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[Antithrombin III deficiency and pregnancy. Apropos of a case].

Congenital deficiency of antithrombin III is a disease inherited as an autosomal dominant which predisposes to thromboembolism. Pregnancy and the postpartum period constitute a major additional risk factor for thromboembolism in deficient women. However, pregnancy may be envisaged without risk since there has been an improvement in knowledge concerning the physiology of the AT III molecule, its exact role in coagulation, the application of accurate laboratory tests which measure the deficiency, and especially the programming of pregnancy under cover of preventive treatment consisting of the perfusion of AT III concentrate in association with heparin. The treatment is restricting and costly but is, nevertheless, the only one to recreate conditions that are similar to physiological conditions, and its effect is therefore more certain.

Adult↗
PubMed1988

Surgery in patients with congenital antithrombin III deficiency.

A retrospective study is presented of 23 patients with congenital antithrombin (AT) III deficiency who underwent 57 operations of various types. Thromboprophylaxis was given in 28 operations. Dextran was used in most cases, sometimes in combination with specific AT III concentrate. No patient given AT III concentrate alone or in combination with other methods had signs of thromboembolism. Deep venous thrombosis followed four of the operations with prophylaxis (3 patients). After the 29 operations without prophylaxis there were three cases of deep venous thrombosis, one with clinical signs of pulmonary embolism and another with superficial thrombophlebitis. Despite its inherent drawbacks, this retrospective study indicated that AT III concentrate can effectively prevent postoperative thromboembolism. But as the selection criteria for thromboprophylaxis are difficult to evaluate, a prospective study should be of great value.

Adult↗
PubMed1988

Changes of antithrombin III (AT III) in AT III deficient patients during long-term anticoagulant treatment.

Antithrombin III deficient patients with manifest thromboembolic diseases need long term coumarin treatment. There are contradictory data on the change of AT III during this therapy. The authors observed 5 patients with severe AT III decrease type I, 3 with functional abnormality and 2 with a pathological heparin binding. AT III function was determined by the Gerendás-Rák method and with chromogenic substrate. AT III antigen was measured with Behring M-Partigen and Laurell rocket electrophoresis. Crossed immunoelectrophoresis was carried out in all patients. In patients with type I AT III decrease, AT III hasn't changed even in a long period of more than 10 years. In the other types AT III became normal. The pathological heparin binding wasn't changed.

Anticoagulants↗
PubMed1989

[Use of antithrombin III concentrates].

Concentrates of antithrombin III (AT III) have been applied in congenital as well as in acquired AT III deficiency. Congenital defects only require substitution during surgery and in the case of pregnancy. Otherwise prophylaxis of thrombosis can be successfully carried out with oral anticoagulants. In acquired AT III deficiency substitution was found to be useful in cases of advanced DIC. When AT III activity was constantly kept around 100% the duration of DIC could be considerably shortened. No beneficial effect of additional administration of heparin was found. In cases of DIC due to septic shock the survival rate could be increased from an average of 20% without substitution to over 70% with AT III substitution as could be shown by different authors.

Antithrombin III↗
PubMed1989

[Familial antithrombin III abnormality accompanied with progressing ischemic stroke].

We report a case of familial antithrombin III (AT-III) abnormality accompanied with progressing ischemic stroke. The patient was a 31-year-old female who developed consciousness disturbance and left hemiparesis on December 1 in 1987. She had a history of two transient ischemic attacks and three episodes of thrombophlebitis of the extremities. Cerebral CT scan showed a low density area on the right temporal lobe that had extended to the right parietal and on the left frontal lobe as clinical symptoms worsened. Cerebral angiogram revealed branch occlusions of the right middle cerebral artery and showed no cerebral venous and sinus obstruction. When her symptoms had been progressing to show semi-comatose state, left hemiplegia and transient Cheyne-Stokes respiration, we found her decreased biological activity and normal immunological level of AT-III. The diagnosis of familial AT-III abnormality had been made by familial investigation. As the treatment of AT-III concentrates transfusion was started from the third day, her symptoms gradually recovered and the low density area stopped extending. Further examinations revealed that she was a homozygote of AT-III abnormality presenting no affinity for heparin and that her parents were heterozygotes. It was suggested that the homozygous AT-III abnormality was the main cause of her progressing ischemic stroke.

Adult↗
PubMed1987

[Prevention of thromboembolism during pregnancy in 3 sisters with congenital antithrombin III deficiency and decreased inducible fibrinolysis].

