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A 7-year-old gypsy girl developed venous and arterial thromboembolism. In this case AT III deficiency of hereditary nature was demonstrated as the cause of thromboembolism.
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Life-long symptoms of venous thromboembolism were present throughout five generations in a large Italian kindred. Eight out of the 22 tested members of the family had reduced plasma levels of antithrombin III (AT III), the main physiological inhibitor of blood coagulation. Three of them, aged 2-28 years, but no thrombotic manifestations. AT III deficiency, which was hitherto thought to be very rare in this country, appeared to be related to a reduced synthesis of the protein without any qualitative abnormality. This view is supported by the concomitant reduction of AT III levels as demonstrated by biological and immunological assays, as well as by a normal pattern of the protein in double-crossed immunoelectrophoresis with and without heparin added to the agarose gel. Long-term treatment with oral anticoagulants appeared to prevent further thromboembolic episodes in two patients, even though plasma AT III levels remained unchanged.
Plasma antithrombin III activity was studied in 22 patients with prostatic cancer who were on estrogen therapy. Normal plasma antithrombin III activity varies between 0.80 and 1.40 U. per ml. A loading dose of 15 mg. diethylstilbestrol daily resulted in a marked decrease in plasma antithrombin III activity (mean 0.24 U. per ml.). Patients with the lower end of normal range of pre-treatment plasma antithrombin III activity may suffer acquired antithrombin III deficiency and, thus, a concomitantly increased risk of thromboembolic complications as a result of estrogen treatment. Patients on maintenance therapy of approximately 1 mg. daily appear to have normal plasma antithrombin III levels. The results obtained suggest that plasma antithrombin III activity should be monitored before and during estrogen therapy in patients with prostatic cancer.
The authors report the case of a young woman aged 29, mother of 2 children, presenting a post-phlebitic syndrome with hyperalgic capillaritic ulcer, a 10 year history of serious thrombophlebitic episodes with repeated pulmonary embolism despite heparin therapy, and reports of similar episodes in the family, some of which proved fatal. Haematological study showed a clear diminution in progressive antithrombin activity. A discussion follows on the clinical and haematological aspects of this constitutional and familial deficiency, which has been known since 1965 (Egelberg). The relative rarity of this condition should not prevent the routine search (by combined functional, immunological and chromogenic estimation) in the presence of repeated thrombosis, and when the thrombosis is biologically resistant to heparin : in such cases, the indication for long term treatment with vitamin K antagonists is undeniable.
We describe a 43-year-old male patient with congenital antithrombin III deficiency requiring hemodialysis due to extension of venous thrombus from recurrent deep vein thrombosis. During dialysis with adequate heparinization, the patient often revealed clot formation in the extracorporeal circuit resulting in unexpected discontinuation of dialysis. When either a combination of antithrombin III concentrate + heparin or the newly developed synthetic antithrombin preparation, MD805, was administered during dialysis, he could be uneventfully dialyzed with either of the two regimens.
A kindred with a history of multiple thromboses was studied for coagulant abnormalities. A deficiency of serum antithrombin III was found in approximately half of the 13 family members by either coagulant or immunologic assay. No clear relationship between antithrombin III deficiency and a history of thrombosis was present. Platelet antithrombin assays were also studied in the same subjects. Ten of the 13 members were deficient. None of the remaining three had a history of thrombosis. On the basis of these findings, the hypothesis is proposed that in some cases familial hypercoagulability may be due to a platelet antithrombin deficiency and that the serum antithrombin III deficiency in some cases is a secondary rather than a primary effect.
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A significant decrease of plasma antithrombin III (AT III) levels, measured with four different biological and immunological methods, was found in 8 of 11 members of a Sicilian family (family DM) and in 3 of 14 members of a northern Italian family (family A). Different behaviour after oral anticoagulant treatment with acenocoumarin was seen in 2 long-term treated subjects. The propositus of family DM, who had had a long history of recurrent thrombosis, did not show any increase of AT III levels. A significant increase was, on the contrary, observed in the propositus of family A, who had suffered a recent thrombosis in a branch of the inferior mesenteric vein.
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Authors report a case of newborn with thrombosis of the pulmonary artery, probably caused by a maternal deficit of antithrombin III. Deficit of antithrombin III (AT III) as the possible cause of thrombosis is discussed.
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