Ulcerative colitis (UC) is one of the two major types of inflammatory bowel disease (IBD), along with Crohn disease (CD). Unlike Crohn disease, which can affect any part of the gastrointestinal tract, ulcerative colitis characteristically involves the large bowel (see the image below). Ulcerative colitis is a lifelong illness that has a profound emotional and social impact on the affected patients.
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Ulcerative colitis. Ulcerative colitis as visualized with a colonoscope.
Signs and symptoms
Patients with UC predominantly complain of the following:
Rectal bleeding
Frequent stools
Mucous discharge from the rectum
Tenesmus (occasionally)
Lower abdominal pain and severe dehydration from purulent rectal discharge (in severe cases, especially in the elderly)
In some cases, UC has a fulminant course marked by the following:
Severe diarrhea and cramps
Fever
Leukocytosis
Abdominal distention
UC is associated with various extracolonic manifestations, as follows:
Uveitis
Pyoderma gangrenosum
Pleuritis
Erythema nodosum
Ankylosing spondylitis
Spondyloarthropathies
Other conditions associated with UC include the following:
Primary sclerosing cholangitis (PSC)
Recurrent subcutaneous abscesses unrelated to pyoderma gangrenosum[1]
Multiple sclerosis[2]
Immunobullous disease of the skin[3]
Physical findings are typically normal in mild disease, except for mild tenderness in the lower left abdominal quadrant (tenderness or cramps are generally present in moderate to severe disease[4] ). In severe disease, the following may be observed:
Fever
Tachycardia
Significant abdominal tenderness
Weight loss
The severity of UC can be graded as follows:
Mild: Bleeding per rectum, fewer than four bowel motions per day
Moderate: Bleeding per rectum, more than four bowel motions per day
Severe: Bleeding per rectum, more than four bowel motions per day, and a systemic illness with hypoalbuminemia (< 30 g/L)
See Presentation for more detail.
Diagnosis
Laboratory studies are useful principally in determining the extent of the disease, excluding other diagnoses, and in assessing the patient’s nutritional status. They may include the following:
Ulcerative colitis (UC) is one of the two major types of inflammatory bowel disease (IBD), along with Crohn disease (CD). Unlike Crohn disease, which can affect any part of the gastrointestinal tract, ulcerative colitis characteristically involves the large bowel (see the images below). Ulcerative colitis is a lifelong illness that has a profound emotional and social impact on the affected patients.
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Ulcerative colitis. Ulcerative colitis as visualized with a colonoscope.
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Ulcerative colitis. Single-contrast enema study in a patient with total colitis shows mucosal ulcers with a variety of shapes, including collar-button....
The exact etiology of ulcerative colitis is unknown, but the disease appears to be multifactorial and polygenic. The proposed causes include environmental factors, immune dysfunction, and a likely genetic predisposition. Some have suggested that children of below-average birth weight who are born to mothers with ulcerative colitis have a greater risk of developing the disease. (See Etiology.)
Histocompatibility human leukocyte antigen (HLA)–B27 is identified in most patients with ulcerative colitis, although this finding is not causally associated with the condition and the finding of HLA-B27 does not imply a substantially increased risk for ulcerative colitis. Ulcerative colitis may also be influenced by diet, although diet is thought to play a secondary role. Food or bacterial antigens might exert an effect on the already damaged mucosal lining, which has increased permeability.
Grossly, the colonic mucosa appears hyperemic, with loss of the normal vascular pattern. The mucosa is granular and friable. Frequently, broad-based ulcerations cause islands of normal mucosa to appear polypoid, leading to the term pseudopolyp (see the image below).
The bowel wall is thin or of normal thickness, but edema, the accumulation of fat, and hypertrophy of the muscle layer may give the impression of a thickened bowel wall. The disease is largely confined to the mucosa and, to a lesser extent, the submucosa. Muscle-layer and serosal involvement is very rare; such involvement is seen in patients with severe disease, particularly toxic dilatation, and reflects a secondary effect of the severe disease rather than primary ulcerative colitis pathogenesis. Early disease manifests as hemorrhagic inflammation with loss of the normal vascular pattern, petechial hemorrhages, and bleeding. Edema is present, and large areas become denuded of mucosa. Undermining of the mucosa leads to the formation of crypt abscesses, which are the hallmark of the disease. (See Presentation.)
The diagnosis of ulcerative colitis is best made with endoscopy and mucosal biopsy for histopathology. Laboratory studies are helpful to exclude other diagnoses and assess the patient's nutritional status, but serologic markers can assist in the diagnosis of inflammatory bowel disease. Radiographic imaging has an important role in the workup of patients with suspected inflammatory bowel disease and in the differentiation of ulcerative colitis from Crohn disease by demonstrating fistulae or the presence of small bowel disease seen only in Crohn disease. (See Workup.)
The initial treatment for ulcerative colitis includes mesalamine, corticosteroids, anti-inflammatory agents, antidiarrheal agents, and rehydration (see Medication). Surgery is considered if medical treatment fails or if a surgical emergency develops. (See Treatment.)
For patient education resources, visit the Digestive Disorders Center. In addition, see the patient education articles Inflammatory Bowel Disease, Crohn's Disease (What Is Crohn's Disease?), and Crohn's Disease FAQs.
Additional information can be found at Colitis Foundation of America (CCFA).
Ulcerative colitis (UC) extends proximally from the anal verge in an uninterrupted pattern to involve part or the entire colon. The rectum is involved in more than 95% of cases; some authorities believe that the rectum is always involved in untreated patients. Rectal involvement occurs even when the rest of the colon is spared.
Ulcerative colitis occasionally involves the terminal ileum, as a result of an incompetent ileocecal valve. In these cases, which may constitute as many as 10% of patients, the reflux of noxious inflammatory mediators from the colon results in superficial mucosal inflammation of the terminal ileum, called backwash ileitis.[8, 9] Up to about 30 cm of the terminal ileum may be affected.
Ulcerative colitis (UC) is a diffuse, nonspecific inflammatory disease whose etiology is unknown.[10] The colonic mucosa proximal from the rectum is persistently affected, frequently involving erosions and/or ulcers, as well as involving repeated cycles of relapse and remission and potential extraintestinal manifestations.[10]
A variety of immunologic changes have been documented in ulcerative colitis. Subsets of T cells accumulate in the lamina propria of the diseased colonic segment. In patients with ulcerative colitis, these T cells are cytotoxic to the colonic epithelium. This change is accompanied by an increase in the population of B cells and plasma cells, with increased production of immunoglobulin G (IgG) and immunoglobulin E (IgE).[11]
Anticolonic antibodies have been detected in patients with ulcerative colitis. A small proportion of patients with ulcerative colitis have antismooth muscle and anticytoskeletal antibodies.
Microscopically, acute and chronic inflammatory infiltrate of the lamina propria, crypt branching, and villous atrophy are present in ulcerative colitis. Microscopic changes also include inflammation of the crypts of Lieberkühn and abscesses. These findings are accompanied by a discharge of mucus from the goblet cells, the number of which is reduced as the disease progresses. The ulcerated areas are soon covered by granulation tissue. Excessive fibrosis is not a feature of the disease. The undermining of the mucosa and an excess of granulation tissue lead to the formation of polypoidal mucosal excrescences, which are known as inflammatory polyps or pseudopolyps.
The exact etiology of ulcerative colitis (UC) is unknown, but certain factors have been found to be associated with the disease, and some hypotheses have been presented. Etiologic factors potentially contributing to ulcerative colitis include genetic factors, immune system reactions, environmental factors, nonsteroidal anti-inflammatory drug (NSAID) use, low levels of antioxidants, psychological stress factors, a smoking history, and consumption of milk products. Certain types of food composition and the use of oral contraceptives may be associated with this condition.[10]
Some evidence exists to indicate smoking may be protective of ulcerative colitis, but a causal association remains unclear.[10] A systematic review and meta-analysis that evaluated the association between smoking and need for surgery in patients with inflammatory bowel disease found that current smokers with Crohn disease had an increased risk of intestinal resection surgery compared to their never-smoking counterparts, whereas in patients with ulcerative colitis, current and never smokers had similar rates of colectomy.[12] However, there was an increased risk for colectomy in former smokers with ulcerative colitis.
Genetics
The current hypothesis is that genetically susceptible individuals have abnormalities of the humoral and cell-mediated immunity and/or generalized enhanced reactivity against commensal intestinal bacteria, and that this dysregulated mucosal immune response predisposes to colonic inflammation.[13]
A family history of ulcerative colitis (observed in 1 in 6 relatives) is associated with a higher risk for developing the disease. Disease concordance has been documented in monozygotic twins.[14] Genetic association studies have identified multiple loci,[10] including some that are associated with both ulcerative colitis and Crohn disease; one relatively recently identified locus is also associated with the susceptibility to colorectal cancer (CDH1).[15]
Chromosomes are thought to be less stable in patients with ulcerative colitis, as measured with telomeric associations in peripheral leukocytes.[16] This phenomenon may also contribute to the increased cancer risk. Whether these abnormalities are the cause or the result of the intense systemic inflammatory response in ulcerative colitis is unresolved.
Immune reactions
Immune reactions that compromise the integrity of the intestinal epithelial barrier may contribute to ulcerative colitis. Serum and mucosal autoantibodies against intestinal epithelial cells may be involved. The presence of antineutrophil cytoplasmic antibodies (ANCA) and anti– Saccharomyces cerevisiae antibodies (ASCA) is a well-known feature of inflammatory bowel disease.[17, 18, 19, 20, 21]
In addition, an immune modulatory abnormality has been assumed to be responsible for the lower incidence of ulcerative colitis in patients who have undergone previous appendectomy. The incidence of previous appendectomy is lower in patients with ulcerative colitis (4.5%) than in control subjects (19%), and a further protective effect is observed if the appendectomy was performed before the patient was age 20 years.[22] Also, patients in whom appendectomy was performed for inflammatory disorders (eg, appendicitis or mesenteric adenitis) seem to have a lower incidence of ulcerative colitis than patients who undergo appendectomy for other disorders such as nonspecific abdominal pain.[23]
Environmental factors
Environmental factors also play a role. For example, sulfate-reducing bacteria, which produce sulfides, are found in large numbers in patients with ulcerative colitis, and sulfide production is higher in patients with ulcerative colitis than in other people. Sulfide production is even higher in patients with active ulcerative colitis than in patients in remission. The bacterial microflora is altered in patients with active disease.[24] A decrease in Klebsiella species is seen in the ileum of patients relative to control subjects. This difference disappears after proctocolectomy.
