PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Platelet Count”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources

Evaluation of automated whole-blood platelet counts and particle sizing.

The Coulter Counter model S-Plus measures the erythrocyte, leukocyte, and platelet counts, and the mean cell volume of erythrocytes and platelets. Two additional features are novel to the instrument: erythrocyte distribution width (RDW), an index of erythrocyte volume heterogeneity, and mean platelet volume. For 677 subjects, we compared these measurements with complete blood counts obtained by a standard instrument, platelet counts from platelet-rich plasma (PRP), and histograms of erythrocyte and platelet volumes generated by free-standing equipment. The two methods correlated well (r = 0.97) for the complete blood count and the mean platelet volume. The whole-blood platelet count correlated well (r = 0.97) with the PRP platelet count, with whole-blood counts on average 5% higher than PRP counts. The whole-blood index of erythrocyte volume heterogeneity, RDW, correlated less well (r = 0.81) with the erythrocyte coefficient of variation measured by histogram. RDW was abnormal for three of 100 normal subjects with normal histograms. RDW was less sensitive (78% vs. 97%) and less specific (94% vs. 97%) than erythrocyte histograms in distinguishing iron deficiency from heterozygous alpha- or beta-thalassemia. We conclude that the Coulter Counter Model S-Plus reliably measures complete blood cell count, platelet count, and mean cell volumes, but analyzes erythrocyte volume distribution less well than does a histogram.

Blood Cell Count↗

Increment of the platelet count in temporal arteritis: response to therapy and ischemic complications.

Temporal arteritis (TA) is a vasculitis involving mainly cranial branches of the aorta that can lead to ischemic complications such as amaurosis or ischemic stroke. Increment in the platelet count has been described in the acute period of the disease. We studied retrospectively the platelet count in patients with TA, its association with ischemic complications and quantified its response to therapy. We found thrombocytosis in 44% of 34 patients with TA, with a mean reduction in the platelet count of 25.1% after therapy. We were also able to quantify the increment in the platelet count at the onset of the disease and its response to prednisone in a group of 5 patients. We did not find any relation between platelet count and ischemic complications of the disease or the result of the temporal artery biopsy. In conclusion TA is associated with an increase in the platelet count, with a 25% reduction after prednisone therapy. These two determinations are not related to ischemic complications of the disease.

Aged↗

Reduced platelet count as a risk factor for intraventricular hemorrhage.

The role of thrombocytopenia as a risk factor for intraventricular hemorrhage in infants of very low birth weight is unclear. This study investigates the relationship between the lowest platelet count and the occurrence of intraventricular hemorrhage in 302 consecutively admitted infants with birth weights under 1500 g. Intraventricular hemorrhage, which occurred in 90 infants (29.8%), was correlated with the lowest platelet count obtained during the first 4 days of life. In 27 infants with intraventricular hemorrhage, the lowest platelet count was less than 100 X 10(9)/L. Statistical analysis of the data demonstrated that reduced platelet count was not associated significantly with intraventricular hemorrhage. Similarly, the severity of intraventricular hemorrhage did not correlate with the lowest platelet count. These data suggest that a reduced platelet count does not play a major role in the pathogenesis of intraventricular hemorrhage in infants of very low birth weight.

Asphyxia Neonatorum↗

Long-term outcome, with monitoring of platelet counts, in patients with chronic hepatitis C and liver cirrhosis after interferon therapy.

OBJECTIVE: Because the determination of the stage of fibrosis depends on rather subjective judgment, more objective parameters are needed. In this study, we followed the long-term outcome, with monitoring of platelet counts, in patients with chronic hepatitis C or liver cirrhosis (LC) who had undergone interferon (IFN) therapy. METHODS: 596 patients who were diagnosed at our institute from 1987 to 1998 with chronic hepatitis C and LC were treated with IFNs. A further 58 patients were not treated (NT). The annual rate of changes in platelet counts were calculated and compared for IFN-treated and NT patients. RESULTS: The relationship between the efficacy of IFN therapy and the incidence of hepatocellular carcinoma (HCC) showed that the patients who were virologic sustained responders (VSR) had a significantly lower incidence of HCC than the nonresponders (NR) and NT patients. The change in platelet counts was +4,350/microl/year in the VSR, +1,010/microl/year in the biochemical sustained responders (BSR), -4,540/microl/year in the NR and -6,180/microl/year in the NT patients, indicating a significant platelet increase in the VSR, a decrease of the same magnitude in the NR and NT patients, and no change in the BSR. The cumulative probability of developing HCC and liver failure was significantly higher in groups with decreased platelet counts than in groups with increased platelet counts among patients who had undergone IFN therapy. Multivariate analyses revealed that a decrease in platelet counts was the cardinal risk factor for development of HCC and liver failure in chronic hepatitis C or LC patients. CONCLUSION: Investigation of platelet counts was useful for determining the long-term outcome of patients who had undergone IFN therapy and for predicting the development of HCC.

