Total Healing of a Partial Rupture of the Supraspinatus Tendon Using Barbotage Technique Associated with Platelet-Rich Plasma: A Randomized, Controlled, and Double-Blind Clinical Trial.

The prevalence of partial rotator cuff tears (PRCTs) is high in the general population. Our hypothesis is that barbotage, when associated with platelet-rich plasma (PRP), is an effective method for healing these tears. The aim of this study was to compare the effects of barbotage with or without PRP on the healing of partial supraspinatus tendon tears (PSTTs). This study assessed the Western Ontario Rotator Cuff Index score and ultrasound (US) images at 6 weeks and 6 months after treatment. Patients in both groups showed clinical improvement, with no significant difference in scores at 6 weeks. However, at 6 months, the PRP group exhibited significant improvement (p = 0.019). Both groups experienced a reduction in ST tear size, but the PRP group demonstrated a significant enhancement at 6 weeks and 6 months. In conclusion, the US-guided barbotage technique, whether associated with PRP or saline solution, proved to be an effective treatment for clinical improvement and reduction in the size of PSTT. Better clinical improvement results were observed with PRP at 6 months. The combination of PRP with barbotage was superior in reducing the size of the ST tear at both 6 weeks and 6 months, resulting in complete healing in 79.3% of the tears.

Podoplanin and CLEC-2 levels in patients with COVID-19.

Introduction: Podoplanin (PDPN gene) and CLEC-2 are involved in inflammatory hemostasis and have also been related with the pathogenesis of thrombosis. Emerging evidence also suggest that podoplanin can exert protective effects in sepsis and in acute lung injury. In lungs, podoplanin is co-expressed with ACE2, which is the main entry receptor for SARS-CoV-2. Aim: To explore the role of podoplanin and CLEC-2 in COVID-19. Methods: Circulating levels of podoplanin and CLEC-2 were measured in 30 consecutive COVID-19 patients admitted due to hypoxia, and in 30 age- and sex-matched healthy individuals. Podoplanin expression in lungs from patients who died of COVID-19 was obtained from two independent public databases of single-cell RNAseq from which data from control lungs were also available. Results: Circulating podoplanin levels were lower in COVID-19, while no difference was observed in CLEC-2 levels. Podoplanin levels were significantly inversely correlated with markers of coagulation, fibrinolysis and innate immunity. scRNAseq data confirmed that PDPN is co-expressed with ACE2 in pneumocytes, and showed that PDPN expression is lower in this cell compartment in lungs from patients with COVID-19. Conclusion: Circulating levels of podoplanin are lower in COVID-19, and the magnitude of this reduction is correlated with hemostasis activation. We also demonstrate the downregulation of PDPN at the transcription level in pneumocytes. Together, our exploratory study questions whether an acquired podoplanin deficiency could be involved in the pathogenesis of acute lung injury in COVID-19, and warrant additional studies to confirm and refine these findings.

Thrombosis Occurrence in COVID-19 Compared With Other Infectious Causes of ARDS: A Contemporary Cohort.

Thrombosis occurrence in coronavirus disease 2019 (COVID-19) has been mostly compared to historical cohorts of patients with other respiratory infections. We retrospectively evaluated the thrombotic events that occurred in a contemporary cohort of patients hospitalized between March and July 2020 for acute respiratory distress syndrome (ARDS) according to the Berlin Definition and compared those with positive and negative real-time polymerase chain reaction results for wild-type severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) using descriptive analysis. The association between COVID-19 and thrombotic risk was evaluated using logistic regression. 264 COVID-19-positive (56.8% male, 59.0 years [IQR 48.6-69.7], Padua score on admission 3.0 [2.0-3.0]) and 88 COVID-19-negative patients (58.0% male, 63.7 years [51.2-73.5], Padua score 3.0 [2.0-5.0]) were included. 10.2% of non-COVID-19 and 8.7% of COVID-19 patients presented ≥ 1 clinically relevant thrombotic event confirmed by imaging exam. After adjustment for sex, Padua score, intensive care unit stay, thromboprophylaxis, and hospitalization length, the odds ratio for thrombosis in COVID-19 was 0.69 (95% CI, 0.30-1.64). We, therefore, conclude that infection-induced ARDS carries an inherent thrombotic risk, which was comparable between patients with COVID-19 and other respiratory infections in our contemporary cohort.

