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Ulcerative Colitis

Diagnosis and Evaluation

Gary R. Lichtenstein, MD, FACP, FACG, AGA; Robert B Stein, MD 
Reviewed on August 15, 2024
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Introduction

The diagnosis of ulcerative colitis (UC) is based on clinical evaluation and medical history and confirmed through laboratory, radiologic, endoscopic and histologic findings. Before making the diagnosis, infectious, ischemic and other etiologies of colitis should be excluded. Important diagnostic criteria are shown in Table 5-1 and discussed in more detail in the sections below.

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Classification Systems for UC

Proper diagnosis of UC, including determination of severity, extent, and prognosis is essential for selecting the most appropriate treatment. Classification systems are also important for standardization of clinical trials, since they play an important role in selecting patient eligibility and exclusion criteria. Several iterations of classification systems for inflammatory bowel disease (IBD) have been proposed and have been refined as our understanding of UC advances. The first classification system, the Rome classification system, was proposed by the…

Introduction

The diagnosis of ulcerative colitis (UC) is based on clinical evaluation and medical history and confirmed through laboratory, radiologic, endoscopic and histologic findings. Before making the diagnosis, infectious, ischemic and other etiologies of colitis should be excluded. Important diagnostic criteria are shown in Table 5-1 and discussed in more detail in the sections below.

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Classification Systems for UC

Proper diagnosis of UC, including determination of severity, extent, and prognosis is essential for selecting the most appropriate treatment. Classification systems are also important for standardization of clinical trials, since they play an important role in selecting patient eligibility and exclusion criteria. Several iterations of classification systems for inflammatory bowel disease (IBD) have been proposed and have been refined as our understanding of UC advances. The first classification system, the Rome classification system, was proposed by the International Working Party in 1991, but it only proposed a classification for patients with Crohn’s disease (CD), not patients with UC. This report was based on anatomical distribution, operative history and clinical behavior (inflammatory, fistulizing, or stenotic disease). However, this classification was felt inappropriate for clinical application in subsequent years and the World Congress of Gastroenterology in Vienna in 1998 provided an opportunity to reconsider and reanalyze this classification, leading to the publication of the Vienna classification system. This classification system was again later revised in 2005 to the Montreal classification system (Table 5-2). Neither the Rome or Vienna classification systems included a classification system for UC, but this changed with the introduction of the Montreal classification, which included three groupings for UC based on extent of disease (ulcerative proctitis, left-sided UC and extensive UC; see Figure 4-1) and four groupings based on disease severity (clinical remission, mild, moderate and severe). The Montreal classification system is the predominant system used today in adult UC patients.

In 2011, the Montreal classification system was modified into the Paris classification system for pediatric IBD patients (Table 5-3). For UC, the Paris classification system modifies the Montreal system in two ways. First, since pediatric-onset UC is characterized by extensive colitis or pancolitis in most cases, extensive disease and pancolitis were assigned to separate disease categories: E3 (extensive disease distal to the hepatic flexure) and E4 (pancolitis proximal to the hepatic flexure). The second difference from the Montreal classification is that only two categories of disease severity are defined: never severe and ever severe, per Pediatric Ulcerative Colitis Activity Index (PUCAI) score of ≥65.

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Enlarge  Figure 4-1: UC Classification by Colonic Involvement (Montreal Classification). Source: Ungaro R, et al. Lancet. 2017;389(10080):1756-1770.
Figure 4-1: UC Classification by Colonic Involvement (Montreal Classification). Source: Ungaro R, et al. Lancet. 2017;389(10080):1756-1770.
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Mayo Score

The Mayo score was originally devised in 1987 by Schroeder and colleagues to assess response to pH-dependent 5-ASA therapy. Although it is unvalidated, The Mayo score correlates closely with quality of life and remains one of the most common assessment tools for UC in current research.

The full Mayo score takes into consideration both clinical and endoscopic aspects of disease, with subscores assigned to four categories: stool frequency, rectal bleeding, inflammatory activity on sigmoidoscopy and overall physician assessment (Figure 5-1A). Each category is assigned a subscore ranging from 0 to 3, so the full Mayo score ranges from 0 to 12, with higher scores corresponding to more severe disease. The resulting score is not intended to predict the need for admission or surgical therapy; instead, it is intended to be compared to previous scores for a given patient and is therefore useful in tracking treatment response and disease progression. In clinical studies, a decrease of the score of ≥3 is typically seen as a therapeutic success.

