Vivostat Platelet-Rich Fibrin® for Complicated or Chronic Wounds-A Pilot Study

Vivostat Platelet-Rich Fibrin(R)(PRF) is an autologous platelet concentrate used for the local treatment of chronic or complicated wounds. Still, its application for this indication is not evidence-based. Therefore, we performed this monocentric retrospective pilot study investigating the clinical outcome of a local treatment of chronic or complicated wounds in 35 patients (23 male, 12 female, mean age 68.7 years) treated with Vivostat PRF(R). This study population is the largest among published studies analyzing the clinical efficacy of Vivostat PRF(R)on chronic wounds so far. Using the perpendicular method we divided the wounds into three sizes (<10, 10-30, and >30 cm(2)). The clinical efficacy of the Vivostat PRF treatment was the primary endpoint and was divided into three groups of increasing degrees of wound improvement: (1) no improvement of the wound (wound area was not reduced > 10% under Vivostat PRF(R)treatment), (2) improvement of the wound (reduced area > 10% under Vivostat PRF(R)treatment) and (3) complete epithelialization (wounds that were completely re-epithelialized after Vivostat PRF(R)treatment). We included patients' diagnosis and concomitant diseases (peripheral arterial occlusive disease (PAOD)), chronic venous insufficiency (CVI)), diabetic foot syndrome (DFS)) in our data analysis in order to investigate their potential impact on the wound healing capacity of Vivostat PRF(R). Our results show that in the entire study population, 13 out of 35 (37.1%) patients experienced wound improvement and 14 out of 35 (40%) patients showed complete epithelialization of their wound under Vivostat PRF(R)treatment. In summary, 77.1% of the treated patients benefited from the Vivostat PRF(R)therapy. These positive wound healing effects were all observed within the first three to six Vivostat PRF(R)applications. Subgroup analyses showed that Vivostat PRF(R)appeared to be more efficient in patients without CVI in comparison to patients with CVI (p= 0.02). Moreover, Vivostat PRF(R)treatment seems to be particularly efficient in PAOD-related wounds with a reduced crural arterial blood supply (p= 0.01). Additionally, we performed an experimental human in vivo study on ten male students where we artificially generated bilateral gluteal wounds and analyzed the influence of the Vivostat PRF(R)treatment on the expression of two genes (human beta Defensin-2, ((hBD-2) and human beta-Defensin-3 (hBD-3)) in keratinocytes of resected wound specimens that are induced during wound healing. Interestingly, this analysis revealed that only seven of out ten individuals showed a relevant hBD-2 and hBD-3 gene induction after Vivostat PRF(R)treatment. This led to the novel "key-lock-hypothesis". With the goal of an individualized precision medicine approach with optimized wound treatment strategies in the future, this is an important observation that demands further experimental and clinical studies.