scholarly journals THE STATE OF PLATELET HEMOSTASIS IN PATIENTS WITH HYPERTENSIVE DISEASE COMBINED WITH NON-ALCOHOLIC FAT LIVER DISEASE

2021 ◽  
Vol 17 (2) ◽  
pp. 47-52
Author(s):  
N.M. Bazhenova
Keyword(s):  
Risk Factors ◽  
Platelet Count ◽  
Liver Disease ◽  
Platelet Aggregation ◽  
Hepatic Steatosis ◽  
Mean Platelet Volume ◽  
The State ◽  
Platelet Volume ◽  
Spontaneous Aggregation ◽  
Spontaneous Platelet Aggregation

Relevance. Platelet activation and platelet aggregation are central processes in the pathophysiology of coronary heart disease and thrombosis. The relationship between cardiovascular morbidity and mortality varies with the presence of other concomitant cardiovascular risk factors. Objective. To determine the state of platelet hemostasis in patients with essential hypertension (HT), with concomitant non-alcoholic fatty liver disease (NAFLD). Materials and methods. 152 patients were examined: 72 men and 80 women. Three groups were identified: I - 46 patients with stage II HT without concomitant NAFLD, II - 54 patients with NAFLD without HT, group III - 52 patients with HT and concomitant NAFLD.  A study of total platelet count, mean platelet volume (MPV), platelet distribution width (PDW), platelet count (PCT) and spontaneous platelet aggregation was performed. Results. The level of mean platelet volume (MPV) in both groups of patients with hepatic steatosis exceeded control values equally - by 6%, both in patients with NAFLD (p<0.001) and in NAFLD with concomitant hypertension (p<0.01). In patients of the NAFLD group and hypertension, the relative width of the platelet distribution by volume (PDW) had high values - 2% (p<0.05) higher than in the control cohort, and 2.4% (p<0.05) than in patients with isolated HT. An increase in the degree of spontaneous aggregation in patients of all surveyed groups compared to controls. So in patients with HT II stage. spontaneous aggregation increased 2.2 times (p<0.001), while in both groups of patients with hepatic steatosis, the increase in spontaneous platelet activity was twice as high: in patients with NAFLD - 4.3 times (p<0.001), in patients with HT II stage. and concomitant NAFLD - 4.1 times (p<0.001). Conclusion. NAFLD is accompanied by an increased in MPV, the size of which correlates with their functional activity. In patients with isolated NAFLD, a statistically significant increase in spontaneous platelet aggregation is also observed, which allows considering NAFLD as one of the risk factors for thrombophilic changes in the primary hemostasis.

Disturbance Of Platelet Function In The Nephrotic Syndrome

1981 ◽  
Author(s):  
E Walter ◽  
D Deppermann ◽  
K Andrassy ◽  
E Weber
Keyword(s):  
Nephrotic Syndrome ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Kidney Function ◽  
Platelet Function ◽  
Platelet Adhesiveness ◽  
Spontaneous Aggregation ◽  
Spontaneous Platelet Aggregation ◽  
Platelet Functions

Thromboembolic phenomena often (30 %) complicate the nephrotic syndrome. It was therefor investigated, wether disturbed platelet functions play a role in this disease.28 normals, 34 patients with nephrotic syndrome and 18 of them with impaired kidney function were tested. In 20 patients the measurements were repeated after administration of aspirin plus dipyridamo1e.Patients with nephrotic syndrome showed in comparison to normals the following changes: 1. increased platelet count (p < 0.01), 2. enhanced platelet adhesiveness (Wright-test: p < 0.001), 3. increased spontaneous aggregation (PAT I: p < 0.001; PAT III: p < 0.01), 4. enhanced PF 4-activity (heparin neutralisation: p < 0.001), 5. elevated β TG-levels only in impaired kidney function. There was no difference in the reaction of platelets against ADP as well as collagen. The changes in platelet function correlated with the severity of the nephrotic syndrome (proteinurea, hypalbuminaemia, hyperlipo- proteinaemia). After aspirin plus dipyridamole administration spontaneous platelet aggregation and adhesiveness were normalized.There is a disturbance of platelet function in patients with nephrotic syndrome, which can be reversed with antiaggregating agents.

