ULCERATIVE COLITIS AND MS - COLITIS RISK FROM MS TREATMENT

[Leonora]

Hello,

I'm writing to ask whether there is anyone out there who has had problem with both MS and ulcerative colitis?

I have both conditions. I got the UC diagnosis first, and the MS more recently. I have been told that in principle I could start on a B-cell depletion treatment (e.g. kesimpta, ocrevus, tsabri...). This would be the most effective way to tackle my MS. But there is a risk that it could trigger a colitis flare - possibly a flare so bad that I would have to have my colon removed.

On the other hand, I could avoid this problem - but only by taking a less effective MS drug.

The only medical evidence to go on seems to be sporadic case reports.

So, do you have UC and MS? Have you ever had a colitis flare in reaction to MS treatment? And if so, did you manage to get it under control without having your colon removed?

[jimmylegs]

hi leonora, sorry to hear about your situation.
if you have not excluded any potential nutrient-related contribution, and would be interested in exploring that angle alongside your other medical inquiries, i might be able to offer some assistance.
if you'd be interested, i'll be here.

[NHE]

Hi Lenora,
Welcome to ThisIsMS.

I have both conditions. I got the UC diagnosis first, and the MS more recently. I have been told that in principle I could start on a B-cell depletion treatment (e.g. kesimpta, ocrevus, tsabri...). This would be the most effective way to tackle my MS. But there is a risk that it could trigger a colitis flare - possibly a flare so bad that I would have to have my colon removed.

For clarification, Tysabri doesn’t deplete B cells. It prevents T cells from crossing the blood brain barrier.

Here’s a description from the Prescribing Information.

https://www.tysabri.com/content/dam/com ... mation.pdf

Natalizumab binds to the alpha-4-subunit of alpha-4-beta-1 and alpha-4-beta-7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the alpha-4-mediated adhesion of leukocytes to their counter-receptor(s). The receptors for the alpha-4 family of integrins include vascular cell adhesion molecule-1 (VCAM-1), which is expressed on activated vascular endothelium, and mucosal addressin cell adhesion molecule-1 (MAdCAM-1) present on vascular endothelial cells of the gastrointestinal tract. Disruption of these molecular interactions prevents transmigration of leukocytes across the endothelium into inflamed parenchymal tissue. In vitro, anti-alpha-4-integrin antibodies also block alpha-4- mediated cell binding to ligands such as osteopontin and an alternatively spliced domain of fibronectin, connecting segment-1 (CS-1). In vivo, natalizumab may further act to inhibit the interaction of alpha-4-expressing leukocytes with their ligand(s) in the extracellular matrix and on parenchymal cells, thereby inhibiting further recruitment and inflammatory activity of activated immune cells.

The specific mechanism(s) by which TYSABRI exerts its effects in multiple sclerosis and Crohn’s disease have not been fully defined.

In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells and their counter- receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be secondary to blockade of the molecular interaction of alpha-4-beta-1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. Data from an experimental autoimmune encephalitis animal model of multiple sclerosis demonstrate reduction of leukocyte migration into brain parenchyma and reduction of plaque formation detected by magnetic resonance imaging (MRI) following repeated administration of natalizumab. The clinical significance of these animal data is unknown.

Note, Tysabri is also used in Crohn’s Disease. See the Prescribing Information for details.