Adult↗

[Estimation of platelet counts and their morphological parameters in patients infected by borrelia burgdorferi].

Platelet counts and their morphologic parameters in patients with Lyme borreliosis before and after antibiotic therapy (4 weeks of treatment) were estimated. 30 patients aged 17-60, x = 41 were evaluated: 7 with Erythema migrans, 3 patients with neuroborreliosis in the from Lymphocytic meningitis and 20 ones with Lyme arthritis. Control group consisted of 19 healthy persons aged 34-52, x = 43. Hematologic analyser Coulter MAXM was used for testing PLT, MPV, PCT and PDW. The results indicated that patients with Lyme boreliosis have decreasing platelet count with simultaneously increasing their volume in comparison with healthy control. It may result from the involement of platelets in defense mechanisms of infected host. The decrease of platelet count after the antibiotic treatment in comparison with the control group may be the reflection of influence of antibiotic treatment on thrombopoesis.

Adolescent↗

Correlation of platelet concentration in platelet-rich plasma to the extraction method, age, sex, and platelet count of the donor.

An important reason to improve methods of isolating platelet-rich plasma (PRP) is the potential use of autologous platelet growth factors. In addition to discontinuous plasma separation, a second method for extraction of PRP has now become available, which can be performed directly by the surgeon. In this study, the suitability of the 2 methods of producing PRP was compared. Whole blood was drawn from 158 healthy donors (112 men, 46 women) aged 20 to 62 years (mean 34, SD 10). The PRP was separated by the discontinuous plasma separation method (by the blood bank) or by the so-called "buffy coat" method (the "self-concentration" method, analogous to the PRP Kit, Curasan, Kleinostheim, Germany). Platelet counts differed significantly according to donor blood (median men 237,500/microL, women 272,000/microL), blood bank PRP preparation (median men 1,302,000/microL, women 1,548,500/microL), and self-concentrated PRP (median men 944,000/microL, women 1,026,000/microL). The platelet concentration of the blood bank PRP correlated with the platelet count in the donor whole blood (Spearman's correlation coefficient r(s) = 0.73). However, there was no significant correlation between the platelet count of self-concentrated PRP and donor whole blood (r(s) = 0.22). Significant but irrelevant influences of sex on platelet concentration were found, but no influence of age was detected.

Adult↗

The relationship between platelet count, sepsis, and survival in pediatric burn patients.

Early identification of sepsis can be difficult in severe burns because of the systemic changes that routinely accompany these burns. This review examined the value of a falling platelet count in predicting the development of sepsis. Thirty-two pediatric patients who sustained lethal burn injuries were compared with 32 patients with similar burns who survived. Daily platelet count was evaluated in conjunction with clinical course. Thirty-one of the 32 non-survivors developed a platelet count less than 0.1 x 10(12)/L. Only 10 of the survivors had a similar occurrence. Platelet count decline preceded other signs of sepsis in all cases. A platelet count below 0.1 x 10(12)/L for more than 4 days was uniformly associated with death. All patients who died succumbed to multisystem organ failure, consistent with sepsis. These results emphasize platelet count as an independent predictor of sepsis and death.

Adolescent↗

The effect of zidovudine on platelet count in HIV-infected individuals.

