Introduction
IBD-related tenesmus, a debilitating urge to pass stool, even when there is no need to do so, is caused by Inflammatory bowel disease (IBD). This chronic condition leads to the inflammation of the digestive system. IBD patients require effective treatment, as this disease can significantly impact a patient's quality of life.1,3
What are the symptoms?
There are two main types of inflammatory bowel diseases: Crohn’s disease (CD) and ulcerative colitis (UC).1 These diseases cause inflammation in the gastrointestinal tract, which mostly happens in adolescents and adults.1
Though CD and UC are similar, there are some differences:
CD can affect the digestive system, from the mouth to the rectum, and affect all the layers of the intestine, through patchy inflammation.2 This can cause symptoms such as: 1,2
- Stomach pain
- Long-term diarrhoea
- Weight loss
- Vitamin D deficiency
- Tenesmus
UC is associated with blood in the stool as it causes the continuous inflammation of the mucosa, the innermost part of the colon, and, depending on how bad the disease is, can lead to symptoms such as:1,2
- Bloody diarrhoea
- Abdominal pain
- Iron deficiency
- Tenesmus
What is tenesmus, and why is it important to address in IBD patients?
Tenesmus is the urge to pass stool without being able to do so.3 This is a common symptom in IBD patients, which is caused by the chronic inflammation of the intestine.3
Patients may find that IBD symptoms, such as tenesmus, have an impact on how they live life and can lead to professional constraints as well as decreased sexual satisfaction due to the constant feeling of tenesmus.2 Over time, IBD can lead to mental health problems such as anxiety and depression, on top of physical constraints.2
Research on the importance of treatment
There was a study carried out to assess stool patterns and symptoms of rectal dysfunction in IBD patients, where it was found that the majority of patients’ tenesmus worsened daily functioning.4 It was also seen that tenesmus in UC patients was significantly higher than in CD patients.4
Additionally, research has also found that tenesmus appears more frequently in response to a change in the activity of the disease and its flare-ups.5 So targeting tenesmus could be a helpful way to treat IBD and improve the quality of a patient’s life, by improving the way the disease is treated.5
What causes IBD?
IBD is an autoimmune disease, which means the immune system attacks healthy tissues.1 Though the specific cause of IBD is unknown, two main factors play a role in its development.1,12
- Genetic factors
- Environmental factors
Research has shown that these factors play a role in causing chronic dysregulation in the immune system.6 This disrupts the mucous system, which then leads to inflammation and tissue damage.1 The health of the intestinal mucosa barrier is important in decreasing inflammation.1
Genetics
Genetics can play a big role in causing IBD. Certain genes can lead to inflammation of the mucosa. This tells us that people with these specific genetics are more likely to develop IBD than those without these genes.6
Environmental factors
Environmental factors such as diet and additives in food can hurt gut health, which can cause inflammation and a higher chance of getting IBD.1,12
How does inflammation contribute to tenesmus?
Inflammation plays a major role in tenesmus development through numerous mechanisms, including:
- Infectious colitis – infections caused by bacteria result in inflammation of the colon7
- Rectal inflammation – continuous inflammation of the mucosa of the rectum6
- Visceral hypersensitivity – continuous inflammation causes hypersensitivity of the colon and rectum8
How to treat IBD-related tenesmus?
The main focus on treating IBD-related tenesmus is using anti-inflammatory therapies. These treatments are used to decrease symptoms such as tenesmus.
