Post-Colonoscopy Perforation in a Patient With Ulcerative Colitis.

Article1 August 1954ULCERATIVE COLITIS: THERAPEUTIC EFFECTS OF CORTICOTROPIN (ACTH) AND CORTISONE IN 120 PATIENTSJOSEPH B. KIRSNER, M.D., Ph.D., F.A.C.P., WALTER L. PALMER, M.D., Ph.D., F.A.C.P.JOSEPH B. KIRSNER, M.D., Ph.D., F.A.C.P., WALTER L. PALMER, M.D., Ph.D., F.A.C.P.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-41-2-232 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptINTRODUCTIONThe effects of corticotropin (ACTH) and cortisone in ulcerative colitis have been characterized as beneficial,1-5 indifferent6-8 and unfavorable.9-14 Numerous studies also have emphasized the complications of therapy and the recurrences.15-20 The observation of 40 patients in 19511 indicated that, while ACTH and cortisone do not cure ulcerative colitis, they may be useful adjuncts, initiating rapid and occasionally dramatic clinical improvement. The present report summarizes our experience with corticotropin and cortisone in 120 patients with ulcerative colitis observed during the past four years.PATIENTS STUDIEDGeneral Data:The series includes 65 females and 55 males; the majority were between 20...Bibliography1. KirsnerPalmerKlotz JBWLAP (a) : ACTH and cortisone in chronic ulcerative colitis. A comparison of clinical effects, J. Lab. and Clin. Med. 36: 846, 1950. (b) Kirsner, J. B., and Palmer, W. L.: ACTH in ulcerative colitis. Report of progress, Gastroenterology 18: 143, 1951. (c) Kirsner, J. B.: Discussion of "ACTH in chronic ulcerative colitis," Proc. Second Clinical ACTH Conference, 1951, The Blakiston Co., Philadelphia, p. 500. (d) Kirsner, J. B., and Palmer, W. L.: Effect of corticotropin (ACTH) in chronic ulcerative colitis. Observations in forty patients, J. A. M. A. 147: 541, 1951. MedlineGoogle Scholar2. 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KirsnerPalmerMaimonRicketts JBWLSNWE: Clinical course of chronic non-specific ulcerative colitis, J. A. M. A. 137: 922, 1948. CrossrefMedlineGoogle Scholar37. LevineKirsnerKlotz MJBAP: A new concept of the pathogenesis of ulcerative colitis, Science 144: 552, 1951. CrossrefGoogle Scholar38. Machella TE: Problems in ulcerative colitis, Am. J. Med. 13: 760, 1952. CrossrefMedlineGoogle Scholar39. KirsnerPalmer JBWL: Ulcerative colitis: consideration of its etiology and treatment, J. A. M. A. 155: 341, 1954. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Chicago, Illinois*Received for publication February 23, 1954. (Presented at Midwest Regional Meeting, American College of Physicians, Milwaukee, Wisconsin, November 21, 1953.)From the Department of Medicine, University of Chicago.†This study was supported in part by the Wallach Fund for Gastrointestinal Research.Dr. David Klein, of Wilson Laboratories, Chicago, Illinois, very generously supplied much of the corticotropin (ACTH).Merck and Company provided a portion of the cortisone. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byInflammatory bowel disease part II: Clinical and therapeutic aspectsBlood eosinophilia and ulcerative colitis--influence of ethnic origin.Clinical Observations on Inflammatory Bowel DiseaseThe Treabnent of Ulcerative ColitisChronic ulcerative colitis in elderly patientsEosinophilia in Peripheral Blood and Inflammatory Exudate in Non-specific ProctocolitisImmediate and Prolonged Therapeutic Effects of Corticotrophin and Adrenal Steroids in Ulcerative ColitisEOSINOPHIL LEUCOCYTES IN ULCERATIVE COLITISCORTICOTROPIN (ACTH) AND THE ADRENAL STEROIDS IN THE MANAGEMENT OF ULCERATIVE COLITIS: OBSERVATIONS IN 240 PATIENTS*†JOSEPH B. KIRSNER, M.D., F.A.C.P., WALTER L. PALMER, M.D., F.A.C.P., JEAN A. SPENCER, M.D., RICHARD O. BICKS, M.D., CHARLES F. JOHNSON, M.D.Response to Drugs and PsychiatryGeneralized scleroderma associated with chronic ulcerative colitisSteroid hormones in the management of chronic ulcerative colitisThe Use of ACTH and Adrenocorticosteroids in Diseases of the Digestive SystemThe Role of Acth and Adrenal Steroids in Perforation of the Colon in Ulcerative Colitis a Clinical-Pathologic StudyUlcerative Colitis; Observations on Its Etiology, Course and ManagementThe Use of the Adrenocorticosteroids in GastroenterologyThe use of ACTH, cortisone, hydrocortisone and related compounds in the management of ulcerative colitisGastroenterologyToxic Psychosis Under Cortisone and CorticotrophinObservations on the Influence of Corticotropins upon the Course of Chronic Ulcerative ColitisTHE PRESENT STATUS OF ACTH AND ADRENAL STEROID THERAPY IN MEDICINE*J. C. BECK, M.D., F.R.C.P.(C)THE RÔLE OF ACTH, CORTISONE AND HYDROCORTISONE IN SURGERY*†WILLIAM E. ABBOTT, M.D., HARVEY KRIEGER, M.D., STANLEY LEVEY, Ph.D.THE USE OF HYDROCORTISONE IN ULCERATIVE COLITIS: PRELIMINARY OBSERVATIONS 1 August 1954Volume 41, Issue 2Page: 232-250KeywordsAdrenocorticotropic hormoneResearch fundingUlcerative colitis Issue Published: 1 August 1954 PDF downloadLoading ...

