Skin Pigmentation Clinical Trial
Official title:
Evaluation of a Tranexamoc Acid Treatment on Post-inflammatory Pigmentation Induced in the Suction Blister Model - Study HPPI
Post-inflammatory hyperpigmentation (PIH) is a common sequela of inflammatory dermatoses. PIH results from the overproduction of melanin or irregular pigment dispersion after skin inflammation. The investigators have developed, validated and published an in vivo model of PIH based on an initial lesion involving suction blisters. In this study, they have demonstrated that the suction blisters model is able to reproduce an epidermal lesion and inflammatory state that, in melanin competent subjects, leads to consistent hyperpigmentation during real sunlight exposure without the need for additional artificial exposure to intense UV light. An increase in vascularisation is demonstrated by histology in early forms of PIH. The investigators have also shown this increase in vascularisation in their PIH model. Furthermore, the transcriptomic study in this model shows that UVA and visible light directly stimulate endothelial cells and increase angiogenesis but act essentially indirectly through the production by fibroblasts of uPA (urokinase-type plasminogen activator), a key factor in the modulation of extracellular matrices, inflammatory processes and angiogenesis. UPA is a serine protease that converts plasminogen to plasmin which promotes angiogenesis. Tranexamic acid (TA) is an antifibrinolytic that reversibly binds to plasminogen, preventing its conversion to plasmin and subsequent fibrin degradation. The aim of the study will be to evaluate the efficacy of tranexamic acid in preventing post-inflammatory hyperpigmentation induced in the suction blisters model in at-risk subjects.
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