Association of heme-oxygenase 1, hemopexin, and heme levels with markers of disease severity in COVID-19.

Heme-oxygenase 1 (HO-1) is an enzyme with well-known anti-inflammatory and antioxidant properties, whose levels have been previously associated with disease severity in the context of sterile and infectious diseases. Moreover, the heme/HO-1 pathway has been associated with prothrombotic changes in other diseases. Accordingly, the potential of modulating HO-1 levels for the treatment of COVID-19 was extensively speculated during the COVID-19 pandemic, but very few actual data were generated. The aim of our study was to explore the association of HO-1, heme, and hemopexin (HPX) levels with COVID-19 severity and with markers of inflammation and coagulation activation. The study was conducted in 30 consecutive patients with COVID-19 admitted due to hypoxemia, and 30 healthy volunteers matched by sex, age, and geographic region. HO-1 and HPX levels were measured by enzyme immunoassay (ELISA) and heme levels were measured by a colorimetric method. A comprehensive panel of coagulation and fibrinolysis activation was also used. Patients with COVID-19 presented increased levels of HO-1 when compared to controls (5741 ± 2696 vs 1953 ± 612 pg/mL, respectively, P < 0.0001), as well as a trend toward increased levels of HPX (3.724 ± 0.880 vs 3.254 ± 1.022 mg/mL, respectively; P = 0.06). In addition, HO-1 and HPX levels reduced from admission to day + 4. HO-1 levels were associated with duration of intensive care unit stay and with several markers of coagulation activation. In conclusion, modulation of HO-1 could be associated with the prothrombotic state observed in COVID-19, and HO-1 could also represent a relevant biomarker for COVID-19. New independent studies are warranted to explore and expand these findings.

Venous thromboembolism in critically ill patients with pneumonia in the pre-COVID-19 era: Data from a large public database.

Background: The magnitude of venous thromboembolism (VTE) risk in severe COVID-19 is a matter of debate because of study heterogeneity, changes in VTE management, and scarce evidence of VTE risk in critically ill patients with pneumonia in the pre-COVID-19 era. Objectives: To evaluate VTE risk in the pre-COVID-19 era in a large intensive care unit (ICU) database. Patients/Methods: Data from consecutive pneumonia patients admitted to the ICU were retrieved from the Medical Information Mart for Intensive Care III. VTE risk was described in the entire cohort and in subgroups. Results: Among 6842 pneumonia patients admitted to the ICU, 486 patients were diagnosed with VTE after a median of 3 (IQR 1-11) days in the ICU. The 30-day cumulative incidence of VTE was 7% and remained at this level across different age groups, sex, and type of ICU. After adjusting for death, the overall cumulative incidence of VTE was 5%. A total of 1788 patients received thromboprophylaxis (of 2958 for whom that data were available). VTE occurred in 10.7% (95% CI 9.0-12.6) of patients without thromboprophylaxis and in 6.4% (95% CI 5.4-7.6) of those with thromboprophylaxis. Mortality was 20.6% among patients with VTE and 19.2% among those without VTE. Conclusions: In the pre-COVID-19 era, VTE risk in ICU patients with pneumonia was high and decreased with thromboprophylaxis. These findings can serve as comparators for future studies aiming at evaluating the impact of COVID-19 or other emerging infections on VTE risk.

Association between interferon-I producing plasmacytoid dendritic cells and thrombotic antiphospholipid syndrome.