In active ulcerative colitis, colonic nitric oxide (NO) generation is enhanced and probably has an important role in its pathogenesis. We tested the reliability of an NO electrode in monitoring colonic NO levels in ulcerative colitis patients and control subjects and its possible usage as a marker of disease activity. Colonic NO level was determined by the NO detection system model NO-501 (InterMedical, Nagoya, Japan). The working electrode was inserted into a 7-mm diameter polyvinyl tube and introduced at a distance 6 cm from the anus. In each subject sigmoidoscopy was performed and mucosal biopsies were obtained. NO synthase (NOS) activity was determined by monitoring the conversion of 3H-arginine to citrulline. Colonic NO level is significantly increased in patients with active ulcerative or Crohn's colitis--more than 2-fold higher than in control subjects. There was good correlation between colonic NO level and NOS activity and the clinical and endoscopic indices of disease activity. Direct determination of colonic NO level is convenient, and reliable, and may help to monitor disease activity in ulcerative colitis.

Nitric oxide (NO) is generated from L-arginine by a family of enzymes called the NO synthases. Previous investigators have proposed that the expression of this inducible enzyme (iNOS) may account for the characteristic vasodilatation, oedema and impairment of get motility seen in active ulcerative colitis. Using a specific antibody to iNOS, we have investigated the distribution of this enzyme in colonic tissue from patients with histologically proven ulcerative colitis. Eight patients with ulcerative colitis expressed calcium-independent citrulline activity (9.96 +/- 2.34 pmol citrulline mg-1 protein min-1) and showed immunoreactivity to the iNOS antibody within the inflammatory infiltrate of the lamina propria, and also within the cytoplasm of the epithelial cells lining the colon. Five age-matched controls showed no calcium-independent citrulline activity (0.2 +/- 0.08 pmol citrulline mg-1 protein min-1) and no immunoreaction to the antibody. We conclude that this enzyme is present in colonic tissue including the epithelium from patients with active colitis. Inhibition of this enzyme may provide a novel therapeutic option for patients with active ulcerative colitis.

