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At least 253 records · Page 14Linked to original sources
PubMed1978

Familial antithrombin III deficiency as pathogenesis of deep venous thrombosis.

A family including 18 members with decreased antithrombin III (AT III), measured with both a biological and an immunochemical method, is described. The pattern found on crossed immunoelectrophoresis, using heparin in the agarose in the first run, was normal, though the peaks were low. This suggests decreased synthesis of a normal protein in the affected members. AT III deficiency occurred in both the paternal and the maternal branch, of the above 18 persons had had at least one thromboembolic episode. Some of the episodes had been precipitated by the presence or occurrence of some predisposing event or circumstance. This suggests the possible occurrence of a gene making some of the maternal family members more susceptible to certain trigger factors, such as surgery, infection, pregnancy, and the puerperium. The mode of inheritance filled all the criteria for autosomal dominant transmission. Prophylactic treatment, preferably oral anticoagulants and/or dextran, is recommended for all persons with a low AT III concentration in any situation known to increase the predisposition to thrombosis. The effect of heparin in these patients is impaired since the heparin co-factor, which is identical with AT III, is lowered.

Adolescent↗
PubMed2006

Vena cava superior syndrome developing in a dialysis patient with antithrombin III deficiency following temporary catheterization.

Despite being widely reported in patients with neoplasms, vena cava superior (VCS) syndrome linked to thrombosis is a major catheter complication that can be encountered during the use of the hemodialysis catheter. Antithrombin III (AT-III), responsible for a large part of thrombin inactivation capacity in plasma, is the most powerful inhibitor of the thrombosis process. This report describes a case of VCS syndrome developing two weeks following the extraction of a right-sided subclavian catheter in a patient transferred from peritoneal dialysis to hemodialysis for one week due to leakage. The patient presented complaining of swelling and pain in the right arm. At Doppler examination, total thrombosis was observed in the subclavian and internal jugular vein. At advanced examinations due to lack of response to heparin and clinical worsening, VCS and AT-III deficiency were determined. Following thrombolytic therapy with streptokinase, AT-III levels were raised by the administration of plasma, and clinical and radiological stabilization was established by continuing heparin and continuous oral anticoagulant therapy.

Antithrombin III Deficiency↗
PubMed1994

Homozygous or compound heterozygous qualitative antithrombin III deficiency.

A male patient of 24 years who had experienced thrombotic episodes since the age of 15 displayed an unusually low antithrombin III (AT III) activity measured as heparin cofactor (13% of the normal), while a similarly decreased value (16% of normal) was found in a 26 year old brother who had suffered from thrombotic events since the age of 12 years. AT III heparin cofactor activities were close to 50% of normal in the father, mother, another brother and a sister, none of whom had experienced thrombotic episodes. Since all available members of the family, including the patient, displayed near normal AT III antigen levels (73-85%) normal total progressive antithrombin activities (92-110%) as assessed by the thrombin agarose diffusion technique and normal total progressive anti-Xa activities, the propositus and his brother could be considered to be homozygotes or compound heterozygotes for a qualitative familial AT III deficiency probably caused by an abnormality of the heparin binding site. Molecular techniques would be required to elucidate the precise mutation giving rise to the deficiency.

Adolescent↗