Background: Thrombotic risk in antiphospholipid syndrome (APS) is conferred by the association of antiphospholipid (aPL) antibodies (first hit) with additional pro-coagulant stimulus (second hit), such as inflammation. Among inflammatory responses, the production of large amounts of interferon (IFN)-I by plasmacytoid dendritic cells (pDCs) is at the basis of the pathophysiology of systemic autoimmune disorders, which raises the hypothesis that this mechanism could also be associated with vascular manifestations of APS. Purpose: Here, we determined the association of pDCs and IFN-I production with thrombotic APS. Research design: Patients with thrombotic primary (t-PAPS) and secondary APS (t-SAPS), asymptomatic aPL carriers and individuals without thrombosis (controls) were included. Data collection and analysis: Circulating pDCs and IFN-α intracellular expression (in the presence or not of oligodeoxynucleotides (CP) stimulus) were quantified by flow cytometry. The expression of five IFN-I inducing genes: ISG15, OASL, Ly6E, MX1, and OAS1 in mononuclear cells was determined by qPCR. Between-group differences were evaluated using chi-square or Kruskal-Wallis tests. Results: A total of 50 patients with t-PAPS, 50 patients with t-SAPS, 20 aPL carriers, and 50 individuals without thrombosis (controls) were included. Intracellular expression of IFN-α was increased after CPG stimulation in both t-SAPS (1.56%; IQR 1.07-2.02) and t-PAPS (0.96%; IQR 0.55-1.24), when compared to aPL carriers (0.71%; IQR 0.42-0.93) and controls (0.48%; IQR 0.24-0.78; p < .0001). ISG15, OASL, Ly6E, MX1, and OAS1 mRNA expressions were higher in t-SAPS (but not in t-PAPS) than in aPL carriers and controls. The expression of proteins and mRNA related to IFN-I response was similar between the triple aPL-positive profile and other aPL profiles. Conclusion: Our results indicate an association of IFN-I response and t-APS. Since IFN-I expression was not increased in aPL carriers or associated with a higher-risk aPL profile, this mechanism does not appear to be related to the presence of aPL alone. IFN-I response could possibly constitute a complementary mechanism for triggering clinical manifestations in APS.

Association between neutrophil extracellular traps (NETs) and thrombosis in antiphospholipid syndrome.

BACKGROUND: The release of neutrophil extracellular traps (NETs) is the basis of immune-mediated thrombosis. Data on the clinical relevance of NETs in antiphospholipid syndrome-related thrombosis are scarce. OBJECTIVE: The aim of this study was to evaluate whether the NET regulator proteins PADI4, ELANE, and MPO are associated with thrombosis in APS. METHODS: A total of 152 thrombotic APS (t-APS) patients and 123 individuals without thrombosis (controls) were included. The following markers of NETs were evaluated: PADI4, ELANE, and MPO gene expression by qPCR and circulating levels of citrullinated histone H3 (H3cit) and myeloperoxidase-DNA complexes (MPO-DNA) by ELISA. RESULTS: The levels of circulating MPO-DNA and MPO mRNA expression and PADI4 mRNA expression were higher in t-APS patients than in controls. The mean differences were 0.05 OD (95% CI 0.01 to 0.09) in MPO-DNA levels, 1.07 AU (95% CI 0.20 to 1.93) for MPO mRNA and 0.20 AU (95% CI 0.03 to 0.36) in PADI4 mRNA fold-change. These differences were more pronounced in triple-positive patients, who had 56% increased levels of MPO-DNA, 44% increased MPO mRNA expression and 69% increased PADI4 mRNA expression compared to controls. Additionally, circulating MPO-DNA levels and MPO mRNA expression were higher in patients with recurrent thrombosis than in patients with incident thrombosis and controls. In recurrent thrombosis, levels of MPO-DNA were 43.8% higher and MPO mRNA expression was 2-fold higher than in controls. Levels of circulating MPO-DNA and PADI4 mRNA expression did not differ substantially between primary and secondary APS. CONCLUSION: Thrombotic APS was associated with increased NET formation, which was more pronounced among patients with poorer prognosis, such as those with triple antiphospholipid positivity and recurrent thrombosis. Our results provide evidence on the association of NETs and the severity of APS-related thrombosis.