There are four main anti-inflammatory treatments currently being used:
Aminosalicylates (5-ASAs)
5-ASAs are one of the first treatments used by doctors for the treatment of tenesmus and IBD, specifically UC, in mild to moderate cases. These drugs suppress specific factors, such as IL-1 and TNF-α, in the immune system, which contribute to chronic inflammation.9 This is to stop tissue damage in the mucosa caused by inflammation and to help start the healing process.9
5-ASAs such as sulfasalazine are typically taken orally. However, there are topical forms such as enemas, foams, and suppositories as well, which are administered in the rectum and are very effective in treating inflammation related to tenesmus.9,10
Research has shown that mucosal healing was induced in about 44% of patients on this treatment. This proves the benefits of 5-ASAs.9
There are side effects of 5-ASAs, but they are generally considered mild. This includes nausea, diarrhoea, and abdominal pain.11 However, the side effects associated with sulfasalazine can be more severe, including infertility and haemolytic anaemia.11
Corticosteroids
Corticosteroids are used for IBD flare-ups in moderate to severe cases.9,10 Corticosteroids do not specifically target tenesmus as they decrease overall inflammation. This helps to decrease the activity of the disease, therefore reducing tenesmus.9,10 Though corticosteroids have not been proven to keep IBD in remission, they induce it, which is when the disease severity is seen to have improved.11
Oral corticosteroids can have several side effects, including diabetes and high blood pressure.11 Research has also shown that corticosteroids can cause IBD patients to become dependent on them, which means stopping the corticosteroids causes physical symptoms.11
Corticosteroids such as prednisolone can be taken orally or used topically.9,10 Topical corticosteroids such as hydrocortisone suppositories are used to decrease rectal inflammation in the area where they are applied, which can alleviate symptoms of tenesmus, especially in UC.9,10
Immunomodulators
Immunomodulators are a group of drugs that focus on suppressing the immune system activity.9 by stopping/decreasing certain immune system factors that ‘attack’ the tissue.10,11 There are three main types of immunomodulators used in IBD:
Calcineurin inhibitors
Calcineurin activates a signalling pathway that causes an inflammatory response.11 Calcineurin inhibitors such as cyclosporine A and tacrolimus prevent calcineurin from initiating this response and reduce the symptoms of tenesmus in IBD patients.
Tacrolimus, however, can have a high chance of side effects such as tremors and damage to renal function.11
Methotrexates (MTX)
Methotrexates stop different enzymes that increase the production of inflammatory cytokines, which are involved in the inflammatory response.9,11
The side effects of MTX include vomiting, rash, and diarrhoea.9,11
Janus kinase (JAK) inhibitors
JAKs are a family of kinases (a type of enzyme) that target cytokine pathways, initiating the inflammatory response. Therefore, stopping these kinases with JAK inhibitors stops the inflammatory response and decreases inflammation.9,11 An example of a JAK inhibitor used in moderate to severe cases of UC is tofacitinib.9.11 It is an effective treatment, but there may be some side effects, such as a herpes zoster infection, otherwise known as shingles.
Biologics
Biologics are a group of drugs that stop/decrease inflammatory mediators such as cytokines. They have shown great success in treating IBD and decreasing tenesmus.9,11 There are three main types:
Anti-TNF therapy
Anti-TNF therapy is a treatment that targets TNF-α, a cytokine that is involved in the inflammatory response.11 Too much of this cytokine can cause long-term inflammation, so anti-TNF therapies such as infliximab are used to decrease TNF-α and therefore lower inflammation.11
This treatment can be used on IBD patients who are dependent on steroids such as corticosteroids.11
Anti-IL-12/23 therapy
Anti-IL-12/23 therapy works similarly to anti-TNF therapy, but instead of decreasing TNF-α, it reduces the inflammatory cytokines IL-12 and IL-23.
Ustekinumab is an example of an Anti-IL-12/23 therapy, which is commonly used to treat mild to moderate CD.
Anti-integrin therapy
Anti-integrin therapy works by blocking integrins (proteins on the surface of the immune cells) that are responsible for moving the cells to areas of inflammation.9,11 By blocking these integrins with anti-integrin therapies such as vedolizumab, the immune cells can’t go to the intestine and cause inflammation, therefore improving symptoms in IBD such as tenesmus.9,11
These do not block the inflammatory response directly, so they can work well in combination with other anti-inflammatory drugs such as immunomodulators.11
Personalising medicine
Best treatment for IBD-related tenesmus depends on the individual patient and the characteristics of the IBD the patient has, as well as their genetics and lifestyle factors.
Personalised medicine tailors to individuals to ensure the best possible treatment for their specific symptoms and side effects is achieved. This can be done in a variety of ways. The most common method is to use more than one anti-inflammatory treatment to ensure inflammation is properly decreased in IBD and its related tenesmus. This also comes with minimal side effects and complications.9,10,11
Summary
In conclusion, anti-inflammatory therapies are important in the management of IBD, specifically in addressing symptoms such as tenesmus. Tenesmus, characterised by a constant urge to pass stool without being able to do so, can significantly impact patients’ quality of life. Therefore, it is important to manage tenesmus with treatments, such as anti-inflammatory therapies including aminosalicylates, corticosteroids, immunomodulators, and biologics.
