Ulcerative colitis

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

Ulcerative colitis (UC) can be classified by both severity and extent.[4] Treatment is guided by both factors.

The treatment goal for patients with active UC is to achieve remission (endoscopic and clinical) by demonstrating complete mucosal healing.[23]

The severity of UC is defined as:[4][26]

Mild: passage of ≤4 stools per day (with or without blood), absence of any systemic illness, and normal levels of inflammatory markers (erythrocyte sedimentation rate [ESR]). C-reactive protein (CRP) ≥12 mg/L has been suggested as a sensitive cut-off that might be considered as an alternative to ESR for determining UC severity.[33]
Moderate: passage of >4 stools per day but with minimal signs of systemic toxicity
Severe: passage of ≥6 bloody stools daily, pulse rate of at least 90 beats per minute (bpm), temperature of at least 37.5ºC (99.5ºF), haemoglobin level of <105 g/L (<10.5 g/dL), and ESR of at least 30 mm/hour.

Fulminant colitis is a rare complication of UC where the inflammation becomes transmural and ulceration extends deeply into the muscle layer with neuromuscular degeneration, potentially leading to toxic dilatation and perforation; this causes extremely severe symptoms and requires urgent treatment.[47][48]

The American Gastroenterological Association (AGA) considers patients as having moderate-to-severe UC if they:[45]

have moderate-to-severe symptoms with mayo endoscopy sub-score (MES) of 2 or 3 (presence of diffuse erythema, friability, erosions or spontaneous bleeding or ulcerations on endoscopy)
have mild symptoms, with high burden of inflammation or poor prognostic features
are dependent on or refractory to corticosteroids.

The extent of UC is defined as follows:[4]

Proctitis: disease limited to the rectum, often extending 15 to 20 cm proximal to the anal verge and distal to the rectosigmoid junction
Left-sided colitis (also called distal UC): disease that extends beyond the sigmoid colon and as far proximally as the splenic flexure or 60 cm from the anal verge
Extensive colitis (also called pancolitis): disease extending proximal to the splenic flexure.

Treatment selection should be based on inflammatory activity and disease prognosis, i.e., patients with factors that impact on disease prognosis (previous hospitalisation or corticosteroid dependence) with mild UC, should be considered for treatments typically recommended for patients with moderate to severely active disease.[23]

Treatment of UC in pregnancy will not be covered here, as it is a complex topic with many varied guidelines. There is a lack of high-quality studies in this population and limited data on drugs approved to treat inflammatory bowel diseases (IBD) during pregnancy.[49] Seek consultant advice for these patients. In August 2025, the Global Consensus Consortium published standardised practical recommendations for providers caring for women with IBD throughout the world, based on best available research.[49]

Acute severe ulcerative colitis (ASUC): initial management

ASUC is the most severe form and a potentially life-threatening condition. The initial risk stratification of patients with ASUC is based on modified Truelove and Witts criteria which defines ASUC in adults as:[26][50][51]

≥6 bloody stools per day and systemic toxicity with at least one additional criteria
temperature >37.8ºC (>100.0ºF)
pulse >90 bpm
haemoglobin <105 g/L (<10.5 g/dL)
Elevated inflammatory markers; ESR >30 mm/h or CRP >30 mg/L. CRP ≥12 mg/L has been suggested as a sensitive cut-off for determining UC severity.[33]

These patients should be admitted to hospital for assessment and intensive management.[51] Patients may be haemodynamically unstable on admission, and need supportive measures such as blood transfusion, fluids, and electrolyte replacement.[51] Prophylactic low molecular weight heparin (LMWH) to prevent venous thromboembolism is recommended.[23][51]

Patients presenting with possible ASUC should have urgent inpatient assessment and blood tests (full blood count, CRP, urea and electrolytes, liver function tests, and serum magnesium level), stool culture, Clostridium difficile assay, radiological imaging (abdominal x-ray to evaluate for toxic megacolon), and flexible sigmoidoscopy. Cross-sectional imaging with a computed tomography (CT) scan should be restricted to patients with a suspected extraluminal complication, perforation, and in those newly diagnosed where the distinction between Crohn’s disease and UC may not be apparent on sigmoidoscopy.[23][52]

Initial treatment

A high-dose intravenous corticosteroid such as methylprednisolone or hydrocortisone is recommended first line to induce remission in patients with ASUC.[23][51][53]
If patients have concomitant C difficile infection, treatment should follow the Infectious Disease Society of America Guidelines (or other appropriate guidelines).[54] See Clostridioides difficile-associated disease.

