Risk of tuberculosis reactivation with interleukin (IL)‐17 and IL‐23 inhibitors in psoriasis – time for a paradigm change

Abstract

Tuberculosis is an infectious disease with a major global impact, ranked in the top 10 mortality causes worldwide. In an immunocompetent individual, the host defence mechanisms control Mycobacterium tuberculosis infection and induce the latent form of the disease. However, in the presence of diseases or therapies, which exert an immunosuppressive effect, latent tuberculosis can be re‐activated. Psoriasis is an immune‐mediated, inflammatory disease, and its treatment has rapidly evolved over the last few years. It has long been recognized that the tumour necrosis factor (TNF)‐α inhibitors are associated with increased risk of reactivation of latent tuberculosis infection. Thus, international guidelines have been suggesting tuberculosis screening before starting the treatment with all biological agents since then. In addition, the institution of chemoprophylaxis in the presence of latent tuberculosis and the annual screening for tuberculosis thereafter have also been indicated. However, anti‐tuberculosis treatments can have significant side‐effects and there are currently several contraindications to their use. The risk benefit of starting anti‐tuberculous treatment should be carefully weighed up. The emergence of new biological drugs for the treatment of psoriasis, such as interleukin (IL)‐17 and IL‐23 inhibitors, has reignited the subject of tuberculosis reactivation as it is possible that IL‐17 and 23 blockade do not carry the same risk of TB reactivation as TNF‐α inhibitors. Although preclinical studies have shown that cytokines IL‐17 and IL‐23 have a possible role against infection with M. tuberculosis, data from clinical trials and post‐marketing surveillance with drugs that inhibit these cytokines appear to suggest that they are not crucial to this response. In this article, we review the available data on tuberculosis reactivation after the treatment of psoriasis with IL‐17 and IL‐23 inhibitors, and its possible impact on the way we currently manage latent tuberculosis infection before or after starting treatment with these new drugs.

Key Signaling Pathways in Psoriasis: Recent Insights from Antipsoriatic Therapeutics

“…Compared to other biologics, the risk of reactivation of tuberculosis may be higher with TNF-α inhibitors. 37 Although IL-23/IL-17 axis inhibitors seem superior in efficacy and safety to TNF-α inhibitors in psoriasis, the more widespread targeting of the immune system may confer advantages to psoriasis complicated with comorbidities, such as arthritis, inflammatory bowel disease, hidradenitis suppurativa and uveitis. 35 , 38 …”

Pathogenic implications, incidence, and outcomes of COVID-19 in autoimmune inflammatory joint diseases and autoinflammatory disorders

“…Thus, patients with RMDs treated with IL-17-targeted agents may be exposed to an increased risk of mucocutaneous candidiasis [42][43][44]. No cases of active tuberculosis have been reported in a review of clinical trial data [37,42,43,45].…”

Serial Quantiferon‐TB Gold test results in 279 patients with psoriasis receiving biologic therapy

“…Turkey is a TB-endemic country for with an incidence rate of 16 [14][15][16][17][18][19] per 100 000 population. 24 Our data underlined the possibility that…”