Psoriasis, long thought to be a chronic immune-mediated dermatological disease, is now being reclassified as a systemic inflammatory disease with substantial metabolic and hepatic complications. Psoriasis affects approximately 2-3% of global population and is associated with up to 50% risk of systemic comorbidities. This mini-review examines the evolving understanding of psoriasis pathogenesis, focusing on the interaction of immunological dysregulation, keratinocyte hyperproliferation, and systemic cytokine release. Tumour necrosis factor- alpha (TNF)-α, IL-17, IL-23, and IL-6 are pro-inflammatory mediators that cause cutaneous plaque formation and reach the systemic circulation, leading to insulin resistance, atherogenesis, and liver inflammation. The review identifies common immuno-metabolic pathways, including TNF-α/NF-κB activation, the IL-23/Th17 axis, and dysregulated PI3K/Akt/mTOR signalling, that contribute to psoriatic illness and associated disorders like metabolic syndrome and metabolic dysfunction-associated steatotic liver disease (MASLD). Epidemiological studies demonstrate that psoriasis patients have a high prevalence of obesity, type 2 diabetes, dyslipidaemia, regardless of established risk factors, supporting the updated classification of NAFLD as MASLD. These findings lend support to the idea that psoriasis is a multi-organ disease caused by chronic low-grade inflammation. Clinically, this requires a transition from skin-centred treatment to thorough systemic examination and customised, multidisciplinary management. Targeted biologic treatments, such as IL-17 and IL-23 inhibitors, offer potential for lowering both systemic inflammation and cutaneous symptoms. This review supports early screening, metabolic monitoring, and lifestyle changes as critical components of long-term psoriatic therapy. Recognising psoriasis as a systemic condition is critical for improving overall patient outcomes, lowering morbidity, and avoiding long-term consequences.