NSAID use
NSAID use is higher in patients with ulcerative colitis than in control subjects, and one third of patients with an exacerbation of ulcerative colitis report recent NSAID use. This finding leads some clinicians to recommend avoidance of NSAID use in patients with ulcerative colitis.[25]
Other etiologic factors
Other factors that may be associated with ulcerative colitis include the following:
Vitamins A and E, both considered antioxidants, are found in low levels in as many as 16% of children with ulcerative colitis exacerbation.[26]
Psychological and psychosocial stress factors can play a role in the presentation of ulcerative colitis and can precipitate exacerbations.[23]
Smoking is negatively associated with ulcerative colitis (although some evidence appears to show it having a protective effect[10] ). This relationship is reversed in Crohn disease.
In the United States, about 1 million people are affected with ulcerative colitis (UC).[27, 28] The annual incidence is 10.4-12 cases per 100,000 people, and the prevalence rate is 35-100 cases per 100,000 people. Ulcerative colitis is three times more common than Crohn disease.
Ulcerative colitis occurs more frequently in white persons than in black persons or Hispanics. The incidence of ulcerative colitis is reported to be 2-4 times higher in Ashkenazi Jews. However, population studies in North America do not completely support this assertion.
Ulcerative colitis is slightly more common in women than in men. The age of onset follows a bimodal pattern, with a peak at 15-25 years and a smaller one at 55-65 years, although the disease can occur in people of any age.[29] Ulcerative colitis is uncommon in those younger than 10 years. Two of every 100,000 children are affected; however, 20%-25% of all cases of ulcerative colitis occur in persons aged 20 years or younger.
International statistics
Ulcerative colitis is more common in the Western and Northern hemispheres; the incidence is low in Asia and the Far East.[4]
In Japan, there are more than 160,000 patients with ulcerative colitis (about 27 per 100,000 people) and, unlike Western nations, a male predominance exists.[10]
In a systematic review and meta-analysis to evaluate patient-reported outcomes for rectal bleeding and stool frequency in 2132 patients with ulcerative colitis (UC) in endoscopic remission, investigators noted that most of these individuals who had normal rectal bleeding and stool frequency subscores attained endoscopic remission, although many had no rectal bleeding.[30] However, despite endoscopic remission, many patients had abnormal stool frequencies.
Ulcerative colitis may result in disease-related mortality. However, overall mortality is not increased in patients with ulcerative colitis, as compared to the general population. An increase in mortality may be observed among elderly patients with the disease. Mortality is also increased in patients who develop complications (eg, shock, malnutrition, anemia). Evidence suggests that mortality is increased in patients with ulcerative colitis who undergo any form of medical or surgical intervention.
Involvement of the muscularis propria in the most severe cases can lead to damage to the nerve plexus, resulting in colonic dysmotility, dilatation, and eventual infarction and gangrene. This condition is termed toxic megacolon and is characterized by a thin-walled, large, dilated colon that may eventually become perforated. Chronic ulcerative colitis is associated with pseudopolyp formation in about 15%-20% of cases. Chronic and severe cases can be associated with areas of precancerous changes, such as carcinoma in situ or dysplasia.
The most common cause of death of patients with ulcerative colitis is toxic megacolon. Colonic adenocarcinoma develops in 3%-5% of patients with ulcerative colitis, and the risk increases as the duration of disease increases. Patients with extensive ulcerative colitis over a long period have a significantly increased risk of colorectal cancer.[10] The risk of colonic malignancy is higher in cases of pancolitis and in cases in which disease onset occurs before age 15 years. Benign stricture rarely causes intestinal obstruction.
Patients with ulcerative colitis (UC) predominantly complain of rectal bleeding, with frequent stools and mucous discharge from the rectum.[31] Some patients also describe tenesmus. The onset is typically insidious. In severe cases, purulent rectal discharge causes lower abdominal pain and severe dehydration, especially in the elderly population.
Ulcerative colitis manifests as an intense inflammatory reaction in the large intestine. Rarely, patients have persistence of small intestinal inflammation following proctocolectomy and pull-through.[32, 33] Constipation may be the main symptom when the inflammation is limited to the rectum (proctitis).[4]
Fulminant disease
In some cases, ulcerative colitis has a fulminant course marked by severe diarrhea and cramps, fever, leukocytosis, and abdominal distention. Fulminant disease occurs more often in children than in adults.[34] An estimated 15% of patients present with an attack severe enough to require hospitalization and steroid therapy.[35, 36] Children may also present with systemic complaints, including fatigue, arthritis, failure to gain weight, and delayed puberty. The differential diagnosis of these symptoms in the pediatric population includes many entities, and definitive diagnosis may be delayed.
Extracolonic manifestations
Extraintestinal manifestations of inflammatory bowel disease include the following[4] :
Musculoskeletal conditions: Peripheral or axial arthropathy
Ulcerative colitis is associated with various extracolonic manifestations. These include uveitis, pyoderma gangrenosum, pleuritis, erythema nodosum, ankylosing spondylitis, and spondyloarthropathies. Reportedly, 6.2% of patients with inflammatory bowel disease have a major extraintestinal manifestation. Uveitis is the most common, with an incidence of 3.8%, followed by PSC at 3%, ankylosing spondylitis at 2.7%, erythema nodosum at 1.9%, and pyoderma gangrenosum at 1.2%.[37] However, reports vary, and some have stated that the incidence of ankylosing spondylitis is as high as 10%. Arthropathies occur in as many as 39% of patients with inflammatory bowel disease. About 30% of such patients have inflammatory back pain, 10% have synovitis, and as many as 40% have radiologic findings of sacroiliitis.[38]
Primary sclerosing cholangitis
PSC is a potentially serious condition associated with ulcerative colitis, often resulting in cholestatic jaundice and liver failure that requires liver transplantation. Of patients with PSC, 75% have inflammatory bowel disease. Of patients with ulcerative colitis, 5% have cholestatic liver disease, and 40% of those have PSC. One interesting hypothesis about the etiology of PSC in patients with ulcerative colitis involves the release of proinflammatory agents in the colon and their absorption into the enterohepatic circulation; they are then concentrated in the biliary system, leading to bile duct damage.[39, 40]
Additional manifestations of disease
Anecdotal reports of recurrent subcutaneous abscesses unrelated to pyoderma gangrenosum exist,[1] and multiple sclerosis also has been weakly associated with ulcerative colitis.[2]
Immunobullous disease of the skin has been associated with ulcerative colitis. One theory regarding this association is the concept of epitope spread. Colonic inflammation leads to mucosal damage, which exposes otherwise hidden antigens. Antibodies to these antigens are then formed; these most likely are cell adhesion molecules, which cross-react with similar antigens in other tissues.[3]
Findings from abdominal examination are usually unremarkable in ulcerative colitis (UC). Physical findings are typically normal in mild disease, except for mild tenderness in the lower left abdominal quadrant (tenderness or cramps are generally present in moderate to severe disease[4] ). The extent and/or the severity of the disease may be reflected by abdominal tenderness, and digital rectal examination may yield mucus and bloody stools.[10]
Patients with severe disease can have signs of volume depletion and toxicity, including the following:
See also the American College of Gastroenterology recommendations in the Guidelines section.
The diagnosis of ulcerative colitis (UC) is best made with endoscopy and mucosal biopsy for histopathology. Laboratory studies are helpful to exclude other diagnoses and assess the patient's nutritional status, but serologic markers can assist in the diagnosis of inflammatory bowel disease. Radiographic imaging has an important role in the workup of patients with suspected inflammatory bowel disease and in the differentiation of ulcerative colitis from Crohn disease by demonstrating fistulae or the presence of small bowel disease seen only in Crohn disease.
Capsule endoscopy is sensitive for early mucosal inflammation, but it can only detect mucosal changes, whereas magnetic resonance imaging (MRI) and intestinal ultrasonography are able to reveal transmural inflammation as well as identify complications.[10, 44] Furthermore, MRI detects fistulas, deep ulcerations, and a thickened bowel wall.[44] Ultrasonography is inexpensive and can be performed at the point of care by the treating gastroenterologist.
Ultrasonography, computed tomography (CT) scanning, and MRI can determine pre- and posttreatment disease activity or identify disease complications.[10] Cross-sectional imaging should be used to detect strictures in the case of complications.[44] Because of radiation associated with CT scanning, the preferred methods are MRI and intestinal ultrasonography. Cross-sectional imaging is also recommended for the detection of abscesses.[44]
Colonoscopy can confirm the diagnosis of suspected ulcerative colitis; it is also the technique of choice to assess disease activity in patients with symptomatic colonic Crohn disease or ulcerative colitis.[44] Note that colonoscopy findings of diffuse inflammatory changes and negative stool cultures are not sufficient for the diagnosis of ulcerative colitis but requires chronic changes over time (ie, 6 months, in the absence of other emerging diagnoses) in addition to histologic signs of chronic inflammation.[4] Complementary cross-sectional imaging can be used to assess phenotype and as an alternative to evaluate disease activity.[44]
As noted, laboratory studies are useful principally for helping to exclude other diagnoses and to assess the patient's nutritional status. However, serologic markers can assist in the diagnosis of inflammatory bowel disease.
