Pre-apheresis donor platelet count: an important platelet yield predictor.
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Platelet aggregation is the key process in primary hemostasis. Certain conditions such as hypoxia may induce platelet aggregation and lead to platelet sequestration primarily in the pulmonary microcirculation. We investigated the influence of high-altitude exposure on platelet function as part of a larger study on 30 subjects with a history of high-altitude pulmonary edema (HAPE) and 10 healthy controls. All participants were studied in the evening and the next morning at low altitude (450 m) and after an ascent to high altitude (4,559 m). Platelet count, platelet aggregation (platelet function analyzer PFA100; using epinephrine and ADP as activators), plasma soluble P (sP)-selectin, and the coagulation parameters prothrombin fragments 1+2 and thrombin-antithrombin complex were measured. High-altitude exposure decreased the platelet count, shortened the platelet function analyzer closure time by approximately 20%, indicating increased platelet aggregation, increased sP-selectin levels to approximately 250%, but left plasma coagulation unaffected. The HAPE-susceptible subjects were prophylactically treated with either tadalafil (a phosphodiesterase 5 inhibitor), dexamethasone, or placebo in a double-blind way. Subgroup analyses between these different treatments and comparisons of the seven placebo-treated individuals developing HAPE and controls revealed no differences in platelet count, platelet aggregation, or sP-selectin values. We conclude that exposure to high altitude activates platelets, which leads to platelet aggregation, platelet consumption, and decreased platelet count. These effects are, however, not more pronounced in individuals with a history of HAPE or actually suffering from HAPE than in controls and therefore may not be a pathophysiological mechanism of HAPE.
Rapid and accurate platelet counting is clinically required in severe thrombocytopenia. Prophylactic platelet transfusions are usually indicated in thrombocytopenia with platelet counts less than 20,000/microliter. It was recently reported that the confidence lower limit of platelet counts by automated blood cell counter is about 14,000/microliter. Clinical blood samples occasionally contain red-cell fragments or large platelets. In these cases, platelets should be counted by the phase-contrast microscopy. However, this manual operation is accurate but not precise and needs complicated technique. Abbott has developed an immunological platelet counting method by CELL-DYN 4000. We measured platelet counts in 137 blood samples from thrombocytopenic patients. These samples included red-cell fragmentation and large platelets on blood smears. We compared platelet counts with the immunological method(PLTimm) to those with Brecher-Cronkite, the optical(PLTo) and the impedance method(PLTi). PLTimm correlated more closely with the phase-contrast microscopy counts than PLTo or PLTi. In patients with microangiopathic hemolytic anemia, PLTo or PLTi could not exclude red-cell fragments, but PLTimm absolutely excluded red-cell fragments. In patients with giant platelets, PLTo or PLTi could not include large platelets but PLTimm included them and coincided well with platelet counts by the phase-contrast microscopy. These results indicate that the immunological method by CELL-DYN 4000 appears to be accurate and a very useful method for accurate platelet counts in severe thrombotybopenia.
As an alternative to liver biopsy, an index of five biochemical markers (alpha2-macroglobulin, apolipoprotein A1, haptoglobin, total bilirubin, gamma-glutamyl-transpeptidase) has been shown to predict the severity of hepatitis C-related fibrosis. The objective of this study was to compare this index with other markers frequently used for this purpose (prothrombin time, platelets, age-platelet index). In 323 hepatitis C-infected patients, the discriminative values of these markers for F2-F4 fibrosis (by the METAVIR classification) were compared. By multiple logistic regression analysis, only the five-marker index (P < 0.0001) and prothrombin time (P = 0.02) were independently predictive of F2-F4 fibrosis. For this outcome, the area under the receiver operating characteristic curve was significantly higher for the five-marker index (0.836 +/- 0.024) than the age-platelet index (P = 0.002), and the platelet count and prothrombin time (P < 0.001), indicating greater diagnostic value. The addition of the latter markers to the five-marker index proved unhelpful for increasing its accuracy. In conclusion, an index of five biochemical markers accurately predicts significant hepatitis C-related fibrosis and is superior to traditional markers.
The evaluation of the number of blood platelets in the left and right heart ventricle observed during haemorrhagic shock has been carried out. It has been stated that the number of blood platelets of the left ventricle outnumber that of the right heart ventricle. The difference is more intense with the prolongation of the time of the survival in the state of shock.
