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Results for “Antithrombin III Deficiency”

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At least 181 records · Page 10Linked to original sources
PubMed2005

Constitutional trisomy 8 mosaicism with myelodysplastic syndrome complicated by intestinal Behcet disease and antithrombin III deficiency.

Trisomy 8 is the most common acquired chromosomal abnormality associated with myeloid malignancy. As a constitutional trisomy 8 mosaicism (T8M), it exhibits an extremely variable phenotype. In addition, Behcet disease (BD) has been reported as an unusual complication of myelodysplastic syndrome (MDS). To our knowledge, 12 case reports of various hematologic malignancies in patients with T8M and 18 case reports of MDS with acquired trisomy 8 complicated by BD have been published to date. We report a case of constitutional T8M with MDS complicated by intestinal BD and antithrombin III deficiency.

Antithrombin III Deficiency↗
PubMedDate not supplied

[Antithrombin III deficiency as a risk factor in postoperative thrombosis].

Hypercoagulation caused by decreased antithrombin III level leads to thrombosis inspite of postoperative prophylactic heparin therapy. Induced low level of antithrombin III is recognised in particular diseases which lead to a reduced ATIII synthesis, high breakdown or loss. Induced forms should be substituted with ATIII transfusions. Congenital forms should be treated lifelong with coumarin derivates. One should always suspect an ATIII deficiency when in spite of full heparin dosage a prolonged plasma thrombin time is not attained. A case history of recurrent thrombosis may also point to such deficiency.

Antithrombin III↗
PubMedDate not supplied

[Treatment of deep venous thrombosis in congenital antithrombin III deficiency with low molecular weight heparin].

A 19-year old male patient with hereditary antithrombin III type I deficiency was admitted for thrombosis of the right iliac, femoral and popliteal veins. Treatment with a low molecular weight heparin resulted in recanalization of the veins confirmed by phlebography. After two weeks of treatment, the drug was replaced by another low molecular weight heparin and this was followed, 3 weeks later, by a documented relapse of thrombosis.

Adult↗
PubMedDate not supplied

Severe preeclampsia in antithrombin III deficiency with no history of venous thromboembolism.

Complications of pregnancy, such as preeclampsia, placental abruption, fetal growth retardation, still-birth and fetal death are associated with an increased frequency of pro-thrombotic abnormalities. We describe a case of severe preeclampsia and multiple placental infarctions in a 28-year-old woman at 31 weeks' gestation. Despite a negative personal history for venous thromboembolism, coagulation screening for thrombophilia detected an isolated antithrombin III deficiency. In view of the high prevalence of pro-thrombotic complications, laboratory screening for thrombophilia would be advantageous in women with complicated pregnancies, to ensure adequate management in high-risk situations, as suggested by larger-scale clinical investigations.

Adult↗
PubMed1989

[Congenital type I antithrombin III deficiency with serious complications in a 7-year-old girl].

This case report concerns a child admitted to the County Hospital of Zalaegerszeg with the symptoms of ataxia, focal convulsions and hemiparesis. Anticonvulsive therapy abolished the epileptic manifestations, but hemiparesis remained unchanged. At the age of six and half years progressive venous thrombosis developed first on the left and some days later on the right lower limb. Phlebography revealed on both sides thrombosis of the vena iliaca which led to stenosis of the right femoral vein and dilated venous collaterals on the abdomen and right thigh. Coeliacography showed an enlarged spleen and varicosity around the portal vein. Later thrombosis of the arteria dorsalis pedis developed indicated by the gangrene the fifth toe. At this stage the child was transfered to the Pediatric Department of the University of Pécs for further evaluation. Examination of the hemostasis showed hypercoagulability due to antithrombin III deficiency pointing towards a common cause, namely thromboembolism of the earlier and recent clinical manifestations. A reduced activity of the antithrombin III was also observed in the mother and two sisters of the child. The response to Syncumar therapy was beneficial, arterial thrombosis regressed and no further thromboembolic complications developed.

Acenocoumarol↗
PubMed1982

Budd-Chiari Syndrome and antithrombin III deficiency.

Presented herein is a case report of a 20-year-old woman with a past history of oral contraceptive use who developed Budd-Chiari syndrome. Onset of her illness was abrupt and stormy, simulating fulminant viral hepatitis or toxic hepatic injury. She died within six months of her initial presentation. Although the patient discontinued the use of oral contraceptives two years prior to the initial presentation of the disease, the morphologic features of the venous thrombosis and hepatic damage were indicative of a chronic, ongoing process of longer than six months' duration, thus raising the possibility of a cause-effect relationship between the "pills" and thrombotic process. Of interest was the finding of persistently depressed antithrombin III levels. While a relationship between oral contraceptive usage, antithrombin III deficiency and the Budd-Chiari syndrome is strongly suggested in this case, prospective studies are needed to substantiate this view.

Adult↗
PubMed1976

Prophylactic and therapeutic use of anticoagulants in inherited antithrombin III deficiency.

A family with a pronounced history of venous thrombotic disease is described. Several members were found to have reduced antithrombin III levels. Heparin cofactor activity was reduced in the antithrombin III-deficient plasma. The proposita, who presented with bilateral iliofemoral vein thrombosis early in pregnancy, was treated initially with heparin, and after the 12th week of pregnancy was maintained on oral anticoagulants until she was 38 weeks pregnant. Heparin was then given and continued throughout the delivery period and for 10 days postpartum with no evidence of recurrent thrombosis. The effect of infusing 5 units of fresh frozen plasma on the antithrombin III level and the response to heparin were minimal and short-lived. Oral anticoagulatns produced a rise in the antithrombin III level. These results demonstrate the importance of maintaining antithrombin III-deficient subjects on long-term oral anticoagulant therapy.

Adult↗
PubMed2001

Budd-Chiari syndrome and extrahepatic portal obstruction associated with congenital antithrombin III deficiency.

We report a patient with Budd-Chiari syndrome (BCS) and extrahepatic portal obstruction (EHO) associated with congenital antithrombin (AT) III deficiency. A 35-year-old man was admitted to Nishi Kobe Medical Center for evaluation of abnormal intrahepatic veins. By various imaging modalities, BCS and EHO were diagnosed. Laboratory data revealed parallel decreases in activity and antigen concentration of AT III despite normal liver function. Taken together, the etiology of both BCS and EHO was considered to be thrombosis, associated with congenital AT III deficiency. Two years after beginning warfarin therapy, the patient has no symptoms and his liver function remains normal. Anticoagulant therapy is considered useful for preventing progression of the disease.

Adult↗
PubMed1990

[Danazol and antithrombin III deficiency].

The study concerned 7 subjects (3 men, 4 women) with nonfamilial antithrombin III deficit which, in the absence of known causes of acquired deficiency, was defined as "sporadic". Danazol (an attenuated synthetic androgen) already shown to be capable of compensating for a lack of certain antiproteases, was given in doses of 200 mg 3 times per day for 10 days, resulting in a rapid rise (mean 21.2%) in antithrombin III values. Unlike results reported in the literature in cases of familial antithrombin III deficit, the levels did not drop below their initial values despite discontinuance of the drug but unexpectedly remained high and even shows a slight subsequent rise. Although our study was limited to 11 cases, these data seem worthy of being reported, with the prospect of other confirmations concerning either this sort of "sporadic" antithrombin III deficit or the favorable effect of Danazol, even at long term.

Antithrombin III Deficiency↗