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PubMed1996

[Hereditary antithrombin III deficiency. Report of an obstetric case and review of the literature].

This case is a gravida 2, para 1, 21 years old, with a 36 weeks pregnancy, complicated with light toxemia, hereditary Antithrombin III (AT III) deficiency, and left iliofemoral thrombophlebitis; the patient was in labor. Two family members had thromboembolic phenomena, one of them had died because of this. The patient have had thrombophlebitis in both lower limbs during the puerperium of her previous delivery. She had received anticoagulants irregularly. Four months before the diagnosis of hereditary AT III deficiency, by laboratory. Labor was normal and had an eutocic delivery, masculine product, 3,250 g, without complications. Three hours before the effect of heparin had been reverted with protamine sulphate. Eight hours after delivery administration of heparin, was reestablished. The patient did not present other complications, and was discharged nine days after delivery. The literature about this subject was reviewed. Special emphasis is given to treatment alternatives in this type of disease that produce hypercoagulability and thromboembolic phenomena. This is the first report in Mexican literature.

Adult↗
PubMed1990

Emergency treatment with recombinant tissue plasminogen activator of pulmonary embolism in a pregnant woman with antithrombin III deficiency.

Thromboembolic complications during pregnancy are frequent in patients with congenital antithrombin III deficiency. We report on a 29-year-old patient with congenital antithrombin III deficiency and severe pulmonary embolism treated with recombinant tissue plasminogen activator. The diagnosis of antithrombin deficiency is retrospective. This case indicates that the risk of thrombolytic therapy in this clinical setting might have been overemphasized.

Adult↗
PubMed1987

[Replacement therapy of acquired antithrombin III deficiency in experimental nephrotic syndrome].

The influence of antithrombin III on hemostasis and renal function was studied in experiments on rats with nephrotic syndrome. The development of nephrotic syndrome was accompanied by the activation of blood coagulation and appearance of acquired antithrombin III deficiency due to its loss with the urine. The replacement therapy by bovine antithrombin III at a dose of 25 U/kg a day for 10 days decreased the signs of excessive thrombinogenesis in experimental animals and increased the amount of thrombin-antithrombin III complexes in the blood flow. The activation of coagulation in rats with nephrotic syndrome predominantly induced the disturbances of the excretory renal function which could be efficiently corrected by antithrombin III.

Animals↗
PubMed1981

Acute aortic thrombosis in antithrombin III deficiency.

Two cases of acute aortic thrombosis, a previously unreported complication of antithrombin III deficiency, are reported. Both patients had abnormally low antithrombin III levels, which improved to normal levels with warfarin ;sodium therapy. The possibility of antithrombin III deficiency should be considered in young patients with acute arterial thrombosis.

Acute Disease↗
PubMed1981

Antithrombin III concentrate: its catabolism in health and in antithrombin III deficiency.

The catabolism of purified radiolabelled antithrombin III (AT III) concentrate was studied in two normals and two patients with congenital AT III deficiency both alone and combined with warfarin. The radiolabelling with iodine monochloride did not change the quality of the concentrate. The half-life varied between 3.4 and 4.8 days. No difference between normals and patients with congenital deficiency in non-acute stage could be observed in the catabolic parameters; nor was there any influence with warfarin.

Adult↗
PubMed1985

The prevalence of hereditary antithrombin-III deficiency in patients with a history of venous thromboembolism.

Antithrombin-III activity was determined in 752 patients with a history of venous thrombosis and/or pulmonary embolism. 54 patients (7.18%) had an antithrombin-III activity below the normal range. Among these were 13 patients (1.73%) with proven hereditary deficiency. 14 patients were judged to have probable hereditary antithrombin-III deficiency, because they had a positive family history, but antithrombin-III deficiency could not be verified in other members of the family. In the 27 remaining patients (most of them with only slight deficiency) hereditary antithrombin-III deficiency was unlikely. The prevalence of hereditary antithrombin-III deficiency was higher in patients with recurrent venous thrombosis.

Antithrombin III Deficiency↗
PubMed1995

Antithrombin III deficiency as a risk factor for catheter-related central vein thrombosis in cancer patients.

