Disturbance of Blood-Brain Barrier After Bone-Marrow Transplantation

Sloane, J P; Lwin, K.Y.; Gore, M.; Powles, R; Smith, J.F.

doi:10.1016/s0140-6736(85)90335-6

Cited by 32 publications

(9 citation statements)

References 6 publications

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“…It would seem likely that PRES acts by way of imparting direct toxicity on to the vascular endothelium, vasoconstriction being caused by elaboration of endothelin, similar to the appearance of microthrombosis, as in the hemolytic-uremic syndrome [4]. The situation for bone marrow-transplant recipients who feature cyclosporine neurotoxicity may be related to abnormalities of the blood-brain barrier, increased blood pressure and renal failure prior to the onset of various neurological symptoms [8]. Under most circumstances, the neurological symptoms and signs associated with cyclosporine use are reversible when the drug's administered dosage is decreased or it is withdrawn altogether, but symptoms may recur when the drug is reintroduced.…”

Section: Discussionmentioning

confidence: 99%

Posterior reversible encephalopathy in a child with Langerhans cell histiocytosis following allogeneic PBSCT treatment with cyclosporine

et al. 2007

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Posterior reversible encephalopathy syndrome (PRES) is associated with a specific disorder of cerebrovascular autoregulation of multiple etiologies. This syndrome had been subsequently described in numerous medical conditions, including hypertensive encephalopathy, pre-eclampsia and the use with immunosuppressive drugs. Here, we report a child suffering from Langerhans cell histocytosis developing into PRES following immunosuppressive therapy. Symptoms and neuroimaging abnormalities were complete resolution subsequent to the withdrawal of cyclosporine. Although PRES is rarely seen among children, it should always be considered in the differential diagnosis of acute neurological illness, especially undergoing immunosuppressive therapy.

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Section: Discussionmentioning

confidence: 99%

Posterior reversible encephalopathy in a child with Langerhans cell histiocytosis following allogeneic PBSCT treatment with cyclosporine

et al. 2007

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“…Evidence for vessel injury has been demonstrated by the finding of vessel wall thickening in medium-sized subarachnoid cerebral arteries in autopsy specimens. 7,8 White matter changes are reversible in most cases. They are usually symmetric, non-enhancing, and located at anastomotic arterial border zones.…”

Section: Discussionmentioning

confidence: 99%

Cyclosporin A-related cerebral vasculopathy

Shbarou

Chao

Morgenlander

2000

Bone Marrow Transplant

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Summary:The use of cyclosporin A has been associated with several side-effects, including neurotoxicity. The mechanism of toxicity is not well known. We report two patients treated with cyclosporin A who developed lesions in the cerebral white matter associated with abnormally elevated cerebral blood flow velocities on transcranial doppler ultrasound and abnormal vascular appearance on magnetic resonance angiography. Bone Marrow Transplantation (2000) 26, 801-804. Keywords: cyclosporin A; toxicity; vasospasm; transcranial doppler ultrasound; magnetic resonance imaging; magnetic resonance angiography Cyclosporin A is an immunosuppressive agent used to prevent graft-versus-host disease (GVHD), to promote engraftment in transplantation and for treatment of multiple auto-immune diseases. [1][2][3] It has been associated with several side-effects, including nephrotoxicity, hepatotoxicity and hypertension. 1 Neurotoxicity has been a recognized complication of the use of cyclosporin A in bone marrow and organ transplantation. Clinical manifestations include seizures, cortical blindness, altered mental status and quadriparesis. 1 CNS lesions caused by cyclosporin A have been localized mainly in watershed zones in the parietal and occipital lobes, and less frequently in the frontoparietal and inferotemporo-occipital junctions, or cerebellum. These lesions are identical to those seen due to cerebral hypoperfusion secondary to cardiac arrest, malignant hypertension or pre-eclampsia/eclampsia. They consist of white matter hypo-attenuation on computed tomography (CT) and hyperintensity on T 2 weighted images on magnetic resonance imaging (MRI). 4 The mechanism of cyclosporin A neurotoxicity is not well known. However the distribution of the lesions suggests a vascular process. We report two patients treated with cyclosporin A in whom we demonstrated abnormally high cerebral blood flow velocities on transcranial Doppler Case reports Case 1A 34-year-old Caucasian woman with myelodysplastic syndrome underwent cord blood transplantation 5 days following treatment with busulfan, mephalan and antithymocyte globulin. She was started on cyclosporin A for GVHD prophylaxis 2 days prior to transplantation at a daily dose of 200 mg i.v. She was also started on i.v. methylprednisolone on the day of the transplant. Immediately following bone marrow transplantation, the patient developed a severe occipital headache. On day 5, she developed acute-onset left-sided weakness and blurred vision in the right eye. Later that day, she developed confusion, incomprehensible speech, and seizure activity of the left side of the body.Physical examination revealed markedly increased tone in the left side with profound weakness, diffuse hyperreflexia and a left Babinski sign. Visual acuity testing using the Snellen's near card showed vision of 20/25 in both eyes. No visual field defects were detected. The patient had an increase in systolic blood pressure (BP) from a baseline of 100 to 120 mm Hg to 150 mm Hg on the day of transplantation. Following that...