Platelet counts were performed in 50 cats presented for diagnostic investigation. For each cat, counts were obtained using a manual haemocytometer method and compared with counts obtained by estimation from a stained blood smear, a QBC VetAutoread analyser, a Zynocyte VS/2000 analyser, impedance automated counts on a Baker System using both EDTA and citrated anticoagulated blood, and use of a Zynostain modified counting chamber kit. None of the methods gave high correlation with the haemocytometer counts. The blood smear estimation of platelet counts had the highest correlation (r = 0.776) and was the only method to have reasonable values for both sensitivity and specificity. With the impedance automated counts, citrated anticoagulated blood had marginally higher correlation than EDTA anticoagulated blood, and the time between blood sampling and platelet count determination had no effect on the count obtained. When in-house analyser or impedance automated platelet counts are abnormal or not consistent with clinical findings, the authors recommend that a manual platelet count using either haemocytometry or examination of a blood smear is performed.
Monitoring of platelet counts 1 hour after transfusion has become standard practice in most centers. In this study, platelet counts obtained 10 and 60 minutes after 48 platelet transfusions were compared. There was a close, linear relationship (r = 0.98) between these values over a wide range of posttransfusion counts, indicating rapid equilibration of transfused platelets. Ten-minute posttransfusion samples are easier to obtain and are convenient for both patients and medical staff.
Thiazole orange (TO) is a fluorescent dye that is commonly used for flow cytometric measurement of erythrocytic reticulocytes. This technique has also been validated for counting "reticulated" platelets, as a measure of bone marrow thrombopoietic activity. Patients with an established diagnosis of idiopathic thrombocytopenic purpura (ITP) have been reported to have a three- to five-fold increase in the percent of circulating reticulated platelets. The current study was conducted to determine if platelet reticulocyte counts predicted recovery of bone marrow thrombopoietic activity following autologous bone marrow transplantation. We found an increase in the percent of circulating reticulated platelets preceding recovery of the platelet count; then, as the patients' platelet counts rose, the percent reticulated platelets fell. In patients with prolonged thrombocytopenia, a persistent increase in the proportion of reticulated platelets suggested a consumptive process, as opposed to failure of engraftment. Moderate transfusion of platelet concentrates did not interfere with the ability of the platelet reticulocyte measurements to detect increased thrombopoietic activity. Platelet transfusions did obscure any decrease in the proportion of reticulated platelets. Our results show that platelet reticulocyte counts could be useful in monitoring the recovery of marrow function following autologous bone marrow transplantation.
Previous reports have shown that a single, oral dose of 50 mg metoprolol (a selective beta-1-receptor antagonist) causes a significant increase in the peripheral platelet count by releasing platelets from the spleen. In the present study 20 healthy volunteers received 50 mg metoprolol and 40 mg propranolol orally. Both drugs induced a statistically significant increase in the platelet count lasting more than 5 h. In addition, the effect of metoprolol and propranolol on beta-adrenoceptor mediated splenic platelet trapping was studied on 7 healthy subjects who received intravenous infusions of isoprenaline before and after the ingestion of these 2 beta-blocking drugs. It was demonstrated that the isoprenaline mediated decrease in the venous platelet count was diminished by both propranolol and metoprolol but the former compound appeared to be more potent in this respect. We conclude that both selective and non-selective beta-receptor blockade causes an increase in the peripheral platelet concentration during rest as well as during beta-adrenoceptor stimulation.
A total of 34 patients, aged 43 to 86 years old (mean 65), consisting of 26 males and 8 females, with thrombotic or arteriosclerotic diseases were orally given highly purified eicosapentaenoic acid ethyl-ester formulation (IPA-E) for 12 weeks without changing regular food intake. Changes in platelet count (PLT), mean platelet volume (MPV), platelet-crit (Pct) and change of distribution width of platelet size (PDW), and factors affecting the changes were studied administration, dose of IPA-E, age, sex, smoking habits, complications of diabetes mellitus and hyperlipidemia, and concomitant drugs such as calcium antagonists or diuretics. With daily administration of 1800 or 900 mg of IPA-E, PLT and Pct began to decrease after four weeks and decreased significantly after eight weeks until the completion of administration. After the 12th week, the MVP became smaller than the preadministration level, while PDW did not change significantly during the entire period of administration. The volume and rates of changes in PLT, MPV and Pct during administration for 12 weeks correlated negatively with those preadministration values. The PLT, MPV and Pct decreased significantly in both the 1800 and 900 mg groups compared to values before administration. There were no significant differences in changes between the two groups. The plasma IPA concentration in the 12th week of the 1800 mg group was significantly higher than that of the 900 mg group. The rate of changes in Pct had a significantly negative correlation with the achieved IPA concentration. The age, smoking habits, complications of diabetes mellitus, or concomitant drugs of calcium antagonists or diuretics did not affect the changes of platelet parameters significantly. The PLT and Pct in male patients decreased significantly, but no significant changes were observed in female patients. The PLT and Pct in patients with IIb and IV hyperlipidemia decreased significantly compared to those in normolipidemic or IIa hyperlipidemic subjects. The study demonstrated that IPA-E improved platelet parameters, suggesting IPA-E could prevent progression of thrombotic and arteriosclerotic diseases, IPA-E was particularly effective in male patients or patients with Type IIb or IV hyperlipidemia. Although a daily dose of 900 mg was effective, 1800 mg was even more effective.
