Welcome to PracticeUpdate! We hope you are enjoying access to a selection of our top-read and most recent articles. Please register today for a free account and gain full access to all of our expert-selected content.
Already Have An Account? Log in Now
Association Between Treatment With Biologics and Cardiovascular Comorbidities in Patients With Psoriasis
abstract
This abstract is available on the publisher's site.
Access this abstract now Full Text Available for ClinicalKey SubscribersPsoriasis increases risk of cardiovascular (CV)-related comorbidities including diabetes, dyslipidemia, and hypertension, and is an independent risk factor for major adverse cardiovascular events (MACE). Systemic immunomodulation with biologics improves psoriatic disease and decreases risk of MACE and psoriatic arthritis in patients with psoriasis, yet, their impact on incident CV-related comorbidities among psoriasis patients remains unclear. We conducted a propensity-score matched (PSM), retrospective-cohort study to investigate whether biologics associate with incident dyslipidemia, hypertension, diabetes, or MACE among psoriasis patients.
Additional Info
Disclosure statements are available on the authors' profiles:
Interleukin-23 inhibition associates with lower incidence of cardiovascular risk factor type diseases compared to biologic naïve patients with psoriasis: A retrospective cohort study
J Am Acad Dermatol 2024 Oct 16;[EPub Ahead of Print], AO Vera, C Ro, W Adawi, A Yap, AS Van Voorhees, CW EnosFrom MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
IL-23 inhibition and the risk of comorbidities in patients with psoriasis
In this retrospective cohort study, Vera et al explored whether treatment with biologic therapies is associated with the incident risk of dyslipidemia, diabetes, hypertension, and major adverse cardiovascular events among patients with psoriasis using TriNetX data. They found that patients receiving treatment with IL-23 inhibitors had a significantly decreased risk of developing all of the above comorbidities compared with propensity score–matched controls. Additionally, sub-analyses found that treatment with IL-23 inhibitors is associated with a decreased risk of developing all of the above comorbidities compared with treatment with other biologic classes (IL-17 inhibitors, IL-12/23 inhibitors, and TNF-α inhibitors). These findings add to the accumulating data that IL-23 inhibition may be uniquely advantageous in the setting of psoriasis.
IL-23 is considered an overarching master cytokine in psoriasis. For one, IL-23 is required for the terminal differentiation and survival of skin-resident memory Th17 cells, which are thought to be the key cell type involved in psoriasis pathogenesis.1 Furthermore, IL-23 is an upstream regulator of several central proinflammatory cytokines involved in psoriasis pathogenesis, including IL-17A and IL-22.1 Thus, inhibition of IL-23 may reduce the number of Th17 pathogenic cells and production of key proinflammatory cytokines in patients with psoriasis. Indeed, a recent small phase II clinical trial found that early treatment with high doses of an IL-23 inhibitor resulted in decreased numbers of lesional skin-resident memory Th17 cells at 1 year.2 Furthermore, several retrospective studies have found a decreased risk of future psoriatic arthritis development in patients with psoriasis treated with IL-23 inhibitors.3,4
There are numerous limitations to this study by Vera et al that preclude definitive statements about the association between IL-23 inhibitor treatment and future risk of dyslipidemia, diabetes, hypertension, and major adverse cardiovascular events. However, this and other studies describing distinct benefits of IL-23 inhibition in patients with psoriasis pave the way for future better-designed trials exploring these associations. If such work supports the findings by Vera et al, it will all but solidify the placement of IL-23 inhibitors at the top of the hierarchy of current psoriasis treatment options.
References