Antithrombin III (AT III) deficiency is associated with a high risk of venous thromboembolism, particularly in pregnancy. As prophylactic treatment it has been recommended that plasma levels of AT III be normalized by use of AT III concentrates, in addition to heparin. - We report on the prophylactic treatment of three sisters (age 21, 25, and 32 years) with congenital AT III deficiency (38-53%, normal 80-120%) and reduced inducible fibrinolytic activity (1.2, 5.8, 1.2%, normal greater than 8.5%), who had already had severe thromboembolism. During pregnancy prophylactic measures were taken individually, depending on the plasma level of beta thromboglobulin (BTG) determined every 2-3 weeks. In two patients prophylaxis with s.c. heparin (2 X 7500 IU/d) was started at the time of the first increase of BTG (around 10th week of gestation), leading to normalization of BTG. When BTG was again elevated, the dose of heparin was increased stepwise to 2 x 15,000 IU/d; in this way functional AT III levels remained in the range of 28-50%. Thus, these two patients received only heparin throughout pregnancy. However, in the third patient BTG levels could not be normalized by heparin alone (60-130 ng/ml, normal less than 43 ng/ml). Injections of AT III concentrate (1000 IU) led to reduction of BTG within 2 hours (60----42,220----61 ng/ml). Therefore, AT III was given from the 25th week of gestation in increasing amounts up to 5000 IU/week (funct. AT III in plasma 51-72%) in addition to heparin (2 x 12,500 IU/d), resulting in BTG levels of 33-51 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Hereditary thrombosis in a Utah kindred is caused by a dysfunctional antithrombin III gene.

Maximum likelihood analysis of linkage between antithrombin III (ATIII) DNA polymorphisms and ATIII deficiency in a large Utah kindred suggests that thrombotic disease in this family is caused by a dysfunctional ATIII gene. ATIII-deficient family members were identified on the basis of: (1) reduced anticoagulant activity and (2) the presence of an electrophoretically abnormal inhibitor molecule in their plasmas. Affected individuals have two copies of the ATIII structural gene, and both alleles appear normal at the resolution of whole genome Southern blotting. However, family studies revealed statistically significant cosegregation of ATIII-deficiency trait and a particular ATIII DNA polymorphism haplotype (lod = 3.35; theta = 0.0); this result is consistent with the presence of a dysfunctional ATIII gene on a chromosome of the +, S haplotype.

Alleles↗
PubMed1988

Management of pregnancy in women with antithrombin III congenital defect: report of four cases.

Four pregnant women with antithrombin III congenital deficiency underwent thrombosis prophylaxis including oral anticoagulants administered from the 16-18th week to the 36-37th week of pregnancy, subcutaneous heparin before the 16-18th week and after the 36-37th week, and a single infusion of AT III concentrate in the peripartum period in order to obtain a minimal level of 0.8 U/ml of AT III functional activity. The level of circulating AT III after the concentrate infusion needs to be evaluated by functional methods, because of a consistent amount in the concentrates of inactive AT III immunoreactive material. No thrombotic or haemorrhagic complication occurred after starting prophylaxis in any woman either in any newborn.

Administration, Oral↗
PubMed1988

Antithrombin III molecular variants with defective binding to heparin or to serine proteases: evidence of two different abnormal patterns identified by crossed immunoelectrofocusing.

Molecular heterogeneity of antithrombin III (AT III) was investigated by a technique of crossed immunoelectrofocusing (CIEF) in plasma samples of patients from 16 families with AT III congenital defect, including 8 AT III molecular variants. The AT III CIEF pattern was normal in all the patients with AT III quantitative deficiency, showing a balanced decrease of all the peaks. Out of the 8 AT III variants investigated, 6 had an abnormal pattern: the three variants with defective binding to heparin (AT III Roma, AT III Barcelona, AT III Malmö) shared a similar abnormal pattern; three variants with defective binding to serine proteases (AT III Pescara, AT III Milano, AT III Tampere) had a common abnormal pattern clearly different from the first one, whereas the other two variants deficient in the inactivation of the serine proteases (AT III Chicago, AT III Milano 2) showed a normal pattern. The first type of pathological pattern (type Roma) was characterized by the presence of an abnormal peak overlapping the normal isoforms present at pH 4.8-4.6 and by an additional peak at pH 4.5. The second type of pattern (type Pescara) showed an additional peak at pH 4.5 and an abnormal quantitative distribution of the isoantithrombins all throughout the pH range (5.2-4.6). In order to separate the abnormal AT III fraction from the normal one, plasma of a patient with Roma defect and serum of a patient with Pescara defect were passed throughout an heparin-ultrogel column.(ABSTRACT TRUNCATED AT 250 WORDS)

Antithrombin III↗
PubMed1988

Oxymetholone therapy in patients with familial antithrombin III deficiency.

