Ulcerative colitis (UC), along with Crohn’s disease (CD), are the main subtypes of a group of conditions known as inflammatory bowel diseases (IBDs).
UC is a chronic, relapsing disease of the gastrointestinal tract in which there is superficial inflammation of the lining (mucosa) of the colon that generally occurs in a continuous pattern.1
Symptoms of UC commonly include diarrhea (bloody), abdominal cramping, anemia, weight loss, and fatigue. Onset of UC peaks between the ages of 15 and 40.2
UC and CD share similar characteristics; however, the location and depth of inflammation varies. UC typically affects continuous patches of colon and is characterized by superficial inflammation, whereas CD may affect any area of the gastrointestinal tract, often following a discontinuous pattern, with inflammation extending through all layers of the gut wall.3
Some patients have features of both UC and CD, and are given a diagnosis of indeterminate colitis.4
In the healthy gut, mucin-covered epithelium provides an important barrier between commensal gut microbiota and host immune cells. In UC, however, damage to the mucinous layer increases permeability of the epithelial barrier thereby allowing commensal bacterial and microbial products to cross the gut lumen into the bowel wall.5
This results in acute intestinal inflammation characterized by immune-cell activation and cytokine production. If initial acute inflammation is not resolved, chronic inflammation ensues, which can cause disease complications and tissue destruction, driven by mucosal cytokine responses.2
Cytokines play a central role in the pathogenesis of UC, where they exert various proinflammatory functions in the inflamed mucosa.2
IEC, intestinal epithelial cell; IL, interleukin; ILC, intestinal lymphoid cell; NK, natural killer; TGFβ, transforming growth factor beta; TNF, tumor necrosis factor.
Adapted from Neurath, 2014.2
Health related quality of life (HRQoL) is significantly lower in patients with UC than the general population due to the negative effects of the disease on physical, psychological, and social well-being.6
Factors that influence the HRQoL of patients with UC include disease course (extent, severity, and relapse pattern), medical therapy (efficacy, adverse events, and adherence issues), and demographic, psychosocial, and socioeconomic characteristics. HRQoL is worse in patients with active disease.6
UC affects 2.2 to 19.2 individuals per 100 000 per year.2
IBD is slightly more prevalent in women than in men (relative risk 1.53).7
In the last 50 years, there has been a steady increase in the incidence in Western countries and newly industrialized countries, possibly reflecting the westernization of diets and lifestyles.8
UC can be classified by the extent of disease (proctitis, left-sided, extensive), and by disease activity/disease phenotype.4
The best validated and most widely used index for identifying severe UC remains that of Truelove and Witts. The Montréal scoring system may also be used. A further scoring system - the Mayo score - is a combined endoscopic and clinical scale used to assess the severity of UC, most commonly used in clinical trials.9
Classification by disease activity adapted from Truelove and Witts
|Erythrocyte sedimentation rate
*Moderate = in between mild and severe
Source: Magro et al, 2017.4
| ||S0 Remission||S1 Mild||S2 Moderate||S3 Severe|
||May be present
||Minimal or no signs of systemic toxicity
|Erythrocyte sedimentation rate
Source: Magro et al, 2017.4
Extraintestinal manifestations are observed in 25% to 40% of patients with IBD.10
The most common manifestations involve the muscles, skeleton, and the skin. Other manifestations involve other organs, such as the liver, pancreas, kidneys, lungs, and eyes.
The treatment strategy for UC is mainly based on the severity, distribution (proctitis, left-sided, extensive), and pattern of disease (relapse frequency, disease course, response to previous medications, side effects of medication, and extra-intestinal manifestations).11
Age at onset and disease duration should also be taken into consideration. The general approach involves stepping up treatment according to response to the previous modality.
TNF, tumor necrosis factor.
Adapted from Magro et al, 20174 and Harbord et al, 2017.11
Biologics are administered when the patient no longer responds to, or experiences adverse events with, alternative treatment options. They are designed to inhibit specific components of the inflammatory immune response.
Anti-tumor necrosis factors (TNFs)
Anti-TNF agents, such as adalimumab and infliximab, bind soluble and transmembrane TNF-α, preventing it from interacting with its two receptors (TNFRI and TNFRII), and preventing TNF-α mediated signaling.
Anti-TNFs may affect various cells of the immune system. Additional, non-TNFR modes of action require binding of the anti-TNF to the transmembrane form of TNF-α and most often result in the death of the target cell.12
IBD, inflammatory bowel disease; mAB, monoclonal antibody; MoA, mode of action; s/tmTNF; soluble/transmembrane tumor necrosis factor; TNFR, tumor necrosis factor receptor.
Adapted from Vande Casteele and Sandborn, 2015.12
Clinical trials data indicate that anti-TNF therapy is effective in achieving and maintaining steroid-free remission in patients with UC with steroid-dependent disease.11
Guidelines for the treatment of UC are available from The European Crohn’s and Colitis Organisation: (https://www.ecco-ibd.eu/publications/ecco-guidelines-science/published-ecco-guidelines.html).11
- The therapeutic goal for UC is to induce and maintain clinical remission
- Treatment generally starts with mesalamine (5-aminosalicylic acid) with the addition of steroids in patients who do not respond
- Thiopurines or anti-TNF therapy is recommended for patients with steroid-dependent disease
You can find additional information about UC by following these links:
Crohn’s & Colitis UK:
European Federation of Crohn's & Ulcerative Colitis Associations
European Crohn’s and Colitis Organisation: