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Results for “Antithrombin III Deficiency”

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At least 757 records · Page 42Linked to original sources
PubMed1990

Screening for hypercoagulable states in vascular surgical practice: a preliminary study.

The prevalence and importance of hypercoagulable states in the general vascular surgical population is unknown. Antithrombin III, protein C, protein S, plasminogen, lupus-like anticoagulant, and heparin-induced platelet activation were determined prospectively in 158 patients with aneurysmal (27), renovascular (1), cerebrovascular (28), aortoiliac (31), or infrainguinal (71) disease. Sixteen abnormal test results were obtained in 15 patients (9.5%) as follows: deficiencies of antithrombin III (2), protein C (4), and protein S (1) and presence of lupus-like anticoagulant activity (5) and heparin-induced platelet activation (4). Reconstructive surgery was performed in 137 of the study patients. Five reconstructions, all infrainguinal bypass grafts, suffered thrombosis within 30 days. Early graft thrombosis occurred in three (27%) of 14 patients with abnormal preoperative test results compared to two (1.6%) of 123 patients with normal testing (p less than 0.01). Of the three patients with abnormal test results and graft thrombosis, lupus-like anticoagulant was detected in two and heparin-induced platelet activation in one. This preliminary study supports routine preoperative screening for lupus-like anticoagulant and heparin-induced platelet activation in patients undergoing infrainguinal reconstruction. Hypercoagulable states appear to be sufficiently common and important in the general vascular surgical population to warrant further investigation.

Adult↗
PubMed1995

Mesenteric venous thrombosis due to coagulation deficiencies - a case report.

Mesenteric venous thrombosis is a rather rare condition posing diagnostic problems and very often with an obscure etiology. Recently, various coagulation deficiencies were found as the main etiologic factor. A case of a 75-year-old man with acute abdomen is presented. Exploratory laparotomy revealed a 250 cm necrosis of the small intestine. Patient was successfully treated by resecting the entire involved segment of the bowel. After a complete coagulation profile examination, deficiencies of protein C and anti-thrombin III were found and were considered as the main cause of the disease. In cases with known coagulation deficiencies the presence of an acute abdomen should raise suspicion of mesenteric venous thrombosis.

Abdomen, Acute↗
PubMed1989

Characterization of antithrombins produced by active site mutagenesis of human alpha 1-antitrypsin expressed in yeast.

Both congenital and acquired antithrombin-III (AT-III) deficiencies are amenable to replacement therapy. We describe two antithrombins produced by recombinant DNA techniques from human alpha 1-antitrypsin (alpha 1AT) cDNA in yeast. Alteration of the alpha 1AT active site, replacing methionine 358 with arginine, results in a thrombin inhibition rate similar to that of heparin-activated AT-III. Alteration of two further residues, to give a five-residue sequence identical to AT-III, does not increase this rate further. Neither antithrombin is activated by heparin; both are unglycosylated and have shorter in vivo half-lives (t1/2) than human alpha 1AT. These antithrombins should be suitable for therapeutic replacement of AT-III in cases of congenital deficiency and in conditions associated with acquired AT-III deficiency, such as disseminated intravascular coagulation.

Amino Acid Sequence↗
PubMed1985

[Significance of antithrombin III in clinical liver transplantations].

The activity of AT III was measured by chromogenous substrates in 18 of 28 patients before, between and after liver transplantation. In half of all cases basic pathological activities could be observed. During transplantation, AT III is on an average decreased to 43% of the initial level. Examples are demonstrated for important AT III deficiencies after liver transplantation in man. Long-time examinations have shown AT III to be in the normal range or higher in 1 to 60 months after transplantation when the graft function is correct.

Adult↗
PubMed1982

[A case of the occlusion of the right middle cerebral artery due to congenital anti-thrombin III (AT III) deficiency (author's transl)].

The authors describe and discuss a case of the occlusion of the right middle cerebral artery due to congenital AT III deficiency. The patient, 23 years old, female, was admitted to our service with episodes of convulsive attacks, disturbance of consciousness and left hemiparesis on the fifth postoperative (laparotomy)day. She had been suffering from recurrent thromnbophlebitis of both legs. Right carotid angiogram revealed the occlusion of the trunk of the right middle cerebral artery about 13mm distal to its bifurcation. Routine laboratory findings on admission, including hematological tests, chemical tests of blood, liver function tests, kidney function tests, chest x-ray film and electrocardiogram, were within normal limits except leukocytosis. But examinations of coagulation and fibrinolysis showed decreased AT III activity and increased AT III antigen concentration. When examined her eight family members on the same examination, six individuals were affected with the decreased AT III activity. On about fourth hospital month, her neurological symptoms took a sudden turn for the worse again. But AT III concentrates transfusion and prescription of warfarin led to her striking clinical improvement. Eight cases of cerebral vessel disease due to congenital AT III deficiency were reported in literature. It is now concluded that AT III deficiency should be considered with one of the etiology of cerebral infarction and cerebral sinus thrombosis in young adults.