Seventy-four HIV-infected homosexual males belonging to CDC groups IIB, III, and IVC2 were treated with increasing doses of zidovudine within the Multicentre Canadian AZT Trial. Following a 3 week observation period, consenting volunteers received 600 mg/day for 18 weeks, 900 mg/day for 9 weeks, and 1,200 mg/day for 9 weeks. This was followed by a 6 week washout period after which zidovudine was restarted at 1,200 mg/day for 18 weeks. Patients were followed for a total of 63 weeks. Every 3 weeks they underwent a full clinical and laboratory assessment. For the purpose of this analysis, subjects were divided according to the mean initial platelet value (greater than or equal to 150,000 or less than 150,000/L) into normals (n = 57) and thrombocytopenics (n = 12), respectively. Analysis of variance was used to compare the mean platelet values at each zidovudine dose. All comparisons were made against baseline values. Zidovudine increased platelet counts in normal and thrombocytopenic subjects. The magnitude of this effect varied depending on the baseline platelet count. Among normals, the platelet count increased from 241,000 +/- 45,000/L at baseline to 261,000 +/- 51,000/L (p less than 0.01). while receiving 600 mg/day of zidovudine. This effect was self-limited, reaching a peak by week 3. The platelet count decreased to baseline values despite increasing the dose of zidovudine to 900 or 1,200 mg/day. The platelet count further decreased to 218,000 +/- 43,000/L during the washout phase (washout vs. 1,200 mg, p less than 0.01).2+ not found to be dose related. The platelet count decreased to 101,000 +/- 34,000/L during the washout phase (washout vs. 1,200 mg/day, p less than 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)

Canada↗

Decreased half-life time of plasma von Willebrand factor collagen binding activity in essential thrombocythaemia: normalization after cytoreduction of the increased platelet count.

Patients with essential thrombocythaemia (ET) exhibit a decrease of large von Willebrand factor (VWF) multimers in plasma, which is inversely related to the platelet count. In the present study we investigated whether the decrease of large VWF multimers in plasma with increasing platelet counts is the consequence of increased turnover of large VWF multimers in vivo. To that end we measured the half-life times of endogenously released VWF:Ag and VWF:CBA (collagen binding activity) after intravenous administration of desmopressin (DDAVP) to nine ET patients and nine control subjects (N). In addition, the half-life times of VWF:Ag and VWF:CBA were also measured in four ET patients after cytoreduction of the increased platelet count to normal or nearly normal values. Estimated half-life times of VWF:Ag did not differ between ET patients and normals (11.0+/-4.0 h v 12.4+/-2.5 h, P>0.05). Estimated half-life times of VWF:CBA were significantly lower in ET patients as compared with normal individuals (6.1+/-2.0 h v 8.4+/-2.5 h, P<0.05). After cytoreduction of the increased platelet count to (nearly) normal values in all four ET patients the half-life time of VWF:CBA significantly (P=0.014) increased from 5.2+/-1.2 h to 8.7+/-2.0 h. Our data suggest that platelets may play a role in the homeostasis of circulating von Willebrand factor, which may compromise normal haemostasis at fairly increased platelet counts.

Aged↗

Alpha-interferon therapy induces improvement of platelet counts in children with chronic idiopathic thrombocytopenic purpura.

PURPOSE: To investigate alpha-interferon (IFN) therapy for children with chronic idiopathic thrombocytopenic purpura (ITP). PATIENTS AND METHODS: Patients with refractory ITP lasting more than 12 months from diagnosis were included if they had platelet counts <50 x 10(9)/L and had received no treatment during the past month. Patients received IFN (3 x 10(6) U/m2 per dose), three times per week for 4 weeks; if partial (<150 x 10(9)/L) or no response was obtained, the same dose was continued for another 8 weeks. In patients with favorable response and subsequent decrease to pre-treatment values, an additional 4 weeks of treatment could be administered. RESULTS: Fourteen patients (ages 4-20 y) receiving 17 IFN courses were included. Mean initial platelet count was 29 +/- 15 x 10(9)/L. A significant increase was achieved during 14 of 17 courses (82.4%). All but two responses were transitory, and platelets returned to initial values after IFN discontinuation (mean 44 +/- 26 days). Considering the best response achieved by each patient, we observed: 1) 10 patients who achieved a sustained improvement of platelet count throughout the treatment period, decreasing to initial values after therapy was stopped; 2) one patient who achieved platelet count >150 x 10(9)/L, remaining with normal platelets at 18 months; 3) one patient who achieved platelet count >150 x 10(9)/L, remaining with platelets between 100 and 140 x 10(9)/L at 48 months; 4) one patient who had no response; and 5) one patient in whom therapy worsened the thrombocytopenia. A mild to moderate flu-like syndrome and a moderate decrease of the absolute neutrophil count were the only side effects observed. CONCLUSION: Interferon therapy induces a significant increase of platelet count and seems to be a valid alternative therapy to attempt the achievement of prolonged remission in refractory ITP, to defer splenectomy in younger children, or to improve platelet count before planned splenectomy.

