Cerebral sinus thrombosis as a potential hazard of antifibrinolytic treatment in menorrhagia.

Achiron, Anat; Gornish, Michael; Melamed, Eldad

doi:10.1161/01.str.21.5.817

Cited by 24 publications

(6 citation statements)

References 14 publications

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“…Thus, in most situations, a causal relationship cannot be established. Most reported cases are related to medications for cancer (asparaginase [196][197][198][199][200][201][202], tamoxifen [203][204][205], and thalidomide [206][207][208]), to hormone stimulation (androgen [209][210][211][212], danazol [213], isoflavone [215], and drugs for ovary stimulation [216][217][218]), stimulation of progenitor cells (erythropoietin [219,220]), or drugs related to homeostasis (heparin [221], heparinoid [222,223], and epsilon aminocaproic acid [224,225]). …”

Section: Drugsmentioning

confidence: 99%

“…A recent review showed that thalidomide, Table 3. Drugs associated with CVST OCs [6][7][8][9][10][11][12][13][14][15] Asparaginase [196][197][198][199][200][201][202] Tamoxifen [136,[203][204][205] Thalidomide [206][207][208] Androgen [209][210][211][212] Danazol (synthetic androgen) [213] Oxymetholone (synthetic androgen) [214] Isoflavone [215] Erythropoietin [219,220] Heparin [221] Pentosan polysulfate [222,223] Epsilon aminocaproic acid [224,225] Intravenous immunoglobulin [226] Clomipramine [227] Lithium [228] Sildenafil [229] Ecstasy [230] Vitamin A [231] Steroids [232][233]…”

Section: Drugsmentioning

confidence: 99%

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Risk Factors of Cerebral Vein and Sinus Thrombosis

Freitas

Bogousslavsky

2007

Handbook on Cerebral Venous Thrombosis

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The risk factors for deep venous thrombosis (and for cerebral vein and sinus thrombosis, CVST) differ from those for arterial disease. The risk factors for venous thrombosis are linked to the Virchow triad of stasis of the blood, changes in the vessel wall, and changes in the composition of the blood, especially the first and third of these. Risk factors are usually divided into acquired (e.g. surgery, trauma, pregnancy, puerperium, lupus anticoagulant, malignant disease, and female hormones) and genetic (congenital thrombophilia). However, the separation of genetic and acquired risk factors is somewhat artificial, since they have additive effects and venous thrombosis is often multifactorial. In this review, we discuss acquired risk factors for CVST. These include hormonal changes (e.g. oral contraceptives use, hormone replacement therapy, pregnancy and puerperium), mechanical precipitants (e.g. head trauma, jugular catheterization, surgery, lumbar puncture), local and generalized infections, cancer, acquired prothrombotic states (e.g. hyperhomocysteinemia, nephrotic syndrome), inflammatory diseases (e.g. vaculitis, intestinal inflammatory disease), hematological disorders, neurological diseases (e.g. dural arteriovenous malformations, spontaneous intracranial hypotension), drugs and other situations. However, only some conditions are consistently present in case series, while many appear only in anecdotal reports. Thus, in most situations, a causal link cannot be established. Determining a cause-and-effect relationship is essential for developing preventive, diagnostic, and therapeutic strategies. Therefore, further multicentered, case-controlled studies are crucial for better understanding the pathogenesis of CVST.

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Section: Drugsmentioning

confidence: 99%

Section: Drugsmentioning

confidence: 99%

Risk Factors of Cerebral Vein and Sinus Thrombosis

Freitas

Bogousslavsky

2007

Handbook on Cerebral Venous Thrombosis

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“…There have been a few studies that suggested an increased risk of thromboembolism in patients receiving EACA [26–28]. The largest series of patients was published by Brown et al .…”

Section: Discussionmentioning

confidence: 99%

Acute promyelocytic leukaemia and acquired α‐2‐plasmin inhibitor deficiency: a retrospective look at the use of epsilon‐aminocaproic acid (Amicar) in 30 patients

Wassenaar

Black

Kahl

et al. 2008

Hematological Oncology

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Bleeding diathesis and a hyper-fibrinolytic state often accompany a diagnosis of Acute Promyelocytic Leukaemia (APML). This complication can have grave effects if not successfully treated, with a 10–20% incidence of haemorrhagic death. We hypothesized that α-2-antiplasmin levels would correlate with the risk for bleeding, and that administration of epsilon-aminocaproic acid (EACA) would attenuate that risk. To assess this, we conducted a retrospective chart review analyzing 30 APML patients, 17 of whom were treated with EACA. Thirty patients were treated, 21 with primary induction therapy. Patients with low α-2-antiplasmin levels were treated with a coagulopathy protocol consisting of low-dose heparin, EACA and blood product support. Seventeen patients (57%) developed haemorrhagic complications during their treatment. The presence and grade of haemorrhage appeared to be associated with the α-2-antiplasmin level. There were no grade IV haemorrhages or episodes of haemorrhagic death. One episode of central venous catheter associated thromboembolism and three deaths from infection during chemotherapy were observed. α-2-Antiplasmin levels are a reliable surrogate for fibrinolysis and haemorrhagic risk in patients with APML. Treatment with EACA is a rational way to pharmacologically inhibit fibrinolysis, is associated with a low incidence of severe haemorrhagic events, and appears to be safe with a low risk of thrombosis. Randomized clinical trials further assessing the efficacy and potential toxicity of EACA in inhibiting fibrinolysis in patients with APML are needed.

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“…The dose in the first patient, aged 31 years, was 3.0-4.5 g per day and in the second patient, aged 32 years, was 0.5-1.0 g per day [23]. In addition, there is a report of a 42-year-old woman treated with EACA, 3 g per day during menstruation, who developed a superior sagittal and left transverse sinus thrombosis [24]. These reports are all isolated and further information about possible underlying thrombophilic defects in these patients is not available.…”

Section: Management At Menarchementioning

confidence: 99%

Menorrhagia from a haematologist's point of view. Part II: management

Siegel

Kouides

2002

Haemophilia

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The management of menorrhagia has until recently been the domain of the gynaecologist. As haematologists, we are now addressing the issue of optimal management of menorrhagia in our patients with bleeding disorders. Addressing three life periods, the menarche, reproductive years, and postchildbearing years, this review will discuss the use of oral contraceptive agents, antifibrinolytics, non-steroidal anti-inflammatory drugs, intranasal DDAVP and the new levonorgestrel-impregnated IUD. Management of specific bleeding disorders will also be reviewed for von Willebrand disease, haemophilia A and B carriers, women with factor XI deficiency and PAI-1 deficiency.

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Cerebral sinus thrombosis as a potential hazard of antifibrinolytic treatment in menorrhagia.

Cited by 24 publications

References 14 publications

Risk Factors of Cerebral Vein and Sinus Thrombosis

Risk Factors of Cerebral Vein and Sinus Thrombosis

Acute promyelocytic leukaemia and acquired α‐2‐plasmin inhibitor deficiency: a retrospective look at the use of epsilon‐aminocaproic acid (Amicar) in 30 patients

Menorrhagia from a haematologist's point of view. Part II: management

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