Psoriasis

Psoriasis is an immune-mediated inflammatory disease that happens to be visible on the skin. The characteristic plaques — thick, silvery-scaled, sharply demarcated, typically on elbows, knees, scalp and lower back — result from keratinocytes turning over in three to five days instead of the usual twenty-eight, driven by a self-sustaining inflammatory loop. The pathogenesis is now well mapped. Dendritic cells release IL-23, which drives T-helper 17 cells to produce IL-17 and IL-22, which in turn stimulate keratinocyte proliferation and recruit more inflammatory cells. That mechanistic clarity is why the IL-17 and IL-23 biologics work so well: they interrupt a specific, identified loop rather than suppressing immunity broadly. Treatment is stratified by severity. Mild disease affecting under 3% of body surface responds to topical corticosteroids and vitamin D analogues such as calcipotriol, usually in combination. Moderate disease adds phototherapy. Moderate to severe disease is where methotrexate, ciclosporin, apremilast and the biologics belong, and where undertreatment is common. Two things are frequently missed. Around a third of people with psoriasis develop psoriatic arthritis, often years after the skin disease, and early treatment prevents irreversible joint damage — so new joint pain or stiffness needs prompt assessment. And psoriasis independently raises cardiovascular risk, roughly in proportion to severity, which makes blood pressure, lipids and glucose part of the management rather than an afterthought.

• •Raised, thickened plaques with silvery-white scale
• •Sharply demarcated edges, unlike eczema
• •Typical sites: elbows, knees, scalp, lower back, gluteal cleft
• •Itch, which affects most patients despite the old teaching that psoriasis does not itch
• •Cracking and bleeding when plaques are stretched
• •Nail pitting, ridging or separation from the nail bed
• •Joint pain, stiffness or swelling, especially in fingers and toes
• •Plaques appearing at sites of skin injury (the Koebner phenomenon)

• •Genetic predisposition, particularly HLA-C*06:02
• •Streptococcal throat infection, a classic trigger for guttate psoriasis
• •Psychological stress
• •Skin trauma, including scratches, tattoos and sunburn
• •Smoking
• •Obesity, which both raises risk and worsens severity
• •Heavy alcohol intake
• •Medications: lithium, beta blockers, antimalarials, and corticosteroid withdrawal
• •Cold, dry weather and reduced sun exposure

Psoriasis is a genetically primed immune disease that requires a trigger to express itself. Around forty susceptibility loci have been identified, with HLA-C*06:02 the strongest, and roughly a third of patients have an affected first-degree relative. But genetics alone is not sufficient — concordance in identical twins is around 65%, leaving substantial room for environment. The immunological engine is the IL-23 / Th17 axis. Once activated, it becomes self-sustaining: IL-17 stimulates keratinocytes to produce antimicrobial peptides and chemokines that recruit more neutrophils and T cells, which produce more IL-17. This is why psoriasis persists in the absence of any ongoing external trigger, and why blocking a single cytokine in the loop can produce near-complete clearance. Obesity deserves specific attention as a modifiable driver. Adipose tissue is metabolically active and secretes IL-6 and TNF-alpha, contributing directly to the inflammatory burden. Weight loss trials in psoriasis have shown improvement in disease severity independent of other treatment, making it one of the few lifestyle levers with genuine evidence behind it.