction. Stercoral ulceration and nonspecific ulcers of the colon are rare but can cause colonic perforation. Infectious causes include tuberculosis and amebiasis. Histology is important to rule out malignancy but is not helpful for diagnosis except in SRUS and certain infections. The approach to isolated colonic ulceration includes biopsy of the ulcer and surrounding tissue, cessation of any NSAIDs, management of constipation, and recognition of the patient with SRUS. Inflammatory bowel disease should be ruled out in appropriate patients.