Mesalamine may work, in part, by this mechanism.

"Mesalamine is a drug used for treating ulcerative colitis and mild to moderate Crohn's disease. The exact mechanism of mesalamine is not known but is believed to be by reducing inflammation in the colon. Ulcerative colitis and other inflammatory diseases cause excessive production of chemicals, for example, prostaglandins, that produce inflammation in the colon. Prostaglandins are produced by the enzymes, cyclooxygenase and lipoxygenase. These enzymes are over-active in individuals with ulcerative colitis. Mesalamine may work by blocking the activity of cyclooxygenase and lipoxygenase, thereby, reducing the production of prostaglandins. Reduced production of prostaglandins decreases inflammation in the colon and the symptoms associated with ulcerative colitis. Available forms of mesalamine differ in their route of administration and how often they are administered. Mesalamine was approved by the FDA in December 1987."

https://www.medicinenet.com/mesalamine/article.htm#what_are_the_side_effects_of_mesalamine

What about aspirin it also block cyclooxygenenase inhibitor too

There are no evidences that would recommend at all, the use of Cox inhibitors in the treatment of IBD patients

Why sir?

Because there are no real mediation by the prostagland routes

OK probably because it's a chronic inflammation which may not be mediated by prostaglandin

No, no evidence for its use in ulcerative colitis

The are enough drugs to treat the UC patients without using COX-2 inhibitors really

What's the action of 5-aminosalicylic acid and sulfasalazine used?

My colleagues works on the effects of Argeratum conyzoides plants on ulcerative colitis and there was improvement just thinking on the mechanism

Hi

For mild form of UC treatment is 5 ASA with local preparation of 5 ASA and steroid. There is need and sistemic corticosteroids (oral drug or injection).

For moderate disease, we must administration of imune regulating drugs such as azathioprin or mercaptopurin.

For severe disease, is need to adminstration Anti TNF alfa to imune suppressing drug such as tacrolimus or cyclosporine. Finally, by complication such as toxic megacolon or severe form of UC non responding in the tratment is need syrgery.

I think that Aspirin is blocator to progress from polyps to malign alteration, but is contraindicated in bleeding form of UC.

Use of Cyclo-Oxygenase Inhibitors Is Not Associated with Clinical Relapse in Inflammatory Bowel Disease: A Case-Control Study Abigail Hensley 1 and Ian L. P. Beales 1,2,*

Pharmaceuticals 2015, 8, 512-524; doi:10.3390/ph8030512

http://www.mdpi.com/journal/pharmaceuticals

Thanks but can we consider gamma interferon antagonist if existing?

Unfortunately, I can not answer this question. I’m a pediatric gastroenterologist and we didn’t need to look for alternative methods of treating ulcerative colitis. We use the latest guideline ESPGHAN(2019).

Ma check your inbox , i message you

You have disponible a big theraputic armamentarium without including COX-2 inhibitors for treating UC

OK but I need to know the mechanism by which it work

There is up-regulation of several cytokines and TNF-alpha factor not meditad tour the COX.2 pathway

Can septicemia leads ulcerative colitis?

Researchers believe bacteria or viruses can mistakenly trigger the immune system to attack the inner lining of the large intestine. This immune system response causes the inflammation, leading to symptoms.

Researchers believe bacteria or viruses can mistakenly trigger the immune system to attack the inner lining of the large intestine. This immune system response causes the inflammation, leading to symptoms.

Alright

Septicemia does not be related as a casual factor with ulcerative colitis

I think that septicemia can lead stress situation that is important factor as trigger for ulcerative colitis in the terren of immunologic response in mucosal change from bacterial and others causes.

There is not a confirmed relationship between both situations

did you know that smoking is protective factor fo ulcerative colitis? can anyone describe the mechanism?

Smoking is not recommended for anybody and there is not a reasonable explanation for recommend its use in UC patients

The majority of patients reported clinical, endoscopic and histological improvement during transdermal nicotine administration (15 mg every day for one month). Transdermal nicotine alone has limited efficacy in active ulcerative colitis and is ineffective as maintenance treatment. A reduction in intestinal blood flow by nicotine has also been described, but it is unlikely that this phenomenon may account for the favourable effects of nicotine in ulcerative colitis, since rectal blood supply in ulcerative colitis patients is already lower than normal. Nicotine influences the cellular and the humoral immune system and interferes with the inflammatory response, perhaps through stimulation of endogenous steroid release. Indeed nicotine has been found to suppress in vivo Th2 cell function as measured by inhibition of interleukin-10 production, and to reduce the synthesis of interleukin-2 and interleukin-8 by mononuclear cells. Nicotine can affect gut motility.

The above quotation is from this 1999 paper in the British Journal of Clinical Pharmacology: Article Nicotine treatment for ulcerative colitis

There doesn't seem to have been much follow-up to this report, and it is little-referenced. The few citations in PubMed are on different topics related to nicotine.

There were no pertinent results when I searched clinicaltrials.gov using the terms ulcerative colitis and nicotine.

From these observations, I would conclude that the medical establishment has not embraced nicotine as a therapy for UC.

The Crohns and Colitis Foundation has this to say on the subject of smoking and IBD:

https://www.crohnsandcolitis.org.uk/about-crohns-and-colitis/publications/smoking-and-ibd

What's the prognosis of UC and crohn's disease in patients with coagulation problems and what are best way of management

@Luis Rodrigo

Mycobacterial therapy is a good option.

Effective antimycobacterial intervention is therefore the first step.

The proportion of coagulation problems is very small and you must treat in the same way as without IBD association