Pharmacogenetics and pharmacogenomics in psoriasis treatment: current challenges and future prospects

Abstract

Presently, no clinically actionable biomarker exists for any therapeutic agent used to treat psoriasis or psoriatic arthritis. The lack of validated outcome measures and conflicting results of open-label studies conducted may be attributed to a multitude of issues that confound discovery. Consequently, studies have been underpowered to identify genes or genetic variants worth translating to clinical practice. In order to achieve a pharmacogenetic/pharmacogenomic signature, improvements in study design of future investigations are required, including carefully designed prospective studies. It is imperative to combine known clinical, serological, and molecular markers with consistent outcomes and an adequate health economic evaluation before they can be adopted widely in clinical practice.

HLA-Cw6 and psoriasis

“…Pharmacogenomic and pharmacogenetic studies have been a recent topic of interest . Common first‐line systemic conventional treatments for psoriasis include ciclosporin, fumaric acid esters, methotrexate, phototherapy and retinoids.…”

A systematic review of pharmacogenetic studies on the response to biologics in patients with psoriasis

“…Sutherland et al . recently published an expert opinion piece on the topic, providing a valuable overview of the current state of affairs in this field of research . We are the first to conduct a systematic review on pharmacogenetics for responses to biologics in patients with psoriasis, summarizing and counterweighing positive and negative findings.…”

Precision therapy for psoriasis patients

“…Выявлены генетические детерминанты нарушения метаболизма метотрексата, ассоциированные с его повышенной токсичностью. К ним относятся полиморфные варианты генов: ABCC1, участвующий в транспорте веществ внутри-и внеклеточно, SLC19A1 -в транспорте фолатов в клетку, ATIC -в биосинтезе пуриновых оснований, CTLA4 -в экспрессии белков на Т-лимфоцитах, SLC12A8 -в регулировании пролиферации кератиноцитов, TAP1 -в лекарственной устойчивости, FBXL19в связывании трансмембранного рецептора интерлейкина-1, ADORA2a -осуществляющий трансмембранную передачу [2], МТНFR -в превращении гомоцистеина в метионин, TYMS -катализирующий превращение уридинового нуклеотида в тимидиновый [24,43].…”