Why the study?
Does insulin-dependent diabetes alter platelet sensitivity to inhibition by PGI2 and PGE1?
Does insulin-dependent diabetes alter platelet sensitivity to inhibition by PGI2 and PGE1?
Insulin-dependent diabetic patients exhibit reduced platelet sensitivity to inhibitory prostanoids, likely due to an impaired c-AMP generating system, which may contribute to their increased thrombotic risk.
May heighten thrombotic risk in IDDM; hypothesis-generating for c-AMP-targeted strategies, pending prospective validation.
In insulin-dependent diabetics (IDDM) and peripheral occlusive arterial disease (POAD), inhibition of platelet aggregation (PA) by PGI(2) and PGE(1) was reduced (p <0.02) compared with non-diabetics and POAD as well as with healthy subjects at a similar extent of PA (in the 3 groups). c-AMP content in resting platelets of IDDM and chronic renal failure was decreased (mean ± SD in pmo1/2.5 × 10(8) platelets): 5.3 ± 1.1 compared with the content in healthy subjects: 8.0 ± 1.12 and P< 0.012. Moreover, c-AMP content in PGE(1)-stimulated platelets was also reduced in these patients. Our results indicate that diabetic patients are characteristically less sensitive to inhibition by the 2 prostanoids, presumably through attenuated activity of the c-AMP generating system.
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Zahavi et al. (1995) studied this question.
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