Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Antithrombin III Deficiency”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 739 records · Page 41Linked to original sources
PubMed1987

Antithrombin III in full-term and pre-term newborn infants: three cases of neonatal diagnosis of AT III congenital defect.

Antithrombin III (AT III) plasma levels were investigated in 18 full term neonates and 14 healthy preterm neonates. A control group of 20 healthy adults was also studied. AT III was measured as antigen concentration (Ag) and antithrombin or anti-factor Xa heparin cofactor (H.C.) activities. Crossed immunoelectrophoresis on heparin-agarose (H-CIE) was carried out on plasma samples; moreover the distribution of isoantithrombins was investigated on whole plasma by a technique of crossed immunoelectrofocusing (CIEF). AT III plasma levels in full term infants were significantly lower as compared to the adult values. The preterm newborns group showed a further significant decrease in AT III levels as compared to the full term neonates. In all infants AT III H-CIE runs displayed a single fast moving anodal peak, so that a normal binding to heparin was demonstrated. The CIEF AT III plasma pattern of the adults as well as of all neonates displayed three major peaks at pH range 5.2-4.9, a small amount of AT III at pH 4.9-4.8 and a minor peak at pH 4.8-4.6, so that it was concluded that the isoantithrombins plasma distribution in neonatal age is identical to that of the adult subjects. Four neonates whose mothers were affected by AT III congenital defect were also investigated: diagnosis of congenital deficiency was established in three cases.

Adult↗
PubMed2000

[Hereditary antithrombin deficiency resulting in severe neonatal thrombosis].

We report a severe vena cava inferior thrombosis in a mature two day-old boy. Pregnancy and birth were event free. The mother had antithrombin deficiency. During pregnancy she was treated with enoxaparin and just before delivery with 2000 IE antithrombin concentrate. At admission the child had unmeasurable antithrombin and low protein C concentrations. He was treated with antithrombin concentrate and heparin. The thrombus disappeared, and now he is on maintenance treatment with warfarin. Risk factors and treatment of inherited antithrombin deficiency are discussed.

Adult↗
PubMed1995

Ectopic transcript analysis in human antithrombin deficiency.

Reverse transcription and amplification of total cellular RNA isolated from peripheral blood mononuclear cells has been used to identify correctly spliced transcripts for human antithrombin. We have explored the potential of this technique for identifying the underlying mutation in five individuals with a Type I deficiency and one individual with a Type II deficiency. In each case correctly spliced transcripts of the correct size were obtained, direct sequencing of which clearly demonstrated the mutation. This method simplifies the detection of mutations in cases of antithrombin deficiency and further extends the use of ectopic transcript analysis.

Antithrombin III↗
PubMed1998

Prevalence of factor V Leiden (APCR) and other inherited thrombophilias in young patients with myocardial infarction and normal coronary arteries.

OBJECTIVE: To investigate the role of activated protein C resistance (APCR, factor V Leiden) in coronary artery thrombosis. METHODS: The prevalence of APCR and of congenital deficiencies of antithrombin III, protein C, protein S, plasminogen, and factor XII was investigated in adult patients under 45 years of age with acute myocardial infarction. The results were compared with those of a group of 53 age and sex matched control subjects. RESULTS: Among 75 patients under the age of 45 years who were admitted from November 1994 to April 1996 for acute myocardial infarction, 22 (29.3%) had normal coronary arteriography (group I) and 53 (70.7%) had significant coronary artery disease (group II). Inherited thrombophilia was more often found in group I (4/22, 18.2%) than in group II (4/53, 7.5%) but the difference was not significant (F test: p = 0.22). The prevalence of APCR was 9.1% (2/22) in group I, 3.8% (2/53) in group 2 (p = 0.57), and 3.8% (2/53) in the normal control group (p = 0.57). CONCLUSIONS: The prevalence of congenital thrombophilias, including APCR, does not seem to be increased in young patients with myocardial infarction and normal coronary angiograms, compared with young patients with coronary atherosclerosis and with normal control subjects. However, the statistical power of the study is too low to detect a significant difference and these results are published to allow a meta-analysis of this problem in the future.

Activated Protein C Resistance↗
PubMed1988

Antithrombin III in surgery.

Monitoring of AT III values and, if necessary, replacement therapy, are particularly important during the peri- and postoperative phase, or after multiple trauma, in order to prevent thromboembolic complications especially in operations on the liver, or when using heart-lung machines and in shock and pronounced DIC. AT III deficiency is partly dependent on the type and severity of the disorder with the resultant increased in turnover and partly on the synthesis capacity of the liver. Life-threatening complications can be prevented by AT III replacement.

