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Thromb Haemost 1973; 30(01): 123-132
DOI: 10.1055/s-0038-1649108
Original Article
Schattauer GmbH

Fibrinocoagulopathy in Maturity Onset Diabetes Mellitus and Atherosclerosis[*]

R.N Banerjee
1   Department of Haematology & Nuclear Medicine, Safdarjang Hospital, New Delhi-16; India.
,
A.L Sahni
1   Department of Haematology & Nuclear Medicine, Safdarjang Hospital, New Delhi-16; India.
,
Vijay Kumar
1   Department of Haematology & Nuclear Medicine, Safdarjang Hospital, New Delhi-16; India.
› Author Affiliations
Further Information

Publication History

Received for publication 16 November 1972

Accepted for publication 25 June 1973

Publication Date:
30 June 2018 (online)

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Summary

Immunofluorescent demonstrations of platelet-free fibrin deposit in the micro and macro-vascular lesions of maturity onset diabetes mellitus and atherosclerosis by earlier workers called for investigations of fibrino-coagulopathy in the two disorders. The present investigation included the determinations of plasma thrombin time (PTCT), fibrinogen concentration (FC), plasma fibrinogen half life (PFT ½) and plasma fibrinogen degradation product (FDP) in (i) the subjects of the two age-onset disorders and their consanguinous family members, and (ii) juvenile diabetes.

The assays were carried out by standard methods. 125Iodine labelled human fibrinogen was used for half life studies.

In a study of 525 subjects, very highly significant (p <0.001) reduction in PTCT, FC and PFT ½ with a very highly significant (p < 0.001) elevation of FDP were observed in the patients of the two age onset disorders. The results were normal in juvenile diabetes.

The study provides convincing evidence of a ‘state of slow consumptive fibrino-coagulopathy’ in the subjects and their siblings with the observed haemostatic defect likely being due to genetically determined Anti-thrombin III deficiency. This observation stimulates a unitary concept of a primary fibrinopathic vascular aetio-pathogenesis, with selective localisation in the macro and microvascular compartment being responsible for the clinical syndromes of ischaemic and metabolic alterations in athersclerosis and maturity onset diabetes mellitus respectively.

* This study was presented in part at the III Congress of International Society of Thrombosis and Haemostasis, Washington DC, USA, August, 1972.


 

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