Cyclosporin A-related cerebral venous sinus thrombosis

Gao, Fei; Zhang, Jun; Wang, Fang; Xin, Xiaoyan; Sha, Dujuan

doi:10.1097/md.0000000000011642

Cited by 7 publications

(10 citation statements)

References 36 publications

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“…Treatment with cyclosporin and corticoids increased the risk of venous thromboembolism, although not specifically for CVST [9][10][11]. The mechanism of cyclosporin thrombogenicity is still controversial.…”

Section: Discussionmentioning

confidence: 99%

Case Report of Cerebral Venous Sinus Thrombosis Complication after Microvascular Decompression Surgery in the Inactive Phase of Ulcerative Colitis

Watanabe¹,

Fachniadine²,

Maruyama³

et al. 2023

AJSCR

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Background: The risk of thrombosis is high in patients with Ulcerative Colitis. The main location of thrombosis is in the extremity and pulmonary vein. Cerebral venous thrombosis is a rare location for thrombosis with high mortality. One of the risk factors for developing thrombosis is in association with surgery, especially during an active phase of Ulcerative Colitis (UC), and very few studies report cases occurring during the inactive phase. Hence, it is important for the surgeon to understand the risk of thrombosis, especially of cerebral sinus thrombosis in the Ulcerative Colitis patient. Case: We are presenting a fatal complication in a male patient of 62, who had sagittal sinus thrombosis and multiple intra-cranial hemorrhages in both frontal lobes 3 weeks after microvascular decompression surgery for hemifacial spasm. Conclusion: The risk of cerebral venous sinus thrombosis is higher in Ulcerative Colitis patients, especially in those who undergo surgery regardless of its type. Careful peri-operative assessment and treatment related to thromboembolism prevention are important to reduce complications in such cases.

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Section: Discussionmentioning

confidence: 99%

Case Report of Cerebral Venous Sinus Thrombosis Complication after Microvascular Decompression Surgery in the Inactive Phase of Ulcerative Colitis

Watanabe¹,

Fachniadine²,

Maruyama³

et al. 2023

AJSCR

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“…We used an isolated working heart model of donor heart preservation that we previously described 69–71 . Male Wister rats (325–395 g) were anesthetized with an intraperitoneal injection of ketamine (80 mg/kg; Cenvet, Australia) and xylazine (10 mg/kg; Provet, Australia), with supplemental doses given as necessary until adequate anaesthesia was achieved.…”

Section: Methodsmentioning

confidence: 99%

“…For genetic ablation studies, ASIC1a -/mice were generated at the Australian Phenomics Isolated working model of donor heart preservation after prolonged cold storage. We used an isolated working heart model of donor heart preservation that we previously described [69][70][71] . The released peptides were purified from the cleavage reaction solutions using reverse phase high-performance liquid chromatography.…”

Section: Animalsmentioning

confidence: 99%

Acid sensing ion channel 1a is a key mediator of cardiac ischemia-reperfusion injury

Scheuer

Saez

et al. 2019

Preprint

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Ischemia reperfusion injury (IRI) is one of the major risk factors associated with primary graft dysfunction, the leading cause of early mortality in heart transplant recipients. Here, we show that the proton-gated acid-sensing ion channel 1a (ASIC1a) plays a key role during cardiac ischemia and demonstrate that ASIC1a is a promising new target to improve the tolerance of cardiac tissue to IRI.Genetic ablation of ASIC1a leads to improved functional recovery following global myocardial IRI in ex vivo mouse hearts, and this effect can be recapitulated by therapeutic blockade of ASIC1a using specific and potent venom-derived pharmacological inhibitors. Using two models of donor heart procurement and storage, we show that ASIC1a inhibition yields improved post-IRI cardiac viability and function as a pre-or post-conditioning agent, with organ recovery equal to benchmark drugs including the sodium-hydrogen exchange inhibitor, zoniporide. Using human pluripotent stem cells, we show that ASIC1a inhibition improves cardiomyocyte viability under conditions of acidosis or ischemia in vitro. At the cellular and whole organ level, we show that acute exposure to ASIC1a inhibitors have no impact on cardiac electromechanical coupling and physiological performance.Consistent with a key role for ASIC1a in human cardiac ischemia, we used summary data from GWAS to show that polymorphisms in the ASIC1 genetic locus are strongly associated with susceptibility to cardiac ischemic injuries. Collectively, our data provide compelling evidence for a novel pharmacological strategy involving ASIC1a blockade as a cardioprotective therapy to improve the viability of donor hearts exposed to myocardial ischemia. Significance StatementIschemia-reperfusion injury (IRI) is the primary reason for early allograft failure after heart transplantation. IRI is also implicated in the pathophysiology of diverse post-ischemic heart diseases that are a leading cause of morbidity and mortality worldwide. There are currently no drugs available to protect the heart from IRI. This study uses genetic approaches to demonstrate a novel role for ASIC1a in mediating the response of the heart to IRI. In addition, we identify venom-derived ASIC1a inhibitors as novel pharmacological therapeutics for cardiovascular medicine, in particular for the preservation of donor hearts destined for transplantation.

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“…Cyclosporine-A (CsA) is widely used as an immunosuppressive agent in organ transplantation ( 1 – 3 ), ulcerative colitis (UC) ( 4 – 6 ), and aplastic anemia (AA) ( 7 ). Most commonly, the high incidences of thromboembolic complications in the renal vascular system were found in patients with CsA use after kidney transplantation ( 8 , 9 ), which might be due to acute and chronic nephrotoxicity of CsA.…”

Section: Introductionmentioning

confidence: 99%

“…However, thrombotic complications in other organs secondary to CsA use are not fully analyzed in the clinical settings ( 10 ). In particular, cases of CsA-induced intracranial thrombotic complications in patients with AA were rather rare ( 7 ). Herein, we presented two cases of AA with CsA-related intracranial thrombotic events, involved in cerebral venous sinuses and cerebral arteries, respectively.…”

Section: Introductionmentioning

confidence: 99%

Cyclosporine-A-Induced Intracranial Thrombotic Complications: Systematic Review and Cases Report

et al. 2021

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This study reported two cases of intracranial thrombotic events of aplastic anemia (AA) under therapy with cyclosporine-A (CsA) and reviewed both drug-induced cerebral venous thrombosis (CVT) and CsA-related thrombotic events systematically. We searched PubMed Central (PMC) and EMBASE up to Sep 2019 for publications on drug-induced CVT and Cs-A-induced thrombotic events. Medical subject headings and Emtree headings were used with the following keywords: “cyclosporine-A” and “cerebral venous thrombosis OR cerebral vein thrombosis” and “stroke OR Brain Ischemia OR Brain Infarction OR cerebral infarction OR intracerebral hemorrhage OR intracranial hemorrhage.” We found that CsA might be a significant risk factor in inducing not only CVT but also cerebral arterial thrombosis in patients with AA.

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Cyclosporin A-related cerebral venous sinus thrombosis

Cited by 7 publications

References 36 publications

Case Report of Cerebral Venous Sinus Thrombosis Complication after Microvascular Decompression Surgery in the Inactive Phase of Ulcerative Colitis

Case Report of Cerebral Venous Sinus Thrombosis Complication after Microvascular Decompression Surgery in the Inactive Phase of Ulcerative Colitis

Acid sensing ion channel 1a is a key mediator of cardiac ischemia-reperfusion injury

Cyclosporine-A-Induced Intracranial Thrombotic Complications: Systematic Review and Cases Report

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