Three patients with familial antithrombin III (ATIII) deficiency, who also have histories of thromboembolism, were treated with oxymetholone in combination with warfarin. Thrombolysis was observed in one patient with acute thrombosis of inferior vena cava during the oxymetholone and warfarin therapy. No further thromboembolic episodes occurred in these patients after initiation of warfarin with or without oxymetholone. The levels of plasma ATIII, alpha 1-antitrypsin, plasminogen and Cl-inactivator were significantly increased in all patients after the introduction of oxymetholone therapy. This suggests that oxymetholone augments anticoagulant and fibinolytic activity. Hence we consider that oxymetholone in combination with warfarin may be possible thrombolytic therapy in patients with familial ATIII deficiency.

Adolescent↗
PubMed1987

Antithrombin III deficiency: clinical relevance and replacement therapy.

Inherited antithrombin III (ATIII) deficiency causes a life-long tendency to venous thromboembolism, which is often recurrent and may be life-threatening. In contrast, the clinical importance of acquired ATIII deficiency, whether spontaneous or associated with estrogen-containing oral contraceptive treatment, remains uncertain. Moderately reduced ATIII activity before or immediately after surgery is neither sensitive nor specific for a high risk of postoperative venous thromboembolism (VTE), while moderately reduced ATIII activity during heparin treatment for VTE fails to indicate an unusually large heparin requirement or to predict recurrence. In the absence of good clinical trials, the value of ATIII replacement therapy also remains obscure; its use in congenital deficiency is largely based on anecdote, and while it may cause more rapid correction of the hemostatic defect in patients with disseminated intravascular coagulation (DIC), any improvement in morbidity or mortality resulting from ATIII replacement remains to be demonstrated.

Antithrombin III↗
PubMed1987

[Antithrombin III].

The in vivo regulation of coagulation is mainly controlled by plasma inhibitors in which antithrombin III (AT III) plays an importance role. AT III is a glycoprotein which inhibits all serine proteases, except factor, VIIa, generated during the coagulation process. The proteases are inactivated by formation of an equimolecular complex and this reaction is greatly enhanced in the presence of heparin. A similar catalytic process could occur in vivo, involving heparin-like substances present on the surface of the surface of the endothelial cell. The physiological importance of AT III is clearly demonstrated by the high incidence of thromboembolic disease in patients with congenital AT III défficiency.

Antithrombin III↗
PubMed1987

Plasma heparin cofactor II, protein C and antithrombin in elective surgery.

The coagulation inhibitors heparin cofactor II (HC II), protein C (PC) and antithrombin (AT) were measured in 14 patients undergoing uncomplicated abdominal, orthopedic or vascular surgery. Marked transient decrease of all the inhibitors was found after all surgical procedures, most prominently in vascular surgery. The greatest mean reduction was in HC II. The fall in PC and AT showed a pattern similar to that of albumin. In contrast to some earlier suggestions our results indicated that, except for HC II, the reduction probably was not due to consumption. Redistribution, hemodilution and, probably, reduced synthesis were the most important contributing factors. Serial measurements of the three coagulation inhibitors may be of prognostic value, but the present study's observed mean decrease of c. 25% in abdominal and 50-62% in vascular surgery must be borne in mind. Still lower inhibitor levels suggest consumption and a complicated postoperative course.

Adult↗
PubMed1986

[Clinical aspects of acquired antithrombin III deficiency].