Research has shown that all of these treatments decrease or stop inflammation and target immune system dysregulation linked to IBD-related tenesmus. What therapies are used for the treatment depends on the individual IBD patients, what type of IBD they have, whether it is UC or CD, and the side effects and complications they may experience.
References
- Saeid Seyedian S, Nokhostin F, Forogh Nokhostin, Dargahi Malamir M. A review of the diagnosis, prevention, and treatment methods of inflammatory bowel disease. JMedLife [Internet]. 2019 [cited 2025 Mar 3];12(2):113–22. Available from: https://medandlife.org/wp-content/uploads/JMedLife-12-113.pdf
- Nóbrega VG, Silva IN de N, Brito BS, Silva J, Silva MCM da, Santana GO. The onset of clinical manifestations in inflammatory bowel disease patients. Arq Gastroenterol [Internet]. 2018 [cited 2025 Mar 3];55:290–5. Available from: https://www.scielo.br/j/ag/a/GJPykqyP38drZjHTrVjSbwL/?lang=en
- Andreyev HJN, Muls AC, Norton C, Ralph C, Watson L, Shaw C, et al. Guidance: The practical management of the gastrointestinal symptoms of pelvic radiation disease. Frontline Gastroenterol [Internet]. 2015 [cited 2025 Mar 3];6(1):53–72. Available from: https://fg.bmj.com/lookup/doi/10.1136/flgastro-2014-100468
- Petryszyn PW, Paradowski L. Stool patterns and symptoms of disordered anorectal function in patients with inflammatory bowel diseases. Adv Clin Exp Med [Internet]. 2018 [cited 2025 Mar 3];27(6):813–8. Available from: https://advances.umw.edu.pl/en/article/2018/27/6/813/
- Joyce JC, Waljee AK, Khan T, Wren PA, Dave M, Zimmermann EM, et al. Identification of symptom domains in ulcerative colitis that occur frequently during flares and are responsive to changes in disease activity. Health Qual Life Outcomes [Internet]. 2008 [cited 2025 Mar 3];6(1):69. Available from: https://hqlo.biomedcentral.com/articles/10.1186/1477-7525-6-69
- Goyette P, Labbé C, Trinh TT, Xavier RJ, Rioux JD. Molecular pathogenesis of inflammatory bowel disease: Genotypes, phenotypes and personalized medicine. Annals of Medicine [Internet]. 2007 [cited 2025 Mar 4];39(3):177–99. Available from: http://www.tandfonline.com/doi/full/10.1080/07853890701197615
- Azer SA, Tuma F. Infectious colitis. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 [cited 2025 Mar 5]. Available from: http://www.ncbi.nlm.nih.gov/books/NBK544325/
- Scott SM, Van Den Berg MM, Benninga MA. Rectal sensorimotor dysfunction in constipation. Best Practice & Research Clinical Gastroenterology [Internet]. 2011 [cited 2025 Mar 5]; 25(1):103–18. Available from: https://linkinghub.elsevier.com/retrieve/pii/S1521691811000023.
- Otte ML, Lama Tamang R, Papapanagiotou J, Ahmad R, Dhawan P, Singh AB. Mucosal healing and inflammatory bowel disease: Therapeutic implications and new targets. World J Gastroenterol [Internet]. 2023 [cited 2025 Mar 5; 29(7):1157–72. Available from: https://www.wjgnet.com/1007-9327/full/v29/i7/1157.htm.
- Klotz U, Schwab M. Topical delivery of therapeutic agents in the treatment of inflammatory bowel disease. Advanced Drug Delivery Reviews [Internet]. 2005 [cited 2025 Mar 5];57(2):267–79. Available from: https://linkinghub.elsevier.com/retrieve/pii/S0169409X04001978
- Cai Z, Wang S, Li J. Treatment of inflammatory bowel disease: a comprehensive review. Front Med [Internet]. 2021 [cited 2025 Mar 5];8:765474. Available from: https://www.frontiersin.org/articles/10.3389/fmed.2021.765474/full
- Lakatos PL. Environmental factors affecting inflammatory bowel disease: have we made progress? Dig Dis [Internet]. 2009 [cited 2025 Mar 6];27(3):215–25. Available from: https://karger.com/DDI/article/doi/10.1159/000228553

