Clinical findings and magnetic resonance imaging in severe cyclosporine‐related neurotoxicity after allogeneic bone marrow transplantation

Trullemans, Fabienne; Grignard, F.; Camp, Benjamin Van; Schots, Rik

doi:10.1034/j.1600-0609.2001.t01-1-00440.x

Cited by 66 publications

(62 citation statements)

References 7 publications

(13 reference statements)

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“…All of our patients received cyclosporine for a period of 4-10 years, but blood levels of cyclosporine were kept in the normal range, and there was no clinical evidence for cyclosporine-induced neurotoxicity. Patients with neurotoxic effects of cyclosporine typically have lesions in the white matter of the cerebellar hemisphere [Bartynski et al, 1997;Trullemans et al, 2001]. Furthermore, cerebellar abnormalities are usually not seen in children without SIOD treated with cyclosporine after renal transplantation.…”

Section: Discussionmentioning

confidence: 98%

Cerebellar atrophy in Schimke‐immuno‐osseous dysplasia

Lücke

Clewing

Boerkoel

et al. 2007

American J of Med Genetics Pt A

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Schimke-immuno-osseous dysplasia is an autosomal-recessive multisystem disorder with the prominent clinical features disproportionate growth failure, progressive renal failure, and T-cell immunodeficiency. Neurological symptoms caused by transient ischemic attacks (TIAs) and strokes are a typical clinical finding in severe SIOD. Cerebral ischemia and white matter changes, moyamoya phenomena and absence of a cerebellar hemisphere and partial absence of the cerebellar vermis have been described in patients with severe SIOD. We present three SIOD patients with atrophy of the caudal parts of the cerebellar vermis (posterior lobule) and of the cerebellar hemispheres. We hypothesize that these cerebellar abnormalities are a continuum of the ongoing vascular disease in severe SIOD.

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Section: Discussionmentioning

confidence: 98%

Cerebellar atrophy in Schimke‐immuno‐osseous dysplasia

Lücke

Clewing

Boerkoel

et al. 2007

American J of Med Genetics Pt A

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“…Among several medications used in transplant patients, CsA is a major one known to cause neurotoxicity. [4][5][6]8 In the present study, CsA toxicity was defined according to the clinical, electrophysiological and imaging findings (most often involving the occipital lobe), regardless of CsA levels. Six of 11 neuro( þ ) patients in this study suffered from CsA toxicity.…”

Section: Discussionmentioning

confidence: 99%

“…7 The clinical presentation in the early post-transplant period has most frequently included convulsions, cranial palsies and symptoms consistent with increased intracranial pressure. 1,3,6,8,9 Cyclosporine A (CsA) metabolic encephalopathy has been described as one of the most important etiological factors for development of neurological symptoms. 4,8 Other causes leading to neurological complications have been reported to be systemic infection, cerebrovascular lesions, microangiopathy, busulfan-induced seizures, or other transplant-related factors.…”

mentioning

confidence: 99%

“…1,3,6,8,9 Cyclosporine A (CsA) metabolic encephalopathy has been described as one of the most important etiological factors for development of neurological symptoms. 4,8 Other causes leading to neurological complications have been reported to be systemic infection, cerebrovascular lesions, microangiopathy, busulfan-induced seizures, or other transplant-related factors. 5,6 Previous studies have suggested unrelated or alternative donor allogeneic transplantation as the most important risk factor for development of neurological complications in children 1,2 and adults.…”

mentioning

confidence: 99%

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Life-threatening neurological complications after bone marrow transplantation in children

Uçkan

Çetin

Yigitkanli

et al. 2004

Bone Marrow Transplant

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Summary:Neurological complications may occur in BMT recipients (11-59%), frequently contributing to morbidity or mortality. They are the main causes of death in 10-15%. Lifethreatening neurological complications were seen in 11 out of 113 (9.7%) children who underwent BMT from HLAmatched family (n ¼ 7) or mismatched donors (n ¼ 4) at our institution. Diagnoses of patients with neurological complications were acute myeloblastic leukemia (AML) (five), thalassemia major (two), Fanconi anemia (two), Omenn syndrome (one) and leukodystrophy (one), and the neurological events were seen between days þ 13 and þ 85 after transplantation. Minor symptoms including reversible, nonrepetitive seizures were excluded. Cyclosporine A toxicity was diagnosed in six children. The rest of the complications were brain abscess/meningoencephalitis (two), severe hypomagnesemia (one), busulfan toxicity (one), sustained hypertension (three), and intracranial hemorrhage (three). Six patients with neurological complications suffered from 4grade II graft-versus-host disease (GvHD), and all were high risk for transplantrelated complications. In this study, risk status of the underlying disease, mismatched transplantation, a diagnosis of AML (advanced stage), older age and 4grade II GvHD were important adverse factors for the development of severe life-threatening neurological complications. Bone Marrow Transplantation (2005) 35, 71-76.

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“…Severe neurotoxicity includes symptoms of confusion, disorientation, decreased responsiveness, visual hallucinations, delusions, seizures, pyramidal motor weakness, cortical blindness, aphasia, and ataxia. Severe neurotoxicity has been reported in 4% to 11% of HSCT patients 17,18 and at both therapeutic and high CsA levels. 17,19,20 Therefore, routine clinical examination or even interviewing patients would be highly valuable in detecting such effects.…”

Section: Discussionmentioning

confidence: 99%

Untitled

2015

Exp Clin Transplant

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Objectives: The use of cyclosporine for graft-versushost disease prophylaxis is a major factor in successful allogeneic hematopoietic stem cell transplantation. However, despite the drug being in clinical practice for more than 3 decades, there is no current global and consistent protocol for its optimal method of administration. In this study, we recorded situations related to cyclosporine administration and associated adverse reactions to aid in the development of more precise future guidelines. Materials and Methods: We monitored 22 candidates for allogeneic stem cell transplant during their hospitalization for a 1-year period, acquiring data recorded from predefined questionnaires prepared according to accredited literature, which included daily clinical and laboratory examinations. Results: Despite active attempts toward adherence to a standard protocol for cyclosporine administration, we found numerous occasions of deviations or mistakes, which may have led to adverse reactions. Conclusions: Our study, as one of the first published "drug utilization evaluations" for cyclosporine in stem cell transplant setting, proposes that educating involved clinical staff regarding a standard method of cyclosporine administration and providing efficient facilities would be highly valuable to implementation of a better practice.

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Clinical findings and magnetic resonance imaging in severe cyclosporine‐related neurotoxicity after allogeneic bone marrow transplantation

Cited by 66 publications

References 7 publications

Cerebellar atrophy in Schimke‐immuno‐osseous dysplasia

Cerebellar atrophy in Schimke‐immuno‐osseous dysplasia

Life-threatening neurological complications after bone marrow transplantation in children

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