“Spontaneous” Platelet Aggregation in Whole Blood in Diabetic and Non Diabetic Survivors of Acute Myocardial Infarction

1993 ◽  
Vol 70 (06) ◽  
pp. 0932-0936 ◽  
Author(s):  
Rosaire P Gray ◽  
Timothy J Hendra ◽  
David L H Patterson ◽  
John S Yudkin
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Whole Blood ◽  
Significant Difference ◽  
Platelet Thrombi ◽  
Spontaneous Aggregation ◽  
Spontaneous Platelet Aggregation ◽  
Normal Controls

SummaryThere is increasing evidence that platelet thrombi play an important role in the pathogenesis of acute myocardial infarction (AMI). We compared “spontaneous” platelet aggregation in whole blood in 17 non-diabetic and 12 diabetic subjects on admission with AML There was no significant difference in the fall in platelet count between the two groups, expressed as platelets remaining (75.2 ± 7.9% vs 77.3 ± 6.9% at 10 min, 66.6 ± 8.9% vs 68.5 ± 6.3% at 20 min, 63.5 ± 8.2% vs 64.9 ± 6.7% at 30 min and 59.4 ± 10.3% vs 61.3 ± 7.6% at 60 min). The rate of “spontaneous” aggregation was increased in subjects with evidence of heart failure on admission compared to those without (59.9 ± 7.9% vs 66.2 ± 6.6% at 30 min [p = 0.05] and 55.4 ± 9.6% vs 63.1 ± 7.7% at 60 min [p = 0.04]). There was no correlation between the fall in platelet count and admission plasma glucose, glycated heaemoglobin or peak aspartate aminotransferase. The subjects studied on admission with AMI had greater rates of “spontaneous” aggregation than 8 subjects studied between 6 and 12 months after acute myocardial infarction (75.9 ± 7.4% vs 85.8 ± 5.4% at 10 min; p = 0.001 and 64.3 ± 7.5% vs 75.0 ± 7.8% at 30 min; p = 0.006) and compared to normal controls (90.7 ± 4.4% at 10 min; p <0.001 and 83.4 ± 6.5 at 30 min; p <0.001). This study provides evidence of increased “spontaneous” platelet aggregation in subjects admitted with acute myocardial infarction but no difference between diabetic and non-diabetic subjects was observed.

A Sex Difference in the Effect of Aspirin on “Spontaneous” Platelet Aggregation in Whole Blood

1983 ◽  
Vol 50 (04) ◽  
pp. 773-774 ◽  
Author(s):  
M J G Harrison ◽  
E Weisblatt
Keyword(s):  
Clinical Trials ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Sex Difference ◽  
Whole Blood ◽  
Antithrombotic Agent ◽  
Male And Female ◽  
Spontaneous Aggregation ◽  
Spontaneous Platelet Aggregation

SummaryPlatelet aggregation can be measured in whole blood by monitoring the fall in single platelet count in an electronic platelet counter. The aggregation that occurs when whole blood is stirred in a small cuvette (“spontaneous aggregation”) or upon the addition of collagen has been studied in citrated whole blood from male and female volunteers. Aspirin 40 μg ml/1 inhibited aggregation induced by collagen in both sexes but spontaneous aggregation was only affected by aspirin in males. These results may help explain the sex difference apparent in the results of some clinical trials of aspirin as an antithrombotic agent.

