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Article: Neurophysiologic study of β-thalassemia patients

TitleNeurophysiologic study of β-thalassemia patients
Authors
Issue Date1993
PublisherSage Publications, Inc.. The Journal's web site is located at http://jcn.sagepub.com
Citation
Journal Of Child Neurology, 1993, v. 8 n. 4, p. 330-335 How to Cite?
AbstractNeurophysiologic investigations were performed in 34 Chinese patients with β-thalassemia major maintained on long-term desferrioxamine treatment to look for subclinical toxicity in the auditory, visual, peripheral, or central neural pathways. In the auditory pathway study, four patients (12%) had mild sensorineural hearing impairment. Two patients (6%) had increased P 100 latencies in the visual evoked potential study, and nine patients (26%) had abnormal electroretinogram results. All had normal electrooculograms. Ophthalmoscopic examination was abnormal in three patients (9%), and three (9%) had a visual field defect. In the peripheral or central nervous pathways, seven patients (21%) had sensory neuropathy, of which three cases were probably related to diabetes mellitus. All had normal motor conduction velocities. Four patients (12%) had increased cortical latencies of median or posterior tibial somatosensory evoked potential. Abnormalities in multiple neural pathways were seen in four patients (12%). There was a significant association between subclinical toxicity to the peripheral or central nervous systems and serum ferritin level (P ≤ .03) and the presence of diabetes mellitus (P < .002). There was no significant relationship between the age, dosage, or duration of desferrioxamine used and the increased risk of neurotoxicity to the auditory, visual, peripheral, or central nervous systems. There was also no association between the risk of neurotoxicity and the serum zinc, copper, or fructosamine levels.
Persistent Identifierhttp://hdl.handle.net/10722/143596
ISSN
2023 Impact Factor: 2.0
2023 SCImago Journal Rankings: 0.683
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWong, Ven_HK
dc.contributor.authorLi, Aen_HK
dc.contributor.authorLee, ACWen_HK
dc.date.accessioned2011-12-12T03:52:11Z-
dc.date.available2011-12-12T03:52:11Z-
dc.date.issued1993en_HK
dc.identifier.citationJournal Of Child Neurology, 1993, v. 8 n. 4, p. 330-335en_HK
dc.identifier.issn0883-0738en_HK
dc.identifier.urihttp://hdl.handle.net/10722/143596-
dc.description.abstractNeurophysiologic investigations were performed in 34 Chinese patients with β-thalassemia major maintained on long-term desferrioxamine treatment to look for subclinical toxicity in the auditory, visual, peripheral, or central neural pathways. In the auditory pathway study, four patients (12%) had mild sensorineural hearing impairment. Two patients (6%) had increased P 100 latencies in the visual evoked potential study, and nine patients (26%) had abnormal electroretinogram results. All had normal electrooculograms. Ophthalmoscopic examination was abnormal in three patients (9%), and three (9%) had a visual field defect. In the peripheral or central nervous pathways, seven patients (21%) had sensory neuropathy, of which three cases were probably related to diabetes mellitus. All had normal motor conduction velocities. Four patients (12%) had increased cortical latencies of median or posterior tibial somatosensory evoked potential. Abnormalities in multiple neural pathways were seen in four patients (12%). There was a significant association between subclinical toxicity to the peripheral or central nervous systems and serum ferritin level (P ≤ .03) and the presence of diabetes mellitus (P < .002). There was no significant relationship between the age, dosage, or duration of desferrioxamine used and the increased risk of neurotoxicity to the auditory, visual, peripheral, or central nervous systems. There was also no association between the risk of neurotoxicity and the serum zinc, copper, or fructosamine levels.en_HK
dc.languageengen_US
dc.publisherSage Publications, Inc.. The Journal's web site is located at http://jcn.sagepub.comen_HK
dc.relation.ispartofJournal of Child Neurologyen_HK
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshBrain/drug effectsen_US
dc.subject.meshCopper/analysis/blood/metabolismen_US
dc.subject.meshDeferoxamine/pharmacology/*therapeutic useen_US
dc.subject.meshDiabetes Mellitus/blood/metabolismen_US
dc.subject.meshElectrooculographyen_US
dc.subject.meshElectroretinographyen_US
dc.subject.meshEvoked Potentials/drug effectsen_US
dc.subject.meshEvoked Potentials, Auditory, Brain Stemen_US
dc.subject.meshFemaleen_US
dc.subject.meshFerritins/analysis/blood/metabolismen_US
dc.subject.meshFructosamineen_US
dc.subject.meshHexosamines/analysis/blood/metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshNeural Pathways/drug effectsen_US
dc.subject.meshZinc/analysis/blood/metabolismen_US
dc.subject.meshbeta-Thalassemia/blood/*drug therapyen_US
dc.titleNeurophysiologic study of β-thalassemia patientsen_HK
dc.typeArticleen_HK
dc.identifier.emailWong, V:vcnwong@hku.hken_HK
dc.identifier.authorityWong, V=rp00334en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1177/088307389300800407-
dc.identifier.pmid8228027en_HK
dc.identifier.scopuseid_2-s2.0-0027452378en_HK
dc.identifier.volume8en_HK
dc.identifier.issue4en_HK
dc.identifier.spage330en_HK
dc.identifier.epage335en_HK
dc.identifier.isiWOS:A1993MA26000007-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, V=7202525632en_HK
dc.identifier.scopusauthoridLi, A=7403291810en_HK
dc.identifier.scopusauthoridLee, ACW=7405631431en_HK
dc.identifier.issnl0883-0738-

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