Thromb Haemost 1985; 54(02): 415-417
DOI: 10.1055/s-0038-1657862
Original Article
Schattauer GmbH Stuttgart

Antithrombin III Activity and Concentration in Diabetes Mellitus

G M Patrassi
The Institute of Medical Semeiotics, Second Chair of Medicine, University of Padua Medical School Padua, Italy
,
R Picchinenna
The Institute of Medical Semeiotics, Second Chair of Medicine, University of Padua Medical School Padua, Italy
,
R Vettor
The Institute of Medical Semeiotics, Second Chair of Medicine, University of Padua Medical School Padua, Italy
,
G Cappellato
The Institute of Medical Semeiotics, Second Chair of Medicine, University of Padua Medical School Padua, Italy
,
D Coccarielli
The Institute of Medical Semeiotics, Second Chair of Medicine, University of Padua Medical School Padua, Italy
,
A Girolami
The Institute of Medical Semeiotics, Second Chair of Medicine, University of Padua Medical School Padua, Italy
› Author Affiliations
Further Information

Publication History

Received 13 February 1985

Accepted 24 April 1985

Publication Date:
18 July 2018 (online)

Summary

Antithrombin III (AT III) levels have been reported to be low, normal, and high in diabetes mellitus. Furthermore, a dicrepancy between AT III activity and antigen concentration was reported. We have evaluated the behaviour of AT III activity and antigen level both in type 1 and type 2 diabetes, either in uncontrolled or in well controlled patients. AT III activity and antigen levels showed values similar to normal. No difference was seen between type 1 and type 2 diabetes. Similar results were observed in the group of well controlled diabetic patients. AT III activity and antigen did not correlate with blood glucose and glycosylated haemoglobin (HbA1). No difference was observed between AT III activity and antigen levels in any group. Therefore the hypercoagulable state found in diabetes mellitus does not depend on AT III modifications. A discrepancy between AT III activity and antigen was not confirmed. A dysantithrombinaemia, explained on the basis of an inactivation of protein glycosylation in diabetes mellitus has not been confirmed.

 
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