We report the case of a pregnant woman for whom the platelet count (77 x 10(9)/L) was underestimated by Coulter STKS analyzer during the third trimester because of large platelets. The microscopic counting of platelets revealed an isolated thrombocytopenia (120 x 10(9)/L). When not pregnant, the patient has low but normal platelet count (155 x 10(9)/L) with high mean platelet volume (MPV > 12 fL). This case report recalls that concomitantly to the decrease in platelet count, the MPV significantly increases at the end of pregnancy. This poorly known phenomenon does not impair platelet count by blood cell analyzers in as much as the platelet volume is in the range of measurement but may be responsible for underestimation of the platelet count if the MPV is already high before pregnancy. We describe how to detect this anomaly and propose simple guidelines for thrombocytopenia in normal pregnancy.
A survey of 44 laboratories was conducted to evaluate current testing proficiency in the diagnosis of von Willebrand disorder (vWD) and to assess recent changes in test practices. Laboratories performed their usual panel of tests for vWD and interpreted results for the likelihood of vWD and potential subtype. Samples were as follows: normal plasma; borderline normal or abnormal levels of von Willebrand factor (vWF) and factor VIII; type 3 vWD; type 2A vWD; and 2 samples from a healthy person, processed after handling at 22 degrees C and 4 degrees C, respectively. Interassay and within-method coefficients of variation were similar for all assays (approximately 15%-25%). Most laboratories reported test values consistent with expected findings and made correct interpretations, although discrepant results for 5% to 10% of responses are of concern. For the sample stored at 4 degrees C, all laboratories detected low or borderline levels of vWF and factor VIII coagulant, and no laboratory identified this sample as from a healthy person. In contrast, for the sample stored at 22 degrees C, most laboratories reported normal results. Compared with previous results, performance of some assays has declined while that of others has increased. Laboratories generally are proficient in tests for vWD, and transport of samples at 4 degrees C before processing may lead to false identification of vWD, suggesting that NCCLS guidelines should be reviewed.
OBJECTIVE: The risk of stroke in patients with recently symptomatic carotid stenosis is considerably higher than in patients with asymptomatic stenosis. In the present study it was hypothesised that excessive platelet activation might partly contribute to this difference. METHODS: A full blood count was done and whole blood flow cytometry used to measure platelet surface expression of CD62P, CD63, and PAC1 binding and the percentage of leucocyte-platelet complexes in patients with acute (0-21 days, n = 19) and convalescent (79-365 days) symptomatic (n = 16) and asymptomatic (n = 16) severe (> or =70%) carotid stenosis. Most patients were treated with aspirin (37.5-300 mg daily) although alternative antithrombotic regimens were more commonly used in the symptomatic group. RESULTS: The mean platelet count was higher in patients with acute and convalescent symptomatic compared with asymptomatic carotid stenosis. There were no significant differences in the median percentage expression of CD62P and CD63, or PAC1 binding between the acute or convalescent symptomatic and asymptomatic patients. The median percentages of neutrophil-platelet (p = 0.004), monocyte-platelet (p = 0.046), and lymphocyte-platelet complexes (p = 0.02) were higher in acute symptomatic than in asymptomatic patients. In patients on aspirin monotherapy, the percentages of neutrophil-platelet and monocyte-platelet complexes (p = 0.03) were higher in acute symptomatic (n = 11) than asymptomatic patients (n = 14). In the convalescent phase, the median percentages of all leucocyte-platelet complexes in the symptomatic group dropped to levels similar to those found in the asymptomatic group. CONCLUSION: Increased platelet count and leucocyte-platelet complex formation may contribute to the early excess risk of stroke in patients with recently symptomatic carotid stenosis.