Extracellular matrix-derived and low-cost proteins to improve polyurethane-based scaffolds for vascular grafts.

Vascular graft surgeries are often conducted in trauma cases, which has increased the demand for scaffolds with good biocompatibility profiles. Biodegradable scaffolds resembling the extracellular matrix (ECM) of blood vessels are promising vascular graft materials. In the present study, polyurethane (PU) was blended with ECM proteins collagen and elastin (Col-El) and gelatin (Gel) to produce fibrous scaffolds by using the rotary jet spinning (RJS) technique, and their effects on in vitro properties were evaluated. Morphological and structural characterization of the scaffolds was performed using scanning electron microscopy (SEM) and atomic force microscopy (AFM). Micrometric fibers with nanometric rugosity were obtained. Col-El and Gel reduced the mechanical strength and increased the hydrophilicity and degradation rates of PU. No platelet adhesion or activation was observed. The addition of proteins to the PU blend increased the viability, adhesion, and proliferation of human umbilical vein endothelial cells (HUVECs). Therefore, PU-Col-El and PU-Gel scaffolds are promising biomaterials for vascular graft applications.

The role of platelet-rich plasma in the mild and severe stages of atherosclerotic disease in mice.

Background: Platelet-rich plasma (PRP) has a high concentration of growth factors (GFs), which present a therapeutic wound healing effect. Despite having been correlated with an immunomodulatory function, the administration of PRP has not yet been investigated in atherosclerosis models. Aim: Evaluate the effect of lyophilized PRP on atherosclerosis in mice models through serum analysis. Methods: Animals received a high-fat diet for disease induction and a weekly PRP retro-orbital application. Effectiveness was evaluated by measuring inflammatory markers in plasma following the treatment of mice with either PRP or saline solution. Results: PRP was well characterized for platelet and GF concentrations; the atherosclerotic profile was established. Cytokine concentrations were altered after PRP applications. Conclusion: PRP could modulate the inflammatory pattern in the early stages of atherosclerosis.

Platelet-rich plasma (PRP) contains growth factors, which stimulate normal wound healing. This product seems to be a good modulator of white blood cells and has not been investigated in atherosclerosis. This study aimed to evaluate PRP in atherosclerosis using mice models. The PRP was produced from animals and preserved using the lyophilization technique; the product was then applied weekly in the vein. For atherosclerosis induction, genetically modified animals were fed a high-fat diet. The effectiveness was evaluated by measuring plasma inflammatory markers after treatment, and PRP seemed to alter cell-signaling molecules (cytokines). This study concluded that PRP was capable of modulating the inflammatory pattern during the early stages of atherosclerosis.

Contact and intrinsic coagulation pathways are activated and associated with adverse clinical outcomes in COVID-19.

Coagulation activation is a prominent feature of severe acute respiratory syndrome coronavirus 2 (COVID-19) infection. Activation of the contact system and intrinsic pathway has increasingly been implicated in the prothrombotic state observed in both sterile and infectious inflammatory conditions. We therefore sought to assess activation of the contact system and intrinsic pathway in individuals with COVID-19 infection. Baseline plasma levels of protease:serpin complexes indicative of activation of the contact and intrinsic pathways were measured in samples from inpatients with COVID-19 and healthy individuals. Cleaved kininogen, a surrogate for bradykinin release, was measured by enzyme-linked immunosorbent assay, and extrinsic pathway activation was assessed by microvesicle tissue factor-mediated factor Xa (FXa; MVTF) generation. Samples were collected within 24 hours of COVID-19 diagnosis. Thirty patients with COVID-19 and 30 age- and sex-matched controls were enrolled. Contact system and intrinsic pathway activation in COVID-19 was demonstrated by increased plasma levels of FXIIa:C1 esterase inhibitor (C1), kallikrein:C1, FXIa:C1, FXIa:α1-antitrypsin, and FIXa:antithrombin (AT). MVTF levels were also increased in patients with COVID-19. Because FIXa:AT levels were associated with both contact/intrinsic pathway complexes and MVTF, activation of FIX likely occurs through both contact/intrinsic and extrinsic pathways. Among the protease:serpin complexes measured, FIXa:AT complexes were uniquely associated with clinical indices of disease severity, specifically total length of hospitalization, length of intensive care unit stay, and extent of lung computed tomography changes. We conclude that the contact/intrinsic pathway may contribute to the pathogenesis of the prothrombotic state in COVID-19. Larger prospective studies are required to confirm whether FIXa:AT complexes are a clinically useful biomarker of adverse clinical outcomes.