Impaired iron absorption or increased loss of iron was found to correlate with disease activity and markers of inflammation in inflammatory bowel disease (IBD). Red cell distribution width (RDW) could be a reliable index of anisocytosis with the highest sensitivity to iron deficiency. The importance of RDW in assessment of IBD disease activity is unknown. In this study, we aimed to determine if RDW could be useful in detecting active disease in patients with IBD. A total of 74 patients with ulcerative colitis (UC) and 22 patients with Crohn's disease (CD) formed the study group with 20 age- and sex-matched healthy volunteers as the control group. CD activity index higher than 150 in patients with CD was considered to indicate active disease. Patients with moderate and severe disease according to the Truelove-Witts scale were accepted as having active UC. In addition to RDW, serum C-reactive protein (CRP) and fibrinogen levels, erythrocyte sedimentation rates (ESR), leukocyte, and platelet counts were measured. Fourteen (63.6%) of the patients with CD and 43 (58.1%) of the patients with UC had active disease. RDW, fibrinogen, CRP, ESR, and platelet counts were all significantly elevated in patients having active IBD compared with those without active disease and controls (P < 0.05). The study subjects were further classified into two subgroups: cases with active and inactive UC and those with active and inactive CD. A subgroup analysis indicated that for an RDW cutoff of 14, the sensitivity for detecting active UC was 88% and the specificity was 71% (area under curve [AUC] 0.81, P = 0.0001). RDW was the most sensitive and specific parameter indicating active UC. However, the same was not true for CD since CRP at a cutoff of 0.54 mg/dl showed a sensitivity of 92% and a specificity of 63% (AUC 0.92, P = 0.001), whereas RDW at a cutoff of 14.1 showed 78% sensitivity and 63% specificity to detect active CD. Among the laboratory tests investigated, including fibrinogen, CRP, ESR, and platelet counts, receiver operating characteristic (ROC) curve analysis indicated RDW to be the most significant indicator of active UC. For CD, CRP was an important marker of active disease.

Apoptosis plays a role in epithelial and mucosal injury, which is 1 of the mechanisms in the pathogenesis of ulcerative colitis. Apoptotic cells increase as a result of injured mucosa in ulcerative colitis and serum M 30 levels increase in epithelial cell apoptosis. In this study, we aimed to evaluate the relation between M 30 serum levels and ulcerative colitis activity. Eighty patients with ulcerative colitis and 40 healthy controls were enrolled into the study. The patient group consisted of 31 extensive colitis, 30 left-sided colitis, and 19 proctitis. The activity of ulcerative colitis was determined with clinical and endoscopic findings. Serum M 30 levels, acute phase reactants, and biochemical tests were analyzed in all subjects. Serum M 30 levels in patients with active ulcerative colitis were significantly higher when compared with the healthy controls (165.6 ± 60.6 and 129.6 ± 37.4; P = 0.003). Serum M 30 levels in active left-sided colitis patients was significantly higher when compared with patients in remission phase (180.6 ± 58.5, 141.5 ± 35.4; P = 0.044). When we exclude patients with ulcerative proctitis, M 30 levels in active ulcerative colitis patients were significantly higher than that the patients in remission phase (174.0 ± 63.5, 135.0 ± 29.9; P = 0.017). We found that M 30 levels increase in patients with active ulcerative colitis. Our findings support the role of apoptosis demonstrated by serum M 30 levels in the pathogenesis of active ulcerative colitis.

