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.

Reduced platelet function in subarachnoid hemorrhage

1986 ◽  
Vol 64 (6) ◽  
pp. 907-910 ◽  
Author(s):  
Sotirios A. Tsementzis ◽  
Jaswinder S. Gill ◽  
Edward R. Hitchcock ◽  
Jennifer A. Hartley ◽  
Surinder K. Gill ◽  
...  
Keyword(s):  
Platelet Count ◽  
Subarachnoid Hemorrhage ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Maximum Rate ◽  
Adenosine Diphosphate ◽  
Platelet Adhesiveness ◽  
Content Type ◽  
Aneurysmal Rupture ◽  
Fine Print

✓ The hypothesis that abnormalities of platelet function may relate to the occurrence or recurrence of subarachnoid hemorrhage (SAH) has been examined. Seventy patients with SAH and 65 control individuals were studied. The adenosine diphosphate (ADP) threshold for secondary platelet aggregation was significantly higher in the SAH group than in the controls. In tests using 4.0 µg/ml ADP, the percent platelet aggregation (at 2 minutes) and the maximum rate of platelet aggregation (over 20 seconds) were significantly lower in the SAH patients. There was no difference in total platelet count between the two groups. Platelet adhesiveness was lower in the SAH patients when compared to controls. Circulating microaggregates did not differ between the two groups. The results indicate that reduced platelet function does relate to SAH and may either contribute to aneurysmal rupture in cases of SAH or be a consequence of it.

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.

“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.

Oral Contraceptives and Platelet Function

1972 ◽  
Vol 28 (02) ◽  
pp. 213-220 ◽  
Author(s):  
L Mettler ◽  
Meseck B. Selchow
Keyword(s):  
Platelet Count ◽  
Oral Contraceptive ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Oral Contraceptives ◽  
Platelet Adhesiveness ◽  
Predisposing Factor ◽  
Platelet Counts ◽  
Contraceptive Therapy ◽  
Oral Contraceptive Therapy

SummaryPlatelet function was studied in women receiving two oral oestrogen-progestagen compounds (Neogynon and Noracyclin-22). Platelet count, adhesiveness, spreading, aggregation (PAT) and thromboelastography (TEG) were studied twice monthly for six months in 186 cycles. Platelet counts in rotated plasma were decreased in both groups. A significant increase in non-spread platelets was found in the Neogynon group only. PAT-degrees were significantly increased in both groups. Platelet adhesiveness and thromboelastographic measurements were not affected. Increased platelet aggregation during oral contraceptive therapy is regarded as a predisposing factor to thrombosis.

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.

Follow-Up of Clinical Manifestations and Platelet Function Test in Patients with Essential Thrombocythemia on Anagrelide Treatment.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4970-4970
Author(s):  
Patricia S. Vassallu ◽  
Nora P. Goette ◽  
Ana C. Glembotsky ◽  
Paula G. Heller ◽  
Laura I. Kornblihtt ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Gastrointestinal Bleeding ◽  
Platelet Function ◽  
Essential Thrombocythemia ◽  
Clinical Manifestations ◽  
Spontaneous Aggregation ◽  
Spontaneous Platelet Aggregation ◽  
Hematological Remission

Abstract Introduccion: Patients with essential thrombocythemia (ET) may have abnormalities of platelet function (PF), the most frecuently are reduced response to epinephrine and ADP-induced aggregation and spontaneous aggregation. Anagrelide (A) has a phosphodiesterase inhibitor activity and may inhibit PF. Therefore, we evaluated the follow-up of clinical manifestations (CM) and the PF in a group of 42 ET patients before treatment and on hematological remission. Materials and methods: 42 ET patients (33/9, F/M) who meet de PVSG criteria, were studied before treatment with A and on hematological remission. The CM were grouped into thrombosis (T), hemorrhages (H), microcirculation disturbances (MD) and combined (C), that included H plus MD or H plus T. Platelet function tests were perfomed with different agonists such as epinephrine, ADP, ristocetine, arachidonic acid and bovine vWF. Results: are shown in Table I. Abbreviations: T≠ (4 TIAs, 1 stroke, 1 AMI), H* (1 upper gastrointestinal bleeding, 4 minor hemorrhages) C± (1 mesenteric, portal and splenic vein thrombosis plus minor hemorrhage, 4 minor hemorrhages plus MCD), Tψ (1 TIA, 1 stroke), H§ (1 lower gastrointestinal bleeding) C† (1 AIT plus minor hemorrhage). During hematological remission spontaneous platelet aggregation disappeared in all patients except one. Abnormal epinephrine response desappeared in 16 patients, was not corrected in 10 and this abnormality appeared in 2 whose response were previously normal. Abnormal ADP response disappeared in 4 cases during treatment and this abnormality was found in 5 previously normal cases. No correlation was found between spontaneous platelet aggregation and clinical manifestations p= NS. No correlation was found between both epinephrine and ADP response and hemorrhages. No significant abnormalities were found in the response to arachidonic acid, ristocetin, and bovine vWF before or during treatment with anagrelide. Conclusions: In this group of ET patients platelet function was not affected by the phosphodiesterase inhibibitor activity of anagrelide. Similarly bleeding manifestations were not worsen during this therapy. As previously shown spontaneous platelet aggregation desappeared in all but one patient. We have not yet an explanation for the increased microvascular disturbances during treatment. Table I Pre treatment On treatment Clinical Manifestations (42 patients ) Asymptomatic 16 18 Thrombosis 6≠ 2ψ Hemorrhages 5* 4§ Microvascular disturbances 10 17 Combined 5± 1† Platelet function Spontaneous aggregation 17/42 1/41 Abnormal epinephrine response 26/41 12/42 Abnormal ADP response 17/41 9/41

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.

