No abstract

Angiotensin-converting enzyme (ACE) is secreted by the vascular endothelium and serum activity may reflect endothelial damage. A study of 48 insulin-dependent diabetics, 15 with and 33 without evidence of diabetic retinopathy and 41 non-diabetic controls was performed. ACE activity was significantly elevated in the diabetics compared with controls (mean +/- SD 46 +/- 14 vs 35 +/- 9 U/l, p less than 0.001) (units in micromoles substrate converted/min/l serum). This elevation was more marked in diabetics with such evidence of microangiopathy as retinopathy or raised albumin excretion rate (AER) (51 +/- 14 U/l, p less than 0.0001), and also in those with raised AER alone (47.2 +/- 15 U/l, p less than 0.002). Patients with both raised AER and retinopathy had significantly higher ACE activities than those with no complications (53 +/- 15 vs 41.2 +/- 15 U/l, p less than 0.05). No correlation was found with glycosylated haemoglobin or smoking habits. We conclude that mean serum angiotensin converting enzyme activity is increased in insulin-dependent diabetes, particularly in those with evidence of microangiopathy and this may reflect microvascular damage.

No abstract

Abnormalities of platelet aggregation and coagulation have been reported in insulin dependent diabetes mellitus (IDDM), although there is controversy concerning their relationship to microangiopathy. We have studied platelet function and haemostasis in 55 patients with IDDM, 23 without, 14 with mild (background retinopathy) and 18 with severe (proliferative retinopathy, or background retinopathy plus proteinuria) complications. Studies were done on 2 occasions 8 weeks apart and the results compared with 28 control subjects. There was evidence of increased in vivo platelet aggregation in the diabetic group v controls shown by raised values of beta-thromboglobulin (61 +/- 42, mean +/- SD, v 18 +/- 14 micrograms/ml, p less than 0.001), platelet factor 4 (62 +/- 76 v 14 +/- 11 micrograms/ml, p less than 0.01), and platelet micro-aggregates (20 +/- 16 v 12 +/- 11%, p less than 0.01). There was no significant difference in fibrinogen and fibrinopeptide A levels, nor in 'in vitro' tests of platelet aggregation between the groups. Dilute whole blood clot lysis time was increased in the diabetic group v controls (6.4 +/- 2.6 v 4.8 +/- 0.5 hours, respectively, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Both diabetic nephropathy and retinopathy result from microangiopathic processes although there is controversy as to whether this is true for neuropathy. Increased platelet aggregation has been reported in diabetics with nephropathy and retinopathy. The presence of increased platelet aggregation in diabetics with neuropathy could be due to the other coincident microvascular complications. We have, therefore, studied in vitro platelet aggregation in 10 diabetics with chronic symptomatic neuropathy but no other complications, 10 with neuropathy and severe retinopathy, 17 with retinopathy alone, and 23 diabetics with no complications. Increased platelet aggregation to adenosine diphosphate (ADP) and adrenaline was seen in diabetics with neuropathy alone (peak responses 85.0 +/- 5.5% and 82.9 +/- 6.2%, respectively) when compared with uncomplicated diabetics (peak response 74.9 +/- 10.1%, p less than 0.005, and 74.3 +/- 12.5%, p less than 0.01, respectively). The increased platelet aggregation in the patients with neuropathy alone was similar to that found in the diabetics with severe retinopathy. We conclude that increased platelet aggregation is associated with established microangiopathy and is also present in otherwise uncomplicated patients with neuropathy, and this may have pathogenic and therapeutic implications.