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PubMed1983

Fatal pulmonary embolism and antithrombin III deficiency in adult lymphoblastic leukaemia during L-asparaginase therapy.

We describe 2 adult patients with acute lymphoblastic leukaemia (ALL) who died from pulmonary embolism following L-asparaginase treatment. Since this drug is known to cause a decrease in antithrombin III, the most important protein physiologically involved in the neutralization of thrombin, we studied the behaviour of this inhibitor in 14 ALL patients treated with a protocol including a 14-day course of L-asparaginase. A significant but transient fall of biological and immunological antithrombin III and a concomitant reduction of fibrinogen were documented.

Acute Disease↗
PubMed1984

Persistent antithrombin III deficiency: risk factor for thromboembolic complications in neonates small for gestational age.

Coagulation and fibrinolytic factors were investigated daily in 24 SGA and 26 AGA neonates. The results were correlated with placental form and structure and with hematologic values. In the SGA infants, a higher incidence of placental infarction (P less than 0.01), polycythemia (P less than 0.005), and thrombocytopenia (P less than 0.001) was present. During the first 9 days, the mean antithrombin III level in the AGA group increased from 0.36 to 0.53 U/ml, whereas in SGA neonates this value was initially significantly lower (0.27 U/ml) and remained at that level for the entire observation period. The same pattern was found for alpha 2-antiplasmin. The persistent AT-III deficiency and reduced blood flow associated with polycythemia may explain the increased risk of thromboembolic complications in SGA infants described by others.

Antithrombin III Deficiency↗
PubMed1989

Neonatal antithrombin III deficiency.

Hemorrhagic and thrombotic complications are common in sick preterm infants and may reflect inadequate regulation of coagulation. All neonates have low levels of the pivotal regulator antithrombin III (ATIII) compared with adults. Plasma levels of ATIII are very low in preterm infants and are further diminished in infants with respiratory distress, necrotizing enterocolitis, sepsis, or disseminated intravascular coagulation. Babies with lower levels of ATIII in the cord blood have been shown to have a worse outcome than neonates with levels appropriate for gestational age, including higher mortality and increased incidence of intracranial hemorrhages and catheter-related thromboses. The origin of severe ATIII deficiency is unknown. Therapies with plasma replacement or anticoagulation have decreased the incidence and severity of hemorrhagic and thrombotic complications in high-risk infants in several clinical trials. These data lay the groundwork and rationale for potential use of ATIII replacement in deficient preterm infants.

Antithrombin III↗
PubMed1983

L-asparaginase induced antithrombin III deficiency: evidence against the production of a hypercoagulable state.

L-asparaginase, a chemotherapeutic agent employed in the treatment of acute lymphocytic leukemia (ALL), is known to depress the synthesis of numerous plasma proteins. The plasma concentration of the major protease inhibitor of the coagulation mechanism, antithrombin III, is substantially decreased in patients receiving this drug. This observation has generated speculation that L-asparaginase may induce a hypercoagulable state in humans. To examine this hypothesis, we studied ten patients with ALL in remission who were being treated with the above chemotherapeutic agent. Our data revealed that infusion of this enzyme leads to a marked decrease in the plasma concentrations of prothrombin as well as antithrombin III. However, we have also observed a constant level of thrombin generation during the same period of time as monitored by plasma levels of prothrombin activation fragment (F1 + 2) and thrombin-antithrombin complex (TAT). Based upon these findings we suggest that administration of L-asparaginase does not usually lead to the induction of a hypercoagulable state.

Adolescent↗
PubMed1997

Acquired protein S and antithrombin III deficiency caused by nephrotic syndrome: an unusual cause of graft thrombosis.

Thrombotic phenomena are well-recognized complications of nephrotic syndrome attributable to loss of intermediate-sized antithrombotic proteins in the urine, resulting in a hypercoaguable state. As such, nephrotic syndrome may be associated with a reduction in circulating antithrombin III and free protein S levels. Associated spontaneous thrombotic complications are generally venous in nature, with arterial thrombosis occurring less frequently. Hypercoagulability caused by acquired nephrotic syndrome has not generally been recognized as a cause of acute thrombosis of arterial bypass grafts. We report two patients who after having nephrotic syndrome sustained acute thrombosis of their arterial bypass grafts. Pathogenesis and management are discussed.

Antithrombin III Deficiency↗
PubMed1999

Protein C, protein S and antithrombin III deficiencies in retinal vein occlusion.

