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PubMed1990

Inferior vena cava thrombosis in a child with nephroblastoma and combined deficiency of antithrombin III and free protein S.

A 3 1/2-year-old girl developed thrombosis of the inferior caval and renal veins several weeks after complete resection of a nephroblastoma. Her mother had suffered from pulmonary embolism at the age of 18 years. Familial antithrombin III deficiency and persistently lowered free protein S levels in the proposita were found. It is assumed that the combination of these two regulatory defects of hemostasis contributed to the early occurrence of this severe thrombotic event.

Antithrombin III Deficiency↗
PubMed1987

[Significance of the thrombin-antithrombin III complex in the diagnosis of pulmonary embolism and deep venous thrombosis--comparison with fibrinopeptide A, platelet factor 4 and beta-thromboglobulin].

In 22 patients with suspected pulmonary embolism and 19 patients with suspected deep vein thrombosis, thrombin-antithrombin III complex (TAT) as an indicator of thrombin activation was measured using a newly developed ELISA. For comparison fibrinopeptide A (FPA), as a marker of an activated coagulation, as well as platelet factor 4 (PF4), and beta-thromboglobulin (beta-TG), as markers of platelet activation, were determined. In all patients in whom pulmonary embolism was confirmed by perfusion lung scan and in 15 of 16 patients in whom deep vein thrombosis was confirmed by phlebography, TAT exceeded the upper limit of normal (3.0 ng/ml). FPA was increased in 71% of the pulmonary embolism patients, PF4 in 53%, and beta-TG in 59%. The data for the patients with deep vein thrombosis were comparable. PF4 and beta-TG were increased in more than 25% of the normal controls, FPA in 17%, and TAT in 9%. TAT is very sensitive in detecting an activation of the coagulation system in patients with suspected thromboembolic events. The test, however, is not specific for thromboembolism; it only indicates an activation of the coagulation system. Acute pulmonary embolism or deep vein thrombosis would appear to be unlikely if TAT is normal. The measurement of TAT is easier and less susceptible to disturbances than that of FPA, PF4, and beta-TG.

Antithrombin III↗
PubMed1986

Low antithrombin III in neonatal shock: DIC or non-specific protein depletion?

Low antithrombin III (AT III) levels in shock are usually ascribed to disseminated intravascular coagulation (DIC). However, decreased activities of clotting factors and their inhibitors could reflect a generalised fall in plasma proteins rather than DIC. AT III and albumin were compared in 48 asphyxiated and non-asphyxiated newborn rabbits (pH 6.70-7.30). Both AT III and albumin were markedly decreased in the sickest animals and there was a direct linear relationship between the two proteins (P less than 0.001). Similar results were obtained in ten newborn infants suffering from shock and haemorrhagic diathesis. In all cases AT III and albumin were decreased below the normal range and significantly correlated (P less than 0.01). Our findings suggest that AT III is not a useful diagnostic marker of DIC. Further, a similar fall of clottable and non-clottable proteins in shock questions the general assumption that the ensuing coagulopathy is due to intravascular coagulation.

Animals↗
PubMed1990

Meningococcemia and purpura fulminans in adults: acute deficiencies of proteins C and S and early treatment with antithrombin III concentrates.

It has been recently suggested that an acquired deficiency of proteins C and S could contribute to the pathogenesis of meningococcemic purpura fulminans (PF) in children. Our study was designed to measure the levels of antithrombin III (AT III), protein C, and protein S during adult PF and to determine the effects of an early infusion of high doses of AT III concentrates on clinical and biological alterations of PF. We studied five consecutive adult patients with meningococcemia (type B) and PF. The levels of AT III, protein C (antigen and activity), and protein S (total and free) were measured at admission and 24 h and 1 month later. The treatment included in each case: amoxycillin, dobutamine and high doses of AT III concentrates. All patients survived and were discharged without any sequelae. At admission, biological data were consistent with severely depressed protein C and protein S levels and moderately decreased AT III levels, without any discrepancy between protein C antigen and activity. After 24 h, AT III and protein S levels were within normal ranges, whereas protein C levels were still depressed. These data are consistent with the theory of a particular imbalance in the anticoagulant systems during meningococcemic PF, contrasting with the usual findings observed during septic disseminated intravascular coagulation. The possibility must be considered that high doses of one anticoagulant (AT III concentrates) could compensate for the acute decrease in the other (protein C system).

