Psoriasis Reframed as Systemic Disease With Metabolic and Hepatic Implications
Psoriasis should be recognized as a systemic inflammatory disease requiring management beyond cutaneous symptoms, according to a mini-review examining the immunologic pathways linking psoriasis with metabolic and hepatic comorbidities.
The review describes psoriasis as a multi-organ condition driven by chronic inflammation, with approximately 2% to 3% of the global population affected and up to a 50% risk of systemic comorbidities. The authors focused on interactions among immune dysregulation, keratinocyte hyperproliferation, and systemic cytokine release.
Proinflammatory mediators, including tumor necrosis factor-alpha (TNF-α), IL-17, IL-23, and IL-6, contribute to cutaneous plaque formation but can also enter systemic circulation, where they promote insulin resistance, atherogenesis, and liver inflammation.
The authors identified several shared immunometabolic pathways implicated in psoriasis and associated conditions, including TNF-α/NF-κB activation, the IL-23/Th17 axis, and dysregulated PI3K/Akt/mTOR signaling. These pathways may contribute to comorbid metabolic syndrome and metabolic dysfunction-associated steatotic liver disease.
According to the review, epidemiologic evidence also demonstrates a high prevalence of obesity, type 2 diabetes, and dyslipidemia among patients with psoriasis, independent of established risk factors. “These findings lend support to the idea that psoriasis is a multi-organ disease caused by chronic low-grade inflammation,” the authors wrote.
Reference
Karmbir, Faisal SM, Narang RK, Kurmi BD, Kaur K, Sharma A. Psoriasis beyond the skin: systemic inflammation as a bridge to metabolic and hepatic comorbidities. Inflammopharmacology. 2026;34(3):1317-1330. doi:10.1007/s10787-025-02027-y
