L-Asparaginase, Antithrombin Iii, and Thrombosis

Conard, J.; Cazenave, B.; Maury, J. P.; Horellou, Marie‐Hélène; Samama, M

doi:10.1016/s0140-6736(80)91538-x

Cited by 35 publications

(15 citation statements)

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“…The most frequent site of vascu lar occlusion was the ileo-femoral venous district and the incidence was around 10% [Conard et al, 1980;Tura et al, 1981], Very recently, Steinherz et al [1981] re ported 2 children with ALL developing dural sinus thrombosis during induction treatment with vincristine, prednisone and asparaginase. The authors found this com plication in only 2 out of 187 previously untreated children with ALL.…”

Section: Discussionmentioning

confidence: 99%

“…First, the massive destruc tion of leukaemic blast cells may cause the release of procoagulant material, as is ty pically seen in acute promyelocytic leu kaemia; second, chemotherapy may im pair the synthesis of proteins physiologi cally involved in the neutralization of acti vated procoagulant factors. Following Lasparaginase therapy, a significant de crease of plasma antithrombin III (AT III) has been described and this may ac count for the thromboembolic manifesta tions described in rare cases of acute lym phoblastic leukaemia (ALL) [Pitney et al, 1980;Conard et al, 1980;Vellenga et al, 1980;Turaet al, 1981].…”

Section: Introductionmentioning

confidence: 99%

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Fatal Pulmonary Embolism and Antithrombin III Deficiency in Adult Lymphoblastic Leukaemia during L-Asparaginase Therapy

et al. 1983

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We describe 2 adult patients with acute lymphoblastic leukaemia (ALL) who died from pulmonary embolism following L-asparaginase treatment. Since this drug is known to cause a decrease in antithrombin III, the most important protein physiologically involved in the neutralization of thrombin, we studied the behaviour of this inhibitor in 14 ALL patients treated with a protocol including a 14-day course of L-asparaginase. A significant but transient fall of biological and immunological antithrombin III and a concomitant reduction of fibrinogen were documented.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Fatal Pulmonary Embolism and Antithrombin III Deficiency in Adult Lymphoblastic Leukaemia during L-Asparaginase Therapy

et al. 1983

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“…We have demonstrated another effect of L-asparaginase on hemostasis, namely reduction in both functional and immunologic levels of antithrombin 111. Conard and coworkers in France have previously reported tremendous decreases in functional antithrombin Ill activity in patients treated with high daily doses of L-asparaginase [20] .…”

Section: I Scussl Onmentioning

confidence: 99%

“…Yet, thrombosis or thromboembolism secondary to L-asparaginase is infrequently commented upon in the literature cited [19,20,31,321. It seems likely that concomitant reductions in both antithrombin 111 and levels of multiple clotting factors may be mutually "protective" against both excessive bleeding and thrombosis during L-asparaginase treatment.…”

Section: I Scussl Onmentioning

confidence: 99%

Reduced antithrombin III levels during L‐asparaginase therapy

Buchanan¹,

Holtkamp

1980

Med. Pediatr. Oncol.

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Antithrombin III levels were measured in serum before, during, and after therapy with three different dosage regimens of L-asparaginase in 11 children with acute lymphoblastic leukemia. Levels determined by both functional and immunologic methods were transiently reduced during alternate-day or daily L-asparaginase treatment but not affected when the drug was administered only every 10 days. The probable mechanism of this effect is impaired hepatic synthesis of antithrombin III, resembling the acute and transient deficiency of other asparagine-rich proteins during L-asparaginase administration.

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“…Thromboembolic manifestations have been described following L-ASE therapy with a significant decrease of antithrombin III by other authors [Pitney, 1980;Conard, 1980;Vellenga, 1980;Tura, 1981].…”

Section: Pulmonary Embolism and L-asparaginase Therapymentioning

confidence: 92%