The full Mayo score can be subdivided into its invasive and noninvasive components, which are sometimes used on their own. The clinical, or partial Mayo score (PMS), considers stool frequency, rectal bleeding and physician’s global assessment, whereas the Mayo endoscopic subscore considers only the sigmoidoscopic component. Endoscopy is an essential tool for evaluating disease severity and the efficacy of new treatment interventions in patients with UC, so the Mayo endoscopic subscore is often used alone to assess endoscopic mucosal response, with a subscore of 0 or 1 indicating mucosal healing (Figure 5-1B). Although a subscore of 1 can mean clearly visible remaining inflammatory activity, recall that the Mayo score was developed well before the advent of high-definition endoscopes, which are the current standard.

Enlarge  Figure 5-1: The Mayo Score. Key: <sup>a</sup> Each patient serves as his or her own control to establish the degree of abnormality of the stool frequency. <sup>b </sup>The daily bleeding score represents the most severe bleeding of the day. <sup>c </sup>The physician’s global assessment acknowledges the three other criteria, the patient’s daily recollection of abdominal discomfort and general sense of well-being, and other observations, such as physical findings and the patient’s performance status. Source: Adapted from Schroeder KW, et al. <em>N Engl J Med</em>. 1987;317:1625-1629. Images from Endoscopy Campus Magazine. https://www.endoscopy-campus.com/en/. Accessed November 2019.
Figure 5-1: The Mayo Score. Key: a Each patient serves as his or her own control to establish the degree of abnormality of the stool frequency. b The daily bleeding score represents the most severe bleeding of the day. c The physician’s global assessment acknowledges the three other criteria, the patient’s daily recollection of abdominal discomfort and general sense of well-being, and other observations, such as physical findings and the patient’s performance status. Source: Adapted from Schroeder KW, et al. N Engl J Med. 1987;317:1625-1629. Images from Endoscopy Campus Magazine. https://www.endoscopy-campus.com/en/. Accessed November 2019.

Ulcerative Colitis Endoscopic Index of Severity (UCEIS)

In addition to the Mayo endoscopic subscore, the UCEIS represents a reliable evaluative instrument of endoscopic disease activity. The UCEIS consists of the following three descriptors: vascular pattern (scored 0 to 2), bleeding (scored 0 to 3) and erosions and ulcers (scored 0 to 3; Figure 5-2A). Example endoscopy images of the UCEIS criteria are shown in Figure 5-2B.

If scoring systems are not properly validated, then clinical trial outcomes risk being affected by inter- and intra-investigator variation in endoscopic assessment of disease severity; however, unlike the Mayo score, the UCEIS has been extensively validated. Developed by Travis and colleagues in 2012, the UCEIS captures 90% of the variance in the overall assessment of endoscopic severity. It was later shown to have satisfactory intra- and inter-investigator reliability (0.96 and 0.88, respectively), to be minimally affected by knowledge of clinical details and to strongly correlate with patient-reported symptoms.

In terms of clinical relevance, Ikeya and coworkers compared the UCEIS with the Mayo endoscopic subscore in the evaluation of UC severity and outcomes in patients undergoing remission induction with tacrolimus during routine clinical practice. They found that, based on the UCEIS, a significant reduction in score was observed in the response and remission groups; however, no significant change was observed in the response group with the Mayo endoscopic subscore. This was found to be due to ulcers becoming smaller and shallower during the early stages of healing, a factor the Mayo endoscopic subscore does not account for. In patients with acute severe colitis, Corte and coworkers found higher UCEIS scores to be associated with worse outcomes. For UCEIS ≥5, 50% of patients required rescue therapy compared to 27% for UCEIS ≤4; for UCEUS ≥5, 33% of patients required a colectomy during follow-up compared to 9% with UCEIS ≤4. When the UCEIS was ≥7 on admission, almost all patients required treatment with infliximab or cyclosporin beyond steroids, possibly marking a threshold for an early decision to initiate rescue therapy.

In a retrospective study, Xie and colleagues compared the Mayo endoscopic subscore to the UCEIS as a predictor for the need of colectomy in patients with acute severe colitis. Both UCEIS and Mayo endoscopic subscore scores were significantly higher in colectomized patients compared to non-colectomized patients; however, only UCEIS was found to be an independent risk factor for colectomy in multivariate analysis (P <0.001; odds ratio: 3.25). When the UCEIS was 3, colectomy rate was 0%, which increased to 17.4% and 80.0% when UCEIS increased to 4 and 7-8, respectively. For Mayo endoscopic subscore, colectomy rate was 13.8% when 2 and 60.0% when 3. Thus, UCEIS outperformed Mayo endoscopic subscore as a predictor for colectomy in patients with acute severe colitis. These results also suggest benefits of considering early colectomy in patients with acute severe colitis and baseline UCEIS ≥7.

