Core Framework & Diagram Psoriasis

Absolutely not. Psoriasis is an autoimmune disease, not an infectious disease. Skin lesions have no infectivity. This is the most common misconception and the root of social discrimination that many patients face.

There's a genetic factor but it's not simple inheritance. If one parent has psoriasis, child risk is approximately ten percent; if both parents, approximately fifty percent. But over half of psoriasis patients have no family history — genetics provides susceptibility, not destiny. Environmental factors (like repeated streptococcal infection) are especially important in triggering childhood psoriasis.

Long-term follow-up data (over ten years) shows biologics' overall safety is acceptable with appropriate screening and monitoring. Main concerns include infection risk (especially tuberculosis — must be screened before use), injection site reactions, and specific drug-specific risks (anti-IL-17 class may worsen in IBD patients). Compared to the cardiovascular and systemic risks of severe psoriasis itself, benefit usually exceeds risk.

Nail psoriasis (pitting, nail separation, subungual hyperkeratosis) is usually harder to treat than skin psoriasis; topical medication effects are limited. Biologics (especially anti-IL-17A and anti-IL-23 types) have some effect on nail psoriasis but improvement is slower than skin lesions, requiring over six months to see significant change.

Both need serious management, but psoriatic arthritis (PsA) treatment is more urgent — because joint erosion damage is irreversible; delayed treatment causes permanent joint functional damage. PsA symptoms include joint pain, morning stiffness (over thirty minutes), 'sausage fingers' (entire finger/toe swelling), heel or sole pain, and spine symptoms. Any psoriasis patient with these symptoms should promptly seek rheumatology evaluation.