Recovery of Donor Peripheral Blood Platelet Count Following Platelet Apheresis.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2892-2892
Author(s):  
Larry J. Dumont ◽  
L. Lassahn ◽  
Peter A. Tomasulo ◽  
Dennis Harpool ◽  
S. Pinkard ◽  
...  

Abstract BACKGROUND: Apheresis platelet collection from healthy normal blood donors can reduce the donor peripheral blood platelet concentration by 50% or more. The kinetics of peripheral blood platelet count (PLT) recovery in the apheresis donors over the first 24 hours has not been described. The objective of this study was to determine the recovery kinetics of the donor peripheral blood platelet count following apheresis platelet donation. METHODS: Healthy apheresis platelet donors were enrolled following informed consent. The apheresis platelet collection was performed using the Gambro Trima system (Gambro BCT, Lakewood, CO) following local SOP and manufacturer’s directions for use. The minimum predicted post-count was configured in the Trima to no less than 78K plt/μL. PLT was determined pre-procedure (Pre), immediately post procedure (Post), 4–11 h (FU1) and 11–41 h (FU2) post-donation using standard methods. The PLT recovery was evaluated as the increase in PLT following the donation (Delta). The effects of study site, time of sample, and the fraction of platelets collected (Fpc) at donation on Delta were evaluated using a random effects generalized linear regression model. A full regression model of Delta as a function of study site, follow-up period and Fpc with all main and interaction effects was used to test hypotheses. RESULTS: 548 subjects were entered into the study at 3 study sites; Pre-PLT 276±59 × 103 plt/μL, Post-PLT 205±47 × 103 plt/μL, Fpc 25±10%. No adverse events were reported by any subjects. Recovery of platelet count following apheresis platelet donation is variable between subjects; and the independent variables of study site, follow-period and Fpc accounted for 25% of the total variation in Delta. PLT increased 12.4±0.9 × 103 plt/μL by the time of follow-up sampling (p=0.01), although there was no difference between PLT at FU1 (214±49 × 103 plt/μL) and FU2 (212±47 × 103 plt/μL; p=0.15). None of the donors reached their pre-donation platelet count during the follow-up period. There was no difference in Delta between centers (p=0.23). Fpc had a significant affect on Delta (p<0.0001); with estimated Delta of 5.2±0.9 × 103 plt/μL at Fpc=15% and 16.0±.8 × 103 plt/μL at Fpc=30%. CONCLUSION: Platelet recovery following apheresis platelet donation was observed to be dependent on the fraction of platelets donated. Surprisingly, the recovery observed within the first 11 h was equivalent to that observed between 11–42 h, averaging 17.5% of the drop observed during apheresis. Recovery was not complete when observed for up to 41 h following donation in this study. Additional investigation of PLT recovery following apheresis donation is indicated to describe and differentiate the potential roles of de novo production, early pro-platelet release and platelet release from peripheral pools over the early post-donation period.

Author(s):  
V. O. Tsvetkov ◽  
V. V. Malovichko ◽  
A. S. Stupin ◽  
S. O. Arkhireev

We are to present a rare occurrence of large limb-threatening ulcer of the leg and foot in patient with thrombocytosis. Essential thrombocythemia was diagnosed based on peripheral blood platelet count and gen test findings. The improving of platelet count was obtained by oral hydroxyurea. Complex surgical treatment, including free-skin grafting, was performed with the excellent result. Two-year follow-up was retraced without any sign of ulcer recurrence. 


2012 ◽  
Vol 142 (5) ◽  
pp. S-1006
Author(s):  
Wissam Bleibel ◽  
Wael Saad ◽  
Daniel Sheeran ◽  
Curtis L. Anderson ◽  
Patrick G. Northup ◽  
...  

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3283-3283
Author(s):  
Chang Liu ◽  
Dorina Kallogjeri ◽  
Marian Dynis ◽  
Brenda J. Grossman