Adolescent↗
PubMedDate not supplied

Increased alpha 2-macroglobulin in diabetes: a hyperglycemia related phenomenon associated with reduced antithrombin III activity.

Increased alpha 2-macroglobulin (alpha 2M) activity and concentration, and decreased antithrombin III (ATIII) plasma concentration are reported in diabetic subjects. In diabetes an inverse correlation between ATIII activity and blood glucose, HbA1, alpha 2M activity and alpha 2M concentration, and a direct correlation between both alpha 2M activity and alpha 2M concentration with blood glucose and HbA1 are found. Moreover, a direct correlation between alpha 2M activity and alpha 2M concentration fails. In both diabetic and normal subjects induced hyperglycemia increases alpha 2M activity and alpha 2M concentration reduces ATIII activity, while ATIII concentration is not affected. These data which show that hyperglycemia may increase alpha 2M molecule levels while altering only the biological function of ATIII, provide evidence that hyperglycemia may decrease, directly, the biological function of some proteins and may condition the levels of some risk factors for the development of diabetic complications such as alpha 2M.

Adult↗
PubMed2003

Budd-Chiari syndrome due to antithrombin III deficiency.

Budd-Chiari syndrome is a disease complex with varied etiology and is one of the causes of post-hepatic portal hypertension. We report a 2 year-old boy who presented with Budd-Chiari syndrome due to congenital antithrombin III deficiency, who was managed with an expandable metal stent placed in the inferior vena cava and oral anticoagulation.

Antithrombin III Deficiency↗
PubMed1983

Usefulness of antithrombin III and alpha 2-plasmin inhibitor in early differentiation of fulminant hepatitis and severe form of acute hepatitis.

To evaluate the usefulness of antithrombin III (AT III) and alpha 2-plasmin inhibitor (alpha 2PI) in early differential diagnosis of fulminant hepatitis from the severe form of acute hepatitis, the activities of AT III and alpha 2PI were measured in plasma of 15 patients with fulminant hepatitis and 6 patients with severe form of acute hepatitis. The activities of prothrombin time (PT), hepaplastintest (HPT) and thrombotest (TT) were also evaluated. The mean values and the standard errors (SE) for PT, HPT and TT were 21.1 +/- 2.6%, 14.0 +/- 1.6% and 10.3 +/- 1.7%, respectively, in the early stage of fulminant hepatitis and 25.3 +/- 2.4%, 21.6 +/- 4.6% and 15.8 +/- 3.6%, respectively, in the severe form of acute hepatitis. No significant difference in the tests between these two diseases was noted. On the other hand, the mean values +/- SE for AT III and alpha 2PI were 13.7 +/- 4.6% and 25.6 +/- 8.6% in fulminant hepatitis and 70.2 +/- 28.5% and 98.7 +/- 9.7% in the severe form of acute hepatitis. A significant difference between the two diseases was observed. From the above, it is concluded that measuring AT III and alpha 2PI along with PT, HPT and TT is useful for early diagnosis of fulminant hepatitis.

Acute Disease↗
PubMedDate not supplied

Elevation of thrombin-antithrombin complexes during thrombolytic therapy in patients with myocardial infarction.