Effects of Halothane on Platelet Function

1980 ◽  
Vol 44 (03) ◽  
pp. 143-145 ◽  
Author(s):  
J Dalsgaard-Nielsen ◽  
J Gormsen
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Platelet Rich Plasma ◽  
Human Platelets ◽  
Halothane Anaesthesia ◽  
Inhibition Of Platelet Aggregation ◽  
Transient Impairment ◽  
High Concentrations ◽  
Uptake And Release ◽  
Platelet Functions

SummaryHuman platelets in platelet rich plasma (PRP) incubated at 37° C with 0.3–2% halothane for 5–10 min lost the ability to aggregate with ADP, epinephrine and collagen.At the same time uptake and release of 14C-serotonin was inhibited. When halothane supply was removed, platelet functions rapidly returned to normal. However, after high concentrations of halothane, the inhibition of platelet aggregation was irreversible or only partially reversible.The results suggest that halothane anaesthesia produces a transient impairment of platelet function.

scholarly journals Influence of Hepatocellular Carcinoma on Platelet Aggregation in Cirrhosis

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1150
Author(s):  
Alberto Zanetto ◽  
Marco Senzolo ◽  
Elena Campello ◽  
Cristiana Bulato ◽  
Sabrina Gavasso ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Adenosine Diphosphate ◽  
Compensated Cirrhosis ◽  
Impedance Aggregometry ◽  
Child Class ◽  
Von Willebrand ◽  
Willebrand Factor

Hyper-functional platelets are being proposed as a potential therapeutic target in multiple cancers. Whether this can be considered in patients with cirrhosis and hepatocellular carcinoma (HCC) is unknown as their platelet function has not yet been investigated. We evaluated platelet function in cirrhosis patients with HCC. Patients with cirrhosis with and without HCC were prospectively recruited. Platelet aggregation, a marker of platelet function, was assessed by impedance aggregometry with adenosine diphosphate (ADP), arachidonic acid (ASPI), and thrombin (TRAP) stimulation. Plasmatic levels of Von Willebrand factor antigen (VWF) were also determined. One-hundred patients were recruited (50 cirrhotics with and 50 without HCC). Cirrhosis severity by Child class and platelet count were comparable between cirrhotics with and without HCC. Cirrhotics with HCC had higher ADP- (45 vs. 28; p < 0.001), ASPI- (47 vs. 28; p < 0.001), and TRAP- (85 vs. 75; p = 0.01) induced platelet aggregation than cirrhotics without HCC, all indicative of platelet hyper-function. The relatively increased platelet aggregation in patients with HCC was confirmed after adjusting the analysis for platelet count/severity of thrombocytopenia. Levels of VWF were higher in patients with vs. without HCC (348 vs. 267; p = 0.006), particularly in compensated cirrhosis. In patients with cirrhosis, HCC is associated with increased platelet aggregation and higher VWF. The clinical implications of these findings deserve further investigation.

Enhanced platelet aggregation and activation under conditions of hypothermia

2007 ◽  
Vol 98 (12) ◽  
pp. 1266-1275 ◽  
Author(s):  
Ruben Xavier ◽  
Ann White ◽  
Susan Fox ◽  
Robert Wilcox ◽  
Stan Heptinstall
Keyword(s):  
Cardiac Surgery ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Whole Blood ◽  
Platelet Rich Plasma ◽  
Baseline Levels ◽  
Spontaneous Aggregation ◽  
High Concentrations ◽  
Induced Aggregation ◽  
P2y12 Antagonist

SummaryThe effects on platelet function of temperatures attained during hypothermia used in cardiac surgery are controversial. Here we have performed studies on platelet aggregation in whole blood and platelet-rich plasma after stimulation with a range of concentrations of ADP, TRAP, U46619 and PAF at both 28°C and 37°C. Spontaneous aggregation was also measured after addition of saline alone. In citrated blood, spontaneous aggregation was markedly enhanced at 28°C compared with 37°C. Aggregation induced by ADP was also enhanced. Similar results were obtained in hirudinised blood. There was no spontaneous aggregation in PRP but ADP-induced aggregation was enhanced at 28°C. The P2Y12 antagonist AR-C69931 inhibited all spontaneous aggregation at 28°C and reduced all ADP-induced aggregation responses to small, reversible responses. Aspirin had no effect. Aggregation was also enhanced at 28°C compared with 37°C with low but not high concentrations of TRAP and U46619. PAF-induced aggregation was maximal at all concentrations when measured at 28°C, but reversal of aggregation was seen at 37°C. Baseline levels of platelet CD62P and CD63 were significantly enhanced at 28°C compared with 37°C. Expression was significantly increased at 28°C after stimulation with ADP, PAF and TRAP but not after stimulation with U46619. Overall, our results demonstrate an enhancement of platelet function at 28°C compared with 37°C, particularly in the presence of ADP.

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