Abstract Abstract 3283 Background: Plasma exchange (PEX) is the first line therapy for patients presenting with thrombotic thrombocytopenic purpura (TTP). Since the therapeutic response and prognosis vary among patients, it is important to predict early and late outcomes in order to optimize treatment for each individual. We have recently reported (Transfusion, in press) that initial platelet recovery rate by day 3 (PRR3) of or above 5 × 109/L per 24 hr is an independent predictor for complete remission in response to PEX and for short-term exacerbations. This study was designed to examine whether PRR3 of or above 5 × 109/L per 24 hr can predict relapse of TTP and long-term survival in these patients. Methods: We reviewed the medical records of 64 consecutive patients with de novo TTP who received PEX in our institution between Decembers of 2003 and 2010. Standard regimen of PEX typically included 1–1.5 volumes of PEX daily with fresh frozen plasma until sustained normalization of platelet count. Time at the start of the first PEX was set as time zero. Complete remission is defined as platelet count rising above 150 × 109/L during PEX and maintain for more than 2 weeks after stopping PEX. Exacerbation is defined as a decrease of platelet count below 150 × 109/L or a 50% drop from the previous count within 1 month of the initial platelet recovery. Relapsed TTP is defined as recurrence of thrombocytopenia and microangiopathic hemolytic anemia over 1 month after the previous remission. PRR was derived as the slope of the linear regression of series of platelet counts at a designated interval, e.g. PRR3 means the rate of platelet recovery during the first 3 days after time zero. The date of death or when alive the date of the most recent visit of the patients was recorded. Kaplan-Meier analysis was used to compare overall survival between different categories of potential prognostic factors. All computation and statistical analysis were performed using SPSS, Version 19.0.0.1 (IBM). Results: Four patients relapsed between 1.4 – 29.4 months after presenting with de novo TTP. All of these patients had PRR3 ≥ 5 × 109/L per 24 hr and ADAMTS13 activities ≤ 10%. A total of 13 deaths occurred during a median follow up of 11.8 months. The survival was significantly better in patients with PRR3 ≥ 5 × 109/L per 24 hr as compared to patients with PRR3 below the cutoff by Kaplan-Meier analysis (p<0.001, Figure 1A). In patient with PRR3 < 5 × 109/L per 24 hr, the estimated rates of survival were 74.7% at 1 month, 64.8% at 3 months, and 58.9% at 1 year, as compared with rates of 100%, 100% and 100%, respectively, in the patients with PRR3 ≥ 5 × 109/L per 24 hr. The survival was not significantly different among groups stratified based on ADAMTS13 activity (cutoff=10%), race (African Americans versus Caucasians), or gender. After adjustment for age and ADAMTS13 activities using Cox proportional hazard regression analysis, PRR3 < 5 × 109/L per 24 hr was associated with a 23-fold increase in mortality rate compared to PRR3 ≥ 5 × 109/L per 24 hr (95% CI for the hazard ratio, 2.7 – 203.3; p<0.005, Figure 1B). Conclusion: We conclude that PRR3 with a cutoff of 5 × 109/L per 24 hr provides a practical approach to risk stratify TTP patients receiving PEX. Patients with PRR3 above the cutoff have increased chance of long-term survival. However, relapses tend to occur exclusively in this group, which may necessitate close follow up and adjunctive therapy to suppress the production of autoantibodies. In contrast, patients with PRR3 below this cutoff may eventually fail the PEX therapy and have significantly increased mortality rate. They may benefit from prompt re-evaluation and exploration of additional therapies other than PEX. Knowing the platelet recovery rate early in the disease's course allows tailoring therapy to the individual patient. Disclosures: No relevant conflicts of interest to declare.


1982 ◽  
Vol 48 (01) ◽  
pp. 041-045 ◽  
Author(s):  
H Ireland ◽  
D A Lane ◽  
S Wolff ◽  
M Foadi

SummaryThe in vivo platelet release reaction in 22 patients with myeloproliferative disorders has been studied by measuring plasma concentrations of the platelet release product β-throm-boglobulin (βTG). Mean βTG and mean βTG:whole blood platelet count ratio were significantly raised in the patient group taken as a whole compared to an age matched control group. No significant increases were observed in the plasma concentrations of thrombin and plasmin sensitive fibrinogen fragments fibrinopeptide A (FpA) and Bβ1-42. The patients were divided into those who had normal, increased or decreased responses to in vitro ADP-induced platelet aggregation. Mean βTG and the mean βTG:whole blood platelet count ratio were higher in the increased and decreased responders to ADP than in the normal aggregation group, but the differences in means were not statistically significant. Aspirin given to six patients at a dose sufficient to eliminate the secondary phase of ADP-induced platelet aggregation reduced mean βTG and the mean βTG : whole blood platelet count ratio but did not alter mean FpA and Bβ1-42. It is concluded that the enhanced platelet release reaction seen in myeloproliferative disorders is independent of plasma protease activity that arises when coagulation and fibrinolytic systems are activated.


