Enhanced Platelet Release Reaction in Insulin-Dependent and Insulin-Independent Diabetic Patients

Davı̀, Giovanni; Rini, G. B.; Averna, Maurizio; Novo, Salvatore; Fede, Gaetana Di; Mattina, Alessandro; Notarbartoló, A; Strano, A

doi:10.1159/000214683

Cited by 12 publications

(3 citation statements)

References 8 publications

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“…An increased platelet aggregation has been reported in Type 1 (insulin-dependent) diabetic patients with poor metabolic control [34]. This phenomenon is accompanied by an increase in the circulating levels of some indices of platelet activation such as fl-thromboglobulin [35] and platelet factor 4 [36]. The results on the production of thromboxane are, on the other hand, conflicting; an increase was reported in Type 1 and Type 2 diabetic patients, but seems to be affected by metabolic control only in the latter group [37,38].…”

Section: Plateletsmentioning

confidence: 99%

Coagulation activation in diabetes mellitus: the role of hyperglycaemia and therapeutic prospects

1993

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Numerous studies have shown that coagulation abnormalities occur in the course of diabetes mellitus, resulting in a state of thrombophilia. These observations are supported by epidemiological studies which demonstrate that thromboembolic events are more likely to occur in diabetic patients. The coagulation abnormalities observed in diabetic patients seem to be caused by the hyperglycaemia, which also constitutes the distinguishing feature of this disease. These data are also supported by in vitro studies which demonstrate how glucose can directly determine alterations in the coagulation system. The abnormalities observed involve all stages of coagulation, affecting both thrombus formation and its inhibition, fibrinolysis, platelet and endothelial function. The final result is an imbalance between thrombus formation and dissolution, favouring the former. Hyperglycaemia probably determines the onset of these abnormalities through three mechanisms which are, respectively, non-enzymatic glycation, the development of increased oxidative stress and a decrease in the levels of heparan sulphate. The first seems to affect the functionality of key molecules of coagulation in a negative sense. Oxidative stress constitutes an important pro-thrombotic stimulus, while the decrease in heparan sulphate determines a reduction in antithrombotic defenses. Good metabolic control could play a key role in controlling the coagulation irregularities in diabetes. However, considering the difficulties in achieving such an objective, it is possible that the use of drugs may represent a valid alternative. In fact, several drugs exist which are of potential interest. It is, however, necessary to perform long-term studies which demonstrate unequivocably that by controlling the coagulation abnormalities in diabetic patients, prolongation of life is possible.

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Section: Plateletsmentioning

confidence: 99%

Coagulation activation in diabetes mellitus: the role of hyperglycaemia and therapeutic prospects

1993

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“…Exaggerated increases in platelet [Ca2+Ii, phosphoinositide turnover, intracellular Ca2+ mobilization and protein phosphorylation have been described in patients with NIDDM (26,86,87,88,157,189,190,261,375,409). Recently, enhanced platelet [Ca2+], response to low density lipoprotein (LDL) cholesterol have been observed in NIDDM patients with and without hypertension (375).…”

Section: Picitelet Adhesion and Platelet Aggregationmentioning

confidence: 99%

Diabetes Mellitus and Hypertension, Emerging Therapeutic Perspectives

Sowers

Epstein

1995

Cardiovascular Drug Reviews

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“…From the results of this study, it appears that platelet aggregation and arachidonic acid metabolism are stimulated in psoriatics with active disease. Hyperaggregatory platelets have also been reported in patients with diabetes mellitus [5] and in cigarette smokers [16]. Furthermore, the 12-lipoxygenase activity of platelets can be stimulated by cigarette smoking [4].…”

Section: Discussionmentioning

confidence: 99%

Increased aggregation and arachidonic acid transformation by psoriatic platelets: evidence that platelet-derived 12-hydroxy-eicosatetraenoic acid increases keratinocyte DNA synthesis in vitro

Kragballe

Fallon

1986

Arch Dermatol Res

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Certain arachidonic metabolites may play a pathogenic role in psoriasis. Platelets are rich sources of 12-hydroxy-eicosatetraenoic acid (12-HETE) and thromboxane A2, mediators of skin inflammation and platelet aggregation, respectively. We have studied untreated psoriatic patients without a history of diabetes mellitus and smoking. In psoriatics, platelet aggregation elicited by thrombin, ADP, and ristocetin was significantly enhanced as compared with healthy adult volunteers. Enhancement of platelet aggregation was detected in patients with both minimal and widespread disease. The formation of 12-hydroxy-5,8,10-heptadecatrienoic acid (HHT), a cyclooxygenase product, and 12-HETE, a 12-lipoxygenase product, was increased in psoriatics with widespread disease but not in those with minimal disease. Formation of 12-HETE was stimulated to a higher degree (125%) than HHT (98%) in psoriasis (P less than 0.05). Addition of platelet-derived 12-HETE to cultured human epidermal keratinocytes resulted in a stimulation of the DNA synthesis (68% at 10(-7) M). These data suggest that platelet activation occurs in psoriasis, and that release of inflammatory and mitogenic compounds by activated platelets may play a role in the pathophysiology of psoriasis. Whether enhanced platelet aggregation in psoriasis is associated with occlusive vascular disease needs further investigation.

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Enhanced Platelet Release Reaction in Insulin-Dependent and Insulin-Independent Diabetic Patients

Cited by 12 publications

References 8 publications

Coagulation activation in diabetes mellitus: the role of hyperglycaemia and therapeutic prospects

Coagulation activation in diabetes mellitus: the role of hyperglycaemia and therapeutic prospects

Diabetes Mellitus and Hypertension, Emerging Therapeutic Perspectives

Increased aggregation and arachidonic acid transformation by psoriatic platelets: evidence that platelet-derived 12-hydroxy-eicosatetraenoic acid increases keratinocyte DNA synthesis in vitro

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