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“…The most common factors are immunosuppressive drugs (cyclosporine, anti-thymocyte globulin, tacrolimus, rituximab, interferon), and chemotherapeutic agents (methotrexate, L-asparaginase, adriamycin, cyclophosphamide, cytosine arabinoside, vincristine) [2,4,7,[8][9][10][11]. Sickle cell disease, hypertension, acute blood pressure changes, renal failure, TLS, infection, sepsis, shock, and organ transplantation are some factors that can also cause PRES [3,5,[12][13][14][15]. The exact etiopathogenesis of posterior leukoencephalopathy syndrome is still unknown.…”

Section: Resultsmentioning

confidence: 99%

“…Immunosuppressive agents could damage the blood-brain barrier by various means: direct toxic effects on the vascular endothelium, vasoconstriction caused by elaboration of endothelin and microthrombosis [1]. The situation for bone marrow transplant recipients who feature cyclosporine neurotoxicity may be related to abnormalities of the blood-brain barrier, increased blood pressure and renal failure prior to the onset of various neurological symptoms [13]. Under most circumstances, the neurological symptoms and signs associated with cyclosporine use are reversible when the drug's administered dosage is decreased or stopped, but symptoms may recur when the drug is reintroduced.…”

mentioning

confidence: 99%

Posterior reversible leukoencephalopathy syndrome in children with hematologic disorders

Malbora

Avcı²,

Dönmez³

et al. 2010

Turk J Hematol

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Objective: Posterior reversible leukoencephalopathy syndrome (PRES) is characterized by headache, altered mental status, cortical blindness, and seizures associated with neuroradiological findings. It involves predominantly white matter of the parieto-occipital lobes. Several medications and disorders play a role in the etiology of PRES. In this study, we aimed to show how the prognosis of PRES in hematological diseases of childhood might be according to the etiological factors. Materials and Methods: Here, we report PRES in six patients, aged 4 to 14 years, with diagnoses of leukemia and aplastic anemia. Results: Suggested causes in our patients were chemotherapeutics, hypertension, infection and antimicrobial drug administration, tumor lysis syndrome, acute renal failure and hemodialysis, immunosuppressive drug administration, and hypomagnesemia. One of the patients died of sepsis, renal failure and pulmonary hemorrhage and another died of relapse after total recovery from PRES. The other four patients are under follow-up without problems. Conclusion: We suggest that PRES can recover fully with early diagnosis and treatment whereas it can show poor prognosis depending on the etiology. (Turk J Hematol 2010; 27: 168-76) Key words: Acute leukemia, aplastic anemia, posterior reversible leukoencephalopathy syndrome, tumor lysis syndrome

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Disturbance of Blood-Brain Barrier After Bone-Marrow Transplantation

Cited by 32 publications

References 6 publications

Posterior reversible encephalopathy in a child with Langerhans cell histiocytosis following allogeneic PBSCT treatment with cyclosporine

Posterior reversible encephalopathy in a child with Langerhans cell histiocytosis following allogeneic PBSCT treatment with cyclosporine

Cyclosporin A-related cerebral vasculopathy

Posterior reversible leukoencephalopathy syndrome in children with hematologic disorders

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