In patients with acute myocardial infarction (AMI) treated with streptokinase (SK) or recombinant tissue-type plasminogen activator (rtPA) we found high levels of thrombin-antithrombin (TAT) complexes signalling a significant activation of the coagulation cascade. In the SK-treated group the median pretreatment TAT complexes levels were 5.0 micrograms/l and in all patients, whatever the pretreatment level, TAT complexes increased following treatment. A statistically significant increase (medians = 20.3 and 12.0 micrograms/l) was observed 90 and 180 min after starting SK. The mean pretreatment level in the rtPA-treated group was also 5.0 micrograms/l and in all but one patients TAT complexes increased following treatment. A statistically significant increase (medians = 37.0 and 30.5 micrograms/l) was observed 90 and 180 min after starting rtPA. There was no statistically significant difference between TAT complexes in the two groups of patients either before or 90 min after treatment, whereas at 180 min the median concentration of TAT complexes was significantly higher for rtPA- than for SK-treated patients. We did not find an association between coronary vessels patency after thrombolysis and concentrations of TAT complexes; however, the rate of occluded vessels was very low (4 out of 30 patients), so that a difference was perhaps lost due to the insufficient size of the sample. In conclusion, we found thrombin activity during thrombolytic therapy in patients with AMI. There is no important difference in this respect between rtPA and SK. Whether or not this phenomenon is responsible for early rethrombosis remains to be explored by larger studies.

Antithrombins↗
PubMedDate not supplied

Antithrombin III concentrates in intensive care.

Antithrombin III concentrates offer a new therapeutic possibility for immediately increasing the inhibitory potential of plasma. Although heparin activates ATIII, thereby accelerating its consumption, it cannot increase the overall inhibitory capacity towards coagulation. The anticoagulant effect of heparin is in relation with the presence of sufficient amounts of ATIII. The intensive care of patients with liver failure, amniotic fluid embolism, heavy bleedings and septicemia was greatly aided by the substitution of ATIII. Disseminated intravascular coagulation was prevented or interrupted and there are observations suggesting that also shock lung and shock kidney are avoided. The substitution of ATIII allows an extremely extensive therapeutic plasmapheresis without the risk of thromboses.

Acute Kidney Injury↗
PubMed1993

Obstetrical analgesia in a parturient with antithrombin III deficiency.

Antithrombin III (AT III) deficiency is a rare inherited disorder which predisposes patients to thrombotic complications. Anticoagulation is necessary to prevent recurrent thrombosis and high doses of heparin are often required. Anticoagulation complicates analgesia in parturients with the condition. We describe such a patient, in pre-term labour, who was successfully managed during labour with intravenous nalbuphine and inhaled nitrous oxide (N2O).

Administration, Inhalation↗
PubMed1999

The treatment of heparin resistance with Antithrombin III in cardiac surgery.

PURPOSE: To report three patients who developed heparin resistance during cardiac surgery which was successfully managed with 1000 U Antithrombin III (AT III). CLINICAL FEATURES: We observed heparin resistance prior to cardiopulmonary bypass (CPB) in one patient and during the CPB in two patients. In the first patient who was scheduled for mitral valve replacement, although heparin was administered sequentially up to 500 U x kg(-1) prior the CPB, the ACT value was 354 sec. After 1,000 U ATIII were administered the ACT was 395 sec and CPB was initiated. The ACT remained between 496 and 599 sec throughout CPB and a total of 260 mg protamine sulfate was given. In the other two patients following 300 U x kg(-1) heparin, the ACT was up to 400 sec and CPB was initiated. During CPB, ACT were decreased 360 sec and 295 sec in patients II and III respectively. Although heparin was added 1,500 U, ACT increased to > or = 400 sec could not be achieved. In the second patient ATIII activity was found 10%. After the administration of 1,000 U ATIII, ATIII activity was found to be 67% 40 min later and ACT were increased up to 400 sec. There was no thrombosis within the extracorporeal circuit, additional heparin was not required, less protamine was administered (< or = 3 mg x kg(-1)) and no excessive postoperative bleeding was observed in all patients. CONCLUSION: We recommend that AT III supplementation should be considered to manage heparin resistance prior or during CPB in patients undergoing open heart surgery.

Adult↗
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↗
PubMedDate not supplied

Effect of sulfated xylans during the interaction of [125I]-thrombin with antithrombin III or heparin cofactor II of human plasma.