Adult↗
PubMed1984

Low antithrombin III levels in neonates with idiopathic respiratory distress syndrome: poor prognosis.

Automated microanalytic chromogenic coagulation assays allow serial monitoring of critically ill newborn infants. In this study 84 premature infants [26 healthy prematures and 58 neonates with idiopathic respiratory distress syndrome (IRDS)] were studied daily during the first week of life, to investigate the possible significance of hemostatic abnormalities in IRDS. In neonates with IRDS, coagulation factors II and X, antithrombin III (AT-III), plasminogen, and alpha 2-antiplasmin were significantly lower than control values. Recovery of the initially low AT-III levels was delayed relative to the other coagulation parameters measured. An AT-III less than or equal to 0.15 U/ml was present within the first 6 h of life in eight patients who developed IRDS, seven of whom died within 48 h. Autopsy of these neonates showed widespread fibrin deposition and hemorrhage in vital organs consistent with intravascular coagulation. These findings indicate that very low levels of AT-III are associated with disseminated intravascular coagulation in neonates with IRDS and suggest that a deficiency of AT-III is predictive of a poor outcome.

Antithrombin III Deficiency↗
PubMed1981

Antithrombin III profiles in malignancy, relationship primary tumors and metastatic sites.

Variations of antithrombin III were studied in a non-randomized population of consecutive cancer cases admitted to a referral hospital. Differences between functional and immunologic assay were observed. Decreases were observed in both assays when compared to a population of hospitalized controls. Patients with cancer of the colon, ovary and prostate showed a deficiency of antithrombin III more frequently than other common tumors. When all tumor cases were subdivided into those in remission compared to those with metastases, a significant decrease in antithrombin III also could be shown. Metastases to the liver were strikingly common in cancer patients with decreased antithrombin III. In these patients, the decrease in antithrombin III could be statistically correlated with reduction in serum albumin.

Antithrombin III↗
PubMed1990

The confirmation of preclinical familial antithrombin deficiency using polymorphism and specific oligonucleotide probes .

Familial deficiency of antithrombin causes venous thromboembolism which may not become clinically apparent until the third or fourth decade of life. In affected families conventional tests of antithrombin activity and antithrombin antigen levels may not be sufficiently accurate to discriminate with certainty between those young people who have inherited the abnormal gene and those who have not. Molecular probes for polymorphisms linked to the gene of interest may be informative but in some families are not. We have used the knowledge of the precise molecular defect in antithrombin Glasgow to design and manufacture DNA probes and have used these probes to detect the presence of the abnormal gene in DNA from clinically unaffected family members and thus confirm their inheritance of antithrombin deficiency and their predisposition to venous thromboembolic disease.

Antithrombin III↗
PubMed2006

The deficiencies of protein C, protein S and antithrombin III in patients with retinal vein occlusion: a Turkish sample.

The aim of this study was to test the role of the decreased levels of protein C (PC), protein S and antithrombin III on the pathogenesis of retinal vein occlusion (RVO). Of 54 patients with RVO, seven had the decreased levels of PC. We found statistically significant differences for the rate of cases with PC deficiency between the patients with RVO and controls (P < 0.05).

Adult↗
PubMed1988

Antithrombotic properties of heparin in a neonatal piglet model of thrombin-induced thrombosis.

The relative deficiency of antithrombin III (AT III) in neonatal plasma results in lower recovery of heparin in some assay systems. It is uncertain whether low AT III levels also limit the antithrombotic effects of heparin in this age group. We therefore compared the antithrombotic properties of heparin in mature pigs and newborn piglets, whose coagulation and inhibitor system closely resembles that of the human neonate. Animals were pretreated with saline, 10 or 25 U/kg heparin (n greater than or equal to 16 per age group and dose). Following an injection of 100 U/kg thrombin, systemic 125I-fibrinogen consumption and local 125I-fibrinogen incorporation into jugular venous stasis thrombi were measured. Significantly more 125I-fibrinogen was consumed in piglets than in pigs systemically (p less than 0.0001), as well as within the occluded vein segment (p = 0.0112), largely because heparin was less effective in piglets than in pigs. This neonatal resistance to heparin could not be explained by lower heparin levels in the newborn animals. However, pretreatment with AT III concentrate significantly improved the antithrombotic properties of heparin in this age group (p less than 0.0001). We conclude that physiologically low AT III levels reduce the efficacy of heparin in neutralizing thrombin activity in newborn piglets. We speculate that AT III deficiency may also limit the antithrombotic properties of heparin in newborn infants with thrombotic disease.