Rescue therapy

If patients do not respond adequately to intravenous corticosteroid treatment within 3-5 days, rescue therapy with either intravenous infliximab or ciclosporin should be added to the corticosteroid.[23][51][53] Although evidence indicates comparable efficacy, the adverse effect profile of ciclosporin is less favourable than that of infliximab.[55][56]
There is growing interest in accelerated infliximab induction for ASUC, but US guidance does not routinely recommend accelerated infliximab induction for patients with ASUC; dose intensification of infliximab can be considered in patients who have a low serum albumin, and only with careful disease monitoring and ongoing assessment.[23] The British Society of Gastroenterology recommends that in patients who do not respond to initial intravenous corticosteroid treatment, an intensified dosing regimen of infliximab can be considered in a select group of patients, especially if serum albumin levels are low.[26][51]

Surgery

The absolute indications for colectomy for patients with ASUC are complications such as toxic megacolon, perforation, uncontrolled severe haematochezia, or multiorgan dysfunction.[23][51][53]
Any patients with severe intractable symptoms or intolerable drug adverse effects should be considered for colectomy.[51][53]
Delay in surgery is associated with an increased risk of surgical complications.[23]

Moderate-to-severe ulcerative colitis: induction therapy

Recommended treatments to induce remission in patients with moderate-to-severe disease include systemic corticosteroids, immunosuppressants, tumour necrosis factor (TNF)-alpha inhibitors (e.g., golimumab, infliximab, adalimumab), selective adhesion-molecule inhibitors (e.g., vedolizumab), interleukin (IL)-12/23 inhibitors (e.g., ustekinumab), IL-23 inhibitors (e.g., mirikizumab, guselkumab, risankizumab), sphingosine 1-phosphate (S1P) receptor modulators (e.g., etrasimod, ozanimod), and Janus kinase (JAK) inhibitors (e.g., tofacitinib, upadacitinib). These drugs may be used as monotherapy or as part of combination therapy, depending on the drug and guideline recommendations.[23][51][53][57][58][59]

AGA guidance focuses on immunosuppressants, biologicals, and small molecules for induction of remission.[45] Check local guidelines as practice may vary.

Corticosteroids

Oral corticosteroids can be used to induce remission in patients with moderate-to-severe UC of any extent and have typically been first-line induction treatments in moderate-to-severe disease[23][24]
In patients with moderately active UC, oral budesonide multi-matrix system (MMX), a locally acting corticosteroid, can be considered before the use of systemic therapy.[23]

Biological and targeted disease-modifying therapies

In patients with moderate-to-severe UC, early use of biological treatment with or without immunosuppressant therapy is suggested.[45]
Combination treatment with a TNF-alpha inhibitor, vedolizumab, or ustekinumab plus an immunosuppressant (a thiopurine or methotrexate) is suggested rather than biological monotherapy.[45][51] Monotherapy with a TNF-alpha inhibitor, vedolizumab, ustekinumab, or tofacitinib is preferred to monotherapy with a thiopurine.[45]
Patients with less severe disease may prefer to begin with TNF-alpha inhibitor monotherapy, but this increases the risk of drug antibody formation.[45]
For patients who respond to TNF-alpha inhibitors but lose response, serum drug levels and antibodies (if there is not a therapeutic level) should be measured to assess the reason for the loss of response.[23][60]
Biosimilars for some biological agents may be available and you should consult your local guidelines for more information.

Specific biological and targeted disease-modifying therapies (also known as advanced therapies) for induction therapy are discussed in detail below.

Moderate-to-severe ulcerative colitis: TNF-alpha inhibitors

TNF-alpha inhibitors are an option for induction therapy in patients with moderate-to-severe UC. Options include golimumab, infliximab, and adalimumab.

Golimumab

In adult outpatients with moderate-to-severe UC, the AGA suggests the use of golimumab over no treatment. In patients who are naive to advanced therapies, the AGA suggests using an intermediate-efficacy drug such as golimumab, rather than a lower efficacy drug (such as adalimumab).[45]
Recommended for inducing and sustaining clinical remission in adult patients with moderate-to-severe active UC who have had an inadequate response to immunosuppressants such as corticosteroids.[23][45]
Golimumab has been shown to induce clinical remission and mucosal healing in patients with moderate-to-severe active UC with a similar safety profile to other TNF-alpha inhibitors.[61][62]