Plain abdominal radiographs are a useful adjunct to imaging in cases of ulcerative colitis of acute onset. In severe cases, the images may show colonic dilatation, suggesting toxic megacolon, evidence of perforation, obstruction, or ileus.
Radiologic findings in cases of acute enterocolitis from infection caused by Entamoeba histolytica (amebiasis), cytomegaloviral colitis, and Isospora, Salmonella, Shigella, or Yersinia may be similar to the findings seen in cases of ulcerative colitis; this is especially true with CT scans.
Double-contrast barium enema examination is a valuable technique for diagnosing ulcerative colitis and Crohn disease, even in patients with early disease, because of its ability to depict fine mucosal detail. Traditionally, barium enema examination has been the mainstay of radiologic investigation for suspected ulcerative colitis.[45, 46, 47, 48]
Colonic biopsy samples from patients with ulcerative colitis may show significantly increased levels of platelet-activating factor (PAF). PAF release, stimulated by leukotrienes, endotoxin, or other factors, may be responsible for the mucosal inflammation; however, this process is not clear.
Much work in the past decade has focused on the development of serologic markers for inflammatory bowel disease. Antineutrophil cytoplasmic antibodies (ANCA) and anti–Saccharomyces cerevisiae antibodies (ASCA) have been the most intensely studied.
ANCA is most commonly associated with ulcerative colitis (UC). Specifically, perinuclear ANCA (pANCA), found on the inside of the nuclear membrane, is highly associated with ulcerative colitis. Positive pANCA and negative ASCA findings suggest ulcerative colitis, whereas negative pANCA and positive ASCA suggest Crohn disease.[4] ANCA assay results are positive in 60%-80% of patients with ulcerative colitis. The presence of pANCA is associated with an earlier need for surgery. The finding of ANCA is roughly 50% sensitive, is 94% specific, and has a 76% positive predictive value for ulcerative colitis.[16, 17, 19]
ASCA is more highly associated with Crohn disease and is present in 60% of cases, whereas ASCA is present in only 12% of patients with ulcerative colitis. ANCA is present in only about 40% of patients with Crohn disease. ANCA and ASCA titers are not correlated with disease activity.
In children with ambiguous and mild complaints in whom ulcerative colitis is part of the differential diagnosis, algorithms have been proposed in which the presence of ANCA is used to identify those who may require more invasive diagnostic tests.[18]
Attempts have been made to correlate ANCA titers with postoperative complications, although this association has not been proven.[20]
Anemia (ie, hemoglobin < 14 g/dL in males and < 12 g/dL in females)
Thrombocytosis (ie, platelet count >350,000/µL)
Comprehensive metabolic panel
Findings on the comprehensive metabolic panel may include the following:
Hypoalbuminemia (ie, albumin < 3.5 g/dL)
Hypokalemia (ie, potassium < 3.5 mEq/L)
Hypomagnesemia (ie, magnesium < 1.5 mg/dL)
Elevated alkaline phosphatase: More than 125 U/L suggests primary sclerosing cholangitis (usually >3 times the upper limit of the reference range).
Inflammatory markers
Elevation of the erythrocyte sedimentation rate (variable reference ranges, usually 0-33 mm/h) and C-reactive protein level (ie, >100 mg/L) correlates with disease activity.[10] Fecal calprotectin is a marker of activity of inflammation[4, 10] ; it can also be used to determine mucosal healing 3-6 months after treatment initiation.[44] Fecal lactoferrin and alpha-1-antitrypsin studies are used to exclude intestinal inflammation.[4]
Stool assays
Stool studies are used to exclude other causes (see Differentials) and to rule out infectious enterocolitis.[10] These tests include evaluation of fecal blood or leukocytes, ova and parasite studies, viral studies, culture for bacterial pathogens, and Clostridium difficile titer.[4]
Once ulcerative colitis (UC) is suspected, endoscopy must be performed. Flexible sigmoidoscopy may be performed if the symptoms are mild, and the physician is likely to initiate therapy on the basis of the results obtained. However, most physicians perform a full colonoscopy if inflammation is found with flexible sigmoidoscopy. Therefore, in most circumstances in which ulcerative colitis is suspected, directly proceeding to full colonoscopy is more cost effective.[49] This practice may be especially applicable in young children, in whom flexible sigmoidoscopy is likely to require the same degree of sedation as that of colonoscopy.
Endoscopic findings of ulcerative colitis include the following[10] :
Loss of vascular pattern
Granular and fragile mucosa
Ulceration, erosions, and/or pseudopolyposis
Multiple biopsy samples should be obtained from both inflamed and normal-appearing mucosa. Despite reports that biopsy results are sensitive and specific in the diagnosis of ulcerative colitis, the inherent failure rates of rectal reconstruction in ulcerative colitis due to the late diagnosis of Crohn disease or indeterminate colitis indicate that biopsy results may not be as accurate as originally thought. However, the diagnosis of Crohn disease on the basis of granuloma identification is reliable.[50]
Findings on colonoscopy with biopsy confirm a diagnosis (see the image below). Also, this evaluation is useful for documenting the extent of the disease, for monitoring disease activity, and for surveillance for dysplasia or cancer. However, be cautious in attempting colonoscopy with biopsy in a patient with severe disease because of the possible risk of perforation or other complications. Although diagnostic colonoscopy has been,[51] and continues to be, a relatively safe procedure,[52] the rate of perforation is higher in patients with severe colitis.[53]
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Ulcerative colitis. Increased postrectal space is a known feature of ulcerative colitis.
The extent of disease is defined by the following:
Extensive disease: Evidence of ulcerative colitis proximal to the splenic flexure
Left-sided disease: Ulcerative colitis present in the descending colon up to, but not proximal to, the splenic flexure
Proctosigmoiditis: Disease limited to the rectum with or without sigmoid involvement
Guidelines on the use of endoscopy in the diagnosis and management of inflammatory bowel disease are available from the American Society for Gastrointestinal Endoscopy.[54]
Histologically, most of the pathology in ulcerative colitis (UC) is limited to the mucosa and submucosa. In fulminant cases, the muscularis propria can be affected. Pathologic features that are typically seen include intense infiltration of the mucosa and submucosa with neutrophils and crypt abscesses, lamina propria with lymphoid aggregates, plasma cells, and mast cells and eosinophils, as well as shortening and branching of the crypts. Goblet cell depletion is also notable. These features are not unique to ulcerative colitis[10] : Except for crypt distortion, the same cellular response can be seen in acute infectious colitis or Crohn disease.
Imaging has an important role in the workup of patients with suspected inflammatory bowel disease and in the differentiation of ulcerative colitis (UC) and Crohn disease.
Plain abdominal radiographs are a useful adjunct to imaging in cases of ulcerative colitis of acute onset. Because of its ability to depict fine mucosal detail, double-contrast barium enema examination also is a valuable technique for diagnosing ulcerative colitis and Crohn disease, even in patients with early disease.
Cross-sectional imaging studies (eg, ultrasonography [US], magnetic resonance imaging [MRI], computed tomography [CT] scanning) are useful for showing the effects of these conditions on the bowel wall.
Radionuclide studies are useful in cases of acute fulminant colitis when colonoscopy or barium enema examination is contraindicated.
Angiography may be helpful because evidence suggests microcirculatory disturbances may play an important role in the pathophysiology of ulcerative colitis.
See Ulcerative Colitis Imaging for more detailed information.
See also the American College of Gastroenterology and American Gastroenterological Association recommendations in the Guidelines section.
The treatment of ulcerative colitis (UC) is made on the basis of the disease stage (active, remission), extent (proctitis, distal colitis, left-sided colitis, pancolitis), and severity (mild, moderate, severe).[10] In general, it relies on initial medical management with corticosteroids and anti-inflammatory agents, such as sulfasalazine, in conjunction with symptomatic treatment with antidiarrheal agents and rehydration.[55] Surgery is contemplated when medical treatment fails or when a surgical emergency (eg, perforation of the colon) occurs. Surgical options include total colectomy (panproctocolectomy) and ileostomy, total colectomy, and ileoanal pouch reconstruction or ileorectal anastomosis. In an emergency situation, subtotal colectomy with end-ileostomy is recommended.[5, 6, 7]
Chronic ulcerative colitis is associated with an increase in the risk of carcinoma, and colonic carcinoma may easily be missed in the setting of ulcerative colitis. Patients with ulcerative colitis must be made aware of the significant risk of colon cancer, and surgical intervention in nonacute cases should be encouraged after 10 years of disease or when symptoms are refractory or steroid dependent. Indications for surgery in ulcerative colitis vary and are discussed in detail under Indications for Surgery.
As yet, no evidence suggests that regular endoscopic screening of patients with ulcerative colitis improves survival. However, the current standard of practice by many gastroenterologists is to continue screening these patients at regular intervals, owing to the risk of cancer development and possible legal implications if malignancy is not detected. Mucosal healing should be determined endoscopically or using fecal calprotectin levels approximately 3 to 6 months after treatment initiation.[44]
Consultations
Consultations include a gastroenterologist, as well as a surgeon for severe or fulminant colitis.
In mild ulcerative colitis (UC) disease confined to the rectum, topical mesalazine (Asacol) given by suppository is the preferred therapy. Enemas and foams are less effective because their concentration in the rectum rapidly diminishes. Left-sided colonic disease is best treated with a combination of mesalazine suppository and an oral aminosalicylate. Combined oral and topical therapy is better than either route alone. Of the oral aminosalicylates, sulfasalazine has the longest history. Sulfasalazine is 5-aminosalicylate (5-ASA) coupled to a sulfapyridine. It is poorly absorbed in the proximal bowel, and the bacteria in the colon uncouple the 5-ASA from the sulfa moiety, allowing 5-ASA to exert its anti-inflammatory effect on the colonic mucosa by inhibiting prostaglandin synthesis.
Mesalazine, another 5-ASA-containing molecule, is better tolerated orally than sulfasalazine and has become the preferred medication. A meta-analysis previously suggested that doses of at least 2 g per day are more effective in inducing remission and preventing relapse, but that exceeding 2.5 g per day might not have any additional benefit.[56] However, more recent studies have shown that higher doses are beneficial in patients not responding to lower doses (eg, 2.4 g vs 4.8 g).[57, 58, 59]
After remission, long-term maintenance therapy is encouraged, but compliance rates are low. One systematic review analyzed the outcomes of once-daily dosing of mesalazine compared to a conventional dosing schedule (minimum of twice daily). It was concluded that once-daily dosing is as effective as divided dosing for relapse prevention, and such daily dosing may increase compliance, although this has not been formally evaluated.[60, 61]
Systemic steroids are indicated when the disease fails to quickly respond to aminosalicylates.
In January 2013, the US Food and Drug Administration (FDA) approved an extended-release oral formulation of budesonide for the treatment of active mild-to-moderate ulcerative colitis in adults patients.[62] Because budesonide is a potent corticosteroid that exerts only minimal systemic activity, this formulation provides the benefit of a powerful anti-inflammatory drug delivered locally while avoiding many of the systemic side effects associated with systemic steroids.
A pooled analysis of the efficacy and safety outcomes from two phase 3 studies of oral budesonide MMX (Multi Matrix colonic delivery) 9 mg and 6 mg and placebo in 672 patients with mild-to-moderate ulcerative colitis found that budesonide MMX 9 mg was safe, efficacious, and well tolerated for inducing remission in these patients.[63] The budesonide MMX 9 mg resulted in significantly greater combined clinical and colonoscopic remission rates compared with placebo, whereas the budesonide MMX 6 mg did not. Symptom resolution and colonoscopic improvement rates were also significantly greater with budesonide MMX 9 mg compared with placebo.[63]
Budesonide rectal foam was FDA approved in October 2014 and is indicated for the induction of remission in adults with active mild-to-moderate distal ulcerative colitis extending up to 40 cm from the anal verge. Approval was based on two randomized, placebo-controlled trials (N = 546) that showed that more participants who received the budesonide rectal foam achieved remission and a rectal bleeding score of 0 at 6 weeks of therapy than placebo.[64]
Acute, severe ulcerative colitis (UC) (ie, >6 bloody bowel movements/day, with one of the following: fever >38°C [100.4°F], hemoglobin level < 10.5 g/dL, heart rate >90 bpm, erythrocyte sedimentation rate >30 mm/h, or C-reactive protein level >30 mg/dL) requires hospitalization and treatment with intravenous high-dose corticosteroids (hydrocortisone 400 mg/d or methylprednisolone 60 mg/d). A meta-analysis supports the use of glucocorticosteroids in inducing remission in acute severe ulcerative colitis.[65]
Alternative induction medications have been evaluated. Cyclosporine, tacrolimus, infliximab, adalimumab, and golimumab are often effective in bringing steroid-resistant disease under control. Infliximab has been shown to be superior to placebo in inducing remission of moderate-to-severe ulcerative colitis.[66] These agents have not been compared in a randomized, controlled fashion, and therefore, one drug cannot be recommended over the others. They have all been associated with overwhelming sepsis.
A systematic review and meta-analysis comprising eight randomized controlled studies of biologics in patients with inflammatory bowel disease found that primary nonresponse to anti-tumor necrosis factor (anti-TNF) agents was associated with an inferior response to second-line non-TNF biologics, relative to therapy discontinuation owing to secondary loss of response after initial response or intolerance.[67]
Cyclosporine is effective for inducing remission in severely active and refractory ulcerative colitis, with an efficacy equivalent to that of infliximab.[10] Tacrolimus is effective for inducing remission in active disease, but no long-term safety and efficacy data exist.[10] Cyclosporine and tacrolimus are both nephrotoxic and should not be used for long-term therapy. Infliximab requires the coadministration of an antimetabolite to limit the development of human anti-mouse antibody (HAMA).
In the Active Ulcerative Colitis Trial (ACT)-1 and ACT-2, colectomy incidence was found to be 10% for the infliximab group, as compared to 17% for the placebo group through 54 weeks, and additional benefits of infliximab included fewer colitis-related hospitalizations and surgeries/procedures. In these two randomized, double-blind, placebo-controlled trials, the benefit of infliximab induction and maintenance therapy in moderate to severe ulcerative colitis was demonstrated in 728 patients.[68]
In a systematic review of 76 randomized controlled trials as well as cohort, cross-sectional, and case-controlled studies (years 2000-2016) that evaluated the pharmacokinetics of infliximab and/or infliximab dose intensification strategies in the setting of acute severe ulcerative colitis, investigators noted an increased infliximab clearance in patients.[69] Moreover, it appeared that in some cohort studies, at least half of the patients with acute severe disease showed clinical improvement from an infliximab dose-intensified regimen, whereas findings from case-controlled studies suggested that this type of regimen plus an additional 1-2 infusions in the first 3 weeks of therapy potentially led to up to an 80% reduction in the early (3-month) colectomy rate.
A more recent study found that accelerated clearance of infliximab was associated with treatment failure in those with corticosteroid-refractory acute ulcerative colitis.[70] The investigators indicated that their findings support using accelerated infliximab induction regimens in those with corticosteroid-refractory acute disease that has failed conventional dosing regimens.
Adalimumab was approved by the FDA in September 2012 for ulcerative colitis unresponsive to immunosuppressants. Approval was based on two phase 3 clinical studies. Both studies enrolled patients who had moderate-to-severe active ulcerative colitis despite concurrent or prior treatment with immunosuppressants (ie, corticosteroids, azathioprine, 6-mercaptopurine). Clinical remission was achieved in each study by week 8 and maintained in the long-term maintenance study at week 52.[71, 72]
Golimumab was approved for induction and maintenance of ulcerative colitis in May 2013. In the Program of Ulcerative Colitis Research Studies Utilizing an Investigational Treatment (PURSUIT) trial, a significantly higher proportion of patients receiving induction treatment with subcutaneous administrations of golimumab 200 mg at week 0 and 100 mg at week 2, or golimumab 400 mg at week 0 and 200 mg at week 2, met the primary endpoint of clinical response at week 6 compared with the placebo (51.8%, 55%, and 29.7% of patients achieving clinical response, respectively [P < 0.0001]).[73]
The FDA approved tofacitinib, a Janus kinase (JAK) inhibitor, in May 2018 for induction and maintenance of adults with moderately to severely active ulcerative colitis.[74] It is the first oral biologic agent approved for long-term use for this condition. Approval was based on the OCTAVE phase 3, randomized, double-blind, placebo-controlled induction 1 and 2 trials (N = 1139).[74, 75] In the OCTAVE Induction 1 trial, remission at 8 weeks occurred in 18.5% of the tofacitinib group compared to 8.2% in the placebo group (P = 0.007); in the OCTAVE Induction 2 trial, remission occurred in 16.6% versus 3.6% (P < 0.001). In addition, the OCTAVE Sustain trial reported remission at 52 weeks in 34.3% of the 5-mg tofacitinib group and 40.6% in the 10-mg tofacitinib group compared to 11.1% in the placebo group (P < 0.001 for both comparisons with placebo).[75]
Some evidence suggests that in carefully selected patients whose condition fails both steroids and either cyclosporine or infliximab, a crossover to second-line treatments may avoid colectomy in the short term (within 2 months).[76]
The long-term outcome in such patients is less clear, and further followup studies are required both to assess the frequency with which such rescued patients progress to colectomy and to compare the overall outcomes in the longer term in such patients after crossover of second-line therapy compared with transition to colectomy after the first failure of second-line therapy.
Vedolizumab is a recombinant humanized monoclonal antibody that binds to α4β7 integrin. Integrins are proteins involved in regulating cellular movement including migration of leukocytes to the gut. Vedolizumab is indicated for moderate to severe ulcerative colitis in patients who have had an inadequate response with, lost response to, or were intolerant to a TNF blocker or immunomodulator; or had an inadequate response with, were intolerant to, or demonstrated dependence on corticosteroids. Approval was based on a large phase 3 clinical trial conducted to simultaneously evaluate vedolizumab for both ulcerative colitis and Crohn disease, and included several clinical studies involving 2700 patients in nearly 40 countries.
In patients with ulcerative colitis who had a response to vedolizumab induction, 41.8% continued to be in clinical remission at 52 weeks compared with 15.9% of patient taking placebo (P < 0.001).[77]
For induction, other treatments have been proposed—but are not standard therapy—and include the following:
Antibiotics have been used as an adjunct to steroid therapy but have not altered outcomes. However, a systemic review and meta-analysis by Khan et al and evidence-based guidelines by the Japanese Society of Gastroenterology indicate that antibiotic therapy may induce remission in active ulcerative colitis.[10, 78] However, selection of the type and duration of antibiotics remains undetermined.[10]
Helminth ova have not been shown to be superior to placebo.
Heparin may promote epithelial repair but is not effective given current delivery systems.
Leukocytapheresis has shown some potential and is quite popular in Japan, where it has been used to induce remission[79] and prevent postoperative septic complications.[80] Confirmatory studies in adults[81] and pediatric patients[82] are very promising. Intensive therapy (two sessions weekly) provides more rapid induction of remission and a better remission rate for moderate to severe ulcerative colitis than weekly therapy.[10] However, it remains a resource-intensive treatment.A randomized, multicenter open trial that compared seven weekly sessions of granulocyte/monocyte apheresis (GMA) plus oral prednisone (40 mg/day and tapering) with prednisone alone in patients with active steroid-dependent ulcerative colitis found that although clinical relapse was delayed with GMA/prednisone, the proportion of steroid-free remissions in these patients did not increase.[83]
Historically, surgery has been viewed as definitive therapy for ulcerative colitis (UC). Indications for surgery in ulcerative colitis are varied. Failure of medical management is the most common indication for surgery.