PURPOSE: The role of decreased levels of protein C, protein S and antithrombin III were investigated in patients with branch and central retinal vein occlusion. METHODS: Forty-five patients with retinal vein occlusion and 20 healthy subjects as a control group was studied. Fourteen patients (31%) had central retinal vein occlusion and 31 (69%) had branch retinal vein occlusion. The concentrations of protein C, protein S and antithrombin III were measured. RESULTS: Plasma levels of protein C, protein S and antithrombin III were not reduced in the control group. Six of the 14 central retinal vein occlusion cases and 3 of the 31 retinal branch vein occlusion cases had decreased levels of protein C. One of the 14 central retinal vein occlusion cases and 1 of the 31 retinal branch vein occlusion cases had decreased levels of protein S. Antithrombin III was reduced in 1 patient of the 31 retinal branch vein occlusions. We found statistically significant differences for number of cases with protein C deficiency between the central retinal vein occlusion cases and the branch retinal vein occlusion cases (p<0.05). CONCLUSION: Deficiency of anticoagulant proteins, especially protein C, may play a role in the etiology of retinal vein occlusion. Measurement of these parameters may be useful in preventing venous thrombosis elsewhere in the body.

Biomarkers↗
PubMed1994

Prothrombin fragment 1 + 2, thrombin-antithrombin III-complexes and fibrinopeptide A in spontaneously clotting whole blood in vitro. Effects of heparin addition and antithrombin III deficiency.

Previous in vitro studies using spontaneously clotting whole blood revealed thrombin formation and high fibrinopeptide A (FPA) concentrations measured during incubation time. This occurred in spite of normal concentrations of thrombin antagonists present in the blood of the healthy subjects examined. However, there are several reports showing that in vivo increased thrombin-antithrombin III-complex (TAT) concentrations and relatively low FPA concentrations may occur e.g. in patients with (pre)thrombotic disorders. These in vivo findings indicate more effective thrombin inhibition by antithrombin III, with almost no fibrin formation. To find an explanation for the differences observed in vitro and in vivo, we extended the in vitro studies by measuring concentrations of prothrombin fragment 1 + 2 (F1 + 2), TAT and FPA at several time points until 30 min. Our goal was to test whether thrombin at least initially is neutralized by antithrombin III, resulting in a lack of fibrin formation, either in the absence or in the presence of heparin (0.2 and 0.5 U/ml whole blood, respectively). In the absence of heparin a simultaneous increase in the concentrations of F1 + 2, TAT and FPA was observed. Thrombin was only partially neutralized by antithrombin III and large amounts of fibrin were formed. The addition of heparin virtually suppressed thrombin formation since the F1 + 2 concentration remained low. Moreover, the small amounts of thrombin formed were neutralized by antithrombin III to a greater extent than in the absence of heparin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

[Mesenteric infarction secondary to antithrombin III deficiency].

AT III is a physiologic inhibitor of blood clot formation: its deficiency is manifested by venous thrombosis. The authors reported case of mesenteric venous infarction in a 42-years-old woman. AT III deficiency was transient and caused by an oral contraceptive. In patients with AT III acquired deficiency it is necessary to suppress any risk factors of venous thrombosis.

Adult↗
PubMedDate not supplied

[Antithrombin III deficiency induced by heparin and constitutional protein C deficiency. Apropos of a case].

Major mesenteric venous thrombosis in a young man who had already had spontaneous thromboembolic accidents prompted the diagnosis in 1982 of 'Antithromin III' deficiency. The initial reduction of this inhibitor proved to be secondary to a consumption raised abnormally by Heparin. Research into the family antecedents made it possible in 1983 to discover a constitutional 'Protein C' deficiency without stopping the antivitamins K for this patient.

Adult↗
PubMed1998

A case report of heparin resistance due to acquired antithrombin III deficiency.

A case of heparin resistance and its management during cardiopulmonary bypass is reported. A patient with a history of post-infarct angina and arrhythmias was treated with intravenous heparin infusion for five days prior to myocardial revascularisation surgery. He required 13,500 IU/kg of heparin to increase his activated clotting time to a therapeutic level for safe institution of cardiopulmonary bypass. This phenomenon of heparin resistance was postulated to be due to consumption of circulating antithrombin III as a result of prior heparinisation. Treatment with fresh frozen plasma restored heparin effectiveness.

Aged↗