Infliximab

In adult outpatients with moderate-to-severe UC, the AGA recommends the use of infliximab over no treatment. In patients who are naive to advanced therapies, the AGA suggests using a higher-efficacy drug such as infliximab, rather than a lower efficacy drug (such as adalimumab).[45]
Should be considered as an alternative to induce and maintain disease remission.[63][64] When infliximab is used as induction therapy for patients with moderate to severely active UC, combination therapy with azathioprine is recommended.[23][51]

Adalimumab

In adult outpatients with moderate-to-severe UC, the AGA suggests the use of adalimumab over no treatment.[45]
A large-scale, prospective, multicentre study in Japan confirmed the safety and effectiveness of adalimumab to induce and maintain clinical remission in patients with moderate to severe UC.[65]

TNF-alpha inhibitors have been associated with a risk of serious infections and malignancy.

Moderate-to-severe ulcerative colitis: selective adhesion-molecule inhibitors

Selective adhesion-molecule inhibitors are an option for induction therapy in patients with moderate-to-severe UC. Vedolizumab is currently the only drug available in this class.

Vedolizumab

A monoclonal antibody against alpha-4-beta-7 integrin. It has been shown to be more effective than placebo as induction and maintenance therapy for UC.[66][67]
In adult outpatients with moderate-to-severe UC, the AGA recommends the use of vedolizumab over no treatment. In patients who are naive to advanced therapies, the AGA suggests using a higher-efficacy drug such as vedolizumab, rather than a lower efficacy drug (such as adalimumab).[45]
The American College of Gastroenterology (ACG) recommends vedolizumab for induction of remission for patients who have previously failed TNF-alpha inhibitor therapy.[23]
One Cochrane review found vedolizumab to be more effective than placebo for inducing clinical remission, clinical response, and endoscopic remission in patients with moderate-to-severe active UC, and for preventing relapse in patients with quiescent UC.[68] In another systematic review and meta-analysis, vedolizumab efficacy for the induction and maintenance of mucosal healing in UC was similar to that of TNF-alpha inhibitors.[69] Network meta-analysis suggested that vedolizumab may lead to a more sustained clinical response than other biological agents approved for UC.[70] Vedolizumab appears to have a favourable safety profile.[71]

Moderate-to-severe ulcerative colitis: IL-12/23 inhibitors

IL-12/23 inhibitors are an option for induction therapy in patients with moderate-to-severe UC. Ustekinumab is currently the only drug available in this class.

Ustekinumab

In adult outpatients with moderate-to-severe UC, the AGA recommends the use of ustekinumab over no treatment. In patients who are naive to advanced therapies, the AGA suggests using an intermediate-efficacy drug such as ustekinumab, rather than a lower efficacy drug (such as adalimumab). The AGA also suggests using a higher efficacy drug, such as ustekinumab, in patients who have previously been exposed to one or more advanced therapies, particularly TNF-alpha inhibitors (infliximab), rather than a lower efficacy drug (such as adalimumab, vedolizumab, ozanimod, and etrasimod).[45]
The interim results of a phase 3 study of ustekinumab in biological-naive and biological-experienced adults with moderate to severely active UC indicate that ustekinumab is more effective than placebo for inducing and maintaining remission. Significantly more patients treated with ustekinumab achieved endoscopic improvement and mucosal healing.[72][73]

Moderate-to-severe ulcerative colitis: IL-23 inhibitors

IL-23 inhibitors are an option for induction therapy in patients with moderate-to-severe UC. Options include mirikizumab, guselkumab, and risankizumab.

Mirikizumab

In adult outpatients with moderate-to-severe UC, the AGA suggests the use of mirikizumab over no treatment. In patients who are naive to advanced therapies, or in patients who have previously been exposed to one or more advanced therapies, particularly TNF-alpha inhibitors, the AGA suggests using an intermediate-efficacy drug such as mirikizumab, rather than a lower efficacy drug (such as adalimumab, vedolizumab, ozanimod, and etrasimod).[45]
In two phase 3, randomised, double-blind, placebo controlled trials it was found that mirikizumab was more effective than placebo in inducing and maintaining clinical remission in patients with moderately to severely active UC.[58]

Guselkumab

In adult outpatients with moderate-to-severe UC, the AGA recommends the use of guselkumab over no treatment. In patients who are naive to advanced therapies, the AGA suggests using a higher-efficacy drug such as guselkumab, rather than a lower efficacy drug (such as adalimumab). The AGA also suggests using an intermediate efficacy drug, such as guselkumab, in patients who have previously been exposed to one or more advanced therapies, particularly TNF-alpha inhibitors, rather than a lower efficacy drug (such as adalimumab, vedolizumab, ozanimod, and etrasimod).[45]
In a phase 3, double blind, randomised, placebo-controlled induction and maintenance study, guselkumab was found to be effective and safe compared to placebo as induction and maintenance therapy.[74]