[125I]-Labeled thrombin was incubated with human plasma and its interactions with the two plasma protease inhibitors antithrombin III (AT-III) or heparin cofactor II (HC-II) were investigated in the presence of oat spelts xylan sulfate (OSXS), sodium pentosan polysulfate (SP-54), and the results were compared with heparin and dermatan sulfate. Addition of OSXS or SP-54 enhanced the complexation of thrombin with HC-II or with both AT-III and HC-II depending upon the concentration and the duration of the interactions of the sulfated compounds with plasma. During the 30 s interaction, OSXS and SP-54 enhanced both AT-III-thrombin and HC-II-thrombin interaction while heparin was more selective and enhanced only the AT-III-thrombin interaction. However after a 2 min interaction, heparin showed an increase in the HC-II-thrombin interaction at higher concentrations. The complexations of AT-III-thrombin and HC-II-thrombin were reversed in the presence of 200 micrograms/ml of SP-54 during a 30 s interaction or in presence of 100 micrograms/ml of OSXS during a 2 min interaction. The Western blotting method of detecting thrombin showed that during the 10 s interaction, heparin enhanced the thrombin-AT-III complex formation while OSXS enhanced the thrombin-HC-II complex formation.

Antithrombin III↗
PubMed1998

Chronic pulmonary thromboendarterectomy complicated by antithrombin III deficiency and antiphospholipid syndrome.

Pulmonary thromboendarterectomy was performed on two patients with chronic pulmonary thromboembolism showing thrombotic tendency. Patient 1 was a 25-year-old male with the disease complicated by congenital antithrombin III deficiency. Patient 2 was a 21-year-old male with the disease complicated by antiphospholipid syndrome. Both patients were admitted to the center upon showing dyspnea. Lung perfusion scintigraphy revealed multiple defects in the right and left lungs. Pulmonary arteriography showed occlusion and stenosis from lobar to segmental arteries. Cardiac catheterization showed marked pulmonary hypertension. Pulmonary angioscopy confirmed the presence of organized thrombi while an intravascular ultrasound revealed a thickening of the pulmonary arterial walls in both lungs. After the insertion of an inferior vena cava filter in each patient, surgery was performed. Following a median sternotomy, a cardiopulmonary bypass was utilized to induce deep hypothermia at a pharyngeal temperature of 16 degrees C, after which a thromboendarterectomy of the bilateral pulmonary arteries was performed under intermittent circulatory arrest. A large amount of organized thrombi was extracted from these arteries. After surgery, both patients showed good postoperative outcome with improved blood flow in both lungs, reduced pulmonary arterial pressure and increased cardiac output.

Adult↗
PubMed1999

Antithrombin treatment of severe hepatic veno-occlusive disease in children with cancer.

UNLABELLED: Hepatic veno-occlusive disease (VOD) is a well-known complication of chemotherapy in Wilms tumor patients, particularly young children. Although this complication resolves uneventfully in most patients, fatal cases have been reported. Severe VOD after transplantation has a high mortality rate ranging from 45% to 98%. New hemostatic therapeutic strategies have significantly improved the prognosis of VOD. Chemotherapy-related VOD in Wilms tumor usually has a good prognosis. We describe two patients with Wilms tumor and one with acute lymphoblastic leukemia, who developed severe veno-occlusive disease of the liver according to the Baltimore criteria while undergoing chemotherapy; the symptoms were hepatomegaly, ascites, hyperbilirubinemia, weight gain and, in one patient, short-term lethargy. Elevated LDH levels of 872 to 12,000 U/l were observed in our patients. All patients had thrombocytopenia between 29,000 and 40,000/microl and decreased antithrombin (AT) and protein C levels; two patients had gastrointestinal bleeding. All patients developed a coagulopathy because of severe hepatic dysfunction. Two patients received low-dose heparin at the onset of VOD. The thrombolytic therapy was rapidly changed to AT supplementation (20-80 IU/kg bw 2x per day) without heparin when thrombocytes were very low or gastrointestinal bleeding occurred. Resolution of VOD was observed in all patients receiving AT alone. The chemotherapy was discontinued in a patient with accidental actinomycin D overdosage in view of the severity of symptoms. The remaining two patients received chemotherapy according to the therapy protocol after restitution. All patients survived without sequelae with a median follow-up of 28 months (range 8-48 months). CONCLUSION: Hepatic veno-occlusive disease is a rare but increasingly recognized complication in pediatric cancer patients receiving conventional chemotherapy. AT supplementation constitutes a good alternative treatment of severe VOD in comparison with other thrombolytic therapies, particularly in patients at high risk of bleeding.

