Alteration of oxide reductive and haemostatic factors in type 2 diabetics.
OBJECTIVE
To assess any pathogenic role of radical activity and haemostatic alteration in the early cardiovascular disease of microalbuminuric type 2 diabetics (non-insulin dependent).


METHODS
A selected cohort of type 2 diabetics was identified, divided according to urinary albumin excretion and compared with a healthy control group depending on some haemostatic factors and radical activity.


METHODS
All the subjects were studied as outpatients.


METHODS
Eighty diabetics and 84 healthy controls were interviewed and underwent blood tests to exclude standard cardiovascular risk factors before follow up.


METHODS
The subjects were males, age range 43-55 years, and divided according to albumin excretion (microalbuminuria > 30-200 mg L-1; normoalbuminuria < 15 mg L-1). The mean duration of diabetes referred by the patients was 9.3 years in albuminuric and 11.1 years in normoalbuminuric patients with a good control of plasma glucose level. Neither the diabetics nor the control group showed clinical evidence of renal and cardiovascular diseases.


RESULTS
Microalbuminuric patients presented elevated malondialdehyde concentration, glutathione peroxidase activity, phospholipidic fatty acid levels, fibrinogen, plasminogen activator inhibitor, tissue plasminogen activator and von Willebrand factor compared with normoalbuminuric patients and controls. More collagen was required in microalbuminuric diabetics than in normoalbuminurics and controls.


CONCLUSIONS
Our results confirm that both free radical activity and changes in haemostatic factors can be observed in type 2 diabetes and particularly in patients with albuminuria. Our very selected series with short duration, good control of diabetes and lack of clinical evidence of cardiovascular disease may suggest that these abnormalities develop earlier and may be associated with, and/or implicated in, the pathogenesis of microvascular complications which can be related to a higher and early cardiovascular morbidity and mortality rate in microalbuminuric diabetics.
Neri
S
S
Department of Internal and Emergency Medicine, School of Medicine, Catania University, Italy.
Bruno
C M
CM
Raciti
C
C
D'Angelo
G
G
D'Amico
R
R
Cristaldi
R
R
D000328:Adult; D001779:Blood Coagulation Factors / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000503:physiopathology; D005227:Fatty Acids / Q000097:blood; D005340:Fibrinogen / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000097:blood; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D010743:Phospholipids / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D010974:Platelet Aggregation; D010959:Tissue Plasminogen Activator / Q000097:blood; D014841:von Willebrand Factor / Q000378:metabolism
D001779:Blood Coagulation Factors; D005227:Fatty Acids; D010743:Phospholipids; D017395:Plasminogen Activator Inhibitor 1; D014841:von Willebrand Factor; D008315:Malondialdehyde; D005340:Fibrinogen; D005979:Glutathione Peroxidase; D010959:Tissue Plasminogen Activator