1979
DOI: 10.1016/s0140-6736(79)90084-9
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Subcutaneous Heparin for Thrombosis in Pregnant Women With Hereditary Antithrombin Deficiency

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Cited by 40 publications
(18 citation statements)
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“…Similarly, heparin is reported to prevent the toxicity of thromboplastin injection in mice [23]. However, heparin increases the turnover rate of anti thrombin [24], and the administration of heparin to AT-111 -deficient patients may therefore paradoxically increase an existing risk of thrombosis [25], While the aetiology of HUS remains undetermined, our data support the existence of a stage of disseminated intra vascular coagulation as a factor of pathogenetic signifi cance [2-4,8.10], Several members of the patient's family had shown a disposition to thrombotic disease during pregnancy and delivery, but the family does not suffer from hereditary antithrombin deficiency [26], Since HUS in adults occurs mostly in women in association with preg nancy, parturition or oestrogen treatment [2,4], there are reasons to believe that changes in the hormonal balance in combination with a thrombogenic stress (pregnancy, par turition) predispose to this syndrome. Although not con sistently accepted, several authors have reported a de creased level of AT-III during pregnancy, parturition or oestrogen treatment [27,28].…”
Section: Discussionsupporting
confidence: 59%
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“…Similarly, heparin is reported to prevent the toxicity of thromboplastin injection in mice [23]. However, heparin increases the turnover rate of anti thrombin [24], and the administration of heparin to AT-111 -deficient patients may therefore paradoxically increase an existing risk of thrombosis [25], While the aetiology of HUS remains undetermined, our data support the existence of a stage of disseminated intra vascular coagulation as a factor of pathogenetic signifi cance [2-4,8.10], Several members of the patient's family had shown a disposition to thrombotic disease during pregnancy and delivery, but the family does not suffer from hereditary antithrombin deficiency [26], Since HUS in adults occurs mostly in women in association with preg nancy, parturition or oestrogen treatment [2,4], there are reasons to believe that changes in the hormonal balance in combination with a thrombogenic stress (pregnancy, par turition) predispose to this syndrome. Although not con sistently accepted, several authors have reported a de creased level of AT-III during pregnancy, parturition or oestrogen treatment [27,28].…”
Section: Discussionsupporting
confidence: 59%
“…Although not con sistently accepted, several authors have reported a de creased level of AT-III during pregnancy, parturition or oestrogen treatment [27,28]. Women with hereditary AT-III deficiency of moderate degree seem to be particularly prone to develop thromboembolism under these circum stances [26], perhaps because the AT-III deficiency is further accentuated. The marked decrease in plasma AT-111 reported here may be of diagnostic significance in the postpartum HUS.…”
Section: Discussionmentioning
confidence: 99%
“…The use of prostacycline has been proposed [12], as has the application of low-dose aspirin [13], Recently, it was reported that haemodialysis can be carried out without heparin with little risk of dialyzer clotting [14], but in most places one would probably prefer to increase the safety by using some form of anticoagulant protection. We may suggest a re placement of the intravenous application of heparin with an administration to the patients prior to haemodialysis of low-dose, subcutaneous heparin, which gives a cumu lative anticoagulant effect, and with which good results have been obtained in the treatment of thrombotic episodes in pregnant women deficient in AT-III [7]. Such studies are currently being initiated.…”
Section: Discussionmentioning
confidence: 99%
“…A direct thrombotic effect of the hormones has never been demonstrated, and the influence on blood coagulation and fibri nolysis has been mild, causing fluctuations mostly within the normal ranges, which would suggest a causal relationship to the occurrence of epi sodes of thrombosis only in vulnerable individuals. The problem of causal ity thus remains enigmatic [2], The reported decrease in the concentration in plasma of antithrom bin III following administration of OC [3] gained increased interest when it was found that women with hereditary antithrombin III deficiency exhib ited a particularly high risk of thromboembolism during pregnancy or when treated with OC [4][5][6], but the particular mechanism by which this vulner ability is expressed remains a puzzle. A delayed resolution of fibrin might contribute to the increased risk, and several studies report on the effect of hormones on the fibrinolytic activity of blood [7][8][9][10][11][12].…”
Section: Introductionmentioning
confidence: 99%