Key result
Diabetes increases platelet interaction with injured vessels and accumulation in thrombi in animal models, though its contribution to vascular complications in humans remains unclear.
This review highlights the altered behavior of platelets in diabetes, noting increased interaction with injured vessels in animal models, while emphasizing the need for further research to clarify its clinical impact on vascular complications.
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Animal models link diabetes to platelet hyperactivity at injury sites; human vascular relevance remains hypothesis-generating and requires targeted trials.
There is considerable information to indicate that when there is vessel injury, platelets can play a major role in the development of atherosclerosis and its thromboembolic complications in the non-diabetic population. Diabetes is a disease associated with an increased risk of vascular complications, but the nature of this association is unclear. Platelets from diabetic humans and animals are hypersensitive to agonists in vitro, but it is unclear if this hypersensitivity persists in vivo. Platelets survival and turnover in the circulation have been used as indicators of platelet behaviour in vivo, but platelet survival measurements do not necessarily correlate with platelet sensitivity in vitro and these measurements may be too insensitive to reflect platelet turnover on injured vessels or in thrombi, unless there is extensive vascular disease. Studies in rats and rabbits indicate that diabetes causes increased platelet interaction with experimentally-injured vessels and accumulation in thrombi. It is unclear, however, whether this altered behaviour of platelets at the injured vessel surface reflects changes in the platelets or in the vessel wall and whether it contributes to the increased risk for vascular complications in diabetic patients.
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P.D. Winocour (1994) conducted a review in Diabetes. Diabetes vs. Non-diabetic population was evaluated. Diabetes increases platelet interaction with injured vessels and accumulation in thrombi in animal models, though its contribution to vascular complications in humans remains unclear.
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