Adult↗
PubMed1992

Septic shock, multiple organ failure, and disseminated intravascular coagulation. Compared patterns of antithrombin III, protein C, and protein S deficiencies.

STUDY OBJECTIVE: Our aim was to document the following in patients with septic shock and disseminated intravascular coagulation (DIC): (1) the influence of DIC in the mortality rate and the occurrence of organ failure; (2) the comparative prognostic value of initial antithrombin III (ATIII), protein C (PC), and protein S (PS) levels; and (3) the compared pattern of sequential ATIII, PC, and PS levels according to clinical outcome. DESIGN: Demographic data, criteria of severity, mortality in ICU, frequency of organ failure, hemodynamic and oxygenation parameters, and laboratory findings were compared in patients with septic shock according to the occurrence of DIC. Initial and sequential levels of ATIII (activity), PC (antigen and activity), PS (total and free), and C4b binding protein (C4bBP) were compared according to the outcome in patients with DIC. PATIENTS: Sixty patients with septic shock were studied. Forty-four entered the group DIC+; 16 entered the group DIC-. RESULTS: Simplified acute physiologic score (SAPS), frequency of acquired organ failure, blood lactate, and transaminase values were significantly higher in the group DIC+. The mortality rate reached 77 percent in group DIC+ vs 32 percent in DIC- (p less than 0.001). In patients with DIC, a fatal outcome was associated with higher bilirubin and transaminase levels, lower PaO2/FIo2 ratio, Vo2, Do2 and O2 extraction. In the group DIC+, all patients but two had severe deficiencies in ATIII and PC levels. Significant correlations were found between initial ATIII and PC levels, PC and free PS levels, and free PS and C4bBP levels. Initial ATIII levels had the best prognostic value for prediction of subsequent death. Serial measurements were consistent with a prolonged ATIII and PC deficiency with significantly different levels between survivors and nonsurvivors. CONCLUSIONS: DIC is a strong predictor of death and multiple organ failure in patients with septic shock. Sequential ATIII, PC, and PS measurements were consistent with prolonged consumption or inhibition that might account for a sustained procoagulant state and inhibition of fibrinolysis. The initial ATIII level was the best laboratory predictor of death in these patients.

Antithrombin III Deficiency↗
PubMed1997

Antithrombin: molecular basis of deficiency.

Antithrombin is a plasma protein regulator of coagulation proteinase activity, particularly that of thrombin. Its deficiency is a risk factor for venous thromboembolism. Considerable progress has been made in understanding the organisation and function of the antithrombin gene and protein, and the molecular basis of deficiency, all of which are reviewed, but briefly, here.

Antithrombin III↗
PubMed2003

Influence of modest endotoxemia on postoperative antithrombin deficiency and circulating secretory immunoglobulin a levels.

OBJECTIVE: To evaluate the influence of modest endotoxemia on postoperative antithrombin deficiency and cholestasis. SUMMARY BACKGROUND DATA: It has not been determined whether endotoxin translocation in small amounts is a physiological phenomenon or whether it is a potential health hazard. METHODS: Blood endotoxin, antithrombin III (ATIII), secretory immunoglobulin A (sIgA), which was selected as a marker of cholestasis, C-reactive protein (CRP), and alpha-1-antitrypsin (AAT) concentrations were measured from the 20 patients undergoing curative gastrectomy for gastric cancer preoperatively and postoperatively. Portal and systemic blood samples were taken for the analysis of endotoxin and interleukin-6 (IL-6) concentrations during surgery in these patients. RESULTS: Although plasma endotoxin levels showed a significant increase during surgery, we did not find a correlation with ATIII, sIgA, CRP, and IL-6 levels. Systemic blood endotoxin levels during surgery correlated with a postoperative rise of serum AAT levels. Plasma ATIII levels transiently decreased on the first and third postoperative day, and sIgA levels were shown to increase on the seventh postoperative day. There was a weak relationship between the extent of postoperative endotoxemia and a reduction in ATIII concentrations. CONCLUSIONS: The influence of modest endotoxemia on postoperative antithrombin deficiency and cholestasis was limited, and increased translocational endotoxemia during abdominal surgery may be a physiological phenomenon to trigger off an acute-phase protein response.

Adult↗