Risankizumab

In adult outpatients with moderate-to-severe UC, the AGA recommends the use of risankizumab over no treatment. In patients who are naive to advanced therapies, the AGA suggests using a higher-efficacy drug such as risankizumab, rather than a lower efficacy drug (such as adalimumab). The AGA also suggests using an intermediate-efficacy drug, such as risankizumab, in patients who have previously been exposed to one or more advanced therapies, particularly TNF-alpha inhibitors, rather than a lower efficacy drug (such as adalimumab, vedolizumab, ozanimod, and etrasimod).[45]
In two phase 3 randomised controlled trials (RCTs), risankizumab improved clinical remission rates in an induction trial and in a maintenance trial for patients with moderately to severely active ulcerative colitis, compared with placebo.[75]

Moderate-to-severe ulcerative colitis: immunosuppressants

A thiopurine (e.g., azathioprine, mercaptopurine) or methotrexate, in combination with a TNF-alpha inhibitor, vedolizumab, or ustekinumab, is recommended for induction of remission in patients with moderate-to-severe UC.[23][45][51] Immunosuppressant monotherapy is not recommended for induction therapy.[23][45]

Methotrexate

Dose-dependent adverse effects of methotrexate include bone marrow suppression, particularly leukopenia, which can develop suddenly and have an unpredictable course; liver injury; and infections.[76] Other adverse effects (not dose-dependent) include pancreatitis, headache, fatigue, anorexia, weight loss, stomatitis, alopecia, arthralgia, muscular weakness, and rash.[76]

Thiopurines

Thiopurines are associated with a small but statistically significant increased risk for lymphoma among adults with IBD compared with patients not receiving thiopurine.[77] Persistent use of thiopurines is also is associated with an increased risk of non-melanoma skin cancer; therefore, patients should be educated in primary skin cancer prevention (e.g., reduced ultraviolet exposure).[78]
Azathioprine and mercaptopurine doses should be lowered in patients with heterozygous thiopurine methyltransferase variant genotype.[79]
Allopurinol should be avoided (or patients monitored closely), as it inhibits the breakdown of azathioprine and increases the risk of myelosuppression.[80] However, adjunctive treatment with low-dose allopurinol, in addition to a 25% to 50% thiopurine dose reduction, is required for select patients in whom thiopurine is preferentially metabolised via the hepatotoxic methylmercaptopurine pathway.[81][82][83]

Moderate-to-severe ulcerative colitis: JAK inhibitors

JAK inhibitors are an option for induction therapy in patients with moderate-to-severe UC. Options include tofacitinib and upadacitinib.

Tofacitinib

In adult outpatients with moderate-to-severe UC, the AGA recommends tofacitinib over no treatment.[45]
In patients who are naive to advanced therapies, the AGA suggests using an intermediate-efficacy drug, such as tofacitinib, rather than a lower efficacy drug. However, JAK inhibitors have restricted use in advanced therapy-naive patients. The prescribing information recommends the use of JAK inhibitors in patients with prior failure or intolerance to TNF-alpha inhibitors.[45]
In patients who have previously been exposed to one or more advanced therapies, particularly TNF-alpha inhibitors, the AGA suggests using a higher-efficacy drug such as tofacitinib.[45]
Guidelines recommend tofacitinib for induction of remission in patients with moderate-to-severe UC who have previously been exposed to infliximab, particularly those with primary non-response, or those who are intolerant to TNF-alpha inhibitor therapy.[23][45]

Upadacitinib

In adult outpatients with moderate-to-severe UC, the AGA recommends upadacitinib over no treatment.[45]
In patients who are naive to advanced therapies, the AGA suggests using an higher efficacy drug, such as upadacitinib, rather than a lower efficacy drug. However, JAK inhibitors have restricted use in advanced therapy-naive patients. The prescribing information recommends the use of JAK inhibitors in patients with prior failure or intolerance to TNF-alpha inhibitors.[45]
In patients who have previously been exposed to one or more advanced therapies, particularly TNF-alpha inhibitors, the AGA suggests using a higher-efficacy drug such as upadacitinib.[45]
Guidelines recommend upadacitinib for induction of remission in patients with moderate-to-severe UC who have previously been exposed to infliximab, particularly those with primary non-response, or those who are intolerant to TNF-alpha inhibitor therapy.[23][45]
Data from three phase 3 RCTs show clinical remission at 8 weeks (primary end point) with upadacitinib (26% and 34%) compared with placebo (5% and 4%, respectively) and at 52 weeks (42% or 52%, depending on the dose of upadacitinib compared with placebo 12%).[84][85]
One recent systematic review suggested that upadacitinib was the best performing agent for the induction of clinical remission compared with other biologics and small molecule drugs; however, it was also the worst performing agent in terms of adverse effects.[86]