Indications for urgent surgery in patients with ulcerative colitis include (1) toxic megacolon refractory to medical management, (2) fulminant attack refractory to medical management, and (3) uncontrolled colonic bleeding. Indications for elective surgery in ulcerative colitis include (1) long-term steroid dependence, (2) dysplasia or adenocarcinoma found on screening biopsy, (3) and the presence of disease for 7-10 years.
A retrospective study (2002-2013) of data from 758 patients who underwent ileal pouch-anal anastomosis for ulcerative colitis in a high-volume Canadian inflammatory bowel institution found this procedure to be safe and effective for surgical management of ulcerative colitis.[84] Four hundred sixty pelvic pouches were created in 2 stages, 285 in 3 stages, and 13 in nontraditional staged operations. The most common early, same hospital stay complications were pelvic abscess (17.8%), small bowel obstruction (17.7%), and wound infection (14.3%), whereas anal stricture and pouch fistula were the most common late, post-discharge complications. The investigators reported an overall 12.1% pouch leak rate.[84]
Once remission has been achieved, maintenance therapy is recommended for all patients with ulcerative colitis (UC) to prevent relapse. Oral aminosalicylates are indicated for disease that responded to acetylsalicylic acid (ASA) or steroids. Aminosalicylates are effective for induction and maintenance of remission in ulcerative colitis; the efficacy of these preparations for preventing ulcerative colitis-associated colorectal cancer remains inconclusive.[10] Patients who do not continue with maintenance therapy experience high rates of relapse. Some patients are unable to maintain remission or are intolerant of 5-aminosalicylic acid (5-ASA) (mesalamine). Azathioprine and 6-mercaptopurine are alternatives with proven effectiveness for maintenance of remission, particularly for those who are steroid dependent or unable to maintain remission with 5-ASA preparations.[10] For patients who were induced with infliximab, maintenance therapy should continue with infliximab or azathioprine.
Anti-tumor necrosis factor (anti-TNF) agents are effective for the induction of remission in steroid-refractory or steroid-dependent moderate to severe ulcerative colitis.[10] If golimumab was used for induction with a good response, monthly maintenance therapy should continue with golimumab. In the PURSUIT maintenance trial (Program of Ulcerative Colitis Research Studies Utilizing an Investigational Treatment), patients responding to golimumab induction were randomized to receive golimumab or placebo for maintenance. Subcutaneous (SC) golimumab 100 mg every 4 weeks maintained a clinical response through week 54 in 51% of patients compared with 31% of patients taking placebo (P< 0.001).[85]
Daily oral maintenance with tofacitinib may be considered if an adequate therapeutic response was observed with tofacitinib induction. In the OCTAVE Sustain trial (Oral Clinical Trials for tofAcitinib in ulceratiVE colitis), remission at 52 weeks occurred in 34.3% of the 5-mg tofacitinib group and 40.6% in the 10-mg tofacitinib group compared to 11.1% in the placebo group (P< 0.001 for both comparisons with placebo).[75]
Corticosteroids may be used for induction of remission of active ulcerative colitis[10] and continued for up to 8 weeks; however, these agents have no efficacy for maintenance of remission and should not be used for this purpose.[10] A novel formulation of slow-release budesonide (Uceris) was approved by the FDA in January 2013. Approval was based on results from the CORE 1 (colonic release budesonide) study that showed endoscopic improvement at 8 weeks, increased remission rates, and clinical improvement with budesonide 9 mg once daily.[86]
Probiotics also appear to be effective at maintaining remission. Escherichia coli strain Nissle 1917 has been compared with mesalazine and proved to be similarly effective.[87] Bio-Three, a commercially available probiotic supplement (Enterococcus T-110, C butyricum TO-A, B mesentericus TO-A) produced remission in 45% of patients tested with mild-to-moderate ulcerative colitis.[88] Trials of fish oil to produce or maintain remission have shown no benefit over placebo.
No specific diet restrictions are required for patients with ulcerative colitis. However, many patients with ulcerative colitis can have concurrent lactose intolerance. No specific diet can maintain remission.[10]
Elemental nutrition and parenteral nutrition have no primary therapeutic role in ulcerative colitis, although parenteral nutrition is often used in patients who are severely ill as effective nutritional support.
Several complications have been reported after ileal pouch–anal anastomosis procedures in patients with ulcerative colitis (UC). The anastomotic leak rate is 7%-9%.[89] If anastomotic leak occurs, fecal diversion, percutaneous drain placement, or repeat surgery with removal or revision of the reservoir is required. Pelvic abscess, which frequently accompanies an anastomotic leak, occurs in about 5% of cases (reports vary from 0% to 25%). Among patients with a pelvic abscess, 26% require excision of the pouch. Only 5.9% of patients without an abscess have pouch failure that requires removal.
If the abscess is managed with diversion and drainage, the pouch may be spared. However, these patients have higher rates of long-term incontinence and pain compared with those without abscesses.[90] In patients who require pouch excision due to an abscess, a gracilis muscle interposition flap has been used to maintain the anal canal and allow future attempts at pouch procedures.[91] Pouch-vesicle, pouch-vaginal, pouch-anal, and enterocutaneous fistulas occur with a frequency of about 1% each.
Outcomes of pouch procedures are classified as good to excellent in as many as 90% of patients. Stool frequency is less than five per day in as many as 74%. Difficulty with evacuation occurs in 20%. About 77% of patients require no dietary restrictions; the remaining patients have a lower stool frequency with a low-fat diet.[92] Complete incontinence is reported in only 2%. Bulk-forming agents are required in as many as 30%.
Sexual dysfunction, manifested by retrograde ejaculation or impotence, occurs in 3% of males. Although Meagher et al reported sexual dysfunction in only 6% of females,[93] Ogilvie et al reported that 47% of females have low Female Sexual Function Index (FSFI) scores, indicating sexual dysfunction.[94] Additionally, Cornish et al described a 25% incidence of sexual dysfunction manifested by dyspareunia or psychological aversion to intercourse for fear of stool leakage.[95] Their report also documented an increase in infertility from 8% preoperatively to 26% postoperatively.
Pouchitis
Pouchitis is defined as a clinical syndrome in which the patient has increased stool frequency, malaise, fever, or incontinence. This syndrome has a reported incidence of 40%-60% but usually responds to antibiotic therapy (ciprofloxacin or metronidazole is most frequently used). The risk of pouchitis increases with time; 18% of patients have pouchitis at 1 year, and 48% have pouchitis at 10 years.[93] Pouch dilatation and pouch-anal anastomotic stricture may lead to fecal stasis and predispose the patient to pouchitis. Clostridium difficile and Clostridium perfringens have been disproportionately found in patients with ulcerative colitis after ileal pouch–anal anastomosis. Treatment of these infections has led to decreases in inflammation.[96, 97]
Toxic megacolon
Toxic megacolon occurs in less than 2% of cases and can be induced by hypokalemia, opiates, anticholinergics, and barium enemas. Patients are acutely ill. Conservative treatment can be tried for 24-48 hours with administration of intravenous (IV) fluids, IV steroids, antibiotics, and IV cyclosporine. Patients may eventually require a total colectomy.
Carcinoma
Carcinoma is a known complication of ulcerative colitis in the small group of patients who have had the disease for approximately 10 years. The cancer tends to be multicentric, atypical in its appearance, and rapidly metastasizing. The risk of colorectal cancer increases by 0.5%-1% per year. Regular surveillance is needed.
Although the incidence of colon adenocarcinoma is greatly reduced with total proctocolectomy and ileal pouch–anal anastomosis, it is not zero. The residual colonic mucosa is at risk for dysplasia and neoplastic transformation.[98]
Because of the increased risk of colorectal cancer, guidelines from the American College of Gastroenterology recommend that after 8-10 years of colitis, patients with ulcerative colitis should undergo annual or biannual surveillance colonoscopy with multiple biopsies at regular intervals.[31] The finding of high-grade dysplasia in flat mucosa, confirmed on review by an expert pathologist, is an indication for colectomy; the finding of low-grade dysplasia in flat mucosa may also be an indication for colectomy to prevent progression to a higher grade of neoplasia.[31]
In a study that aimed to identify a panel of markers associated with the long-term outcome of infliximab therapy for patients with refractory ulcerative colitis (UC) (median follow-up, 5 y), Arias et al confirmed that short-term clinical response and mucosal healing—as well as baseline levels of C-reactive protein (CRP) of 5 mg/L or less and albumin of 35 g/L or greater—were independent predictors of colectomy-free survival.[99] Moreover, infliximab levels over 2.5 μg/mL at week 14 of treatment predicted both relapse-free survival and colectomy-free survival. A combined risk panel that included clinical response, mucosal healing, and levels of perinuclear antineutrophil cytoplasmic antibodies (pANCA), CRP, and albumin identified patients at risk for disease relapse or colectomy.[99]
In patients with chronic pouch inflammation, villous hypertrophy and dysplasia may occur. Although dysplasia has never been found within the pouch of a pediatric patient, chronic inflammatory changes have been identified, leading to the supposition that dysplasia may develop. Yearly screening endoscopy has been recommended for the first 5 years after the procedure. In children who have chronic inflammatory changes in the pouch reservoir, annual screening endoscopy should be performed. If no inflammation is present, screening endoscopy may be performed every 2 years.[100]
Patients with extensive colitis or left-sided colitis with negative findings on screening colonoscopy should begin surveillance colonoscopy in 1-2 years. For patients with ulcerative colitis and primary sclerosing cholangitis, screening and subsequent surveillance colonoscopy should begin on an annual basis at the time of onset of primary sclerosing cholangitis.
Patients with proctosigmoiditis have no increased risk for colorectal cancer compared to the general population. However, these patients should be managed according to the current guidelines on colorectal cancer screening. If high-grade dysplasia or cancer is found, colectomy is performed. The management of low-grade dysplasia is controversial[101] ; however, most experts would recommend colectomy.
