Psoriasis vulgaris is a chronic, immune-mediated inflammatory disease in which dysregulation of the TNF-α and IL-23/Th17 axes drives keratinocyte hyperproliferation and systemic comorbidities. Targeted biologic drugs-TNF-α inhibitors, the IL-12/23 p40 inhibitor ustekinumab, IL-23 p19 inhibitors, and IL-17 pathway inhibitorssuccessfully control the disease. Network meta-analyses (NMA) demonstrate that these drugs show high efficacy in the short term and are generally well tolerated. Long-term use, however, raises concerns about serious infection, tuberculosis ( TB) and hepatitis B virus (HBV ) reactivation, malignancy, inflammatory bowel disease (IBD), major adverse cardiovascular events (MACE), and rare paradoxical reactions. This review integrates randomized trial data, long-term extensions, pharmacovigilance signals and real-world cohorts to appraise the safety of biologic agents in psoriasis vulgaris. TNF-α inhibitors carry class-typical risks of serious infection and opportunistic mycoses, particularly in older or comorbid patients, but large registries demonstrate stable long-term profiles when screening and prophylaxis are optimized. Ustekinumab and IL-23 inhibitors show low serious-infection and TB-reactivation rates, reassuring data in patients with prior TB or cancer, and neutral MACE signals. IL-17-pathway inhibitors are associated with predictable, mostly mild mucocutaneous candidiasis and rare IBD onset or exacerbation, with very high skin-clearance rates and durable safety in trials and real-world studies. Observational data suggest that age, baseline comorbidity and concomitant immunosuppression drive absolute risk more strongly than molecule choice. When agents are selected according to comorbidity profile, supported by structured screening, vaccination and close monitoring, modern biologics for psoriasis vulgaris appear broadly safe, with rare but important class-specific adverse events that require proactive counselling and early recognition.
Engin et al. (Sun,) studied this question.