Putamina involvement in Wernicke encephalopathy induced by Janus Kinase 2 inhibitor
The aim of the study was to report a case of Wernicke encephalopathy (WE) due to fedratinib (Janus Kinase 2 inhibitor) treatment with atypical neuroimaging findings. We present a detailed report of the case and literature review. A 68-year-old woman under treatment with fedratinib (investigational J...
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| Veröffentlicht in: | Clinical neuropharmacology 2015-05, Vol.38 (3), p.117-118 |
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| container_title | Clinical neuropharmacology |
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| creator | Rodríguez-Pardo, Jorge Puertas-Muñoz, Inmaculada Martínez-Sánchez, Patricia Díaz de Terán, Javier Pulido-Valdeolivas, Irene Fuentes, Blanca |
| description | The aim of the study was to report a case of Wernicke encephalopathy (WE) due to fedratinib (Janus Kinase 2 inhibitor) treatment with atypical neuroimaging findings.
We present a detailed report of the case and literature review.
A 68-year-old woman under treatment with fedratinib (investigational JAK2 inhibitor) developed memory impairment, diplopia, and ataxia compatible with WE. Brain magnetic resonance imaging showed extensive lesions involving medial thalami, periaqueductal gray, caudate nuclei, and putamina. Thiamine supplementation provided clinical recovery and radiological improvement of the lesions described. Basal ganglia lesions have been previously described in children with this disease, but this is rarely found in adults. Clinical trials including fedratinib have been recently discontinued, and its involvement in pathogenesis of WE may be related to thiamine-transporter inhibition.
Our case represents an example of drug-related WE, with a rare radiological pattern. Precocious diagnosis and treatment are essential to prevent irreversible brain injury. |
| doi_str_mv | 10.1097/WNF.0000000000000083 |
| format | Article |
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We present a detailed report of the case and literature review.
A 68-year-old woman under treatment with fedratinib (investigational JAK2 inhibitor) developed memory impairment, diplopia, and ataxia compatible with WE. Brain magnetic resonance imaging showed extensive lesions involving medial thalami, periaqueductal gray, caudate nuclei, and putamina. Thiamine supplementation provided clinical recovery and radiological improvement of the lesions described. Basal ganglia lesions have been previously described in children with this disease, but this is rarely found in adults. Clinical trials including fedratinib have been recently discontinued, and its involvement in pathogenesis of WE may be related to thiamine-transporter inhibition.
Our case represents an example of drug-related WE, with a rare radiological pattern. Precocious diagnosis and treatment are essential to prevent irreversible brain injury.</description><identifier>ISSN: 0362-5664</identifier><identifier>EISSN: 1537-162X</identifier><identifier>DOI: 10.1097/WNF.0000000000000083</identifier><identifier>PMID: 25970282</identifier><language>eng</language><publisher>United States</publisher><subject>Aged ; Brain - drug effects ; Brain - pathology ; Female ; Humans ; Janus Kinase 2 - antagonists & inhibitors ; Magnetic Resonance Imaging ; Pyrrolidines - administration & dosage ; Pyrrolidines - adverse effects ; Sulfonamides - administration & dosage ; Sulfonamides - adverse effects ; Thiamine - therapeutic use ; Thiamine Deficiency - chemically induced ; Thiamine Deficiency - complications ; Thiamine Deficiency - drug therapy ; Treatment Outcome ; Wernicke Encephalopathy - chemically induced ; Wernicke Encephalopathy - diagnosis ; Wernicke Encephalopathy - diet therapy ; Wernicke Encephalopathy - pathology</subject><ispartof>Clinical neuropharmacology, 2015-05, Vol.38 (3), p.117-118</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c340t-a1e12ceb61199d3087db30a734559057081a832ce2092a6dce978eaebfbef9393</citedby><cites>FETCH-LOGICAL-c340t-a1e12ceb61199d3087db30a734559057081a832ce2092a6dce978eaebfbef9393</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25970282$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rodríguez-Pardo, Jorge</creatorcontrib><creatorcontrib>Puertas-Muñoz, Inmaculada</creatorcontrib><creatorcontrib>Martínez-Sánchez, Patricia</creatorcontrib><creatorcontrib>Díaz de Terán, Javier</creatorcontrib><creatorcontrib>Pulido-Valdeolivas, Irene</creatorcontrib><creatorcontrib>Fuentes, Blanca</creatorcontrib><title>Putamina involvement in Wernicke encephalopathy induced by Janus Kinase 2 inhibitor</title><title>Clinical neuropharmacology</title><addtitle>Clin Neuropharmacol</addtitle><description>The aim of the study was to report a case of Wernicke encephalopathy (WE) due to fedratinib (Janus Kinase 2 inhibitor) treatment with atypical neuroimaging findings.
We present a detailed report of the case and literature review.
