Impedance Aggregometry Reveals Increased Platelet Aggregation during Liver Transplantation

In patients presenting for liver transplantation, increased platelet aggregation as well as thrombocytopenia have been demonstrated, but bedside assays have not been investigated. We compared platelet aggregation in liver transplantation patients and control surgical patients using impedance aggregometry. We hypothesized that platelet activity is not altered during liver transplantation. After the allowance of the ethics committee, platelet aggregation was determined using impedance aggregometry with the activators ristocetin, adenosine diphosphate (ADP), arachidonic acid, collagen, and thrombin receptor-activating peptide (TRAP) in liver transplantation patients at four time points (start of surgery, anhepatic phase, reperfusion, end of surgery) and in control surgical patients. Moreover, platelet count was determined using a Coulter counter. To compensate for the thrombocytopenia often present in patients presenting for liver transplantation, the ratio between impedance aggregometry finding and platelet count was used. For statistical evaluation, the t-test or the Mann–Whitney U-test were used, as appropriate. Platelet aggregation ratio showed a 3.1-fold increase in liver transplantation patients (n = 37) in comparison to control surgical patients (n = 10) when ristocetin was used as the activator (p = 0.001). Moreover, an approximately twofold increase of ADP-, arachidonic acid-, collagen-, and TRAP-induced platelet aggregation ratio was determined. Platelet aggregation normalized at the end of the transplantation procedure. Impedance aggregometry revealed a markedly increased platelet aggregation in some liver transplantation patients and might be suitable to guide platelet transfusion and antiplatelet therapy.

Platelet Function Tests in Relation to Retinopathy and Neuropathy in Well Controlled Diabetic Patients

The following tests were done in 61 well controlled diabetic patients: Platelet survival time (PST), platelet aggregation ratio acc. to Wu and Hoak (PAR), platelet aggregation test 1 acc. to Breddin (PAT 1), ADP-threshold concentration and filtragometer aggregation time acc. to Hornstra (Ta). The mean PST in 20 healthy volunteers was 99 hours ± 13,4 hrs.: in 12 pat. wihtout retinopathy 88,6 ± 12,8 hrs.; in 28 pat. with non-proliferative retinopathy 103,9 ± 18,2 hrs. and in 1 par. with proliferative retinopathy 105,8 ± 7,5 hrs. In 16 pat. with a disturbed nerve conduction time the mean PST was 102,2 ± 21,5 hrs. and 96,0 ± 21,9 hrs, in 28 pat. with a normal time. The PST was shortened (mean-1 ED) in 12 pat. out of 44 pat. The mean PAR was 0,37 ± 0,11 in 27 normal volunteers and 0,78 ± 0,12 in 61 diabetics. The PAR was < 0,71 in 16 out of 61 pat. The mean PAT 1 was 1,7 in 27 normal volunteers and 1,5 in 61 diabetics; the test was abnormal in 6 out of 61 pat. The ADP-threshold concentration was < 0,75 mumol ADP/L in only 4 out of 61 pat. The mean Ta was 242 ± 50,5 sec. in 16 normal volunteers and 167 ± 83 sec. in 44 pat.; the Ta was < 150 sec. in 23 out of 44 pat. There was no correlation between the severity of retino- and/or neuropathy with the PST, PAR, PAT 1, ADP-threshold or Ta or between the laboratory values. There was no abnormal laboratory test in 2 3 pat., one in 19, two in 16 and three in 3 pat. There was no relationship between the severity of retino- and/or neuropathy and number of abnormal laboratory tests.