Enlarge  Figure 5-2: Ulcerative Colitis Endoscopic Index of Severity. Source: Adapted from Travis SP, et al. <em>Gut</em>. 2012;61(4):535-542. Images from Endoscopy Campus Magazine. https://www.endoscopy-campus.com/en/. Accessed November 2019.
Figure 5-2: Ulcerative Colitis Endoscopic Index of Severity. Source: Adapted from Travis SP, et al. Gut. 2012;61(4):535-542. Images from Endoscopy Campus Magazine. https://www.endoscopy-campus.com/en/. Accessed November 2019.

Additional Severity Indices

Numerous other UC activity indices exist for the classification and prognosis of UC, including the modified Truelove and Witts severity index, the Lichtiger score, the Simple Clinical Colitis Activity Index and others. However, in clinical practice it is typically sufficient to describe disease activity in adults as clinical remission, mild, moderate, or severe, as outlined in the Montreal classification. In pediatric patients, the PUCAI is also commonly used to assess severity (Table 5-4).

Current severity indices only account for disease activity at a single timepoint and do not accurately encompass the comprehensive impact of UC on patient life. As such, there is a desire to redefine disease severity using composite criteria to account for disease course, extraintestinal manifestations, measurable inflammatory burden using markers of disease activity and extent and disease effect on patient symptoms, quality of life and disability.

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Differential Diagnosis

It is essential to exclude the presence of other possible causes of colitis in patients presenting with symptoms of UC. Possible causes include infectious colitis caused by bacterial, viral, or parasitic pathogens, in addition to other causes of gastrointestinal inflammation (Table 5-5).

Stool studies should be performed in all patients to exclude the presence of infectious causes, especially Clostridioides difficile. Bacterial colitis should be routinely considered, with increased suspicion in patients with history of exposure. Amebic dysentery should be suspected in patients who traveled to endemic areas and in those exposed to the illness. The most widespread diagnostic test for Entamoeba histolytica is identification of cysts in stool samples by microscopy; however, the most accurate test is for serum amebiasis antibodies. Amebic colitis can also be identified with the presence of classic microscopic findings on endoscopic mucosal biopsy. Viral or parasite-induced colitis should be considered in the immunocompromised. CD and microscopic colitis—a common cause of nobody diarrhea, abdominal pain and weight loss in adults—should be routinely considered as causes. Ischemic colitis should be considered in patients with risk factors for vascular disease. Length of time with illness may assist in making a correct diagnosis, as UC often is reported over weeks to months of illness, whereas, infectious or ischemic colitis are often shorter in duration of illness. Evaluation of endoscopic biopsies aid in differential diagnosis, with the finding of crypt architecture distortion less common in acute, self-limited colitis and almost always seen in idiopathic IBD such as UC.

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Laboratory Investigations

Laboratory features are not disease-specific markers—they help assess disease activity and complications by assessing inflammatory processes or deficiencies due to malnutrition. Although many studies have evaluated the utility of laboratory tests as surrogate markers of IBD activity, none (alone or in a panel) have been shown to be sensitive or specific enough to establish the diagnosis of UC.

Erythrocyte Sedimentation Rate (ESR) and C-Reactive Protein (CRP)

Elevated inflammatory markers, such as ESR and CRP, increase in occurrence with severity and extent of disease. However, normal CRP levels do not rule out disease activity, since fewer than 50% of UC patients have abnormal findings on these tests at diagnosis. Due to the relative insensitivity of inflammatory markers in detecting UC, they cannot be relied on to exclude or make the diagnosis.

Fecal Calprotectin and Lactoferrin

Noninvasive stool biomarkers, such as fecal calprotectin or fecal lactoferrin, are more sensitive and specific for intestinal inflammation. Fecal calprotectin, a protein in stool that correlates with increased neutrophils in the intestine, is strongly correlated with histologic grade of mucosal inflammation, with 94% sensitivity and 64% specificity for active mucosal inflammation. Since patients with low levels of fecal calprotectin have <1% chance of having IBD, this test is useful for ruling out IBD when the differential diagnosis is uncertain as to whether a patient has IBS or IBD. Fecal calprotectin does not distinguish between different causes of intestinal inflammation, so it cannot be used as a definitive diagnostic tool for UC.