Adolescent↗

The platelet count as a predictor of variceal hemorrhage in primary biliary cirrhosis.

BACKGROUND: Variceal bleeding is a common, life-threatening complication of primary biliary cirrhosis (PBC) that remains difficult to predict. OBJECTIVE: The aim of this study was to identify whether certain biochemical and hematological parameters may be used as predictors of variceal bleeding in patients with PBC. METHODS: Cox proportional hazard regression analysis was used to test whether various prognostic factors were significantly associated with the time of first bleeding in 63 patients with proven PBC, of whom 11 had subsequent bleeding. RESULTS: Both the first available platelet count and the bilirubin level were of significant value in predicting variceal bleeding, but only the platelet count was an independent predictor of bleeding. In the group of patients who subsequently bled, there was a progressive drop in the platelet count over the follow-up period, with a proportional increase in the risk of bleeding; a platelet count below 200 x 10(9)/L was strongly associated with variceal bleeding (p < 0.001). None of the patients with platelet count above 200 x 10(9)/L bled over a total of 136 patient-years follow-up. In the group who did not bleed, no change in platelet count was identified during follow up. CONCLUSION: We conclude that the platelet count can be used as a predictor of variceal bleeding in PBC.

Aged↗

Platelet count in normal, small, and anemic fetuses.

A reference range for fetal platelet count with gestation was established from the study of samples obtained by cordocentesis from 229 pregnancies that had prenatal diagnosis. The mean platelet count increased from 187 +/- 47 x 10(9)/L at 15 weeks to 274 +/- 47 x 10(9)/L at 40 weeks' gestation. In 113 red cell-isoimmunized pregnancies, the moderately anemic fetuses were significantly thrombocythenic, whereas the severely anemic fetuses were thrombocytopenic. In 136 small-for-gestational-age fetuses the platelet count was reduced and there were significant correlations between the magnitude of the thrombocytopenia and the degree of fetal smallness, hypoxemia, and acidemia.

Anemia↗

Effect of heparin in arterial line flushing solutions on platelet count: a randomised double-blind study.

INTRODUCTION: Arterial catheters are widely used in intensive care units for continuous blood pressure monitoring and blood sampling. Studies have examined the effect of heparin on patency of arterial catheters but not on platelet counts. Heparin is a naturally occurring anticoagulant that helps prevent clotting and is given to prevent and treat thrombosis. It has many other effects, including reducing platelet counts. METHODS: A prospective, randomised, double-blind study compared the effects of heparinised and normal saline (both administered via a continuous flush device to an arterial catheter) on patients' platelet counts. All patients admitted to a mixed medical-surgical ICU between April and December 2003 were eligible for entry. Exclusion criteria were age under 16 years, known sensitivity to heparin, pre-existing coagulopathy that precluded heparin, or requirement for therapeutic heparin. Lines were inserted into radial, brachial or femoral arteries. A 500 mL bag of saline for the flush was injected with numbered syringes, containing either normal saline (NS, 35 patients) or 500 IU heparin (HS, 30 patients), and pressurised. Platelet count was assessed daily. RESULTS: Mean platelet counts were 234.6 x 10(9)/L (NS) versus 256.6 x 10(9)/L (HS). Comparison using the central limit theorem showed means were not different at the 95% confidence interval (- 77.6 to 37 x 10(9)/L). CONCLUSION: Use of heparin in normal saline as a continuous flush for an arterial catheter does not reduce platelet counts in critically ill patients.

Anticoagulants↗

Platelet count monitoring and laboratory testing for heparin-induced thrombocytopenia.

