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Paradoxical Platelet Behaviour in Diabetic Ketoacidosis
Author(s) -
Campbell R. R.,
Foster K. J.,
Stirling C.,
Mundy D.,
Reckless J. P. D.
Publication year - 1986
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.1986.tb00729.x
Subject(s) - medicine , platelet , diabetic ketoacidosis , ketoacidosis , endocrinology , prostacyclin , diabetes mellitus , adenosine diphosphate , platelet factor 4 , platelet aggregation , type 1 diabetes
Thrombotic events may occur in patients who present with severe uncontrolled diabetes or with diabetic coma. As a possible explanation for this, platelet function was investigated at presentation with diabetic ketoacidosis and during treatment in 10 patients. Concentrations of the platelet‐specific proteins, platelet factor 4 (PF4) and betathromboglobulin (betaTG) were elevated and fell towards normal with treatment. Despite evidence of increased aggregation in vivo , platelets from subjects with ketoacidosis were insensitive to adenosine 5′‐diphosphate (ADP), sensitivity increasing with correction of ketoacidosis. Platelets from ketoacidotic diabetics were initially insensitive to the anti‐aggregatory action of prostacyclin (PGI 2 ) and became normal with treatment. Initial blood glucose concentrations correlated with log 10 ADP concentrations ( r = 0.72, p < 0.01) and with log 10 PGI 2 ID 50 (the PGI 2 concentration required to half‐inhibit ADP‐induced aggregation) ( r = 0.66, p < 0.025). Glucose concentrations throughout the 2‐week study period correlated with all log 10 ADP concentrations ( r = 0.32, p < 0.005) and all log 10 PGI 2 ID 50 concentrations ( r = 0.51, p < 0.001). The decrease in ADP sensitivity in ketoacidosis, paradoxical in view of the evidence of increased in vivo platelet aggregation, may result from an acquired platelet storage pool deficiency.