The effects of healthy donor platelet apheresis on the some biochemical parameters and QTc dispersion

It?s known that apheresis process causes hypocalcemia and the prolongation of the QT related to the citrate that is given in process in donors. The prolongation of the QT and corrected QT (QTc) is related to important arrhythmia and mortality also QTc dispersion (QTcd) is a better indicator of non-uniform ventricular repolarization and it is suggested that it can be evaluated as an independent risk factor for ventricular arrhythmia. It is known that apheresis process causes decreasing of the ionized calcium and magnesium level and increasing of the parathormon (PTH) level in healthy donors. At the same time there are publications that shows the relation between PTH level and osteoprotegerin (OPG)/RANKL system that are the parameters of bone formation and resorption. Recently studies are reported that shows the relation between OPG and cardiovascular and atherosclerotic events. In this study we purposed to search the effects of the healthy donor platelet apheresis on the QTc dispersion, serum PTH, magnesium (Mg), calcium (Ca) and OPG/RANKL systemIn our study we measured QTc dispersion of 36 healthy platelet apheresis donor before apheresis process, at the first hour of the process and thirty minutes after the process according to the electrocardiography (ECG) results. At the same time we took blood samples to measure serum sodium (Na), potassium (K), calcium, ionized calcium, magnesium, alkaline phosphatase (ALP), bone ALP (BALP), OPG, RANKL, C-reactive protein (CRP) and parathormon levelsIn QTc dispersion measurements, while mean QTc dispersion value was 57.722 ±24.742 before apheresis process, at the first hour of the apheresis process it is measured as 46.167±25.892. This decrease is statistical significant (p=0.009). But the mean value of QTc dispersion thirty minutes after the apheresis process was 61.639±24.643 that was same as the values before apheresis process. At the first hour of the apheresis, statistical significant more prolongated QTcd was observed in 40 years old and older group in comparison with 40 years old group (p=0.035In measurements before apheresis, at the first hour of the apheresis and thirty minutes after the apheresis process we could?nt determine statistical significant variation in sodium, potassium, calcium, magnesium, ionized calcium, CRP and RANKL levels of the donors. For OPG when. we compare the levels before apheresis with the levels at first hour and after the apheresis we found a significant decrease ( respectively, p=0.027 and p=0.013). It was observed that PTH level at the first hour of the apheresis increases, after the apheresis this increasing continued (respectively, p=0.000 and p=0.001). In alkaline phosphatase measurements, both serum total ALP and bone alkaline phosphatase levels showed statistical significant decreasing during apheresis and after the apheresis process (respectively, for ALP p=0.0001 and p=0.0001; for BALP p=0.018 and p=0.014In literature, as we could?nt find any publication about the effects of the donor platelet apheresis process to the QTc dispersion, also we could?nt find any publication about the effects of the donor platelet apheresis process to the OPG/RANKL system. In our study, there was no clincally important ECG changes associated with apheresis. Although mean age of the our donor population is low, in our study observing significant more prolonged QTcd during the apheresis process in 40 years old and older group makes think we need to follow these individuals closely during the process. Also in this study, showing PTH/ OPG/RANKL system was effected by donor platelet apheresis makes think it can be useful to research in the long term effects of this process in donors and repetitive apheresis process results.