The fibrin sleeve of venous catheters (VC) and parietal thrombi represent frequent and dangerous side-effects of central venous catheterization (CVC), due to the risk of embolism. Reduced levels of coagulation clotting factors inhibitors (such as Antithrombin III) are known to be associated with increased thrombogenic risk. The aim of this study was to evaluate the role of Antithrombin III (AT III) deficiency as a risk factor for thrombosis in cancer patients undergoing CVC. The study groups included patients with a reduced AT III activity (< 70%, 20 consecutive patients) and with normal AT III values (> 70%, 20 randomly selected patients), requiring a VC for chemotherapy and/or total parenteral nutrition. The study protocol included evaluation of Hb, PLTs, PT (INR), aPTT, Fibrinogen and AT III at days 0, 1, 3 and 8 after CVC and upon VC removal. Peripheral and pullout phlebographies were performed in all patients on catheter withdrawal. A quantitative scale was developed to evaluate both VC and parietal thrombus degree in each catheter-containing venous segment (subclavian, innominate, superior vena cava); the sum of the mean values was defined as overall thrombus. The average VC dwelling time was similar in both groups. There were no significant differences in Hb, PLTs, PT (INR), aPTT, Fibrinogen and in the remaining parameters of the study between the two groups. The group with AT III deficiency presented a higher degree of both parietal (p < 0.05) and overall thrombus (p < 0.02). Data showed a higher severity of CVC-related thrombosis in patients with AT III deficiency than in the control group. Further studies are needed to evaluate whether the therapeutically-induced normalization of AT III levels can reduce the thrombosis degree.

Adult↗
PubMed1984

Antithrombin III deficiency as a reflection of dynamic protein metabolism in patients undergoing vascular reconstruction.

Antithrombin III (AT-III) deficiency has been associated with increased risk of venous and arterial thromboses and arterial graft failure. Deficiency of this circulating glycoprotein may be congenital; however, acquired deficiencies may develop in protein-losing or protein-wasting states. In the present study, AT-III levels of 108 patients undergoing vascular surgical procedures were determined preoperatively and at intervals (third, fifth, and seventh days) postoperatively. The mean AT-III level was then compared to the patient's protein status. The effect of reduced AT-III activity on early graft failure was also noted. A low preoperative AT-III level (less than 80%) was found in 16.3% of the patients studied. Among 83 patients with serum albumin levels greater than 3.0 gm/dl or transferrin levels greater than 180 mg/dl, reduced AT-III activity was present in only 10 (12%). In contrast, when serum albumin levels were less than 3.0 gm/dl, AT-III deficiency was found in 12 of 25 patients (48%) (p less than 0.01). Early thrombosis of a femorodistal graft occurred in 5 of 15 patients (33%) with reduced AT-III levels. When AT-III levels were normal, early bypass failure occurred in only 9 of 67 grafts (13.4%). However, this difference was not statistically significant. An additional 15 patients had sequential pre- and postoperative measurements (up to 3 weeks) of serum protein and AT-III levels to illustrate the relationship between the dynamics of protein metabolism and AT-III levels. There was a clear temporal relationship between albumin, transferrin, and AT-III levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Cerebral thromboembolism due to antithrombin III deficiency in two children.

Despite numerous well-described causes of stroke in infancy and childhood, a significant proportion remains unexplained. Venous thromboembolism is a common complication in adult patients undergoing surgery, and after severe trauma, but not in otherwise healthy children less than 10 years old. However, it may also occur spontaneously without recognizable cause. It has been known for a long time that some patients are particularly prone to venous thrombosis and in recent years great efforts have been made to identify the risk factors. The attention of haematologists has been focused on the possibility that certain abnormalities of coagulation may be associated with a tendency to thrombosis, but only in a few instances a clear causal relationship has been established. One such example is a deficiency of antithrombine III, but such a deficiency has hitherto been recognized as a cause for thrombosis in children only in very particular circumstances. We present two young children with stroke of which one was purely ischemic and the other ischemic with secondary hemorrhage. Both our patients showed an AT III deficiency. Patient one also had a cyanotic congenital heart disease with right to left shunting which made cerebral embolism originating from a thrombus in the iliac vein possible to occur. We consider her hematocrit values too low to be a predisposing factor for this thrombosis. AT III deficiency may be caused by several different mechanisms. Either it exists as a congenital (hereditary) or as an acquired disorder. In patient two the family history was positive for hereditary AT III deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Antithrombin III Deficiency↗
PubMed1980

Heparin anticoagulation during cardiopulmonary bypass in an antithrombin-III deficient patient. Implications relative to the etiology of heparin rebound.

A case of antithrombin-III (AT-III) deficiency was diagnosed on the basis of a diminished anticoagulant effect following the administration of heparin for cardiopulmonary bypass. The clinical evaluation and interpretation of a diminished response to heparin is discussed, as are considerations relative to the treatment of AT-III deficient persons whose disorder is not manifest until they are already anesthetized for cardiovascular bypass. The implications of AT-III deficiency relative to the mechanism of heparin rebound are also discussed.

Aged↗
PubMed1995

Acute promyelocytic leukemia developed in a patient with congenital antithrombin III deficiency.

