NICE guidance - Vedolizumab for treating moderately to severely active Crohn's disease after prior therapy

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NICE guidance states (1):

Vedolizumab is recommended as an option for treating moderately to severely active Crohn's disease only if:

  • a tumour necrosis factor-alpha inhibitor has failed (that is, the disease has responded inadequately or has lost response to treatment) or

  • a tumour necrosis factor-alpha inhibitor cannot be tolerated or is contraindicated.

    Vedolizumab is recommended only if the company provides it with the discount agreed in the patient access scheme.

Vedolizumab should be given as a planned course of treatment until it stops working or surgery is needed, or until 12 months after the start of treatment, whichever is shorter. At 12 months, people should be reassessed to determine whether treatment should continue. Treatment should only continue if there is clear evidence of ongoing clinical benefit. For people in complete remission at 12 months, consider stopping vedolizumab, resuming treatment if there is a relapse. People who continue vedolizumab should be reassessed at least every 12 months to decide whether continued treatment is justified.

Vedolizumab in Crohn's disease:

  • interaction between alpha4beta7 and mucosal vascular addressin cell adhesion molecule-1 (MAdCAM-1) activates the gut-specific migration of lymphocytes to Peyer's patches
    • important leukocyte involved in the pathogenesis of both Crohn's disease and ulcerative colitis is the alpha4beta7-integrin-expressing T cell. When activated, these cells preferentially adhere to endothelial surfaces within the GI tract as well as the associated lymphoid tissues
  • is a humanized immunoglobulin (Ig) G1 monoclonal antibody, which binds to alpha4beta7
    • does not involve alpha4beta1-VCAM (vascular cell adhesion molecule) interactions or T-cell trafficking to the brain or kidney. As such, it is not directly linked with risk of progressive multifocal leukoencephalopathy (PML), which is a rare viral disease associated with high mortality
    • prevents leukocyte binding to the endothelial surface and, as a result, extravasation into affected tissue

Reference:

Last edited 10/2021 and last reviewed 10/2021

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