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At least 199 records · Page 11Linked to original sources
PubMed1985

Acquired factor X and antithrombin III deficiency in a patient with primary amyloidosis and nephrotic syndrome.

A 45-year-old man with primary amyloidosis was initially seen with nephrotic syndrome. Factor X was found to be 5% and antithrombin III (AT III) 45% of normal plasma values. During an 11-month period, despite severe factor X deficiency, the patient did not have any bleeding complications. He developed progressive renal failure and AT III levels increased to normal, at which time he developed severe bleeding complications. These findings suggest a protective role of AT III deficiency against bleeding in a patient with severe factor X deficiency.

Amyloidosis↗
PubMed2003

The prevalence of protein C, protein S, and antithrombin III deficiency in non-APS/SLE Chinese adults with noncardiac cerebral ischemia.

Protein C (PC), protein S (PS), and antithrombin III (AT-III) are vital thrombin antagonists in circulation. However, the prevalence of these natural inhibitors for cerebral ischemia is barely mentioned in the Chinese population. The prevalence of PC, PS, and AT-III deficiency in Chinese adults with cerebral ischemia is reported. The study subjects were free of antiphospholipid antibody syndrome or systemic lupus erythematosus. Cardiac, liver, and renal function were normal. An overall rate of thrombophilia was 27%. PS deficiency was the most common disorder, followed by PC with PS and PC deficiency. There was only one patient with AT-III deficiency. No gender was specific for thrombophilia. However, PS deficiency was predilected in young adults. A positive correlation between PC and AT-III was achieved in patients with a normal PC activity but not PC deficiency. There was no correlation between AT-III or PS. The odds ratios of PC and PS were 5.29 and 2.86, respectively. Accordingly, an inability for thrombin antagonization by the PC/PS axis may relate to the occurrence of cerebral ischemia in the Chinese population. AT-III seems to display a minor role only.

Adult↗
PubMed1990

[Antithrombin III deficiency as a cause of unexplained thrombosis recurrences in vascular surgery].

Antithrombin deficit may be a cause of spontaneous vascular thrombosis or rethrombosis, following vascular operations, which remain inexplicable to clinicians. Three cases are reported of A III deficit, in two of whom vascular rethrombosis resulted from considerable fall in A III activity, measured by kinetic method and in the third patient this severe postoperative complication was averted. The importance of measuring A III in patients with arterial insufficiency in whom vascular reconstruction is forthcoming is discussed. The substituting therapy in patients with this pathology and arterial reconstruction is given due consideration. Substituting therapy is recommended as means for avoiding rethrombosis in patients with proven A III deficit, as well as a method of treatment, together with heparin therapy, after successful reoperation of such patients.

Aged↗
PubMed2002

[Cerebrovascular accidents with familial antithrombin III deficiency--gene analysis study].

We report two cases of the cerebral infarction with familial antithrombin III type I deficiency. Case 1 is a 47-year-old woman presenting deep cerebral vein thrombosis. Case 2 is a 20-year-old man presenting the top of the basilar syndrome. Beside them, substantial number of members had cerebral infarction in this pedigree. We measured AT III activity and quantity for 18 persons in this pedigree. As a consequence, 6 of 18 persons in this pedigree had AT III type I deficiency. Analysis of PCR products of AT III gene derived from the case 1's leukocyte DNA revealed a novel frame shift insertion was demonstrated as mutant alleles with 4-base CTTT in nt 2,420 or nt 2,424 in exon 2 domain on the AT III gene. AT III type I deficiency caused by frame shift insertion has been reported only twelve pedigrees. This is the first case report of AT III type I deficiency caused by frame shift insertion in Japan.

Adult↗
PubMed1980

Plasminogen and antithrombin III deficiencies in the childhood nephrotic syndrome associated with plasminogenuria and antithrombinuria.

Three of four patients with the childhood nephrotic syndrome were found to have low plasma plasminogen concentrations; all four had low plasma antithrombin III concentrations. In the two patients who were tested, urinary concentrations of these proteins exceeded the plasma concentrations. As the urinary losses of plasminogen and antithrombin III decreased over the course of illness, the plasma concentrations of antithrombin III and plasminogen rose. One patient had multiple thromboembolic episodes. We conclude the deficiencies of antithrombin III and plasminogen, probably secondary to urinary excretion of these proteins, may contribute to the thrombotic diathesis associated with nephrotic syndrome.

Adolescent↗
PubMedDate not supplied

Prevalence of antithrombin III deficiency in blood donors selected for personal or familial history of venous thrombosis.

Antithrombin III (ATIII) was measured using a functional assay in 692 (6.7%) out of 10,332 blood donors selected for their personal or familial history of venous thrombosis. Three subjects with low levels of the protein were observed. Thus, the prevalence of ATIII deficiency was of 0.43%, corresponding to a prevalence of 0.03% in the general population. On the basis of family studies and of clinical and laboratory investigations, inherited ATIII deficiency was excluded and reduced levels of the inhibitor were attributed to an impaired liver function, despite normal blood coagulation tests. Therefore, in this study inherited ATIII deficiency cases were not found; however, acquired ATIII deficiency associated with normal clotting tests might represent a rare but definite risk factor for thrombosis.

Antithrombin III Deficiency↗
PubMed1983

Heparin cofactor activities in a family with hereditary antithrombin III deficiency: evidence for a second heparin cofactor in human plasma.

Plasma levels of antithrombin-heparin cofactor, determined by heparin-dependent antithrombin assay, and antithrombin III antigen were measured in 22 members of a large kindred predisposed to venous thrombosis. While 11 members had reduced plasma levels of both antithrombin-heparin cofactor and antithrombin III antigen, the levels of antithrombin-heparin cofactor were always greater than the levels of antithrombin III antigen: 66% (+/- 7%) and 49% (+/- 5%) of normal plasma, respectively. Pooled normal plasma and plasma from one of the affected family members (60% antithrombin-heparin cofactor and 47% antithrombin III antigen) were fractionated by heparin-agarose affinity chromatography. Antithrombin-heparin cofactor, which eluted from heparin-agarose with buffer containing 0.4 M NaCl and did not cross-react with antibody specific for antithrombin III and did not inhibit factor Xa at an appreciable rate in the presence of heparin, was designated heparin cofactor A. Antithrombin-heparin cofactor, which eluted from heparin-agarose with buffer containing 2.0 M NaCl, was functionally and antigenically identified as antithrombin III. The concentrations of heparin cofactor A in normal and patient plasma were similar (4.5 x 10(-7) M), while the concentration of antithrombin III in patient plasma (8.0 x 10(-7) M) was only 50% of normal (1.6 x 10(-6) M). The functional properties of both heparin cofactor A and antithrombin III obtained from patient plasma were normal. From the results of the present study it would appear that the antithrombin-heparin cofactor concentrating measured in patient plasma reflects the combined concentrations of heparin cofactor A and antithrombin III. Since heparin cofactor A does not cross-react with antibody to antithrombin III, the concentration of antithrombin III antigen in patient plasma is thus lower than the concentration of antithrombin-heparin cofactor.

Antithrombin III↗