Association Between Cyclosporin Neurotoxicity and Hypomagnesaemia

Thompson, C. E. R.; Sullivan, Katherine; June, CarlH.; Ed, Thomas

doi:10.1016/s0140-6736(84)91556-3

Cited by 312 publications

(115 citation statements)

References 20 publications

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“…Considering the above reported findings, [1][2][3][4][5][6][7] we suspected that there were various factors closely related to the encephalopathy in this patient, such as acute hypertension, a high serum concentration of CsA, atypical metabolism induced by chronic hepatitis B, co-administration of FLCZ, and PSL used for prevention of allergic reaction to ATG (days −6 to day 0). Moreover, we had to reduce the dose of CsA on day −1, because of the history of a high concentration of CsA before BMT.…”

Section: Discussionmentioning

confidence: 98%

“…It has been shown that the damage exacerbates hypertension in recipients and that acute hypertension, hypocholesterolemia, hypomagnesemia, co-administration of PSL or antibiotics (penicillin, cephalosporine) and elevated serum concentrations of CsA can cause CsA-induced encephalopathy. 2,4,5 However, some patients receiving CsA show neurotoxic symptoms with therapeutic concentrations of CsA, 1,2 and only 20% of patients with CsA-induced encephalopathy show high serum concentrations of the drug. Although blood levels of CsA do not always correspond to tissue concentrations, the high serum concentration observed in this patient on day 0 might have induced high tissue concentrations.…”

Section: Discussionmentioning

confidence: 99%

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Cyclosporin A-induced encephalopathy after allogeneic bone marrow transplantation with prevention of graft-versus-host disease by tacrolimus

Takahata

Hashino

Izumiyama

et al. 2001

Bone Marrow Transplant

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Summary:A 21-year-old woman with severe aplastic anemia received an allogeneic bone marrow transplant (allo-BMT) from an HLA-matched and ABO-matched sibling donor after conditioning with cyclophosphamide, rabbit ATG (Lymphoglobuline; Aventis-Pharma), and total lymphoid irradiation. She had a long history of cyclosporin A (CsA) therapy before conditioning. She complained of severe headache and convulsions on day 0, and findings on magnetic resonance images suggested CsA-induced encephalopathy. CsA was immediately stopped, and tacrolimus for prevention of graft-versushost disease (GVHD) was started on day 2. Hematological engraftment was observed on day 14 without serious GVHD. Prompt diagnosis, replacement of immunosuppressive agents, and careful monitoring of serum drug concentrations are thought to have contributed to the patient's good clinical course, since CsA-induced encephalopathy tends to be recurrent but to improve completely without any sequelae. Bone Marrow Transplantation (2001) 28, 713-715.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Cyclosporin A-induced encephalopathy after allogeneic bone marrow transplantation with prevention of graft-versus-host disease by tacrolimus

Takahata

Hashino

Izumiyama

et al. 2001

Bone Marrow Transplant

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“…The etiology of CSP-associated neurotoxicities is unknown, although hypocholesterolemia, 34 hypertension, 35 hypomagnesemia, 36 concomitant high-dose glucocorticoids 37,38 and microangiopathic hemolytic anemia 39 have been reported as clinical factors which may contribute. Neurotoxicity can occur in patients with CSP levels in the recommended target range.…”

Section: Discussionmentioning

confidence: 99%

Clinical outcome after conversion to FK 506 (tacrolimus) therapy for acute graft-versus-host disease resistant to cyclosporine or for cyclosporine-associated toxicities

Furlong

Storb

Anasetti

et al. 2000

Bone Marrow Transplant

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Summary:This retrospective study describes the outcome in 53 patients who had immunosuppressive treatment changed from cyclosporine (CSP) to tacrolimus for resistant acute GVHD (n = 23), hemolytic uremic syndrome (HUS) (n = 13) or CSP-associated neurotoxicity (n = 17). Tacrolimus was administered at doses of 0.03 mg/kg/day intravenously or 0.12 mg/kg/day orally in divided doses, as tolerated. Median time of conversion to tacrolimus after transplant was day 47. Nineteen patients had treatment changed to tacrolimus for resistant acute GVHD grades III or IV, with the median day of conversion being day 49 after transplant. Two of 20 evaluable patients had a complete resolution of GVHD after changing treatment to tacrolimus, with 18 showing no improvement. Eleven evaluable patients had therapy changed to tacrolimus for CSP-associated neurotoxicity at a median of 36 days after transplant. Eight patients had resolution of neurotoxicity and three had partial improvement. Eleven evaluable patients had therapy changed to tacrolimus for HUS at a median of 46 days after transplant. One patient had complete resolution of HUS and 10 showed no response. Side-effects related to tacrolimus included renal toxicity (34%), neurotoxicity (15%) and HUS (9%). Nine (17%) patients remain alive, including six patients who had therapy changed to tacrolimus for CSP-associated neurotoxicity. While often successful for dealing with neurotoxicity, only a rare patient improved after therapy was changed from CSP to tacrolimus for HUS or resistant acute GVHD. Bone Marrow Transplantation (2000) 26, 985-991.

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“…Hypocholesterolaemia has also been described as a possible risk factors for RPLS [14][15][16]. Hypomagnesaemia is also a risk factor for RPLS [17]. Hypomagnesaemia can occur as a side effect of cyclosporine treatment because cyclosporine causes intracellular migration and renal wasting of magnesium [18].…”

Section: Risk Factorsmentioning

confidence: 99%

Reversible posterior leukoencephalopathy syndrome

Renard

Labauge

Vandenberghe

2010

Translational Neuroscience

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Reversible posterior leukoencephalopathy syndrome (RPLS) is characterized by subacute onset of headache, decreased alertness, vomiting, seizures, visuoperceptual disturbances, together with bilateral white matter lesions in posterior brain regions on brain imaging. The most frequently associated conditions related to RPLS are arterial hypertension and the use of immunosuppressive or cytotoxic treatment. T2-, Fluid Attenuation Inversion Recovery (FLAIR), and Apparent Diffusion Coefficient (ADC)-weighted magnetic resonance imaging (MRI) reveal hyperintensities in parietooccipital white matter but grey matter and other regions including frontal and temporal lobes, brainstem, cerebellum, basal ganglia, or even spinal cord may also be involved. According to ADC findings, the underlying pathophysiologic mechanism is probably one of vasogenic (rather than cytotoxic) oedema. These MRI findings help in differentiating RPLS from ischaemic events and other diseases resembling RPLS. Failure of cerebral autoregulation, endothelial dysfunction, disrupted blood-brain barrier, vasospasm, and direct toxic drug effects may all play a role in the pathophysiology of RPLS. Treatment consists of discontinuation of the causal drug, treatment of high blood pressure, and antiepileptic therapy. Clinical recovery and regression of radiological abnormalities are typically seen after early treatment. However, delay in diagnosis and treatment can result in irreversible brain damage, often in association with complicating cerebral infarction or haemorrhage.

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Association Between Cyclosporin Neurotoxicity and Hypomagnesaemia

Cited by 312 publications

References 20 publications

Cyclosporin A-induced encephalopathy after allogeneic bone marrow transplantation with prevention of graft-versus-host disease by tacrolimus

Cyclosporin A-induced encephalopathy after allogeneic bone marrow transplantation with prevention of graft-versus-host disease by tacrolimus

Clinical outcome after conversion to FK 506 (tacrolimus) therapy for acute graft-versus-host disease resistant to cyclosporine or for cyclosporine-associated toxicities

Reversible posterior leukoencephalopathy syndrome

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