Pharmacotherapy of Psoriasis

Pharmacotherapy of Psoriasis

1. Definition, scope and disease concept

• Psoriasis is a chronic, immune-mediated, T-lymphocyte–driven systemic inflammatory disease characterised by well-demarcated erythematous scaling plaques; it waxes and wanes, is never cured, and is treated to control — drugs diminish lesions but do not eradicate the disease (DiPiro 12e Ch.118, pp.1639–40; KDT 8e Ch.66, p.950).
• It is the most common immune-mediated inflammatory disease worldwide; US prevalence ≈3% (~8 million people); global prevalence ranges 0.09–11.4% with lower frequencies (0.4–0.7%) in people of African and Asian descent and near-absence in American aboriginal populations (DiPiro 12e Ch.118, p.1639).
• Affects males and females equally; bimodal age of onset — peaks at 20–30 years and again at 50–60 years; ~75% have onset before age 40 (early-onset disease is the more strongly genetically determined form) (DiPiro 12e Ch.118, pp.1639–40).
• Why pharmacology matters here: every effective drug class maps onto a defined step of the psoriatic immune cascade — keratinocyte hyperproliferation (vitamin D₃ analogues, retinoids, anthralin), the TNF-α/IL-23/IL-17 cytokine axis (biologics), T-cell activation/calcineurin (ciclosporin, topical calcineurin inhibitors), DNA/folate metabolism and adenosine (methotrexate), and intracellular second-messenger signalling (PDE-4 and JAK/TYK2 inhibitors) (DiPiro 12e Ch.118, pp.1640–53; Wolverton 4e Ch.14/Ch.18).