Methods: Autologous whole blood collected 72 h before surgery was processed to prepare platelet concentrates and cryoprecipitate. In a closed system, calcium was added to the cryoprecipitate to release autologous thrombin and generate a firm fibrin clot. The fibrin clot, platelets and calcium were then placed in a conical flask in which a PRF glue formed. The protocol was validated through determination of pre- and post-platelet counts and fibrinogen amounts in the product.
Results: Platelets were recovered with 68% efficiency during the preparation. Essentially no platelets or fibrinogen were found in the supernatant of the PRF glue, suggesting that nearly all had been incorporated in a PRF glue having a relatively large (8 cm × 10 cm) size.
Conclusion: The protocol described here is a cost-effective, simple and closed system that can be used to produce large-size PRF glue to promote repair of major surgical defects.
METHODS: A total of 120 healthy volunteers were enrolled (55 adult males, 32 adult females, and 33 children). The volunteers were interviewed for any bleeding history or drug intake which affects coagulation. Kaolin-activated TEG was performed on citrated whole blood, and parameters including R-time, K-time, angle, MA, LY30, and CI were analyzed.
RESULTS: Derived reference range for total volunteers irrespective of age and sex were as follows: R-time: 3.8-10.6, K-time: 1.2-3.1, angle: 44.9-72.0, MA: 41.2-64.5, LY30: 0-9.9, and CI: -3.7 to 3.4. Statistically significant difference was observed in different age and sex groups for R-time, K-time, and angle. About 40% of the volunteers had at least one abnormal parameter according to the manufacturer's reference range which decreased to 12.5% when the derived reference ranges were considered.
CONCLUSION: Gender- and age-related variances were observed in reference ranges of our population and which was also differed from the other ethnic population. Many of our healthy volunteers were categorized as coagulopathic when manufacturer's reference range was considered. So, it is important to derive the reference range of the target population before using the TEG into clinical practice.
METHODOLOGY: A prospective single-center cohort study was conducted in a tertiary care set-up. Transfusion Dependent Thalassemia patients registered with the pediatric unit were screened for hypercoagulability using TEG during six months of the study period and followed up for three years for the development of thromboembolic events. Patient demographics, history of splenectomy, Serum ferritin levels and annual red cell transfusion requirement (mL/kg/year) were assessed. TEG parameters used were R time, K time, alpha angle, Maximum amplitude, Clot index, and Lysis 30. The thrombin generation test (V Curve) obtained from the first-degree derivate of the TEG velocity curve was also used for analysis.
RESULTS: A total of 34 patients were recruited during the six months study period with an average age of 10.6 years ( ± 5.47). The average pre-transfusion hemoglobin level and the volume of packed red cells received were 7.24 g/dL and 152.82 mL/kg/year respectively. The TEG tracing was suggestive of a hypercoagulable state in 58.82% of patients. The mean values of angle (70.74), MA (64.16), CI (2.65) and TG (774.43) in TDT patients compared to age matched reference range (62.81, 57.99, 0.8, 577.83 respectively) was suggestive of prothrombotic changes. Annual blood transfusion requirement was negatively correlated with hypercoagulable status (-0.344, CI= -0.68 to 0.08). One out of 34 patients developed corona radiata infarct (with annual blood requirement; 112.7 mL/kg/Year). The risk to develop a hypercoagulable state appeared to be higher when the volume of RBCs transfused was less than 154 mL/kg/Year.
CONCLUSION: TDT patients are at risk of developing thromboembolism, and screening with TEG may be useful to identify those at high risk.
OBJECTIVES: To estimate the global, regional, and national burden of ischemic heart disease and ischemic stroke attributable to elevated LDL-C (relative to 35-54 mg/dL) from 1990 to 2023 and to quantify the contributions of population growth, aging, risk-deleted burden, and exposure changes to burden trends.
DESIGN, SETTING, AND POPULATION: This comparative risk assessment, part of the Global Burden of Disease Study 2023, estimated population-level LDL-C exposure and associated health loss in 204 countries and territories. Mean LDL-C levels were estimated using spatiotemporal gaussian process regression based on 806 studies across 161 countries. Relative risks were derived from meta-analyses of 38 randomized clinical trials. Population-attributable fractions for deaths and disability-adjusted life-years (DALYs) were estimated by age and sex for adults aged 25 years or older from 1990 to 2023, with 95% uncertainty intervals.
EXPOSURE: Population-level LDL-C concentrations.
MAIN OUTCOMES AND MEASURES: Population-attributable fractions, counts, and rates (all ages and age standardized per 100 000) of LDL-C-attributable deaths and DALYs from ischemic heart disease and ischemic stroke, with uncertainty intervals.
RESULTS: In 2023, elevated LDL-C accounted for 3.6 million deaths (95% uncertainty interval, 2.2-5.4 million; 6.0% of global mortality) and 90.7 million DALYs (95% uncertainty interval, 58.9-123.3 million; 3.2% of DALYs). Although global all-ages rates remained stable, age-standardized death and DALY rates decreased by 45.6% and 39.5%, respectively, since 1990. In 2023, age-standardized LDL-C-attributable DALY rates were highest in Eastern Europe and lowest in high-income Asia-Pacific. One-third of the global LDL-C burden occurred in India and China. Population growth and aging drove the increasing burden, with notable regional disparities in LDL-C exposure and risk-deleted DALY rates shifting toward middle-sociodemographic settings.
CONCLUSIONS AND RELEVANCE: Despite declining age-standardized rates, the absolute LDL-C burden has increased since 1990 due to demographic changes and has shifted toward middle-sociodemographic countries. Measurement and surveillance gaps persist. Strengthened prevention, diagnosis, and treatment access strategies are essential to mitigate the health burden of LDL-C.