A 68-year-old woman under treatment with fedratinib (investigational JAK2 inhibitor) developed memory impairment, diplopia, and ataxia compatible with WE. Brain magnetic resonance imaging showed extensive lesions involving medial thalami, periaqueductal gray, caudate nuclei, and putamina. Thiamine supplementation provided clinical recovery and radiological improvement of the lesions described. Basal ganglia lesions have been previously described in children with this disease, but this is rarely found in adults. Clinical trials including fedratinib have been recently discontinued, and its involvement in pathogenesis of WE may be related to thiamine-transporter inhibition.
Our case represents an example of drug-related WE, with a rare radiological pattern. Precocious diagnosis and treatment are essential to prevent irreversible brain injury.</description><subject>Aged</subject><subject>Brain - drug effects</subject><subject>Brain - pathology</subject><subject>Female</subject><subject>Humans</subject><subject>Janus Kinase 2 - antagonists & inhibitors</subject><subject>Magnetic Resonance Imaging</subject><subject>Pyrrolidines - administration & dosage</subject><subject>Pyrrolidines - adverse effects</subject><subject>Sulfonamides - administration & dosage</subject><subject>Sulfonamides - adverse effects</subject><subject>Thiamine - therapeutic use</subject><subject>Thiamine Deficiency - chemically induced</subject><subject>Thiamine Deficiency - complications</subject><subject>Thiamine Deficiency - drug therapy</subject><subject>Treatment Outcome</subject><subject>Wernicke Encephalopathy - chemically induced</subject><subject>Wernicke Encephalopathy - diagnosis</subject><subject>Wernicke Encephalopathy - diet therapy</subject><subject>Wernicke Encephalopathy - pathology</subject><issn>0362-5664</issn><issn>1537-162X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkNtKAzEQhoMotlbfQGQvvdmawybZXIpYT0UFlXoXstlZGt2Tm91C396UVkHnZgbm-2fgQ-iU4CnBSl4sHmdT_KdStofGhDMZE0Hf99EYM0FjLkQyQkfef2wQlahDNKJcSUxTOkYvz0NvKlebyNWrplxBBXUf5mgBXe3sJ0RQW2iXpmxa0y_XYZUPFvIoW0f3ph589BDCHiIaNkuXub7pjtFBYUoPJ7s-QW-z69er23j-dHN3dTmPLUtwHxsChFrIBCFK5QynMs8YNpIlnCvMJU6JSVkgKFbUiNyCkikYyIoMCsUUm6Dz7d22a74G8L2unLdQlqaGZvCaSMFVSmWSBDTZorZrvO-g0G3nKtOtNcF6o1MHnfq_zhA7230Ysgry39CPP_YNODlwaA</recordid><startdate>20150501</startdate><enddate>20150501</enddate><creator>Rodríguez-Pardo, Jorge</creator><creator>Puertas-Muñoz, Inmaculada</creator><creator>Martínez-Sánchez, Patricia</creator><creator>Díaz de Terán, Javier</creator><creator>Pulido-Valdeolivas, Irene</creator><creator>Fuentes, Blanca</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope></search><sort><creationdate>20150501</creationdate><title>Putamina involvement in Wernicke encephalopathy induced by Janus Kinase 2 inhibitor</title><author>Rodríguez-Pardo, Jorge ; 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We present a detailed report of the case and literature review.
A 68-year-old woman under treatment with fedratinib (investigational JAK2 inhibitor) developed memory impairment, diplopia, and ataxia compatible with WE. Brain magnetic resonance imaging showed extensive lesions involving medial thalami, periaqueductal gray, caudate nuclei, and putamina. Thiamine supplementation provided clinical recovery and radiological improvement of the lesions described. Basal ganglia lesions have been previously described in children with this disease, but this is rarely found in adults. Clinical trials including fedratinib have been recently discontinued, and its involvement in pathogenesis of WE may be related to thiamine-transporter inhibition.
Our case represents an example of drug-related WE, with a rare radiological pattern. Precocious diagnosis and treatment are essential to prevent irreversible brain injury.</abstract><cop>United States</cop><pmid>25970282</pmid><doi>10.1097/WNF.0000000000000083</doi><tpages>2</tpages></addata></record> |
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| ispartof | Clinical neuropharmacology, 2015-05, Vol.38 (3), p.117-118 |
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| source | MEDLINE; Journals@Ovid Complete |
| subjects | Aged Brain - drug effects Brain - pathology Female Humans Janus Kinase 2 - antagonists & inhibitors Magnetic Resonance Imaging Pyrrolidines - administration & dosage Pyrrolidines - adverse effects Sulfonamides - administration & dosage Sulfonamides - adverse effects Thiamine - therapeutic use Thiamine Deficiency - chemically induced Thiamine Deficiency - complications Thiamine Deficiency - drug therapy Treatment Outcome Wernicke Encephalopathy - chemically induced Wernicke Encephalopathy - diagnosis Wernicke Encephalopathy - diet therapy Wernicke Encephalopathy - pathology |
| title | Putamina involvement in Wernicke encephalopathy induced by Janus Kinase 2 inhibitor |
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