Antineoplastic Agents↗
PubMed1997

[D-dimer, thrombin-antithrombin III-complex (TAT) and prothrombin fragment 1+2 (PTF). Parameters for monitoring therapy with low molecular-weight heparin in coagulation disorders].

Two groups of 15 patients each with disseminated intravascular coagulation in association with septic disease were treated with low-molecular-weight heparin (lmw-heparin) in different dosages (group I: 1.5-5 IE/kg body weight (BW) per hour; group II: 8-15 IE/kg BW). We studied the levels of D-dimer, thrombin-antithrombin III complex (TAT), prothrombin fragments 1 and 2 (PTF), and global tests of coagulation like prothrombin time (PT), activated partial thromboplastin time (PTT), thrombin time (TT) and platelet count, plasminogen activation (PA) and fibrinogen concentration to estimate the success of heparin therapy in the two groups. TT and fibrinogen concentration were not suitable to follow the course of the coagulation disorder, PT, PTT, platelet count progressively PA, D-dimer, TAT, and PTF normalised progressively after heparinisation. However, only the last three parameters were sensitive enough to show different effects of variable dosages of lmw-heparin. D-dimer, TAT, and PTF levels declined in proportion with heparin concentrations, and thus appear to be the most useful parameters for monitoring the therapeutic effect of heparin in septic coagulopathies.

Anticoagulants↗
PubMed2003

Combined antithrombin and protein C supplementation in meningococcal purpura fulminans: a pharmacokinetic study.

PURPOSE: To document in patients with meningococcal purpura fulminans (PF), the effects of a combined supplementation with antithrombin (AT) and protein C (PC) plasma concentrates and to estimate the pharmacokinetics and dose requirements of each inhibitor. DESIGN: Retrospective study of 15 patients. SETTING. One paediatric and one adult ICU in a university hospital. INTERVENTIONS: In addition to standard intensive care, all patients received a 100 IU/kg loading dose of AT and PC concentrates, followed by a continuous infusion (AT: 100-150 IU.kg.day; PC: 100 IU.kg.day in adults, and 400 IU/kg in infants). MEASUREMENTS: Clinical data, coagulation, and fibrinolysis parameters, AT and PC activities, and free protein S (PS) levels were sequentially measured. Restitution ratio, median increment after supplementation, and half-life of clearance from plasma were calculated for the two plasma substitutes. RESULTS. At admission, all patients had a severe decrease in AT, PC, and PS levels. The supplementation regimen induced a substantial increase in AT and PC activities, peaking at H18 and H48, respectively. The supplementation procedure did not modify free PS levels. The median values of AT and PC restitution ratio, increment in plasma activity observed after 100 IU/kg concentrate, and apparent half-life of clearance from plasma were 0.85 U.ml.U.kg and 0.59 U.ml.U.kg, 23% and 21%, 16 h and 6 h, respectively. CONCLUSION: If AT and PC concentrates are to be given in fulminant meningococcemia, the doses of supplementation should be at least 150 IU/kg AT and 250 IU/kg PC as loading dose and 150 IU/kg AT and 200 IU/kg PC as daily maintenance therapy. Taking into account the individual variability in inhibitor deficiency and restitution ratio, repeated measurements of plasma levels are mandatory to obtain a patient-based adjustment of the supplementation.

Antithrombins↗