Collagen-induced platelet aggregation and collagen glycosyl-transferase activity in diabetic patients

1977 ◽  
Vol 11 (6) ◽  
pp. 847-858 ◽  
Author(s):  
E. Roux ◽  
G. Cherbit ◽  
F. Regnault
1972 ◽  
Vol 27 (01) ◽  
pp. 114-120 ◽  
Author(s):  
A. A Hassanein ◽  
Th. A El-Garf ◽  
Z El-Baz

SummaryADP-induced platelet aggregation and calcium-induced platelet aggregation tests were studied in 14 diabetic patients in the fasting state and half an hour after an intravenous injection of 0.1 unit insulin/kg body weight. Platelet disaggregation was significantly diminished as compared to a normal control group, and their results were negatively correlated with the corresponding serum cholesterol levels. Insulin caused significant diminution in the ADP-induced platelet aggregation as a result of rapid onset of aggregation and disaggregation. There was also a significant increase in platelet disaggregation. In the calcium-induced platelet aggregation test, there was a significant shortening of the aggregation time, its duration, and the clotting time. The optical density fall due to platelet aggregation showed a significant increase. Insulin may have a role in correcting platelet disaggregation possibly through improvement in the intracellular enzymatic activity.


1979 ◽  
Author(s):  
J. García-Conde ◽  
J.A. Amado ◽  
J. Merino ◽  
I. Benet

We have studied platelet aggregation induced by 0,5 mM. Araquidonic acid (AA) addition to platelet-rich-plasma (PRP) from 21 insulin treated diabetic patients and in 21 non-diabetic controls. The velocity of aggregation was significantly higher in the diabetic group. There was no differences in the velocity of aggregation in patients with or without retinopathy.The incubation of PRP of normal subjects at 37- during 5 minutes with 5,8 10-4 M. Imidazole changed the pattern of aggregation: The velocity of aggregation was slower and appeared a wave of disaggregation. Imida zole had not effect on aggregation in the diabetic group. This data add support to the findings published by COLWLLL showing that platelets from diabetics have hyperactive AA metabolism. Prostaglandin I2 (PGI2) obtained from rat aorta shows an inhibitory effect on ADP or AA induced aggregation. This effect is less marked in diabetic PRP than in PRP of normal controls. PGI2 release in platelet-poor-plasma from diabetics is normal. This can represent a resistance ot diabetic platelet to the anti aggregating effect of PGI 2. A similar finding was also appreciated with the PGE1 in three out of six patients so tar stu


1981 ◽  
Author(s):  
A I Woods ◽  
S S Meschengieser ◽  
N M Sutton ◽  
M A Lazzari

Abnormalities in platelet function tests have already been described in diabetic patients reflecting platelet hyperreactivity. An attempt to determine which of the tests seemed to be more affected in the diabetic population was done in a group of 34 diabetic patients (20 men and 14 women, age range 15-76). The tests performed included assay of Ristocetin Cofactor (McFarlane et al.) circulating platelet aggregates (CPA) (Wu-Hoak) and platelet aggregation induced by ADP in low concentration (0.6 x 10-6M) and Bovine Factor VIII (0.001 U/ml). In matched controls only 3.5% had a positive aggregation induced by Bovine F VIII and with ADP (0.6 x 10-6M% ) the extent of maximum aggregation was 30%.In 15 of the 34 patients (44%) aggregation induced by ADP in high dilution was greater than 50% and this was the test more frequently affected. The level of Ristocetin Cofactor was increased (>160%) in 12 of 34 patients (35%) and aggregation induced by BF VIII was positive also in 12 patients (35%). The detection of CPA was positive in 9 patients (26%). Two patients had spontaneous platelet aggregation and in them all the other tests performed were also positive. Three patients had 3 of the tests altered, and 11 patients only had 2 affected tests.The assay more affected was the ADP induced aggregation followed by the Ristocetin Cofactor levels and BF VIII induced aggregation. The test less affected was the CPA. A correlation with clinical data will be mentioned.


Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4504-4504
Author(s):  
Roger C Munro ◽  
Lisa J Wakeman ◽  
Saad Al-Ismail

Abstract A 58 year old lady with Metabolic Syndrome of 10 years duration presented with post-menopausal PV bleeding, haematuria, occasional epistaxis and ecchymoses. Prescribed medication which had remained unchanged for the preceding two years included daily doses (mgms) of Aspirin (150), Atenelol (50), Metformin (500 × 3), Bendroflumethiazide (2.5), Losartan (50) and Simvastatin (20). Intravenous urogram, cystoscopy, cytological examination of urine sediment, hysteroscopy, a cervical scan and endometrial biopsies showed neither evidence of overt pathology nor any physiological indication for the cause of haematuria or PV bleeding. Tests for urinary infection were negative. Apart from the raised blood glucose (9.1: NR 3.3 – 6.0 mmol/L), the biochemistry profile including liver enzymes, coagulation profile and blood count were normal (Platelets = 265 × 109/L). Bleeding episodes were observed after commencement of a daily intake of 7–8 cups of green tea for a period of six months. Green tea intake was self-instigated in response to reported amelioration of risk factors associated with Metabolic Syndrome (reduction in LDL cholesterol and serum triglyceride levels; elevation of protective HDL; potent antioxidant activity; ACE inhibition and promotion of glucose metabolism). Hot water extract of green tea specifically inhibits platelet adhesion and lowers sub-maximal platelet aggregation and prolongs the lag time in a dose-dependent manner. Previous fractionation studies of these hot water extracts, has revealed that the tea catechins (tannins) actively inhibit thromboxane A2 production and that ester-type catechins are more effective than free-type catechins. One of the ester-type catechins, epigallocatechin gallate (EGCG), suppresses thrombin and collagen-induced platelet aggregation completely at a concentration of 0.2 mg/ml. EGCG also inhibits aggregation by a mechanism which differs from that of aspirin by inhibiting platelet activating factor (PAF). The IC50 values of EGCG and aspirin indicate that their potencies are comparable. Bleeding symptoms ceased two weeks after the patient stopped drinking green tea. Our assumption of the causal effect of green tea on anomalous bleeding in this patient needs to be confirmed by structured platelet function tests in both aspirinised and non-aspirinised patients. Since inhibition of cyclo-oxygenase is an additional anti-thrombotic property of aspirin which differs from that of green tea, diabetic patients taking prophylactic low-dose aspirin should continue to do so and potentially beneficial ingestion of green tea should not be considered without consultation with an appropriate health professional in view of its synergistic potential on the effect of aspirin and the associated haemorrhagic risks.


2005 ◽  
Vol 51 (9) ◽  
pp. 1673-1682 ◽  
Author(s):  
Anna Michno ◽  
Anna Raszeja-Specht ◽  
Agnieszka Jankowska-Kulawy ◽  
Tadeusz Pawełczyk ◽  
Andrzej Szutowicz

Abstract Background: Excessive blood platelet activity contributes to vascular complications in diabetic persons. Increased acetyl-CoA in platelets from diabetic persons has been suggested to be a cause of this hyperactivity. We therefore investigated whether l-carnitine, which up-regulates metabolism of acetyl-CoA in muscles and brain, may affect platelet function in healthy and diabetic individuals. Methods: We obtained platelets from healthy and diabetic persons and measured acetyl-CoA concentrations, malonyl dialdehyde (MDA) synthesis, and platelet aggregation in the absence and presence of l-carnitine. Activities of selected enzymes involved in glucose and acetyl-CoA metabolism were also assessed. Results: Fasting glucose, fructosamine, and hemoglobin A1c were present in significantly higher amounts in the blood of diabetic patients than in healthy individuals. Activities of carnitine acetyltransferase, glucose-6-phosphate dehydrogenase, oxoglutarate dehydrogenase, and fatty acid synthase were 17%–62% higher in platelets from diabetic patients. Mitochondrial acetyl-CoA was increased by 98% in platelets from diabetic patients, MDA synthesis was increased by 73%, and platelet aggregation by 60%. l-Carnitine had no or only a slight effect on these indices in platelets from healthy individuals, but in platelets from diabetic patients, l-carnitine caused a 99% increase in acetyl-CoA in the cytoplasmic compartment along with increases in MDA synthesis and platelet aggregation. Conclusions: Excessive platelet activity in persons with diabetes may result from increased acetyl-CoA, which apparently increases synthesis of lipid activators of platelet function. l-Carnitine may aggravate platelet hyperactivity in diabetic persons by increasing the provision of surplus acetyl-CoA to the cytoplasmic compartment.


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