INTRODUCTION: Proton pump inhibitors (PPIs) are one of the most commonly prescribed medications in the United States. Some recent studies have suggested that PPIs may have a negative effect on the gut microbiome. Dysbiosis of the gut microbiome has been linked with inflammatory bowel disease (IBD). We hypothesized that PPI use is associated with increased IBD flares and activity. This study was aimed to assess the effect of PPIs on IBD flares and activity. METHODS: We conducted a prospective longitudinal study of Veterans from the IBD clinic at the Michael E. DeBakey VA Medical Center from 2014 to 2018. Our eligibility criteria included patients who were at least 18 years of age, who were diagnosed with Crohn's Disease (CD) or Ulcerative Colitis (UC), and who had at least 1 clinic visit. IBD flare was defined by patient self-report of IBD flare between clinical encounters. IBD activity was quantified using the partial Mayo Score (pMayo) for UC, and the Harvey Bradshaw Index (HBI) for CD. Remission was defined by pMayo &lt;2 for UC and HBI &lt;5 for CD. Exposure of PPI was confirmed by chart review. Associations of PPI use with IBD flare and activity were assessed using T-tests and Chi-squared tests. RESULTS: A total of 132 patients were included in the analysis of which 74 had CD and 58 had UC. 40 patients were PPI users, and IBD flares occurred in 60 patients. No significant association between PPI usage and IBD flares were observed: 42.5% of PPI users developed flares compared to 46.7% of non-PPI users who developed flares, P-value = 0.658. In patients with CD, PPI use was associated with non-remission status (RR 2.53; 95% CI 1.04-6.15). In UC patients, PPI use was not associated with non- remission status (RR 1.10; 95% CI 0.67-1.79). 13 CD patients on PPIs discontinued the PPI between encounters, which was associated with a statistically significant decrease in HBI (3.62- &gt;2.54, P-value = 0.005). Among UC patients who discontinued PPIs, there was a non-significant trend towards decreased pMayo (2.26- &gt;1.59, P-value = 0.069). CONCLUSION: Amongst CD patients, PPI use was not associated with interval flare however, it was associated with non-remission status. Cessation of PPIs was associated with a statistically significant decrease in HBI in CD patients. In UC patients, no significant association between PPI use and flare or activity were observed. Decreasing unnecessary PPI use in patients with CD may decrease disease severity.

MicroRNAs Are Differentially Expressed in Ulcerative Colitis and Alter Expression of Macrophage Inflammatory Peptide-2α

In this study, we investigated whether reticulated platelets (RP) would be useful markers in the evaluation of ulcerative colitis (UC) activity and also aimed to gain indirect information about the platelet kinetics. Complete blood count, C-reactive protein, erythrocyte sedimentation rate, and proportion of RP were measured in 16 active, 21 inactive UC patients, and 20 healthy blood donors. UC activity was assessed by Truelove-Witts criteria. Mean platelet count was increased in patients with active compared to inactive UC (p=0.008) or healthy donors (p=0.000). Mean platelet volume (MPV) was significantly decreased in patients with active compared to inactive (p=0.015) and healthy donors (p=0.001). RP values was significantly decreased in active and inactive UC groups compared to healthy donors (p=0.000, p=0.000, respectively), while there was no significant difference between active and inactive UC patients (p=0.980). Significant negative correlation between platelet count and MPV in patients with active UC (r=-0.542, p=0.030) was observed. RP values is reduced in active and inactive UC patients compared to healthy donors. To our knowledge, this is the first study about proportion of RP with UC in literature. However, the role of low RP values have not been determined clinically. Further studies are needed to evaluate the role of platelet abnormalities and changes in megakaryopoiesis caused by inflammatory state on low MPV and RP values during the course of UC.