1978 ◽  
Vol 39 (02) ◽  
pp. 346-359 ◽  
Author(s):  
P D Winocour ◽  
M R Turner ◽  
T G Taylor ◽  
K A Munday

SummaryA major limitation to single-cell protein (SCP) as a human food is its high nucleic acid content, the purine moiety of which is metabolised to uric acid. Rats given a Fusarium mould as a source of SCP in diets containing oxonate, a uricase inhibitor, showed elevated plasma and kidney uric acid concentrations after 21 d, which were related to the level of dietary mould. ADP-induced and thrombin-induced platelet aggregation was greater in the hyperuricaemic rats than in controls and a progressive increase in aggregation with increasing levels of dietary mould was observed. Furthermore a time-lag, exceeding the life-span of rat platelets, was observed between the development of hyperuricaemia and the increase in aggregation. A similar time-lag was observed between the lowering of the hyperuricaemia and the reduction of platelet aggregation when oxonate was removed from the diet.If human platelets react to uric acid in the same manner as rat platelets this might explain the link that has been suggested between hyperuricaemia and ischaemic heart disease. In that event diets high in nucleic acids might be contra-indicated in people at risk from ischaemic heart disease.In rats given a low protein diet (50 g casein/kg) for 21 d ADP-induced and thrombin-induced platelet aggregation and whole blood platelet count were reduced compared with control animals receiving 200 g casein/kg diet but not in rats given 90 or 130 g casein/kg diet. A study of the time course on this effect indicated that the reduction both in aggregation tendency and in whole blood platelet count occurred after 4 d of feeding the low protein diet. These values were further reduced with time.


Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 29-30
Author(s):  
Takahiro Shima ◽  
Teppei Sakoda ◽  
Tomoko Henzan ◽  
Yuya Kunisaki ◽  
Takahiro Maeda ◽  
...  

Peripheral blood stem cell (PBSC) transplantation is a key treatment option for hematological diseases and widely performed in clinical practice. Platelet loss is the major complication of PBSC apheresis, and platelet-rich plasma (PRP) return is recommended in case of severe platelet decrease following apheresis; however, little is known about the frequency and severity of platelet loss nor the efficacy of PRP return post-apheresis. To address these questions, we assessed changes in platelet counts following PBSC-related apheresis in 270 allogeneic (allo)- and 105 autologous (auto)-PBSC settings. We also evaluated efficacy of PRP transfusion on platelet recovery post-apheresis. Platelet counts reduced up to 70% post-apheresis in both allo- and auto-PBSC settings, while severe platelet count decrease (&lt; 50 x 109/L) was only observed in auto-PBSC patients (Figure 1). We next analyzed the relationship between severe platelet (&lt; 50 x 109/L) after apheresis and several clinical factors by using univariate and multivariate analysis for auto-PBSC patients. As shown in Table 1, in univariate analysis, severe platelet counts following auto-PBSC apheresis was found more frequently in patients with lower platelet count, lower percentage of CD34+ cells in PB at pre-apheresis, repeated round of apheresis, and smaller number of collected CD34+ cells. On the other hand, in multivariate analysis, the white blood cell (WBC) counts pre-apheresis was the only significant risk factor of severe platelet count following apheresis (p = 0.038). We finally analyzed the transitions of platelet counts in the setting of apheresis. The median platelet counts at pre-apheresis, post-apheresis, and post-PRP return were 187.0 x 109/L, 132.0 x 109/L, and 154.0 x 109/L for allo-PBSC apheresis, and 147.0 x 109/L, 111.0 x 109/L, and 127.0 x 109/L for auto-PBSC apheresis (p &lt; 0.0001 for all, allo-PBSC donors and auto-PBSC patients, respectively) (Figure 2), indicating that PRP return post-apheresis facilitated a rapid platelet recovery in both allo- and auto-settings. Collectively, our data suggest that WBC counts pre-apheresis is a useful predictor for severe platelet decrease following auto-PBSC apheresis and that PRP return is an effective mean to facilitate platelet recovery post-apheresis. Disclosures No relevant conflicts of interest to declare.


Blood ◽  
1952 ◽  
Vol 7 (9) ◽  
pp. 948-949 ◽  
Author(s):  
KENNETH OTTIS ◽  
OSCAR E. TAUBER

Abstract Healthy, adult male and female golden hamsters, 3 months of age, showed blood platelet count means of 688,000 ± 141,000 per cu. mm. and 742,000 ± 120,000 per cu. mm., respectively, when direct counts were made with siliconized pipets and with Rees and Ecker fluid as a diluent.


Sign in / Sign up

Export Citation Format

Share Document