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Fibrinolysis in diabetes mellitus. Role of overweight and hypertriglyceridemia
Insights
Overweight and high triglycerides significantly delay blood clot lysis time in diabetics, suggesting overweight and lipid metabolism disturbances, not diabetes itself, cause impaired clot breakdown. Enhanced fibrin crosslinking contributes to this delay.
Area of Science:
- Cardiovascular Science
- Metabolic Disorders
- Hematology
Background:
- Diabetes mellitus is associated with increased risk of thrombotic events.
- Impaired fibrinolysis, the breakdown of blood clots, may contribute to this risk.
- Factors influencing fibrinolysis in diabetic patients require further investigation.
Purpose of the Study:
- To investigate variations in dilute blood clot lysis time (DBCLT) in diabetic patients.
- To examine the influence of insulin dependency, body weight, serum lipids, and vascular complications on DBCLT.
- To explore the role of fibrin crosslinking in delayed clot lysis.
Main Methods:
- DBCLT was measured in 103 diabetic patients and 76 normal weight, normolipidemic controls.
- Patients were categorized by body weight, serum lipid levels, and presence of diabetic vascular diseases.
- In vitro experiments using p-chlormercuribenzoate (PCMB) to inhibit plasma factor XIII were conducted.
Main Results:
- DBCLT was significantly longer in overweight diabetic patients compared to normal weight diabetics and controls.
- Hypertriglyceridemic diabetic patients exhibited longer DBCLT than normolipidemic diabetics.
- Higher levels of fibrinolytic inhibitors were found in patients with diabetic small vessel disease.
Conclusions:
- Deficient thrombolysis in diabetics is primarily linked to overweight and lipid metabolism disturbances, rather than diabetes or its vascular complications.
- Enhanced fibrin crosslinking appears to be a contributing factor to delayed blood clot lysis in overweight diabetics.
Abstract:
The variations of dilute blood clot lysis time (DBCLT) in 103 diabetic patients were investigated in terms of insulin dependency, body weight, serum lipids and presence of diabetic vascular diseases. The results showed that DBCLT was significantly longer in the 34 overweight diabetic patients (437 +/- 68 min) than in the 69 diabetics at or below the ideal body weight (240 +/- 28 min) or in the 76 normalipidemic normal weight control subjects (253 +/- 12 min). DBCLT was also longer in the hypertrigliceridemic diabetic patients than in the normolipidemic ones. The mean lysis time was similar in diabetic patients with and without retinopathy. However, a higher level of fibrinolytic inhibitors was found in patients with diabetic small vessel disease. In vitro inhibition of plasma factor XIII by p-chlormercuribenzoate (PCMB) caused an acceleration of DBCLT and the differences between lysis time in the overweight diabetics and in the controls were attenuated. These results suggested that deficient thrombolysis is rather due to overweight and to disturbances of lipid metabolism than to diabets and/or its vascular complications and that enhanced fibrin crosslinking is at least partially responsible for delayed clot lysis.