Study Suggests Interferon-Beta Likely Not a Trigger for Psoriasis


These data do not support the idea that interferon-beta works as a trigger for psoriasis, though it may have a different influence on psoriasis among those with MS versus those without MS.

Credit: Pexels

Credit: Pexels

New findings resulting from a registry-based self-controlled study do not support the hypothesis that interferon-beta serves as a trigger for the development of psoriasis.1

These findings represented the conclusion of research led by Ida M. Heerfordt, of the department of clinical pharmacology at Copenhagen University Hospital – Bispebjerg and Frederiksberg in Denmark. Heerfordt et al. noted that type 1 interferons such as interferon-alpha and interferon-beta, were highlighted as possible triggers of the psoriasis.

The investigators added that case reports had shown that some multiple sclerosis (MS) patients who were given recombinant interferon treatment experienced an increase in existing psoriasis or new disease development.

“Despite anecdotal evidence of interferon-beta potentially inducing psoriasis in patients with MS, a systematic investigation of this association is yet to be conducted,” Heerfordt and colleagues wrote. “Thus, we aimed to assess psoriasis risk among a large cohort of patients with MS treated with interferon-beta.”2

Background and Methods

Within Denmark, every resident maintains a unique civil registration number (CPR) which is implemented in all healthcare interactions. The Danish MS Registry, dating back to 1956, contains MS patient data within Denmark, with such information as age, sex, clinical details, and history of treatment being available.

The research team in this study looked at treatment-naïve individuals with MS who began utilizing interferon-beta or other disease-modifying drugs (DMDs) (with azathioprine, methotrexate, dimethyl fumarate, and methylprednisolone being excluded) from January 1996 - June 2023. The team used a self-controlled cohort trial design and sought to assess psoriasis occurrences in relation to initiation of interferon-beta treatment.

They evaluated study participants from the time period of 2 years before to 2 years following the beginning of treatment. The investigators sought to consider other elements potentially influencing psoriasis risk, so they compared the study subjects with individuals beginning other DMDs for MS.

The research team linked participants’ CPR numbers to the Danish National Patient Register as well as the Danish National Prescription Registry. For this study, they extracted data from the Danish National Prescription Registry on prescriptions connected to psoriasis treatment.

The team defined an ‘event’ as either a primary psoriasis diagnosis or a prescription of antipsoriatic medication. Individuals meeting either of these criteria during the study period were identified as cases.

The investigators assessed the subjects over a period of 2 years preceding and following the initiation or discontinuation of their interferon-beta treatments, excluding subjects with prior psoriasis as defined by specified criteria. Their exposure they looked into was the beginning initiation of a DMD for MS, maintaining a specific focus on interferon-beta.


There had been a group of 7,174 subjects who were undergoing interferon-beta therapy. The investigators found that the rate of newer cases of psoriasis following treatment initiation was shown to be only a marginally higher rate of 2.01 per 1,000 person-years, compared to the before-treatment rate of 1.67 per 1,000 person-years.

A lack of statistical significance (P = .53) was noted by the research team, with the reported incidence rate ratio (IRR) being 1.20 (95% confidence interval [CI] 0.68–2.13). On the other hand, the control arm of the study were shown to have a substantial psoriasis incidence rise after treatment initiation, with a rate of 3.12 per 1,000 person-years.

This was compared to previously (1.11 per 1,000 person-years), and these results yielded an IRR of 2.80 (95% CI 1.36–4.77, P = .0038).

“The mechanisms underlying the development of psoriasis share similarities with those involved in MS, as both conditions are characterized by dysregulated immune responses,” they wrote. “The connection is, however, poorly understood. Treatment with interferon-beta may have a different influence on psoriasis pathogenesis in individuals with MS than in individuals without MS.”


  1. Heerfordt IM, Framke E, Windfeld-Mathiasen J, Mogensen M, Olsen RH, Magyari M, et al. Reevaluating the role of interferon-beta in psoriasis pathogenesis: A registry-based self-controlled study. J Dermatol. 2024; 00: 1–4.
  2. Gu H, Zhang Y, Zeng W, Xia Y. Participation of interferons in psoriatic inflammation. Cytokine Growth Factor Rev. 2022; 64: 12–20.
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