OBJECTIVE: Heparin-induced thrombocytopenia (HIT) is an antibody-mediated adverse drug reaction that paradoxically is associated with a brief but dramatically increased risk for thrombosis (transient acquired thrombophilia). The objective of this article is to provide practical recommendations for platelet count monitoring in patients receiving heparin, as well as for selection of laboratory assays to detect pathogenic HIT antibodies. STUDY SELECTION: Relevant literature that focused on frequency and timing of HIT in various clinical settings and that dealt with laboratory testing for HIT antibodies was critically appraised. DATA EXTRACTION AND SYNTHESIS: The author prepared a preliminary manuscript including recommendations that was presented to participants at the College of American Pathologists Conference XXXVI: Diagnostic Issues in Thrombophilia (November 10, 2001). Support of at least 70% of conference participants was required for recommendations to be adopted. CONCLUSIONS: The risk of immune HIT varies depending on the type of heparin (unfractionated heparin greater than low-molecular-weight heparin) and patient population (surgical greater than medical). Thus, the intensity of platelet count monitoring should be stratified depending on the clinical situation. Platelet count monitoring should focus on the period of highest risk (usually days 5 to 10 after starting heparin) and should use an appropriate platelet count baseline (generally, the highest platelet count beginning 4 days after start of heparin). However, earlier platelet count monitoring is appropriate if the patient received heparin within the past 100 days, as already circulating HIT antibodies can cause rapid-onset HIT with heparin reexposure. Although both antigen and (washed platelet) activation assays are very sensitive for detecting clinically significant HIT antibodies, activation assays have greater diagnostic specificity for clinical HIT.

Blood Platelets↗

The risk of bleeding after percutaneous liver biopsy: relation to platelet count.

We sought to define the risk of bleeding after percutaneous aspiration liver biopsy in patients with low platelet counts but otherwise normal clotting factors. Eighty-seven patients underwent liver biopsy using the Menghini 1-second technique with either a 1.6-mm or a 1.2-mm needle. Bleeding occurred in three out of 13 patients whose platelet counts at the time of biopsy were 60,000/mm3 or less, as compared to no bleeding in 74 patients with higher platelet counts (p = 0.003). A liver biopsy should not necessarily be withheld because of low platelet counts unless they are below 60,000/mm3 and cannot be raised for an adequate time during and after biopsy.

Adult↗

Plasma clot retraction assay with standard platelet count.

After classifying the phases of blood clot retraction within the mechanism of blood coagulation and the factors on which this phenomenon is depending, the authors briefly review the methods employed for its investigation. An improvement based on the determination of plasma clot retraction, performed in a plasma with a standard count of platelets (100,000/mm3) is presented. The authors have employed it for the investigation of 100 normal subjects and 25 patients with platelet dysfunctions, and have obtained very good results.

Adult↗

White blood cell and platelet counts could affect whole blood viscosity.

BACKGROUND: Blood viscosity is correlated with cerebral blood flow and cardiac output, and increased viscosity may increase the risk of thrombosis or thromboembolic events. The relationship between hematocrit and viscosity is well-known, however, the relationships between white blood cell (WBC) or platelet count and viscosity were not fully studied. The aim of the present study was to determine the influences of platelet count and WBC count on blood viscosity. METHODS: One-hundred and 13 subjects with different hemoglobin, WBC and platelet count were enrolled into the study. The variables measured included serum fibrinogen, cholesterol, triglyceride, high-density lipoprotein (HDL), low-density lipoprotein (LDL), complete blood counts including hemoglobin, hematocrit, platelet count, red blood cell (RBC) count, WBC count, whole blood and plasma viscosity. The relationships of these variables with whole blood or plasma viscosity were analyzed. RESULTS: Serum fibrinogen, cholesterol, triglyceride, HDL and LDL did not correlate with whole blood viscosity. Not only hematocrit, hemoglobin and RBC, but also WBC and platelet count, could affect whole blood viscosity. On the other hand, none of the variables could affect plasma viscosity. CONCLUSIONS: All the blood cell components, but not the plasma proteins detected above, could affect whole blood viscosity. When patients are with high leukocytosis and thrombocytosis, impaired blood viscosity should also be considered to obtain appropriate clinical management.

Adult↗