Safety concerns with JAK inhibitors

The US Food and Drug Administration (FDA) has issued a warning about an increased risk of serious cardiovascular events, malignancy, thrombosis, and death with JAK inhibitors.[87] This follows final results from a large randomised safety clinical trial which compared tofacitinib with TNF-alpha inhibitors in patients with rheumatoid arthritis. The study found an increased risk of blood clots and death with the lower dose of tofacitinib (5 mg twice daily); this serious event had previously been reported only with the higher dose (10 mg twice daily - the induction dose for UC) in the preliminary analysis.[88] The FDA advises clinicians to:[87]
- Reserve JAK inhibitors for patients who have had an inadequate response or are intolerant to one or more TNF-alpha inhibitors
- Consider the patient’s individual benefit-risk profile when deciding to prescribe or continue treatment with these drugs, particularly in patients who are current or past smokers, patients with other cardiovascular risk factors, those who develop a malignancy, and those with a known malignancy (other than a successfully treated non-melanoma skin cancer).

The European Medicines Agency (EMA) also recommends measures to minimise the risk of serious adverse effects with JAK inhibitors in patients who are aged >65 years, patients who are current or past smokers, patients with other cardiovascular risk factors, and patients with other malignancy risk factors. The EMA advises that JAK inhibitors should only be used to treat moderate or severe UC in these patient groups if no suitable treatment alternative is available.[89] In addition the EMA recommends that:[89]
- JAK inhibitors should be used with caution in patients at high risk of blood clots (other than those listed above)
- The dose should be reduced in patients who are at risk of venous thromboembolism, major cardiovascular problems, or cancer, where possible.

The UK Medicines and Healthcare products Regulatory Agency (MHRA) supports these recommendations, and also advises patients taking JAK inhibitors to carry out periodic skin examinations, due to an increased risk of non-melanoma skin cancer associated with these drugs.[90]

Patients with less severe disease, who place higher value on the potential safety of drugs, and a lower value on the relative efficacy of drugs, may reasonably choose vedolizumab as an alternative.[45]

Moderate-to-severe ulcerative colitis: S1P receptor modulators

S1P receptor modulators are an option for induction therapy in patients with moderate-to-severe UC. Options include ozanimod and etrasimod.

These drugs are contraindicated in patients with recent (in the last 6 months) myocardial infarction, unstable angina, stroke, transient ischaemic attack, or heart failure.[25] They are also contraindicated in patients with a history or presence of second- or third-degree atrioventricular block, sick sinus syndrome, or sino-atrial block (unless the patient has a functioning pacemaker).[91]

Ozanimod

In adult outpatients with moderate-to-severe UC, the AGA recommends the use of ozanimod over no treatment. In patients who are naive to advanced therapies, the AGA also suggests using a higher efficacy drug, such as ozanimod, rather than a lower efficacy drug (such as adalimumab).[45]

Etrasimod

In adult outpatients with moderate-to-severe UC, the AGA recommends the use of etrasimod over no treatment. In patients who are naive to advanced therapies, the AGA also suggests using a higher efficacy drug, such as etrasimod, rather than a lower efficacy drug (such as adalimumab).[45]

Moderate-to-severe ulcerative colitis: therapeutic drug monitoring (TDM)

To optimise drug concentration and clinical improvement for patients with UC being treated with immunosuppressants and/or biologics, TDM is becoming more frequently used to check drug trough concentration, and assess for the presence of antidrug antibodies.[92][93][94] BMJ Rapid Recommendations: proactive therapeutic drug monitoring of biologic drugs in adult patients with inflammatory bowel disease, inflammatory arthritis, or psoriasis: a clinical practice guideline Opens in new window

TDM can be performed at any point during induction or maintenance therapy, and is conditionally recommended by the AGA to guide treatment changes for patients with IBD.[92][95]

Moderate-to-severe ulcerative colitis: surgery

Any patients with severe intractable symptoms or intolerable adverse effects from pharmacotherapy should be considered for colectomy.[23][51][53]