The American College of Gastroenterology released their guideline on preventive care in inflammatory bowel disease (IBD) in 2017[102] . Their preventive health maintenance recommendations are outlined below.
Strong recommendations
Patients with IBD (both ulcerative colitis and Crohn disease) should undergo screening for melanoma independent of the use of biologic therapy. IBD patients on immunomodulators (6-mercaptopurine or azathioprine) should undergo screening for nonmelanoma skin cancer (NMSC) while using these agents, particularly those older than 50 years.
Patients with conventional risk factors for abnormal bone mineral density with ulcerative colitis and Crohn disease should undergo screening for osteoporosis with bone mineral density testing at the time of diagnosis and periodically after diagnosis.
Adults with IBD older than 50 years should consider vaccination against herpes zoster, including certain subgroups of immunosuppressed patients.
Conditional recommendations
Patients with conventional risk factors for abnormal bone mineral density with ulcerative colitis and CD should undergo screening for osteoporosis with bone mineral density testing at the time of diagnosis and periodically after diagnosis.
Adults with IBD should receive age-appropriate vaccinations before initiation of immune suppression when possible.
Household members of immunosuppressed patients can receive live vaccines with certain precautions.
All adult patients with IBD should undergo annual vaccination against influenza. Those on immunosuppressive therapies and their household contacts should receive the non-live trivalent inactivated influenza vaccine, but not the live inhaled influenza vaccine.
Adult patients with IBD receiving immunosuppressive therapy should receive pneumococcal vaccination with both the PCV13 and PPSV23, vaccines in accordance with national guidelines.
Adults with IBD should be assessed for prior exposure to varicella and vaccinated if naive before initiation of immunosuppressive therapy when possible.
Patients with IBD who are immunosuppressed and traveling to endemic areas for yellow fever should consult with a travel medicine or infectious disease specialist prior to travel
Adolescents with IBD should receive meningococcal vaccination in accordance with routine vaccination recommendations.
Vaccination against tetanus/diptheria, and pertussis (Tdap), hepatitides A and B (HAV, HBV, respectively); and human papillomavirus (HPV) should be administered as per Advisory Committee on Immunization Practice (ACIP) guidelines.
Women with IBD on immunosuppressive therapy should undergo annual cervical cancer screening.
Screening for depression and anxiety is recommended in patients with IBD.
The American College of Gastroenterology (ACG) published recommendations on ulcerative colitis (UC) in adults in March 2019.[103, 104] The focus of management has shifted from symptom-based treatment to symptom management and mucosal healing. The ACG guideline's strong recommendations are outlined below.[103]
Diagnosis, assessment, and prognosis
Stool testing is recommended to exclude Clostridioides difficile when UC is suspected.
Serologic antibody testing is not recommended for the following:
To establish or exclude a diagnosis of UC
To determine the prognosis of UC
Goals for managing patients with UC
Treat patients with UC to achieve mucosal healing (ie, resolution of inflammatory changes [Mayo endoscopic subscore 0 or 1]) to increase the likelihood of sustained steroid-free remission and prevent hospitalizations and surgery.
UC management
Induction and maintenance of remission in mildly active UC
Patients with, or who previously had, mildly active ulcerative proctitis are recommended to receive rectal (PR) 5-aminosalicylate (5-ASA) therapies at a dose of 1 g/d to induce or maintain remission.
To induce remission in patients with mildly active left-sided UC:
Rectal 5-ASA enemas at a dose of at least 1 g/d are preferred over rectal steroids.
In the setting of intolerance or nonresponse to oral (PO) and PR 5-ASA at appropriate doses (PO: ≥2 g/d; PR: ≥1 g/d), use PO budesonide multi-matrix (MMX) 9 mg/d.
Patients with mildly active extensive UC are recommended to receive PO 5-ASA at a dose of at least 2 g/d to induce remission.
Patients with UC of any extent whose condition fails to respond to 5-ASA therapy are recommended to receive PO systemic corticosteroids to induce remission.
Patients with mildly to moderately active UC refractory to PO 5-ASA are recommended to additionally receive budesonide MMX 9 mg/d to induce remission.
Patients with mildly to moderately active UC of any extent using 5-ASA to induce remission are recommend to receive either once-daily or more frequently dosed PO 5-ASA based on patient preference to optimize adherence, as efficacy and safety are no different.
Patients with mildly active left-sided or extensive UC are recommend to receive at least 2 g/d of PO 5-ASA therapy for maintenance of remission.
Systemic corticosteroids are not recommended to maintain remission in patients with UC.
Management of moderately to severely active UC
Induction of remission
For moderately active UC, PO budesonide MMX is recommended to induce remission.
For moderately to severely active UC of any extent, PO systemic corticosteroids are recommended to induce remission.
To induce remission in patients with moderately to severely active UC, note the following:
Monotherapy with thiopurines or methotrexate is not recommended.
Anti-tumor necrosis factor (TNF) therapy using adalimumab, golimumab, or infliximab is recommended.
When infliximab is used as induction therapy, combination therapy with a thiopurine is recommended.
Vedolizumab or tofacitinib (tofacitinib: 10 mg PO twice daily × 8 wk) is recommended (either agent is also recommended when anti-TNF therapy has failed previously).
Maintenance of remission in those with previously moderately to severely active UC
Systemic corticosteroids are not recommended to maintain remission in patients with UC.
Continue anti-TNF therapy using adalimumab, golimumab, or infliximab to maintain remission after anti-TNF induction in patients with previously moderately to severely active UC.
Continue vedolizumab to maintain remission in patients with previously moderately to severely active UC now in remission after vedolizumab induction.
Continue tofacitinib to maintain remission in patients with previously moderately to severely active UC now in remission after tofacitinib induction.
Management of hospitalized patients with acute severe UC (ASUC)
Apply deep venous thrombosis (DVT) prophylaxis to prevent venous thromboembolism (VTE).
Test for C difficile infection (CDI).
In the setting of ASUC and concomitant CDI, treat CDI with vancomycin instead of metronidazole.
Routine use of broad-spectrum antibiotics is not recommended to manage ASUC.
Use methylprednisolone 60 mg/d or hydrocortisone 100 mg 3 or 4 times daily to induce remission.
In the setting of ASUC with inadequate response to intravenous corticosteroids (IVCS) by 3-5 days, medical rescue therapy with infliximab or cyclosporine is recommended.
When remission is achieved with infliximab treatment, maintain remission with infliximab.
Colorectal cancer prevention in UC
When using standard-definition colonoscopes in those with UC undergoing surveillance, dye spray chromoendoscopy with methylene blue or indigo carmine is recommended to identify dysplasia.
American Gastroenterological Association Guidelines
The American Gastroenterological Association (AGA) released new guidelines on the management of mild-to-moderate ulcerative colitis (UC) in February 2019,[105] with a focus on the use of oral (PO) and topical 5-aminosalicylates (5-ASA) agents, rectal (PR) corticosteroids, and PO budesonide.[105, 106]
Strong recommendations
Patients with extensive mild-moderate UC: The AGA recommends using either standard-dose mesalamine (2-3 g/d) or diazo-bonded 5-ASA rather than low-dose mesalamine, sulfasalazine, or no treatment. (Patients already on sulfasalazine in remission or patients with prominent arthritic symptoms may reasonably choose sulfasalazine 2-4 g/d if alternatives are cost-prohibitive, albeit with higher rate of intolerance.)
Patients with mild-moderate ulcerative proctitis who choose rectal therapy over oral therapy: The AGA recommends using mesalamine suppositories.
Conditional recommendations
Patients with extensive or left-sided mild-moderate UC: The AGA suggests adding rectal mesalamine to oral 5-ASA.
Patients with mild-moderate UC with a suboptimal response to standard-dose mesalamine or diazo-bonded 5-ASA or with moderate disease activity: The AGA suggests using high-dose mesalamine (>3 g/d) with rectal mesalamine.
Patients with mild-moderate UC being treated with oral mesalamine: The AGA suggests using once-daily dosing rather than multiple times per day dosing.
Patients with mild-moderate UC: The AGA suggests using standard-dose oral mesalamine or diazo-bonded 5-ASA, rather than budesonide MMX (Multi-Matrix System) or controlled ileal release budesonide for induction of remission.
Patients with left-sided mild-moderate ulcerative proctosigmoiditis or proctitis: The AGA suggests using mesalamine enemas (or suppositories) rather than oral mesalamine. (Patients who have a higher value for convenience of oral medication administration and a lower value on effectiveness could reasonably choose oral mesalamine.)
Patients with mild-moderate ulcerative proctosigmoiditis who choose rectal therapy over oral therapy: The AGA suggests using mesalamine enemas rather than rectal corticosteroids. (Patients who place a higher value on avoiding difficulties associated with mesalamine enemas and a lower value on effectiveness may reasonably select rectal corticosteroid foam preparations.)
Patients with mild-moderate ulcerative proctosigmoiditis or proctitis being treated with rectal therapy who are intolerant of or refractory to mesalamine suppositories: The AGA suggests using rectal corticosteroid therapy rather than no therapy for induction of remission.
Patients with mild-moderate UC refractory to optimized oral and rectal 5-ASA, regardless of disease extent: The AGA suggests adding either oral prednisone or budesonide MMX.
No recommendations
The AGA makes no recommendations for the use of probiotics in those with mild-moderate UC, nor for the use of curcumin in patients with mild-moderate UC despite 5-ASA therapy.
In patients with mild–moderate UC without Clostridium difficile infection, the AGA recommends fecal microbiota transplantation be performed only in the context of a clinical trial.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications. The treatment of ulcerative colitis (UC) relies on initial medical management with corticosteroids and anti-inflammatory agents, such as sulfasalazine, in conjunction with symptomatic treatment with antidiarrheal agents and rehydration.
Clinical Context:
Sulfasalazine is useful in treating mild-to-moderate ulcerative colitis and maintaining remission. It acts locally in the colon to reduce the inflammatory response and systemically inhibits prostaglandin synthesis.
Clinical Context:
Balsalazide is a prodrug that is converted into 5-aminosalicylic acid through bacterial azo reduction. Metabolites of drug may decrease inflammation by blocking the production of arachidonic acid metabolites in colon mucosa.
Clinical Context:
Mesalamine is the drug of choice for maintaining remission. It is useful for the treatment of mild-to-moderate ulcerative colitis. It is better tolerated and has less adverse effects than sulfasalazine. Enema and suppository forms are typically used in patients with distal colitis.
Clinical Context:
Infliximab is a chimeric mouse-human monoclonal antibody to TNF. It binds free and membrane-bound TNF and thus prevents the cytokine from binding to its cell surface receptor and exerting biological activity. Infliximab is indicated for the treatment of moderate-to-severe active ulcerative colitis in patients who have experienced inadequate response to conventional therapy. It has been shown to reduce signs and symptoms, to achieve clinical remission and mucosal healing, and to eliminate corticosteroid use.
Clinical Context:
Golimumab is a human anti-TNF-alpha monoclonal antibody that blocks the inflammatory activity of TNF-alpha. It is indicated for induction and maintenance treatment of adults with moderate-to-severe ulcerative colitis that is resistant to prior treatment or requires continuous corticosteroid therapy. Following a brief induction dosage regimen, the maintenance dose is given SC once each month.
Clinical Context:
Adalimumab is a recombinant human anti-TNF-alpha IgG1 monoclonal antibody that blocks the inflammatory activity of TNF-alpha. It specifically binds to TNF-alpha and blocks its interaction with p55 and p75 cell surface TNF receptors. It is indicated for inducing and sustaining clinical remission in adult patients with moderately to severely active ulcerative colitis who have had an inadequate response to immunosuppressants such as corticosteroids, azathioprine, or 6-mercaptopurine (6-MP). The FDA approved adalimumab-atto, adalimumab-adbm, adalimumab-adaz, adalimumab-bwwd as biosimilars and not as interchangeable drugs.
These agents prevent the endogenous cytokine from binding to the cell surface receptor and exerting biological activity. These agents adversely affect normal immune responses and allow the development of superinfections; reactivation of latent TB has been reported in patients with previous exposure to TB.
Clinical Context:
Azathioprine is effective as a steroid-sparing or steroid-reducing agent and for use in maintenance therapy. Administration is oral. Onset of action can be delayed by up to 3-6 months.
Clinical Context:
Cyclosporine is effective as a means of avoiding surgery in patients with severe ulcerative colitis refractory to intravenous corticosteroids. It is given as an intravenous infusion, but can be switched to PO qd dose as "bridge" therapy for outpatient use.
Clinical Context:
6-Mercaptopurine is effective as a steroid-reducing or steroid-sparing agent and for use in maintaining remission. Administration is oral. Onset of action can be delayed by up to 3-6 months.
Clinical Context:
Immunomodulator produced by the bacteria Streptomyces tsukubaensis. Mechanism of action of tacrolimus is similar to cyclosporine. It is effective in bringing steroid-resistant disease under control. Tacrolimus should not be used for long-term therapy, owing to the risk of nephrotoxicity.
These agents regulate the key factors of the immune system. Agents such as tacrolimus and cyclosporine are often effective in bringing steroid-resistant disease under control.
Clinical Context:
High dose corticosteroids such as hydrocortisone are used in the treatment of acute, severe ulcerative colitis. Hydrocortisone decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
Clinical Context:
Budesonide is a potent glucocorticoid that has poor oral absorption and extensive first-pass metabolism. These properties make it ideal for reducing gastrointestinal inflammation. It is indicated for remission induction of active, mild-to-moderate ulcerative colitis.
Clinical Context:
Budesonide rectal is a corticosteroid available as a 20 mg/metered-dose rectal foam. It is indicated for the induction of remission in adults with active mild-to-moderate distal ulcerative colitis extending up to 40 cm from the anal verge.
Corticosteroids decrease inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability. They are used for induction of remission in moderate-to-severe active ulcerative colitis.[107] They have no role in maintaining remission; long-term use can cause adverse effects.
Clinical Context:
Vedolizumab is a recombinant humanized monoclonal antibody that binds specifically to α4β7 integrin. It blocks the interaction of α4β7 integrin with mucosal addressin cell adhesion molecule-1 (MAdCAM-1) and inhibits the migration of memory T-lymphocytes across the endothelium into inflamed gastrointestinal parenchymal tissue. It is indicated for both ulcerative colitis and Crohn disease.
Integrin inhibitors are emerging as options for moderate-to-severe active IBD in patients who have had an inadequate response with, lost response to, or were intolerant to a TNF blocker or immunomodulator; or had an inadequate response with, were intolerant to, or demonstrated dependence on corticosteroids.
Clinical Context:
Tofacitinib is a JAK inhibitor indicated for adults with moderately to severely active ulcerative colitis. An induction dose for at least 8 weeks is administered orally, followed by a maintenance dose, depending on the patient's therapeutic response.
Janus kinase (JAK) pathway inhibitors consist of a group of intracellular tyrosine kinases that transmit signals from cytokine or growth factor-receptor interactions on the cellular membrane to influence cellular processes of hematopoiesis and immune cell function. Within the signaling pathway, JAKs phosphorylate and activate signal transducers and activators of transcription (STATs) which modulate intracellular activity including gene expression. Tofacitinib is a JAK inhibitor that modulates the signaling pathway at the point of JAKs, preventing the phosphorylation and activation of STATs.
Clinical Context:
A fluoroquinolone, ciprofloxacin has activity against pseudomonads, streptococci, MRSA, Staphylococcus epidermidis, and most gram-negative organisms but no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently, growth.
Clinical Context:
Metronidazole is an imidazole ring–based antibiotic active against various anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents but as monotherapy for C difficile enterocolitis.
In several controlled, trials, antibiotics have not been shown to provide consistent benefits for the treatment of active ulcerative colitis. Thus, they are usually administered on an empiric basis in patients with severe colitis in whom they may help by averting a life-threatening infection. They have been shown to be effective for the treatment of pouchitis after an IPAA procedure
Clinical Context:
This drug combination consists of 2.5 mg of diphenoxylate, which is a constipating meperidine congener, and 0.025 mg of atropine to discourage abuse. The preparation inhibits excessive GI propulsion and motility, but it may exacerbate constipation.
Clinical Context:
Loperamide, which is available over the counter, acts on intestinal muscles to inhibit peristalsis and to slow intestinal motility. It prolongs the movement of electrolytes and fluid through bowel and increases viscosity and loss of fluids and electrolytes. Loperamide improves stool frequency and consistency, reduces abdominal pain and fecal urgency, and may exacerbate constipation.
These agents are nonabsorbable synthetic opioids that provide symptomatic relief in the treatment of ulcerative colitis. They prolong GI transit time and decrease secretion via peripheral mu-opioid receptors. They reduce visceral nociception via afferent pathway inhibition.