Effects of Thalidomide on Platelets: Possible Causes of Hypercoagulability and Thrombocytopenia.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3969-3969
Author(s):  
Holavanahalli Keshava-Prasad ◽  
Varsha Kaushal ◽  
Paulette Mehta
Keyword(s):  
Bone Marrow ◽  
Platelet Aggregation ◽  
Control Subject ◽  
Adhesion Molecules ◽  
Mean Platelet Volume ◽  
Molecular Mechanisms ◽  
Platelet Volume ◽  
Expression Of Genes ◽  
Spontaneous Platelet Aggregation

Abstract Thalidomide(Thal) is often used in hematological disorders and can predispose to thrombosis and rarely cause thrombocytopenia. The mechanisms of these effects are not well known. In order to evaluate these mechanisms, we studied a control subject and patients on thal. including 1 with thal-induced thrombocytopenia(TIT). We evaluated platelet counts, mean platelet volume, and bone marrow megakaryocyte reserve at sequential points, and also performed in vitro studies using platelet rich plasma (PRP). Platelets were studied before and after incubation with varying concentrations of thal from 10 to 20 μg/ml. Spontaneous platelet aggregation was evaluated and remaining PRP was used for studying the expression of genes for adhesion molecules, using cDNA Q-Series Adhesion molecules and ECM array from SuperArray Bioscience Corporation (Frederick, MD). RNA was extracted from untreated and in vitro thal-treated platelets from subjects in the study using mini RNAeasy kit (Qiagen, Valencia, CA) and then, reverse transcription, probe synthesis, hybridization, washes, data acquisition and analyses were performed as suggested in the supplier’s protocol. We compared expression of various genes normalized to the intensity of the ß-actin gene. The patient with TIT was a 59-year-old white male who was on thal maintenance after chemotherapy and tandem autologous stem cell transplants. Platelet count dropped from 148,000/μL to 19,000/μL within 7 days of increasing the dose from 100 to 200 mg daily. Mean platelet volume (MPV) increased from 6.4 to 9.5fL. His Bone marrow showed increased megakaryocytes without myeloma cells. There were no other causes for his thrombocytopenia, suggesting thal-induced platelet destruction, perhaps immune-mediated. In order to evaluate molecular mechanisms of thal-induced thrombocytopenia and other effects of thal on platelet function which may cause thalidomide-induced hypercoagulabilty, we studied genes controlling adhesion molecules in this patient (A) at various times during his recovery from TIT, in another thal-treated myeloma patient without thrombocytopenia (B), and in a normal control (C). Platelets of patient A showed markedly enhanced spontaneous aggregation after incubation with even low concentrations of thal. Repeat testing after cessation of thal therapy no longer demonstrated this phenomenon. No spontaneous platelet aggregation occurred in patients without TIT (B), or the control subject (C). In the control subject, there was no demonstrable expression of any adhesion molecule genes; in contrast, genes for integrin alpha10 (IGTA10), VCAM and MMP15 were expressed in platelets of both patients receiving thal (A, B), but decreased in patient A after recovery from TIT. Incubation with thal increased the gene for IGTA10 by up to 12- fold in platelets of patients on thal (A, B). Expression appeared to be dose dependent (3–4 fold with 10 μg/ml, and 12 fold with 20 μg/ml of thal). Patient B had high baseline expression of the gene for IGTA10, which did not increase on exposure to thal. VCAM and MMP 15 were also expressed on platelets of patients on thal (A, B), and further increased with exposure to in vitro thal. These results suggest that TIT is probably mediated by peripheral destruction, perhaps on immune basis, and is transient. Moreover, myeloma patients on thal may have increased expression of genes regulating some aspects of cell adhesion which may contribute to TIT or to hypercoagulability. Further studies are ongoing to verify these findings in more patients, and to delineate the mechanisms.