ANCA and ASCA

The first and most studied serological markers for IBD are anti-neutrophil cytoplasmic antibody (ANCA) and anti-Saccharomyces cerevisiae antibody (ASCA). The presence of ANCA is more associated with UC, whereas positive ASCA is more associated with CD. Perinuclear ANCA (pANCA) or atypical ANCA (xANCA) is observed in 50% to 70% of UC patients and in <10% of CD patients. As such, ANCA positivity and a negative test for CD-specific ASCA indicate that UC is more likely than CD, which can be useful in making a diagnosis in patients with features of both UC and CD. The ANCA+/ASCA− combination has a specificity of 81% to 98% for UC, whereas the ANCA−/ASCA+ combination has a specificity of 92% to 97% for CD.

Other Investigations

UC patients may have iron deficiency, leukocytosis, anemia, or thrombocytosis. Hypoalbuminemia, a predictor of poor response to biologics and need for colectomy, may be observed in severe disease.

Radiologic Findings

Diagnostic evaluations may include imaging studies, but they are of limited use in diagnosing UC. In patients with acute severe UC, assessment for toxic megacolon should be done using a plain upright abdominal radiograph. CT and MRI are not sensitive or specific enough to be recommended as diagnostic tools.

Endoscopic Evaluation

All patients should undergo endoscopic evaluation since it is the only way to confirm the diagnosis of UC. Colonic inflammation in UC patients almost always begins at the rectum, extending proximally in a contiguous circumferential pattern. This contrasts with patients with CD, who can have regions of disease separated by noninflamed mucosa. Classic endoscopic findings of UC include erythema, loss or normal vascular pattern, erosions, friability, bleeding, granularity and ulcerations (Figure 5-3). There is often a clear demarcation between inflamed and normal tissue in UC, but histologic inflammation can still be observed in normal-appearing mucosa.

Caution should be exercised in patients on topical or systemic medications, since these treatments can result in patchy disease or rectal sparing, which can erroneously be interpreted as evidence of CD. In up to 75% of patients with proctitis, proctosigmoiditis, or left-sided colitis, an area of isolated inflammation called a cecal patch (also called a periappendiceal red patch) may be present around the appendiceal orifice. Although non-contiguous inflammation is a distinguishing feature of CD, the presence of the cecal patch skip-area does not change the diagnosis to CD. Up to 20% of patients with pancolitis may show mild inflammation in the terminal ileum, a feature known as backwash ileitis. In the case scenario where a patient has severe ileitis in the absence of pancolitis, CD should be suspected and an esophagogastroduodenoscopy should be performed in patients with symptoms of upper GI tract involvement to assess this possibility. In 5% to 10% of patients, a definitive diagnosis (UC or CD) cannot be made—these patients are classified as having IBD unclassified (IBDU) or indeterminate colitis. The term indeterminate colitis is often used by pathologists when they are unable to make a definitive diagnosis based on colectomy samples.

Biopsies should be obtained to confirm the correct diagnosis. The optimum number of biopsy samples from a colonoscopy that should be obtained has not been established. In one study it was suggested that two biopsies should be obtained from six different areas, including normal areas, since inflammatory changes may become evidence upon microscopy.

Enlarge  Figure 5-3: Endoscopy Images of Mild, Moderate, and Severe UC. Key: Mild disease with erythema and decreased vascular pattern (A), moderate disease with loss of vascular pattern and erosions (B), and severe disease with diffuse ulcerations (C). Source: Modified from Ungaro R, et al. Lancet. 2017;389(10080):1756-1770.
Figure 5-3: Endoscopy Images of Mild, Moderate, and Severe UC. Key: Mild disease with erythema and decreased vascular pattern (A), moderate disease with loss of vascular pattern and erosions (B), and severe disease with diffuse ulcerations (C). Source: Modified from Ungaro R, et al. Lancet. 2017;389(10080):1756-1770.

Atypical Features in Pediatric Patients

Compared to adults, pediatric UC patients can have more atypical features:

  • Acute severe colitis with deep ulcers and transmural inflammation, features typically present in CD but not UC
  • Macroscopic rectal sparing in 5% to 30% of patients
  • Histologic evaluation showing patchy disease with normal crypt architecture, in 34% of patients, usually under 10 years of age
  • Upper gastrointestinal tract involvement, with ulceration, in 8% of patients
  • Cecal inflammation in 2% of patients with left-sided colitis.

