To the best of our knowledge, this is the first clinical study addressing the use of autologous PL as a treatment measure for knee osteoarthrosis (KOA). There are no studies published regarding the treatment of KOA by intra-articular injections of PL. The previous studies were on the use of platelet-rich plasma (PRP) treatment for KOA. Platelet-rich plasma use has been in place for several years, however, a standardized protocol has not yet been established. Platelet lysate represents a safe, economical, easy to prepare, and easy to apply source of growth factors in the treatment of KOA. A head-to-head study is needed to compare PRP with PL in KOA.
We examined platelet aggregation in platelet-rich plasma (PRP) and in whole blood in nine patients with Thrombasthenia Glanzmann (TG). In PRP, aggregation was measured by monitoring the changes in light absorbance that occurred in response to adenosine 5-diphosphate (ADP), collagen and ristocetin. To measure platelet aggregation in whole blood, we used multiple electrode Impedance aggregometry using the same aggregating agents. In PRP, the patient's platelets showed defective aggregation in response to ADP, collagen, epinephrine and partially to ristocetin in all patients. In whole blood, platelet aggregation in response to the same aggregating agents showed similar response and appeared to be very similar to that which occurred in PRP. Whole blood impedance aggregometry seems to give similar results to PRP light transmission aggregometry in patients with TG. Multiple electrode aggregometry (MEA) is faster and more convenient to use in these patients.
Acetyl salicylic acid (ASA) and clopidogrel are extensively used in the prevention of cardiovascular disease. However, the responsiveness to ASA treatment may vary among individuals. This study was conducted to investigate the profile and prevalence of ASA resistance in cardiac patients. From August 2007 to August 2008, a total of 282 cardiac patients were enrolled. Two study groups were identified: patients taking 100 mg ASA daily but without clopidogrel, and patients taking both 100 mg ASA and 75 mg clopidogrel daily. Platelet function was determined with the Multiplate analyzer to determine platelet responsiveness. Salicylate blood level was measured for all patients on ASA. Seventy-three patients (26%) were determined to be nonresponsive to ASA, and 45 patients (16%) were partially responsive, whereas 164 patients (58.2%) were responsive to ASA. Myocardial infarction and coronary obstruction were both strongly associated with ASA nonresponsiveness (p < 0.001). ASA resistance occurred more in female patients (p = 0.002). The salicylate blood level was found to be low in ASA-resistant patients (35.33 ± 50.22 mg/l) and higher in sensitive patients (54.26 ± 18.7 mg/l; p < 0.001). Quantitative assessment of platelet functions is predictive of ASA treatment failure in individual patients. Dual antiplatelet treatment with clopidogrel and ASA was found to have greater inhibitory effects on platelet aggregation than either agent alone. Non-adherence may be a significant mediator of poor outcome.
In this study, thrombophilic mutations were not increased in patients with RP. Thrombophilic mutations do not seem to be risk factors for RP. Routine investigation of hereditary thrombophilia in these patients is not justified.
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