What is ulcerative colitis (UC)?What are the symptoms of ulcerative colitis (UC)?What are the signs and symptoms of fulminant ulcerative colitis (UC)?Which extracolonic conditions are associated with ulcerative colitis (UC)?What are the physical findings in severe ulcerative colitis (UC)?How is the severity of ulcerative colitis (UC) graded?Which laboratory studies are used in the diagnosis of ulcerative colitis (UC)?Which procedure is most commonly used in the diagnosis of ulcerative colitis (UC), and what are the characteristic findings?How is ulcerative colitis (UC) defined based on the extent of disease?Which imaging studies are useful in the diagnosis of ulcerative colitis (UC)?What treatment options are available for the medical management of mild ulcerative colitis (UC) and acute severe UC?When is surgery indicated in a patient with ulcerative colitis (UC)?What surgical options are available to patients with ulcerative colitis (UC)?Which segment of the bowel is most commonly affected by ulcerative colitis (UC)?What is the etiology of ulcerative colitis (UC)?What are the pathologic features of ulcerative colitis (UC)?What is the initial treatment for patients with ulcerative colitis (UC)?Which segments of the digestive tract are involved in ulcerative colitis (UC)?What types of immunologic changes are associated with ulcerative colitis (UC)?Which antibodies have been associated with ulcerative colitis (UC)?Which microscopic findings are characteristic of ulcerative colitis (UC)?What etiologic factors are associated with ulcerative colitis (UC)?What is the relationship between a patient’s smoking history and the need for surgical intervention in ulcerative colitis (UC)?What is the role of genetics in the development of ulcerative colitis (UC)?Which antibodies are associated with ulcerative colitis (UC)?What is the relationship between appendectomy and ulcerative colitis (UC)?What bacterial factors are associated with the development of ulcerative colitis (UC)?What is the role of NSAIDs in the development of ulcerative colitis (UC)?What are some of the less common factors associated with ulcerative colitis (UC)?What are the prevalence and incidence rates of ulcerative colitis (UC) in the US?Is there a racial predilection in ulcerative colitis (UC) in the US?Is ulcerative colitis (UC) more common in men or women?At what age does ulcerative colitis (UC) most commonly develop?Is there a geographic predilection in ulcerative colitis (UC)?Does ulcerative colitis (UC) increase the risk of mortality?Which comorbidities are associated with ulcerative colitis (UC)?What potentially fatal complications are associated with ulcerative colitis (UC)?What signs and symptoms are associated with insidious onset of ulcerative colitis?What signs and symptoms are associated with fulminant onset of ulcerative colitis?Which extracolonic manifestations are associated with ulcerative colitis (UC)?What is the role of primary sclerosing cholangitis (PSC) in ulcerative colitis (UC)?Which comorbidities have been reported but are not commonly associated with ulcerative colitis (UC)?What are the typical physical findings in patients with ulcerative colitis (UC)?How is the severity of ulcerative colitis (UC) graded?Which conditions should be considered in the differential diagnosis of ulcerative colitis (UC)?How is ulcerative colitis (UC) differentiated from Crohn disease, and why is the distinction important?According to guidelines, which conditions, in addition to Crohn disease, should be excluded in the differential diagnosis of ulcerative colitis (UC)?What are the differential diagnoses for Ulcerative Colitis?Which procedure should be performed for a definitive diagnosis of ulcerative colitis (UC)?What is the role of laboratory studies in the diagnosis of ulcerative colitis (UC)?What is the role of radiographic imaging in the diagnosis of ulcerative colitis (UC)?Why is a double-contrast barium enema exam important in the diagnosis of ulcerative colitis (UC)?What is the role of colon biopsy in the diagnosis of ulcerative colitis (UC)?What is the role of other radiologic studies in the diagnosis of ulcerative colitis (UC)?Which antibodies are the focus of most ulcerative colitis (UC) research?Which antibodies are most commonly associated with ulcerative colitis (UC)?What CBC count findings are associated with ulcerative colitis (UC)?Which comprehensive metabolic panel findings are associated with ulcerative colitis (UC)?Which inflammatory markers suggest ulcerative colitis (UC)?What is the role of stool studies in the diagnosis of ulcerative colitis (UC)?Should endoscopy or sigmoidoscopy be performed prior to colonoscopy when ulcerative colitis (UC) is suspected?Which types of mucosa should be sampled during biopsy when ulcerative colitis (UC) is suspected?How is a diagnosis of ulcerative colitis (UC) confirmed?How is the extent of disease defined in ulcerative colitis (UC)?What histopathologic findings are consistent with ulcerative colitis (UC)?What is the role of imaging in the diagnosis of ulcerative colitis (UC), and which studies are useful?What is the standard medical treatment for ulcerative colitis (UC), and what are the surgical options, when indicated?What is the association between colon cancer and ulcerative colitis (UC)?Is regular endoscopic cancer screening indicated in patients with ulcerative colitis (UC)?What consultations are recommended for patients with ulcerative colitis (UC)?How is mild ulcerative colitis (UC) treated?What are the recommendations for long-term maintenance therapy after remission in mild ulcerative colitis (UC)?What is the role of systemic steroid therapy in the treatment of mild-to-moderate ulcerative colitis (UC)?How is acute, severe ulcerative colitis (UC) treated?What is the role of infliximab in the treatment of acute, severe ulcerative colitis (UC)?What is the role of monoclonal antibody drugs in the treatment of ulcerative colitis (UC)?How is vedolizumab used in the treatment of acute, severe ulcerative colitis (UC)?What nonstandard therapies are available for the treatment of acute, severe ulcerative colitis (UC)?When is surgery indicated in patients with ulcerative colitis (UC), and what are the indications for urgent surgery?Does research support ileal pouch-anal anastomosis for the treatment of ulcerative colitis (UC)?What is the role of maintenance therapy for ulcerative colitis (UC) in patients who are in remission?What treatment options are available for maintenance therapy in ulcerative colitis (UC)?Are dietary restrictions part of the maintenance therapy for ulcerative colitis (UC)?What complications are associated with ileal pouch-anal anastomosis procedures in patients with ulcerative colitis (UC)?What are the outcomes of ileal pouch-anal anastomosis in ulcerative colitis (UC)?How is sexual function affected by ileal pouch-anal anastomosis in patients with ulcerative colitis (UC)?What is pouchitis, how common is it, and how is it treated in patients with ileal pouch–anal anastomosis resulting from ulcerative colitis (UC)?What is the incidence of toxic megacolon in patients with ulcerative colitis (UC), what are its causes, and how is it treated?What is the risk of colorectal cancer in patients with ulcerative colitis (UC), and what are the guidelines for surveillance and treatment?What are the long-term surveillance and treatment options for ulcerative colitis (UC)?What are the guidelines on the treatment of ulcerative colitis?What are the goals of pharmacotherapy in ulcerative colitis (UC)?Which medications in the drug class 5-aminosalicylic Acid Derivative are used in the treatment of Ulcerative Colitis?Which medications in the drug class Tumor Necrosis Factor Inhibitors are used in the treatment of Ulcerative Colitis?Which medications in the drug class Immunosuppressant Agents are used in the treatment of Ulcerative Colitis?Which medications in the drug class Corticosteroids are used in the treatment of Ulcerative Colitis?Which medications in the drug class Alpha 4 Integrin Inhibitors are used in the treatment of Ulcerative Colitis?Which medications in the drug class JAK Inhibitors are used in the treatment of Ulcerative Colitis?Which medications in the drug class Antimicrobials are used in the treatment of Ulcerative Colitis?Which medications in the drug class Antidiarrheal are used in the treatment of Ulcerative Colitis?
Marc D Basson, MD, PhD, MBA, FACS, Senior Associate Dean for Medicine and Research, Professor of Surgery, Pathology, and Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences
Disclosure: Nothing to disclose.
Chief Editor
BS Anand, MD, Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine
Disclosure: Nothing to disclose.
Acknowledgements
Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital
Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons
Disclosure: Nothing to disclose.
Alex Jacocks, MD Program Director, Professor, Department of Surgery, University of Oklahoma School of Medicine
Disclosure: Nothing to disclose.
Tri H Le, MD Assistant Professor of Medicine, Division of Gastroenterology and Hepatology, Penn State Milton S Hershey Medical Center
Tri H Le, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society of Gastrointestinal Endoscopy, and Crohns and Colitis Foundation of America
Disclosure: Nothing to disclose.
Luis M Lovato, MD Associate Clinical Professor, University of California, Los Angeles, David Geffen School of Medicine; Director of Critical Care, Department of Emergency Medicine, Olive View-UCLA Medical Center
Luis M Lovato, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Anil Minocha, MD, FACP, FACG, AGAF, CPNSS Professor of Medicine, Director of Digestive Diseases, Medical Director of Nutrition Support, Medical Director of Gastrointestinal Endoscopy, Internal Medicine Department, University of Mississippi Medical Center; Clinical Professor, University of Mississippi School of Pharmacy
Anil Minocha, MD, FACP, FACG, AGAF, CPNSS is a member of the following medical societies: American Academy of Clinical Toxicology, American Association for the Study of Liver Diseases, American College of Forensic Examiners, American College of Gastroenterology, American College of Physicians, American Federation for Clinical Research, American Gastroenterological Association, and American Society of Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Noel Williams, MD Professor Emeritus, Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; Professor, Department of Internal Medicine, Division of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada
Noel Williams, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada
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Sandborn WJ, et al. A phase III randomized, placebo-controlled, double-blind study to evaluate the safety and efficacy of subcutaneous golimumab maintenance therapy in patients with moderately to severely active ulcerative colitis: PURSUIT-Maintenance. Presented at the American College of Gastroenterology, October 22, 2012 Las Vegas, NV.
Swift D. Updated UC guideline adds mucosal healing to treatment goal. Medscape Medical News. March 4, 2019. Available at https://www.medscape.com/viewarticle/909801. Accessed: March 20, 2019.
American Gastroenterological Association. New guideline provides recommendations for the treatment of mild-to-moderate ulcerative colitis. Available at https://www.gastro.org/press-release/new-guideline-provides-recommendations-for-the-treatment-of-mild-to-moderate-ulcerative-colitis. January 9, 2019; Accessed: March 20, 2019.
Ulcerative colitis. Ulcerative colitis as visualized with a colonoscope.
Ulcerative colitis. Ulcerative colitis as visualized with a colonoscope.
Ulcerative colitis. Single-contrast enema study in a patient with total colitis shows mucosal ulcers with a variety of shapes, including collar-button ulcers (yellow arrow), in which undermining of the ulcers occurs, and double-tracking ulcers (red arrow), in which the ulcers are longitudinally orientated.
Ulcerative colitis. Increased postrectal space is a known feature of ulcerative colitis.
Ulcerative colitis. Increased postrectal space is a known feature of ulcerative colitis.
Ulcerative colitis. Plain abdominal radiograph from a patient with known ulcerative colitis who presented with an acute exacerbation of his symptoms. The image shows thumbprinting in the region of the splenic flexure of the colon.
Ulcerative colitis. Double-contrast barium enema study shows pseudopolyposis of the descending colon.
Ulcerative colitis. Single-contrast enema study in a patient with known ulcerative colitis in remission shows a benign stricture of the sigmoid colon.
Ulcerative colitis. Plain abdominal radiograph in a 26-year-old with a 10-year history of ulcerative colitis shows a long stricture/spasm of the ascending colon/cecum. Note the pseudopolyposis in the descending colon.
Ulcerative colitis. Single-contrast enema study in a patient with total colitis shows mucosal ulcers with a variety of shapes, including collar-button ulcers (yellow arrow), in which undermining of the ulcers occurs, and double-tracking ulcers (red arrow), in which the ulcers are longitudinally orientated.
Ulcerative colitis. Double-contrast barium enema study shows total colitis. Note the granular mucosa in the cecum/ascending colon and multiple strictures in the transverse and descending colon in a patient with a more than a 20-year history of ulcerative colitis.
Ulcerative colitis. Single-contrast barium enema study shows burnt-out ulcerative colitis.
Ulcerative colitis. Intravenous urogram in the same patient as in Image 11 shows features of ankylosing spondylitis.
Ulcerative colitis. Lateral radiograph of the lumbar spine in the same patient as in Images 10-11 shows a bamboo spine.
Ulcerative colitis. Single-contrast barium enema study in a patient with Shigella colitis.
Ulcerative colitis. Postevacuation image obtained after a single-contrast barium enema study shows extensive mucosal ulceration resulting from Shigella colitis.
Ulcerative colitis. Double-contrast barium enema studies show granular mucosa associated with Campylobacter colitis.
Ulcerative colitis. Ulcerative colitis as visualized with a colonoscope.
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