Plasma fatty acid patterns were assessed by gas liquid chromatography in 73 patients with active inflammatory bowel disease and 107 healthy controls. The influence of the disease activity on fatty acid profile was also investigated. Plasma fatty acid patterns in patients with ulcerative colitis and Crohn's disease were similar. Plasma C18:3n3 and C22:6n3 were significantly higher in active ulcerative colitis (p = 0.0143 and p < 0.00001 respectively) and in Crohn's disease (p < 0.00001 for both) than in controls, whereas C20:3n6 was significantly lower in patients than in controls, both in ulcerative colitis (p = 0.0001) and in Crohn's disease (p = 0.0041). In more severe disease, plasma polyunsaturated fatty acid concentrations fell with a significant stepwise decrease in the desaturation index (p = 0.0031 in ulcerative colitis and p = 0.0355 in Crohn's disease). Even in patients with severe disease, however, plasma n3 fatty acids (C18:3n3 and C22:6n3) never fell below those of healthy controls. These findings suggest that in active inflammatory bowel disease, an increased biosynthesis might coexist with an increased consumption of polyunsaturated fatty acids. These observations may be of relevance in the pathogenesis of the disease as polyunsaturated fatty acids are involved in tissue eicosanoid synthesis and cellular membrane function, including that of immunocompetent cells. These results also question the rationale of using n3 polyunsaturated fatty acids in the treatment of inflammatory bowel disease.

CD4+ immune response as a potential biomarker of patient reported inflammatory bowel disease (IBD) activity

目的 探讨活动期溃疡性结肠炎和血小板激活状态的关系.方法对33例活动期溃疡性结肠炎、12例缓解期溃疡性结肠炎、30例肠易激综合征(IBS)患者和正常对照组28例用SH-93智能血液凝聚仪检测血小板聚集率,用酶联免疫法检测P选择素和血栓素B2(TXB2).同时评价45例溃疡性结肠炎内镜下表现和结肠黏膜活检情况.结果33例活动期溃疡性结肠炎患者平均1 min血小板聚集率和最大血小板聚集率均明显高于IBS组和正常对照组(P＜0.01),33例活动溃疡性结肠炎P选择素和TXB2明显高于IBS组和正常对照组,差异有显著意义(P＜0.01或P＜0.05).缓解期溃疡性结肠炎的P选择素也高于正常对照组.结论活动期溃疡性结肠炎患者体内存在血小板激活,血小板可能直接参与结肠黏膜的急性炎症反应.其中P选择素是溃疡性结肠炎的特异性指标,而血小板聚集率和TXB2与疾病的活动度有关.抗血小板药物可能对溃疡性结肠炎有一定的治疗效果。

The aim of this study was to compare in vitro release of eosinophil cationic protein (ECP) from peripheral blood eosinophils during active phases of childhood Crohn disease (CD) and ulcerative colitis with phases of remission. Ten children with CD and nine children with ulcerative colitis were investigated during 55 and 56 clinical visits, respectively. Each patient was investigated during at least one phase of clinically active disease and one phase of remission. Disease activity was assessed by means of the Paediatric Crohn Disease Activity Index (PCDAI) in Crohn disease and according to the clinical activity index of Rachmilewitz in ulcerative colitis. On an intra-individual basis, in vitro ECP release was significantly higher (P < 0.001) during active phases of CD and ulcerative colitis than in phases of remission (CD:median: 24.5 microg/l, range 16.0-61.2 versus median: 5.7 microg/l, range 2.0-16.7; ulcerative colitis: 14.8 microg/l, 8.3-39.8 versus 4.9 microg/l, 2.0-9.9). On an inte-individual basis, in CD and ulcerative colitis a strong and highly significant correlation was observed between disease activity indices and in vitro release of ECP from peripheral eosinophils (r = 0.89, P < 0.0001 and r = 0.82, P < 0.0001, respectively). These results show that in vitro ECP release from peripheral eosinophils reflects disease activity in both CD and ulcerative colitis and therefore can be used as a new appropriate laboratory parameter for assessment of disease activity in chronic inflammatory bowel disease.

