ReviewInflammopharmacology2026
Psoriasis beyond the skin: systemic inflammation as a bridge to metabolic and hepatic comorbidities.
Review in Inflammopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
0 citing papers in PubMed.
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Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
41703364What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.