“Not a biologic, an injection, or a cream” – Oral treatment for Psoriasis shows possibilities for Hidradenitis suppurativa (HS) patients

Apremilast in the treatment of moderate to severe hidradenitis suppurativa

THE ONLY PDE4 INHIBITOR APPROVED TO TREAT PLAQUE PSORIASIS

While the exact way in which Otezla helps improvesymptoms of plaque psoriasis isn’t completelyunderstood, here’s what we do know:

  • Otezla works inside inflammatory cells to reducePDE4 activity
  • A reduction in PDE4 activity is thought to helpreduce the overactive inflammation that happensin people with psoriasis
  • This reduction in overactive inflammation leads to areduction in symptoms of plaque psoriasis
  • Otezla helps decrease redness, thickness, and scaliness of plaques


Otezla Via Wiki
: Apremilast (brand name Otezla) is a medication for the treatment of certain types of psoriasis and psoriatic arthritis. It may also be useful for other immune system related inflammatory diseases. The drug acts as a selective inhibitor of the enzyme phosphodiesterase 4 (PDE4) and inhibits spontaneous production of TNF-alpha from human rheumatoid synovial cells. It is taken by mouth.


Possibilities for Hidradenitis suppurativa (HS) patients via JAAD: Apremilast in the treatment of moderate to severe hidradenitis suppurativa: A case series of 9 patients – Journal of the American Academy of Dermatology

Despite the many therapeutic approaches available for hidradenitis suppurativa, there is still a need for effective medications to treat moderate and severe forms of the disease. In this study, we assessed the efficacy of the oral phosphodiesterase 4 inhibitor apremilast (30 mg, twice a day) in the management of 9 patients with moderate to severe hidradenitis suppurativa (Hurley stage II-III) who had responded poorly to other treatments.

Although it has many antiinflammatory effects, the mechanism by which apremilast may work in hidradenitis suppurativa is unknown. However, therapy with a phosphodiesterase 4 inhibitor, such as apremilast, which can modulate key pro- and antiinflammatory mediators, such as tumor necrosis factor–α, interleukin-23 (IL) and IL-12 and chemoattraction via regulation of IL-8 and interferon-γ–induced protein 10 expression, might suppress the cellular mechanisms involved and expression of many upregulated cytokines in hidradenitis suppurativa.

READ THE FULL SOURCE: jaad.org
© 2017 by the American Academy of Dermatology, Inc.

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