Neutrophil activation and circulating neutrophil extracellular traps are increased in venous thromboembolism patients for at least one year after the clinical event.

Neutrophil activation and neutrophil extracellular traps (NETs) have been associated with the pathogenesis of venous thromboembolism (VTE). Considering VTE-associated chronic sequelae, which suggest that some pathological mechanisms remain after the acute episode, we investigated whether neutrophil activation is increased in patients with a prior VTE at least one year before this investigation. Thirty-seven patients with prior VTE and 37 individuals with no history of VTE were included. Neutrophil activity was evaluated by the expression of the adhesive molecule activation-specific epitopes LFA-1 (CD11a) and MAC-1 (CD11b), chemotaxis, reactive oxygen species (ROS) and by MPO-DNA complexes as markers of NETs. The adhesive molecules sICAM-1 and sVCAM-1, involved in the cross talk between neutrophil and endothelial cells, were also evaluated. Patient neutrophils presented increased CD11a expression before and after TNF-α stimulus, whereas increased CD11b expression was observed only after TNF-α stimulus, as compared to controls. Neutrophil chemotaxis on both, basal state and after IL-8 stimulus, on circulating levels of sICAM-1 and sVCAM-1, and on MPO-DNA complexes were also increased in VTE patients. ROS release was similar between patients and controls. This is, to our knowledge, the first study to investigate neutrophil inflammatory activity in VTE patients a long period after an acute event (approximately 2 years). The results showed altered neutrophil activation patterns in these patients. While activated neutrophils can cause endothelial activation and injury, the activated endothelium can induce the release of NETs with consequent endothelial cytotoxicity, creating a vicious cycle of activation between neutrophils and endothelium that can lead to thrombosis. VTE patients (approximately 2 years after the clinical event) present an altered neutrophil activation state evidenced by increased activity of the LFA-1 and Mac-1 adhesive molecules, as well as increased chemotaxis and circulating levels of NETs remnants. Circulating levels of ICAM-1 and VCAM-1, which are endothelial adhesive molecules, are also increased in VTE patients, suggesting not only an exacerbated endothelial activation and dysfunction, but also an interaction of the neutrophil adhesive molecules with their endothelial ligands, favoring the migration process of neutrophil.

Efficacy of a hypolipid diet in patients with primary antiphospholipid syndrome with dyslipidemia: a prospective study.

Although dyslipidemia is associated with poorer prognosis in antiphospholipid syndrome (APS), the management of lipid disorders can be challenging. While statins may increase the bleeding risk associated with anticoagulation, the effectiveness of hypolipid diet (HD) has not yet been established in patients with autoimmune disorders. In this study, we evaluated whether HD is associated with decreases in cholesterol levels in patients with thrombotic primary APS (t-PAPS) and dyslipidemia. Nutritional and lipid profiles were assessed before HD was initiated (baseline) and after 3 and 6 months with HD. A 24-h dietary recall was applied to assess the adherence to the diet. Forty-four patients were included, mean age was 43 years (± 12.93) and 65% were female. After HD was started, the intake of carbohydrates, lipids, saturated fats and cholesterol decreased, whereas dietary fiber intake increased. Levels of total cholesterol (TC) and non-high density lipoprotein cholesterol (non-HDL-C) decreased after 3 and 6 months of HD, as compared to baseline (P = 0.007 and P = 0.008). Low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-C) values did not change during the study period. The mean body mass index (BMI) decreased from 28.4 to 27.8 kg/m2 after six months of HD (p < 0.0001). In subgroup analysis, the effects of HD were more pronounced in patients with high TC, LDL-C or non-HDL-C levels at baseline and in those without obesity or hypertension. Nutritional intervention is feasible among t-PAPS and could be an alternative therapy to modulate lipid metabolism in this population.