IL-39 (Interleukin-39) is a heterodimeric cytokine composed of IL-23p19 and EBI3 (Epstein-Barr virus-induced gene 3) subunits. Despite the evidence that correlates the role of IL-39 in regulating inflammation, its expression in the intestinal microenvironment of IBD (inflammatory bowel disease) patients is still unknown. Thus, this work was focused on characterizing relative mRNA (messenger RNA) IL-39 expression and intestinal synthesis in IBD patients. This study includes 37 patients diagnosed with ulcerative colitis (UC), 15 with Chron's disease (CD), and 22 controls. Gene expression of IL-39 subunits (IL-23p19/EBI3) was measured by RT-PCR (real time polymerase chain reaction). Intestinal synthesis was evaluated by immunohistochemistry and serum levels by ELISA. Statistical analysis was done using Prism GraphPad V6. Relative mRNA IL-39 expression was increased in patients with active UC and active CD compared to the remission UC, remission CD, and control group. High levels of relative mRNA expression of IL-39 (IL-23p19 subunit) were associated with histological activity. IHQ analysis showed increased IL-39 production in mucosa, submucosa, muscular, and serosa layer of patients with active disease. IL-39 serum production was increased in patients with UC. IL-39 gene's upregulation was found in patients with active IBD and was associated with severe histological activity in UC. This is the first report regarding the role of IL-39 in patients with IBD. The findings suggest that IL-39 might play a role as an inflammatory mediator in active IBD and could be considered a new alternative in treating this condition.

Background Individuals with inflammatory bowel disease (IBD) experience mental health disorders at a rate of 1.5 to 2 times higher than the general population. With the rising incidence of IBD, many people are affected by the disease during significant life stages such as pregnancy. Research on the impact of IBD on anxiety and depression in pregnant people is limited. Aims To assess the impact of active IBD on anxiety and depression during pregnancy. Methods This retrospective survey study analyzed data from patients seen at the ‘Preconception and Pregnancy in IBD’ clinic at Mount Sinai Hospital who conceived prior to January 1st, 2022. Standardized pre-visit surveys included validated measures of mental health (General Anxiety Disorder-7 for anxiety; Patient Health Questionnaire-9 for depression) and IBD disease activity (pMayo6 for ulcerative colitis (UC); mHBI for Crohn’s disease (CD)). Demographic data was also collected (age, marital status, occupational status, smoking habits, alcohol use, cannabis use, previous diagnosis of anxiety and/or depression, IBD type, IBD surgical history, and medication use). Linear regression models were used to assess associations between disease activity and anxiety/depression, adjusting for medication type and stratified by trimester and IBD subtype. Results A total of 94 patients were included in this study, 42 patients had UC (44.7%), and 52 patients had CD (55.3%). The median age for the UC group was 32 (IQR 31-35.8), and the median age for the CD group was 32.7 (IQR 30-35.2). Active CD in the second trimester was significantly associated with higher anxiety (p = 0.024) and depression scores (p = 0.021) compared to those in remission. For CD, 6 patients (35.3%) in trimester 1, 8 patients in trimester 2 (25.8%), and 8 patients (26.7%) in trimester 3 had a GAD-7 score of ≥ 5; 5 patients (29.4%) in trimester 1, 6 patients (19.4%) in trimester 2, and 7 patients (23.3%) in trimester 3 had a PHQ-9 score of ≥ 5. Active UC in the second trimester was associated with significantly higher anxiety (p = 0.034) and depression (p = 0.022) scores compared to inactive UC. In the third trimester, this pattern persisted, with active UC again associated with elevated anxiety (p = 0.030) and depression (p = 0.027) scores. For UC, 4 patients (33.3%) in trimester 1, 9 patients (30%) in trimester 2, and 9 patients (31.0%) in trimester 3 had a GAD-7 score of ≥ 5; 4 patients in trimester 1, 4 patients in trimester 2, and 7 patients in trimester 3 had a PHQ-9 score of ≥ 5. Conclusions Active IBD during pregnancy is significantly associated with increased anxiety and depression, therefore, a multidisciplinary approach including mental health support is imperative for pregnant people with IBD. Funding Agencies None

Studies of prostaglandins and sulphasalazine in ulcerative colitis