The significance of acquired antithrombin III (AT III) deficiency must be interpreted in close relation to the underlying disease process. In patients with acute or chronic liver impairment, the AT III activity is related to a decrease of procoagulatory factors, whereas, in protein loss syndromes such as nephrotic syndrome, the AT III indicates an increased risk of thromboembolic events. The effect of oral contraceptives (OC) on AT III levels in young healthy females (n = 30) was determined prospectively. AT III decreases during OC usage could not be related to the estrogen content of the examined oral contraceptives, and there was no parallel decrease of AT III activity and concentration in each type of OC. In a prospective study, the extent of AT III decrease was determined in patients undergoing cardiopulmonary bypass operations (CPB) receiving different anticoagulant schedules during extracorporeal circulation (n = 49). There was no significant influence on the effectiveness of anticoagulation by the observed AT III decreases. AT III deficiency during CPB was primarily the result of hemodilution. However, the AT III kinetics were significantly influenced by the different protamin dosages and were not affected by the different heparin dosages. Correction of diminished AT III levels by substitution of AT III concentrates is beneficial in cases, in which an interruption of an enhanced coagulatory process such as disseminated intravascular coagulation is necessary or in patients requiring high dosage heparinization as in deep vein thrombosis. In those cases the quality of AT III correction correlates to the course of the disease. However, the potency of concentrates as well as the individual AT III recovery and half-life must be considered for an appropriate treatment with AT III substitution.

Adult↗
PubMed1986

[Significance of antithrombin III in kidney diseases].

This article deals with the clinical importance of antithrombin III (AT III) in renal disease. Patients with nephrotic syndrome demonstrates a high risk of thromboembolism. A renal AT III loss is an important pathogenetic factor in these events. Patients with serumalbumin below 2.0 g/dl are mostly endangered. In patients with acute oligoanuric renal failure low AT III-levels due to consumption were often found that lead to diminished protection against intravascular coagulation processes and can therefore contribute to progression of illness. An AT III-substitution may be of some benefit in these patients. Additionally AT III was given in patients with dialysis-dependent renal failure and low levels of AT III leading to a reduced incidence of thrombosis of the extracorporeal system. Unnecessary high doses were also avoided and a minimal heparinization could be performed more efficiently in bleeding risk patients. Furthermore, AT III-levels during renal transplantation and during organ rejection are reported.

Acute Kidney Injury↗
PubMed1987

Catabolism and distribution of functionally heterogeneous human antithrombin III.

To test the hypothesis that binding to an endogenous heparin-like substance controls breakdown of antithrombin III (ATIII) in vivo, the metabolic behavior of a commercial ATIII concentrate was investigated in three normal volunteers and five subjects with hereditary ATIII deficiency. The concentrate, purified to homogeneity as evidenced by sodium dodecyl sulfate--gel electrophoresis, was a 2:1 mixture of functional ATIII with heparin cofactor activity and dysfunctional ATIII incapable of binding enzymes or heparin. Each subject received intravenously a dose of 75 U/kg of ATIII activity together with iodine 125-labeled tracer. Daily fractional catabolic rates calculated from the three-exponential disappearance curves of plasma radioactivity were similar in all investigated subjects and were within the range obtained in studies using functionally homogeneous tracer. Although all subjects had markedly increased ATIII levels after injection of the concentrate, the relative sizes of their ATIII distribution pools resembled those reported previously for people with normal ATIII concentration. There was, however, a noticeably faster disappearance from plasma of excess functional ATIII compared with that of ATIII antigen, with mean half-lives of 47.5 +/- 9 hours and 62.3 +/- 8 hours, respectively. Assuming that antigenic ATIII represented both functional inhibitor and dysfunctional ATIII incapable of binding heparin, these data are consistent with the supposition that interaction with endogenous heparin or a similar substance may regulate a catabolic pathway marking ATIII for destruction.

Adult↗
PubMed1986

Purified radiolabeled antithrombin III metabolism in three families with hereditary AT III deficiency: application of a three-compartment model.

Purified human radioiodinated antithrombin III (125I-AT III) was used to study its metabolism in six members from three different families with a known hereditary AT III deficiency. Six healthy volunteers served as a control group. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and crossed immunoelectrophoresis (CIE) showed the purified AT III to be homogeneous. Amino acid analysis of the protein revealed a composition identical to a highly purified internal standard. The specific activity was 5.6 U/mg. Analysis of plasma radioactivity data was performed, using a three-compartment model. Neither plasma disappearance half-times nor fractional catabolic rate constants differed significantly between patients and control subjects. The mean absolute catabolic rate in the patient group was significantly lower than that of the control group at 2.57 +/- 0.44 and 4.46 +/- 0.80 mg/kg/day, respectively. In addition, the mean patient alpha 1-phase, flux ratio (k1,2 and k2,1) of the second compartment alpha 2-phase and influx (k3,1) of the third compartment were significantly reduced as compared with control values. It has been tentatively concluded that the observed reduction in the second compartment may be caused by a decrease in endothelial cell surface binding.

Adult↗