Serum Metabolic Profiles Based on Nuclear Magnetic Resonance Spectroscopy among Patients with Deep Vein Thrombosis and Healthy Controls.

Deep venous thrombosis (DVT) is associated with significant morbidity and mortality. Studies on changes in the level of metabolites could have the potential to reveal biomarkers that can assist in the early detection, diagnosis, monitoring of DVT progression, response to treatment, or recurrence of DVT. In this scenario, the metabolomic analysis can provide a better understanding of the biochemical dysregulations of thrombosis. Using an untargeted metabolomic approach through magnetic resonance spectroscopy and multi- and univariate statistical analysis, we compared 40 patients with previous venous thrombosis and 40 healthy individuals, and we showed important serum differences between patients and controls, especially in the spectral regions that correspond to glucose, lipids, unsaturated lipids, and glycoprotein A. Considering the groups depending on risk factors and the local of the previous episode (lower limbs or cerebral system), we also noticed differences in metabolites linked to lipids and lactate. Comparative analyses pointed to altered ratios of glucose/lactate and branched-chain amino acids (BCAAs)/alanine, which might be associated with the fingerprints of thrombosis. Although samples for metabolomic analysis were collected months after the acute episode, these results highlighted that, alterations can still remain and may contribute to a better understanding of the complications of the disease.

Characterization of autologous platelet rich plasma (PRP) and its biological effects in patients with Behçet's Disease.

INTRODUCTION: Behçet's disease (BD) is an immune-mediated chronic systemic vasculitis, characterized by clinical manifestations that include: mucocutaneous ulcers, ocular involvement, immunological alterations, vascular and neurological implications. The available treatments present limitations such as high cost and side effects, and the search for a low-cost biological treatment with immunomodulatory potential becomes of great value. Platelet rich plasma (PRP) has some characteristics that indicate a possible use as an immunomodulator due to the wide range of secreted cytokines, especially through the participation of TGF-ß1 in the differentiation of T regulatory cells (Treg). This study aimed to characterize the PRP poor in leukocytes (P-PRP) of patients with BD and active ulcers and to evaluate its effects as an immunomodulator through a subcutaneous application. METHODS: We selected patients with a diagnosis of BD, with a low dose of prednisone and with no central nervous system or ocular involvement. Platelet and leukocyte count and quantification of 17 cytokines were evaluated in P-PRP. The effects of P-PRP were evaluated by cell frequency of TCD4 +, TCD8 +, Treg, natural killer (NK), and activated NK, as well as by the cytokine profile in patient's plasma, and the clinical manifestations through score and questionnaire. Also, it was evaluated the number and timing of oral ulcer closure. PRP was used as an adjuvant, with 9 applications of 3 mL, over 6 months, with a follow-up of one year. RESULTS: The results using PRP showed adequate values and no significant inter-and intra-individual variations. The systemic evaluations during the use of PRP showed significant alterations, characterized by the increase in Treg cell frequency (p = 0.0416) and a decrease in activated NK cells (p = 0.0010). However, no clinical correlation was observed through score analysis. The most relevant clinical data was the decrease in the closing time of ulcers throughout the application period. CONCLUSION: In a pilot study with BD patients, P-PRP promoted an anti-inflammatory profile characterized by increased Treg cells and decreased activated NK cells and alterations in cytokines. A clinical improvement was observed with a decrease in the number and time of closure of oral ulcers.

A retrospective analysis of 122 immune thrombocytopenia patients treated with dapsone: Efficacy, safety and factors associated with treatment response.

