cris.boxmetadata.label.title
Serologic evolution of neurocysticercosis patients after antiparasitic therapy
cris.boxmetadata.label.dateissued
01 browse.startsWith.months.january 1997
cris.boxmetadata.label.accesslevel
open access
cris.boxmetadata.label.resourcetype
journal article
cris.boxmetadata.label.authors
GARCIA LESCANO, HECTOR HUGO
VERASTEGUI PIMENTEL, MANUELA RENEE
GONZALEZ ZARIQUIEY, ARMANDO EMILIANO
Tsang V.C.W.
Martinez M.
Cuba J.M.
Alban G.
Estrada H.
Rios-Saavedra N.
Soto M.
Torres M.P.
Boero J.
GAVIDIA CHUCAN, CESAR MIGUEL
Universidad Peruana Cayetano Heredia
Universidad Peruana Cayetano Heredia
Universidad Peruana Cayetano Heredia
Universidad Peruana Cayetano Heredia
Universidad Peruana Cayetano Heredia
Universidad Peruana Cayetano Heredia
Universidad Peruana Cayetano Heredia
Universidad Peruana Cayetano Heredia
Universidad Peruana Cayetano Heredia
Universidad Peruana Cayetano Heredia
cris.boxmetadata.label.publisher
Oxford University Press
cris.boxmetadata.label.abstract
Neurocysticercosis is the main cause of acquired epilepsy in developing countries and is an emerging disease in the United States. Introduction of the immunoblot assay provided a new tool for the diagnosis and monitoring of neurocysticercosis. This study analyzed the relationship between clinical characteristics of cerebral infection (number and type of lesions) plus the baseline response on immunoblot and the changes observed after therapy. Reaction to all 7 diagnostic bands was associated with severe infection (more lesions). Seventeen patients (35%) had no active lesions on computed tomography (CT) 3 months after therapy and were considered cured. Although most cured patients remained seropositive after 1 year, 3 became seronegative before 9 months. In these 3 cases, the lesions had resolved on CT at 3 months. Persistent seropositivity does not necessarily indicate active infection. Serologic follow-up will be clinically helpful only in rare cases in which early antibody disappearance occurs.
cris.boxmetadata.label.citationstartpage
486
cris.boxmetadata.label.citationendpage
489
cris.boxmetadata.label.volume
175
cris.boxmetadata.label.issue
2
cris.boxmetadata.label.language
English
cris.boxmetadata.label.ocdeknowledgeArea
Enfermedades infecciosas Neurociencias
cris.boxmetadata.label.doi
cris.boxmetadata.label.scopusidentifier
2-s2.0-0031026717
cris.boxmetadata.label.pubmedidentifier
cris.boxmetadata.label.source
Journal of Infectious Diseases
cris.boxmetadata.label.containerissn
00221899
cris.boxmetadata.label.sponsor
Institut Malarde. UNDP/World BanklWHO. National Institutes of Health. National Institute of Allergy and Infectious Diseases / U01AI035894. SmithKline Beecham Pharma. Financial support: Institut Malarde and UNDP/World BanklWHO Special Programme for Research and Training in Tropical Diseases, Task Force on Operational Research on Filariasis. Received 8 July 1996; revised 23 September 1996. Informed consent was obtained from all patients, and the study was approved by the ethical review boards of the Universidad Peruana Cayetano Heredia and Johns Hopkins University. Financial support: NIH (AI-35894) and SmithKline Beecham Pharmaceuticals (London). Correspondence: Dr. R. H. Gilman, Dept. of International Health, School of Hygiene and Public Health, Johns Hopkins University, 615 N. Wolfe St., Baltimore, MD 21205. Reprints: Dr. H. H. Garcia, Dept. de Microbiologia, Universidad Peruana Cayetano Heredia, Av. Honorio Delgado 430, Lima 31, Peru. * Members are listed after the text.
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