This site is intended for healthcare professionals

Go to /sign-in page

You can view 5 more pages before signing in

Go to /pro/cpd-dashboard page

This page is worth 0.05 CPD credits. CPD dashboard

Go to /account/subscription-details page

This page is worth 0.05 CPD credits. Upgrade to Pro

Aetiology

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

Authoring team

The aetiology of Ulcerative colitis (UC) is unclear.

It is thought to occur due to the interaction of genetic factors and environmental triggers (1).

It is probably an autoimmune disease caused by an inflammatory response to normal colonic microflora (1).

Several risk factors have been identified:

  • not smoking
    • smoking has a universal protective effect resulting in a decrease in the risk of developing UC (a 40% lower risk) than in non smokers (1,2)
    • but in former smokers the risk of developing UC is approximately 1.7 times more higher than in non smokers (2)
    • it is also associated with a milder course of the disease (1)
  • a family history of inflammatory bowel disease
  • non-selective NSAIDs - can cause exacerbation of UC
  • appendicectomy performed for "true" appendicitis at an early age appears to have some protective effect against developing UC (2)

Reference:


Create an account to add page annotations

Annotations allow you to add information to this page that would be handy to have on hand during a consultation. E.g. a website or number. This information will always show when you visit this page.

The content herein is provided for informational purposes and does not replace the need to apply professional clinical judgement when diagnosing or treating any medical condition. A licensed medical practitioner should be consulted for diagnosis and treatment of any and all medical conditions.

Connect

Copyright 2024 Oxbridge Solutions Limited, a subsidiary of OmniaMed Communications Limited. All rights reserved. Any distribution or duplication of the information contained herein is strictly prohibited. Oxbridge Solutions receives funding from advertising but maintains editorial independence.