1274 PLATELET ABNORMALITIES IN DIABETIC PERIPHERAL NEUROPATHY W. R. TIMPERLEY N. R. PORTER F. E. PRESTON
B. C. O’MALLEY J. D. WARD
Departments of Medicine, Hæmatology, and Neuropathology, Royal Infirmary, Sheffield S6 3DA. Abnormal platelet function has been demonstrated in 20 patients with diabetic peripheral neuropathy. The results are compared to those obtained from 19 matched diabetic patients with no clinical evidence of complications and 20 matched normal control subjects. Platelets from patients with diabetic neuropathy showed an increased sensitivity to the aggregating agents adenosine diphosphate and adrenaline. Spontaneous platelet aggregation was demonstrated in both groups of diabetic patients.
Summary
Introduction PERIPHERAL neuropathy is a common and distressing complication of diabetes mellitus, but despite intensive research the precise pathogenesis remains obscure. Currently, the main argument centres round the relative roles of metabolic’-6 and vascular 7-12 factors. In support of the vascular theory, we have recently demonstrated microvascular thrombi in sural-nerve biopsies in a group of patients with diabetic neuropathy. 13 Detailed histological examination of the thrombi revealed clumps of granular material suggestive of platelet aggregates. In view of this observation, a detailed study of platelet function was carried out in the same group of patients.
Patients and Methods Three groups of patients
were
studied:
Group 1.- 20 patients with symptoms and signs of diabetic neuropathy. Group II: 19 diabetic patients without clinical evidence of neuropathy or other complications of diabetes. Group 111.- 20 normal, non-diabetic control subjects.
temperature and tested within 30 minutes of collection. Aggregation studies were performed according to the method described by Born22 using an E.E.L. ’Aggregometer’ and’Telsec’ flat-bed recorder. The aggregating agents used were adenosine diphosphate (A.D.P.) (Sigma Chemical Co.) and adrenaline. Serially increasing concentrations of each agent were added to the platelet-rich plasma until a biphasic response was recorded indicating the platelet-release reaction. The sensitivity of the platelets was expressed in terms of the threshold concentration of the aggregating agent required to room
produce a biphasic response. Spontaneous platelet aggretation was detected by continous stirring of the platelet-rich plasma for 10 to 12 minutes. Statistics.-The results were analysed statistically by a nonparametric method-the Wilcoxon rank sum test. One-way analysis of variance and the two-sample t test were inappropriate in the presence of non-normally distributed data.
Results
A.D.P.-induced platelet aggregation.-Platelets from patients in group i were extremely sensitive to low concentrations of A.D.P. (fig. la). The mean threshold A.D.P. concentration of this group was significantly less than that of either group II (P
B. C. O’MALLEY J. D. WARD
Departments of Medicine, Hæmatology, and Neuropathology, Royal Infirmary, Sheffield S6 3DA. Abnormal platelet function has been demonstrated in 20 patients with diabetic peripheral neuropathy. The results are compared to those obtained from 19 matched diabetic patients with no clinical evidence of complications and 20 matched normal control subjects. Platelets from patients with diabetic neuropathy showed an increased sensitivity to the aggregating agents adenosine diphosphate and adrenaline. Spontaneous platelet aggregation was demonstrated in both groups of diabetic patients.
Summary
Introduction PERIPHERAL neuropathy is a common and distressing complication of diabetes mellitus, but despite intensive research the precise pathogenesis remains obscure. Currently, the main argument centres round the relative roles of metabolic’-6 and vascular 7-12 factors. In support of the vascular theory, we have recently demonstrated microvascular thrombi in sural-nerve biopsies in a group of patients with diabetic neuropathy. 13 Detailed histological examination of the thrombi revealed clumps of granular material suggestive of platelet aggregates. In view of this observation, a detailed study of platelet function was carried out in the same group of patients.
Patients and Methods Three groups of patients
were
studied:
Group 1.- 20 patients with symptoms and signs of diabetic neuropathy. Group II: 19 diabetic patients without clinical evidence of neuropathy or other complications of diabetes. Group 111.- 20 normal, non-diabetic control subjects.
temperature and tested within 30 minutes of collection. Aggregation studies were performed according to the method described by Born22 using an E.E.L. ’Aggregometer’ and’Telsec’ flat-bed recorder. The aggregating agents used were adenosine diphosphate (A.D.P.) (Sigma Chemical Co.) and adrenaline. Serially increasing concentrations of each agent were added to the platelet-rich plasma until a biphasic response was recorded indicating the platelet-release reaction. The sensitivity of the platelets was expressed in terms of the threshold concentration of the aggregating agent required to room
produce a biphasic response. Spontaneous platelet aggretation was detected by continous stirring of the platelet-rich plasma for 10 to 12 minutes. Statistics.-The results were analysed statistically by a nonparametric method-the Wilcoxon rank sum test. One-way analysis of variance and the two-sample t test were inappropriate in the presence of non-normally distributed data.
Results
A.D.P.-induced platelet aggregation.-Platelets from patients in group i were extremely sensitive to low concentrations of A.D.P. (fig. la). The mean threshold A.D.P. concentration of this group was significantly less than that of either group II (P