These atypical presentations increase the likelihood of inappropriately diagnosing pediatric UC patients with IBDU or CD.

Histologic Evaluation

Histologically, the disease is limited to the mucosal layers. In untreated patients, signs of active inflammation and features of chronic mucosal injury are typically present. UC is characterized by diffuse inflammatory cell infiltration of the mucosa (from lymphocytes, plasma cells and granulocytes), distorted crypt architecture (shortening and branching of crypts, crypt atrophy and crypt abscesses), goblet cell/mucin depletion, Paneth cell metaplasia and basal lymphoplasmacytosis. Paneth cells are a normal component of the right colon, but not the left colon and if present represent a metaplastic process. Basal lymphoplasmacytosis is the presence of lymphoplasmacytic infiltrate between crypt bases and the muscularis mucosae. The histologic features observed in patients with chronic active colitis are typically consistent across biopsy samples, in terms of degree of injury and inflammation, due to the uniform nature of UC. Histologic disease activity indices include the Robarts Histopathology index and Nancy index (Table 5-6).

In inactive or quiescent disease, UC is histologically characterized by architectural abnormalities in the absence of active inflammation, the most common of which being atrophy, irregularity and shortening of crypts, thickening of the muscularis mucosae and metaplasia. It is important to recognize; however, that individuals with inactive UC can have endoscopically normal mucosa with complete histologic normalization.

 