One systematic review of outcomes and postoperative complications following colectomy for patients with UC suggests that early and late complications arise in about one third of patients undergoing surgery for UC.[96] While colorectal surgical procedures are recommended for a specific group of patients, the postoperative complications associated with these procedures should not be underestimated.[96]

Mild ulcerative colitis: induction therapy

Treatment to induce remission in patients with mild disease is topical (rectal) or oral aminosalicylates (also known as 5-aminosalicylates or 5-ASA drugs), or a combination of both.[7][23][51][53] Corticosteroids may also be added to aminosalicylate therapy.[51][53] Aminosalicylates include mesalazine, sulfasalazine, balsalazide, and olsalazine. Mesalazine is the only aminosalicylate available as a topical formulation.

An oral aminosalicylate is not as effective as topical; if used, initial treatment of mild UC is with a low-dose oral aminosalicylate.[23][53] Once-daily dosing of oral aminosalicylates is recommended, but more frequent doses can be used based on patient preference to optimise adherence.[23]

Proctitis

First-line treatment to induce remission for patients with mildly active ulcerative proctitis is rectal aminosalicylate.[23][51] A rectal aminosalicylate is recommended over a rectal corticosteroid.[23][51]

Left-sided colitis

First-line treatment for the induction of remission in patients with left-sided colitis is a rectal aminosalicylate (in preference to a rectal corticosteroid) combined with oral aminosalicylate.[7][23][51][53]
For patients with mildly active left-sided UC who are intolerant or non-responsive to an oral and rectal aminosalicylate, the addition of oral budesonide MMX is recommended for induction of remission.[7][23][51][53]

Second-generation corticosteroids, such as budesonide MMX, are starting to emerge as a primary treatment option in mild-to-moderate UC.[51][97][98] They are associated with significantly fewer corticosteroid-related adverse events than conventional corticosteroids.[99] MMX technology may facilitate adherence by reducing the pill burden.[100]

Extensive UC

The ACG suggests that an oral aminosalicylate is the preferred first-line treatment.[23]
In patients with mild UC refractory to optimised oral and rectal aminosalicylate therapy, the addition of either oral prednisolone or budesonide MMX is recommended as an alternative.[23][24][26][51]

Maintenance of remission: general principles

The goal of maintenance therapy is to maintain corticosteroid-free clinical and endoscopic remission; systemic corticosteroids are not recommended for maintenance of remission of UC of any severity.[23][51]

Maintenance of remission: ASUC

Patients with ASUC who achieve remission with infliximab treatment should continue treatment with infliximab for maintenance of remission.[23] However, if patients with ASUC achieve remission with ciclosporin, a thiopurine is suggested for maintenance of remission.[23]

Allopurinol should be avoided (or patients monitored closely) in patients taking thiopurines, as it inhibits the breakdown of azathioprine and increases the risk of myelosuppression.[80] However, adjunctive treatment with low-dose allopurinol, in addition to a 25% to 50% thiopurine dose reduction, is required for select patients in whom thiopurine is preferentially metabolised via the hepatotoxic methylmercaptopurine pathway.[81][82][83]

Maintenance of remission: moderate-to-severe ulcerative colitis

Maintenance therapy should be continued with the drug successful in achieving induction, with the important exception that corticosteroids are not recommended for long-term maintenance.[26] It is assumed that if a drug (excluding corticosteroids and cyclosporine) is effective for induction of remission, it will be continued for maintenance of remission unless otherwise specified.[26][45][51]

Some exceptions and additional considerations include:

Patients with previous moderate-to-severe UC who have achieved remission with TNF-alpha inhibitors and/or immunosuppressants, or JAK inhibitors, should not be given concomitant aminosalicylates for maintenance of remission.[23]
For patients with previously moderate-to-severe UC who achieve remission with corticosteroid induction, a thiopurine is suggested for maintenance of remission in preference to no treatment.[45]
Methotrexate monotherapy is not recommended for maintenance of remission.[23][45]

Maintenance of remission: mild ulcerative colitis

The large majority of patients with mild UC who achieve remission with aminosalicylate therapy continue with aminosalicylate treatment to maintain remission.[23][51]

Patients on maintenance therapy with a high-dose aminosalicylate, who require two or more courses of corticosteroids in 12 months, or who become corticosteroid dependent or refractory, require treatment escalation to a thiopurine, a TNF-alpha inhibitor, vedolizumab, or tofacitinib.[26][51] The treatment choice should be determined by clinical factors and patient preference.[26][51]