Acute and Chronic Changes in Platelet Volume and Count After Cardiopulmonary Bypass Induced Thrombocytopenia in Man

1987 ◽  
Vol 57 (01) ◽  
pp. 55-58 ◽  
Author(s):  
J F Martin ◽  
T D Daniel ◽  
E A Trowbridge
Keyword(s):  
Platelet Count ◽  
Mean Platelet Volume ◽  
Artery Bypass ◽  
Bypass Graft ◽  
Control Group ◽  
Artery Bypass Graft ◽  
Platelet Volume ◽  
Young Males ◽  
The Mean

SummaryPatients undergoing surgery for coronary artery bypass graft or heart valve replacement had their platelet count and mean volume measured pre-operatively, immediately post-operatively and serially for up to 48 days after the surgical procedure. The mean pre-operative platelet count of 1.95 ± 0.11 × 1011/1 (n = 26) fell significantly to 1.35 ± 0.09 × 1011/1 immediately post-operatively (p <0.001) (n = 22), without a significant alteration in the mean platelet volume. The average platelet count rose to a maximum of 5.07 ± 0.66 × 1011/1 between days 14 and 17 after surgery while the average mean platelet volume fell from preparative and post-operative values of 7.25 ± 0.14 and 7.20 ± 0.14 fl respectively to a minimum of 6.16 ± 0.16 fl by day 20. Seven patients were followed for 32 days or longer after the operation. By this time they had achieved steady state thrombopoiesis and their average platelet count was 2.44 ± 0.33 × 1011/1, significantly higher than the pre-operative value (p <0.05), while their average mean platelet volume was 6.63 ± 0.21 fl, significantly lower than before surgery (p <0.001). The pre-operative values for the platelet volume and counts of these patients were significantly different from a control group of 32 young males, while the chronic post-operative values were not. These long term changes in platelet volume and count may reflect changes in the thrombopoietic control system secondary to the corrective surgery.

The Effect of Dimethyl Sulfoxide on In Vitro Platelet Function

1976 ◽  
Vol 36 (01) ◽  
pp. 221-229 ◽  
Author(s):  
Charles A. Schiffer ◽  
Caroline L. Whitaker ◽  
Morton Schmukler ◽  
Joseph Aisner ◽  
Steven L. Hilbert
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Dimethyl Sulfoxide ◽  
Platelet Function ◽  
Platelet Volume ◽  
Short Term ◽  
Platelet Factor ◽  
Short Term Exposure ◽  
Structural Abnormalities

SummaryAlthough dimethyl sulfoxide (DMSO) has been used extensively as a cryopreservative for platelets there are few studies dealing with the effect of DMSO on platelet function. Using techniques similar to those employed in platelet cryopreservation platelets were incubated with final concentrations of 2-10% DMSO at 25° C. After exposure to 5 and 10% DMSO platelets remained discoid and electron micrographs revealed no structural abnormalities. There was no significant change in platelet count. In terms of injury to platelet membranes, there was no increased availability of platelet factor-3 or leakage of nucleotides, 5 hydroxytryptamine (5HT) or glycosidases with final DMSO concentrations of 2.5, 5 and 10% DMSO. Thrombin stimulated nucleotide and 5HT release was reduced by 10% DMSO. Impairment of thrombin induced glycosidase release was noted at lower DMSO concentrations and was dose related. Similarly, aggregation to ADP was progressively impaired at DMSO concentrations from 1-5% and was dose related. After the platelets exposed to DMSO were washed, however, aggregation and release returned to control values. Platelet aggregation by epinephrine was also inhibited by DMSO and this could not be corrected by washing the platelets. DMSO-plasma solutions are hypertonic but only minimal increases in platelet volume (at 10% DMSO) could be detected. Shrinkage of platelets was seen with hypertonic solutions of sodium chloride or sucrose suggesting that the rapid transmembrane passage of DMSO prevented significant shifts of water. These studies demonstrate that there are minimal irreversible alterations in in vitro platelet function after short-term exposure to DMSO.

Evaluation of platelet count and mean platelet volume in type 2 diabetes mellitus

2020 ◽  
Vol 14 (2) ◽  
pp. 34-37
Author(s):  
Priya Bhatt ◽  
◽  
Jignasa Bhalodia ◽  
Mehul Patel ◽  
◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Platelet Count ◽  
Mean Platelet Volume ◽  
Platelet Volume
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