Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2009) 20 P396

Belarussian Medical Academy of Post-Graduate Education, Minsk, Belarus.


Diabetes mellitus and abdominal obesity are considered to be risk factors for venous and arterial thrombosis, but till now it still remains unclear, what factor is a primary in the genesis of these abnormalities: fibrinolysis dysfunction, vascular endothelium impairment or pathology of the platelet homeostasis component.

Forty-two persons included in the study were primary divided into 3 groups: 1 group – nearly healthy (10 males, 12 females), 2 group – overweight with body mass index (BMI) more then 25 kg/m2 (9 males, 11 females), 3 group – patients with diabetes mellitus (10 males, 6 females).

Platelet adhesive and aggregative activity had been evaluated in a quantity method with the help of aggregometer device SOLAR AP 2110, ADP «Renam», Russia had been used as an aggregation activator. Disease compensation stipend in patients with Diabetes Mellitus had been determined according to the level of the glycated hemoglobin that at the average was 7.0±1.5 (12–5.2%).

Through the evaluation of the platelet adhesive and aggregative activity (Table 1) significant evaluation of the aggregation level in overweight and diabetes groups had been detected (P<0.05) in comparison with a control group, the longest time to reach the maximum aggregation level had been seen in diabetes group (P<0.01). Aggregation level in overweight and diabetic patients does not differ significantly.

Table 1
Homeostasis parametersNearly healthyOverweightPI–IIDiabetesPI–IIIPII–III
Aggregation level (%)53.02±10.8962.62±11.96<0.0564.1±15.6<0.05>0.05
Aggregation speed (30), %/min49.5±13.161.2±8.1<0.0546.4±16.44>0.05<0.05
Aggregation time (min)4.14±0744.07±0.6>0.055.12±0.88<0.05<0.01

These dates are proving the fact, that one of the reasons for cardiovascular disease developing in association with diabetes mellitus and abdominal obesity is abnormality of the pathology of the platelet homeostasis component.

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