Changes of the platelet count in liver diseases are described in humans. Thrombocytopenia was observed more frequently than thrombocytosis. There are only a few investigations on platelet counts in liver diseases in dogs. The goal of the present study was to investigate the influence of different liver diseases including degeneration, hepatitis and liver tumours, on the platelet count. Platelet counts of 52 dogs with different liver diseases were measured and compared with 52 healthy dogs. The results showed, that dogs with liver degeneration have thrombocytosis in 41% of the cases and a group of dogs with liver tumours (malignant histiocytosis, hepatoma, malignant lymphoma anaplastic sarcoma, cholangiocarcinoma, hepatocellular carcinoma) had thrombocytopenia in 50% of the cases. The dogs with hepatitis showed no specific changes in the platelet count. The statistical comparison of our patients with liver disease and a control group of healthy dogs showed significantly higher platelet counts in cases of liver degeneration (p < 0.0001) and significantly lower platelet counts in cases of liver tumour (p < 0.001). The comparison between the dogs with different liver diseases showed significantly lower platelet counts in dogs with liver tumours when compared to dogs with liver degeneration (p < 0.0001). There was no significant difference between dogs with liver tumours and dogs with hepatitis and between dogs with liver degeneration and dogs with hepatitis. Based on the results of this study the author recommends to assess platelet counts in all dogs with liver disease, especially if liver biopsy is planed.
To observe the change of quantity and quality of platelets preserved in a full-sealed bag, and explore the difference of platelets preserved in oscillating and static conditions at (22 +/- 2) degrees C, the platelet concentrates were prepared with a CS-3000-plus blood cell separator, the platelet counts were performed with automatic blood cell analyzer and P-selectin in supernatant of platelet concentrates was detected by ELISA. The results showed that both of platelet count and P-selectin content in the platelet concentrates had no significant difference between oscillating and static preservation condition. With prolongation of preserved time, the platelet count decreased and P-selectin content increased gradually in both preserved conditions. There was no difference in the platelet counts during 0 - 72 hours preservation in both conditions, and significant difference was seen in 96 - 120 hours preservation. It was concluded that the expired date for platelet product preserved in CS-3000-plus blood cell separator full-sealed system should be 3 days. Under the condition of (22 +/- 2) degrees C, the quality of the platelet preserved in oscillating state is not superior to static preservation.
This study was undertaken to examine the relationship between cigarette-smoking and total white blood cell count (wbcc) and platelet count (pc) in adult Nigerians. We also studied the relationship of the white blood cell and platelet counts to the duration of the smoking habit and number of cigarette smoked per day. Three hundred and fifty-two healthy male adults, aged 18-52 years, were studied. They were randomly allocated to two groups--176 smokers and 176 non-smokers. The smoking habit was assessed from a minimum period of 1 year and a minimum number of 5 cigarettes per day. Results revealed that platelet count was higher for the regular Nigerian smoker than for non-smoker. The difference between mean platelet counts for smokers and non-smokers was statistically significant (t = 2.64 p = 0.0046). Man WBC count in smokers was slightly higher than for non-smokers. However, unlike in the case of platelet counts, the mean difference in WBC count between smokers and non-smokers is not statistically significant (t = 0.07, p value = 0.9442). Similar studies based on white population has showed statistically significant increases in wbcc and pc in smokers.
Most studies measuring circulating vascular endothelial growth factor (VEGF) have sampled serum rather than plasma. There has been much debate whether the collection of sera (which causes the activation of platelets and VEGF release) is a true reflection of tumor angiogenic activity or whether platelets act as scavengers of VEGF. Addressing this issue, we measured serum and plasma VEGF, before and after colorectal resection, with reference to platelet counts. Serum and plasma samples were collected from 116 colorectal cancer (CRC) and 116 control patients. Ninety CRC and 32 benign resections were performed. Both plasma and serum VEGF were significantly higher in CRC patients (18.5 and 327 pg/ml, respectively) compared with controls (9.0 and 151.5 pg/ml, respectively; P < 0.0001). Paired serum and plasma VEGF measurements correlated in both CRC (r = 0.56) and control patients (r = 0.73; P < 0.0001). Serum and plasma VEGF levels correlated with platelet count in CRC patients (r = 0.58 and 0.44, respectively) but not in controls. Plasma and serum VEGF levels, and VEGF concentration per platelet, increased with advancing disease stage. The correlation of serum and plasma VEGF with platelet counts in CRC but not in benign disease may be attributable to the scavenging of VEGF from the tumor source by platelets, with plasma levels reflecting free circulating VEGF in equilibrium with platelet levels. VEGF levels in citrated plasma are low and lie close to the limits of ELISA sensitivity. We recommend that a standardized measurement of serum VEGF--normalized by the patient's platelet count to give a value of serum VEGF per platelet--be adopted.