Animals↗
PubMed1991

Incidence and clinical characteristics of hereditary disorders associated with venous thrombosis.

At present, different congenital defects in several proteins--antithrombin III (AT III), protein C (PC), protein S (PS), and plasminogen (PLG)--are known to be causes of hereditary predisposition to thrombosis (thrombophilia). The incidence of these hereditary disorders in our 204 patients (106 males and 98 females) with venous thromboembolism were 4% (three cases deficient in PC, three in PS, two in PLG, and one patient in AT III). Their families were studied. In all cases the disorders were inherited as an autosomal dominant trait. The first thrombotic episodes occurred at a age of below 40 years. There was no relationship between protein levels and the occurrence of thrombosis, although a significant relationship was observed between a positive history of thromboembolic disease and a diagnosis of protein deficiencies. We evaluated the differences between primary thrombosis and secondary thrombosis. The most common thrombotic sites were the deep veins. There were no differences between males and females. Evaluation of PC, PS, AT III, and PLG in patients with thromboembolic disease should be considered.

Adolescent↗
PubMed1985

Prenatal diagnosis of hemoglobinopathies by DNA analysis.

Restriction site polymorphisms are normal inherited variations in DNA that can be readily detected by restriction endonuclease analysis. Currently, 17 such polymorphisms are recognized within a 60 kb (kilobase) stretch of DNA which includes the beta-globin gene complex. Because of their proximity to the beta-globin gene, often these restriction site polymorphisms can be used to predict inheritance of beta-globin variants that produce disease. For example, restriction site polymorphisms can be used for prenatal diagnosis for the large majority of couples at risk of having a child with beta-thalassemia. When each member of such a couple is heterozygous at one or more of these 17 sites, family studies are usually successful in determining which forms of the polymorphism are co-inherited with the beta-thalassemia genes in that particular family. Subsequently, study of fetal DNA isolated from amniocytes obtained by midtrimester amniocentesis or from chorionic villi obtained by first trimester chorion biopsy will reveal which DNA polymorphisms that fetus has inherited. By deductive reasoning one can then predict which beta-globin genes it has co-inherited. Because of the general nature of these polymorphisms, which are related to the beta-globin gene and its variants only because of their proximity on chromosome 11, they are potentially useful in the prenatal diagnosis of any beta-chain hemoglobinopathy. Some hemoglobinopathies (including alpha-thalassemia, sickle cell anemia, and some cases of beta-thalassemia) can be detected directly by DNA analysis. In these cases in utero diagnosis does not need to rely on restriction site polymorphisms, which require preliminary family studies and are not applicable in all at risk pregnancies. Recently, genetic probes, which are necessary for detecting restriction site polymorphisms, have been isolated for sequences of several genes whose protein products are important in blood coagulation. These include probes for all three genes whose polypeptide products combine to form the fibrinogen molecule as well as probes for the prothrombin, Factor IX, Factor VIII, and antithrombin III genes. Defects in these genes are expected to be the causes of afibrinogenemia, prothrombin deficiency, hemophilia B, hemophilia A, and antithrombin III deficiency, respectively. From experience with other genes, it is expected that restriction site polymorphisms within and/or flanking these genes will be found.(ABSTRACT TRUNCATED AT 400 WORDS)

Anemia, Sickle Cell↗
PubMed2004

Antithrombin: in control of coagulation.

Antithrombin is a serine proteinase inhibitor (serpin) which controls the process of coagulation. It has a well defined structure, consisting of three beta-sheets, nine alpha-helices and a reactive centre loop (RCL). The RCL contains the reactive centre which harbours a bait sequence for target proteases; cleavage results in inhibition by a unique mechanism. The inhibitory activity of antithrombin is controlled by its interaction with the co-factor, heparin, which accelerates its interaction with target proteases. This ensures that heparin and its newer derivatives, such as heparin pentasaccharide, are the mainstay therapeutics for control of thrombosis or inappropriate clotting. The clinical importance of antithrombin is manifested by its clear association with thrombosis when deficiency states occur.

Animals↗
PubMed2006

Antithrombin Nagasaki (Ser 116 to Pro): a rare antithrombin variant with abnormal heparin binding presenting during pregnancy.

Quantitative antithrombin deficiency constitutes an important risk factor for venous thromboembolism, stillbirth, and other complications of pregnancy. Studies suggest, however, that individuals heterozygous for missense mutations involving the heparin-binding site of antithrombin do not have a significantly increased thrombotic risk. Owing to the rarity of such mutations, it remains unclear whether any specific heparin-binding site defects might be associated with thrombotic potential. We report here the case of a pregnant woman with an exceptionally rare Type II heparin-binding site antithrombin variant. This case highlights the difficult issues that are associated with the management of Type II antithrombin deficiency during pregnancy.

Adult↗