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Clinical and Applied Thrombosis/Hemostasis, Vol. 11, No. 1, 49-53 (2005)
DOI: 10.1177/107602960501100105

Myocardial Infarction and Arterial Thrombosis in Severe (Homozygous) FXII Deficiency: No Apparent Causative Relation

A. Girolami

University of Padua Medical School, Department of Medical and Surgical Sciences, Second Chair of Medicine, Padua, Italy

M. Morello

University of Padua Medical School, Department of Medical and Surgical Sciences, Second Chair of Medicine, Padua, Italy

B. Girolami

University of Padua Medical School, Department of Medical and Surgical Sciences, Second Chair of Medicine, Padua, Italy

A. M. Lombardi

University of Padua Medical School, Department of Medical and Surgical Sciences, Second Chair of Medicine, Padua, Italy

C. Bertolo

University of Padua Medical School, Department of Medical and Surgical Sciences, Second Chair of Medicine, Padua, Italy

Twenty-one patients (12 female and 9 male) with severe (homozygous) factor XII (FXII) deficiency and 58 (32 female and 26 male) with heterozygous FXII deficiency were observed for an average 16.2 years. No patient with homozygous FXII deficiency experienced myocardial infarction or any other arterial thrombosis. The same was true for heterozygotes. The cases of FXII deficiency and arterial thrombosis reported in the literature were evaluated. In every instance, associated risk factors were present that could justify the arterial thrombosis. Dyslipidemia, hypertension, smoking, and diabetes mellitus were the most frequent findings. The examination of the few papers that dealt with the prevalence of arterial thrombosis in patients with severe FXII deficiency showed that only 1 patient of 61 experienced myocardial infarction. In conclusion, it seems that the role of FXII deficiency in the pathogenesis of arterial thrombosis is minor.

Key Words: Coagulation • Arterial thrombosis • Factor XII deficiency • Contact phase


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