BACKGROUND: The optimum second-line treatment or best sequence of treatments for immune thrombocytopenia (ITP) are yet to be determined. Our institution has accumulated extensive experience regarding the use of dapsone as second-line therapy for ITP. OBJECTIVES: We aimed to assess the efficacy rate and safety of dapsone treatment in ITP patients. PATIENTS/METHODS: Here we report our experience in a retrospective study, including 122 patients, with a median treatment duration with dapsone of 6 months and a median follow-up period of 3.4 years. RESULTS: The overall response rate in this cohort was 66%, including 24% of complete responses. Among responders, in 24% a relapse occurred while on treatment. Therefore, a sustained response was observed in 51% of patients. Interestingly, 81% of the responders maintained the response after the interruption of treatment, for a median time of 26 months. Side effects were reported in 16% of the patients in this cohort and treatment was interrupted due to side effects in 11% of patients. The main cause in these cases was hemolytic anemia and methemoglobinemia. Reductions in hemoglobin levels during the use of dapsone were seen in 94% of the patients. Responders presented significantly greater reductions in their hemoglobin levels than nonresponders did: median hemoglobin drop of 1.9 g/dl vs. 1.2 g/dl (p = .004). CONCLUSIONS: Our findings suggest that dapsone has adequate efficacy and is well tolerated. Although the mechanism of action is still unclear, our observation that the degree in the drop of hemoglobin is greater in responders suggest a possible role of the blockage of the reticuloendothelial system in the therapeutic effect of the drug.

A case series of platelet rich plasma in chronic venous ulcers.

INTRODUCTION: Venous ulcers are the most common type of leg wounds (80%) and the main cause is chronic venous insufficiency. Autologous platelet-rich plasma (PRP) is a potential wound healing treatment due to its great variety of growth factors. The aim of this study was to describe in a case series the results of poor-leukocyte PRP (P-PRP) or saline for the treatment of chronic non-healing ulcers of the lower extremity. METHODS: Eight patients were treated according to the topical therapy: saline solution or P-PRP gel. All patients used double compression stocks and were assisted by a vascular practitioner for up to 12 months or until wound healing. The treatment was performed weekly with cleaning of the affected area, macroscopic evaluation (area measurement and photos) and P-PRP or saline application, and closure with Tegaderm®. Trial Registration: Retrospectively approved by Brazilian Clinical Trials, register number RBR-7zhgb3 (http://www.ensaiosclinicos.gov.br/rg/RBR-7zhgb3/). RESULTS: All patients showed signs of wound healing with a reduction in wound size and ulcer numbers, but more evident with P-PRP application. CONCLUSIONS: The results suggested that P-PRP presented a better result when compared to saline solution in the healing process of long clinical course chronic venous ulcers, when associated to compressive stocks and topical care.

The effect of lyophilized platelet rich-plasma on skin aging: a non-randomized, controlled, pilot trial.

Platelet-rich plasma (PRP) showed positive results in the improvement of skin aging. Lyophilized PRP can be interesting in clinical practice due to the facility to obtain many samples in a single blood collection and can be used in multiple injections. To evaluate the effect of lyophilized PRP in the treatment of skin aging, through a Phase II pilot study. Nineteen women (54 years ± 7 years) with Glogau photoaging II and III types were select for this non-randomized, split-face controlled study. They received monthly intradermal injections of lyophilized PRP and saline solution (as control) into the facial skin, during a period of 2 months. The evaluation was performed by imaging method, histological techniques, and multiphoton microscopy. Although lyophilized PRP presented 10 times the platelet baseline value (P < .0001) and growth factors in adequate levels, only saline solution showed an increase of dermis thickness (p = .0009). Collagen pre and post-application remained the same for both types of treatments. The use of lyophilized PRP by mesotherapy showed no improvement on skin aging. TRIAL REGISTRATION APPROVAL: RBR-3n9wxw, UTN U1111-1226-6093-retrospectively registered.