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References

  • Lichtenstein GR, Stein RB, Clinical Management of Ulcerative Colitis, 2nd ed. Professional Communications Inc. 2023
  • Adams SM, Bornemann PH. Ulcerative colitis. Am Fam Physician. 2013;87(10):699-705.
  • Annese V, Daperno M, Rutter MD, et al. European evidence based consensus for endoscopy in inflammatory bowel disease. J Crohns Colitis. 2013;7:982-1018.
  • Appleman HD. What are the critical histologic features in the diagnosis of ulcerative colitis? Inflamm Bowel Dis. 2008;14(S2):S164-S165.
  • Bernstein CN, Shanahan F, Anton PA, et al. Patchiness of mucosal inflammation in treated ulcerative colitis: a prospective study. Gastrointest Endosc. 1995;42:232-237.
  • Bossuyt X. Serologic markers in inflammatory bowel disease. Clin Chem. 2006;52:171-181.
  • Canani RB, Terrin G, Rapacciuolo L, et al. Faecal calprotectin as reliable non-invasive marker to assess the severity of mucosal inflammation in children with inflammatory bowel disease. Dig Liver Dis. 2008;40:547-553.
  • Christensen B, Hanauer SB, Erlich J, et al. Histologic normalization occurs in ulcerative colitis and is associated with improved clinical outcomes. Clin Gastroenterol Hepatol. 2017;15(10):1557-1564.e1.
  • Conrad K, Roggenbuck D, Laass MW. Diagnosis and classification of ulcerative colitis. Autoimmun Rev. 2014;13(4-5):463-466.
  • Conrad K, Schmechta H, Klafki A, et al. Serological differentiation of inflammatory bowel diseases. Eur J Gastroenterol Hepatol. 2002;14:1-7.
  • Corte C, Fernandopulle N, Catuneanu AM, et al. Association between the ulcerative colitis endoscopic index of severity (UCEIS) and outcomes in acute severe ulcerative colitis. J Crohns Colitis. 2015;9(5):376-381.
  • DeRoche TC, Xiao SY, Liu X. Histological evaluation in ulcerative colitis. Gastroenterol Rep (Oxf). 2014;2(3):178-192.
  • Feuerstein JD, Cheifetz AS. Ulcerative colitis: epidemiology, diagnosis, and management. Mayo Clin Proc. 2014;89(11):1553-1663.
  • Ikeya K, Hanai H, Sugimoto K, et al. The Ulcerative Colitis Endoscopic Index of Severity more accurately reflects clinical outcomes and long-term prognosis than the Mayo Endoscopic Score. J Crohns Colitis. 2016;10(3):286-295.
  • Irvine EJ, Feagan B, Rochon J, et al. Quality of life: a valid and reliable measure of therapeutic efficacy in the treatment of inflammatory bowel disease. Canadian Crohn’s Relapse Prevention Trial Study Group. Gastroenterology. 1994;106(2):287-296.
  • Levine A, Griffiths A, Markowitz J, et al. Pediatric modification of the Montreal classification for inflammatory bowel disease: the Paris classification. Inflamm Bowel Dis. 2011;17(6):1314-1321.
  • Lewis JD. The utility of biomarkers in the diagnosis and therapy of inflammatory bowel disease. Gastroenterology. 2011;140(6):1817-1826.
  • Marchal-Bressenot A, et al. Development and validation of the Nancy histological index for UC. Gut. 2017;66(1):43-49.
  • Menees SB, Powell C, Kurlander J, et al. A meta-analysis of the utility of C-reactive protein, erythrocyte sedimentation rate, fecal calprotectin, and fecal lactoferrin to exclude inflammatory bowel disease in adults with IBS. Am J Gastroenterol. 2015;110:444-454.
  • Mosli MH, et al. Development and validation of a histological index for UC. Gut. 2017;66(1):50-58.
  • Panes J, Bouhnik Y, Reinisch W, et al. Imaging techniques for assessment of inflammatory bowel disease: joint ECCO and ESGAR evidence-based consensus guidelines. J Crohns Colitis. 2013;7:556-585.
  • Park SH, Loftus EV, Yang SK. Appendiceal skip inflammation and ulcerative colitis. Dig Dis Sci. 2014;59: 2050-2057.
  • Prideaux L, De Cruz P, Ng SC, et al. Serological anti-bodies in inflammatory bowel disease: a systematic review. Inflamm Bowel Dis. 2012;18:1340-1355.
  • Sandborn WJ, Feagan BG, Wolf DC, et al; TOUCHSTONE Study Group. Ozanimod Induction and Maintenance Treatment for Ulcerative Colitis. N Engl J Med. 2016;374(18):1754-1762.
  • Sands BE. Biomarkers of inflammation in inflammatory bowel disease. Gastroenterology. 2015;149:1275-1285.
  • Satsangi J, Silverberg MS, Vermeire S, et al. The Montreal classification of inflammatory bowel disease: controversies, consensus, and implications. Gut. 2006;55(6):749-753.
  • Schroeder KW, Tremaine WJ, Ilstrup DM. Coated oral 5-aminosalicylic acid therapy for mildly to moderately active ulcerative colitis. A randomized study. N Engl J Med. 1987;317(26):1625-1629.
  • Siegel CA, Whitman CB, Spiegel BM, et al. Development of an index to define overall disease severity in IBD. Gut. 2018;67(2):244-254.
  • Solem CA, Loftus EV Jr, Tremaine WJ, et al. Correlation of C-reactive protein with clinical, endoscopic, histologic, and radiographic activity in inflammatory bowel disease. Inflamm Bowel Dis. 2005;11(8):707-712.
  • Travis SP, Schnell D, Feagan BG, et al. The impact of clinical information on the assessment of endoscopic activity: characteristics of the Ulcerative Colitis Endoscopic Index Of Severity [UCEIS]. J Crohns Colitis. 2015;9(8):607-616.
  • Travis SP, Schnell D, Krzeski P, et al. Developing an instrument to assess the endoscopic severity of ulcerative colitis: the Ulcerative Colitis Endoscopic Index of Severity (UCEIS). Gut. 2012;61(4):535-542.
  • Travis SP, Schnell D, Krzeski P, et al. Reliability and initial validation of the ulcerative colitis endoscopic index of severity. Gastroenterology. 2013;145(5):987-995.
  • Turner D, Otley AR, Mack D, et al. Development, validation, and evaluation of a pediatric ulcerative colitis activity index: a prospective multicenter study. Gastroenterology. 2007;133:423-432.
  • Ungaro R, Mehandru S, Allen PB, et al. Ulcerative colitis. Lancet. 2017;389(10080):1756-1770.
  • Vermeire S, Van Assche G, Rutgeerts P. Laboratory markers in IBD: useful, magic, or unnecessary toys? Gut. 2006;55(3):426-431.
  • Xie T, Zhang T, Ding C, et al. Ulcerative Colitis Endoscopic Index of Severity (UCEIS) versus Mayo Endoscopic Score (MES) in guiding the need for colectomy in patients with acute severe colitis. Gastroenterol Rep (Oxf). 2018;6(1):38-44.
  • Yu YR, Rodriguez JR. Clinical presentation of Crohn’s, ulcerative colitis, and indeterminate colitis: Symptoms, extraintestinal manifestations, and disease phenotypes. Semin Pediatr Surg. 2017;26(6):349-355.
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