A case of acute promyelocytic leukemia (APL) developed in a patient with congenital antithrombin III (AT-III) deficiency is reported. Despite the presence of disseminated intravascular coagulation (DIC), plasma AT-III activity was not decreased at the diagnosis of APL compared to the patient's baseline level (approximately 50% of normal). He was successfully treated with all-trans retinoic acid (ATRA) to achieve complete remission without the use of heparin. Although he developed phlebitis at the site of insertion of the intravenous catheter during remission-induction, no major thrombotic episode was noted. Coagulation parameters including fibrin and fibrinogen degradation products (FDP-E), thrombin-antithrombin complex (TAT), FDP-D dimer (D-D dimer), and plasmin-alpha 2 plasmin inhibitor complex (PIC) improved rapidly after initiation of ATRA. This case is a clear demonstration of the characteristics of DIC developing in APL, i.e. no or minimal decrease in the level of AT-III activity and a predominant increase in the fibrinolytic system, rather than hypercoagulability.

Antithrombin III Deficiency↗
PubMed2001

[Anesthetic management of a patient with congenital antithrombin III Deficiency using temporal inferior vena cava filter].

We described the perioperative management of a patient with congenital antithrombin III deficiency using temporal inferior vena cava filter. A 30-year-old man with congenital antithrombin III deficiency was scheduled for artificial head replacement of the hip joint under general anesthesia. He was diagnosed as having congenital antithrombin III deficiency when he had had an episode of venous thrombosis after artificial head replacement of the right hip joint. He had been taking warfarin as an anticoagulant, and it was discontinued three days before surgery. To prevent perioperative thrombus formation, the plasma AT III activity was maintained above 80% before, during and after surgery using AT III concentrates. We also placed the temporal inferior vena cava filter. There was no serious thrombosis or embolism perioperatively. The use of the filter during the perioperative period helped to avoid development of serious thrombosis and embolism.

Adult↗
PubMed1985

Effect of danazol on the biochemical abnormality of inherited antithrombin III deficiency.

Seven members of a family affected by hereditary antithrombin III deficiency were identified. The disorder was associated with recurrent spontaneous episodes of phlebitis, deep venous thrombosis, and pulmonary embolism in middle age. Danazol, a 17-alkyl derivative of ethinyl testosterone, which has been used to treat other antiprotease deficiency states, was assessed in the management of two men with antithrombin deficiency. In a dose of 600 mg a day danazol appeared to correct the antithrombin deficiency. This drug may provide a useful adjunct to anticoagulant treatment, particularly before surgery.

Adult↗
PubMed1994

Acquired antithrombin III deficiency secondary to asparaginase therapy in childhood acute lymphoblastic leukaemia.

As improved treatment regimens for acute lymphoblastic leukaemia (ALL) continue to improve survival future, therapy must also take into consideration the many secondary problems. Most of these are the direct result of combination chemotherapy and L-asparaginase (ASP), is an example of a highly effective chemotherapeutic agent with serious side-effects such as thromboembolic events. ASP interferes with protein synthesis resulting in an acquired deficiency of antithrombin III. This review explores the effects of ALL and ASP on haemostasis, and the link between ASP and thromboembolic events in childhood ALL.

Adolescent↗
PubMed1989

Acquired antithrombin III deficiency: laboratory diagnosis, incidence, clinical implications, and treatment with antithrombin III concentrate.

Antithrombin III (ATIII) is the predominant naturally occurring inhibitor of serine proteases generated during blood coagulation [Rosenberg RD: Annu Rev Med 1978; 29: 367-378]. Since 1965, several assays have been developed that allow rapid and precise determination of ATIII in plasma. As a consequence, the existence of acquired ATIII deficiency in many pathologic conditions has been described. Acquired ATIII deficiency is based on decreased synthesis, increased loss or increased consumption, or induced by drugs. An inherited ATIII deficiency is associated with a lifelong tendency to venous thromboembolism. In contrast, the clinical significance of acquired ATIII deficiency has been less well defined. A precise estimate of the risk of thromboembolism in the acquired ATIII deficiency state cannot easily be provided, owing to the lack of studies in consecutive patients. In 1978, a purified human ATIII concentrate became available for clinical investigation. Despite numerous small studies, the value of ATIII replacement therapy in patients with acquired deficiency remains to be demonstrated.

Antithrombin III↗
PubMed1978

[Hereditary antithrombin III deficiency causing recurrent thrombo-embolic problems (author's transl)].

A marked deficiency in antithrombin III (AT III) was demonstrated in a 39-year-old man suffering from recurrent thrombo-embolic problems. The patient's father had died following a thrombo-embolic disorder. A certain number of members of the family also showed evidence of a marked decrease in AT III levels. Although it was not possible to study the patient's parents, it would seem reasonable to conclude that the diagnosis was one of hereditary deficiency in AT III. The various aspects of this disorder discovered by Egeberg are reviewed: early onset, in several members of the same family, or recurrent thrombo-embolic problems, accompanied by a decrease in functional activity of one of the principal inhibitors of thrombin (AT III), with autosomal dominant transmission and treatment based upon anti-vitamin K agents.

Adult↗