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Utility of C‐reactive protein and serum amyloid A in the diagnosis of equine protozoal myeloencephalitis

BACKGROUND: Accurate antemortem EPM diagnosis requires evidence of intrathecal antibody production. Some advocate the use of acute phase proteins in addition to serology, which alone results in substantial false positives. HYPOTHESIS/OBJECTIVES: The purpose of this study was to determine if serum C‐...

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Autores principales: Mittelman, Neil S., Stefanovski, Darko, Johnson, Amy L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons, Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6189384/
https://www.ncbi.nlm.nih.gov/pubmed/30216559
http://dx.doi.org/10.1111/jvim.15254
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author Mittelman, Neil S.
Stefanovski, Darko
Johnson, Amy L.
author_facet Mittelman, Neil S.
Stefanovski, Darko
Johnson, Amy L.
author_sort Mittelman, Neil S.
collection PubMed
description BACKGROUND: Accurate antemortem EPM diagnosis requires evidence of intrathecal antibody production. Some advocate the use of acute phase proteins in addition to serology, which alone results in substantial false positives. HYPOTHESIS/OBJECTIVES: The purpose of this study was to determine if serum C‐reactive protein (CRP) or serum amyloid A (SAA) concentrations were elevated in cases of equine protozoal myeloencephalitis (EPM) compared to other neurological diseases. ANIMALS: 25 clinical cases of equine neurological disease: EPM (10), cervical vertebral stenotic myelopathy (CVSM) (10), neuroborreliosis (2), equine motor neuron disease (1), degenerative myelopathy (1), and leukoencephalomalacia (1). METHODS: Serum and CSF CRP and SAA were measured. Selection criteria included neurologic disease, antemortem diagnosis of EPM or CVSM, or postmortem diagnosis of EPM, CVSM, or other neurologic disease, and availability of serological results and archived samples for testing. RESULTS: Serum SAA and serum CRP levels were generally undetectable or low in horses with EPM (median CRP ≤0.1 mg/L, ≤0.1‐14.4 mg/L; median SAA ≤0.1 mg/L, ≤0.1‐6.11 mg/L) and CVSM (median CRP ≤0.1, ≤0.1‐2.41 mg/L; median SAA ≤0.1mg/L, ≤0.1‐13.88 mg/L). CSF CRP and SAA for horses with EPM (median CRP 3.35 mg/l, 0.19‐13.43 mg/l; median SAA ≤0.1 mg/L, ≤0.1‐2.4 mg/L) and CVSM (median CRP 4.015 mg/L, 0.16‐9.62 mg/L; median SAA 0.62 mg/L, ≤0.1‐2.91 mg/L) were also undetectable or low. Kruskal–Wallis test showed no statistically significant differences between serum CRP (P = .14), serum SAA (P = .79), spinal fluid CRP (P = .65), or spinal fluid SAA between horses with EPM and CVSM (P = .52). CONCLUSION: Neither SAA nor CRP in serum or CSF aid diagnosis of EPM.
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spelling pubmed-61893842018-10-22 Utility of C‐reactive protein and serum amyloid A in the diagnosis of equine protozoal myeloencephalitis Mittelman, Neil S. Stefanovski, Darko Johnson, Amy L. J Vet Intern Med EQUID BACKGROUND: Accurate antemortem EPM diagnosis requires evidence of intrathecal antibody production. Some advocate the use of acute phase proteins in addition to serology, which alone results in substantial false positives. HYPOTHESIS/OBJECTIVES: The purpose of this study was to determine if serum C‐reactive protein (CRP) or serum amyloid A (SAA) concentrations were elevated in cases of equine protozoal myeloencephalitis (EPM) compared to other neurological diseases. ANIMALS: 25 clinical cases of equine neurological disease: EPM (10), cervical vertebral stenotic myelopathy (CVSM) (10), neuroborreliosis (2), equine motor neuron disease (1), degenerative myelopathy (1), and leukoencephalomalacia (1). METHODS: Serum and CSF CRP and SAA were measured. Selection criteria included neurologic disease, antemortem diagnosis of EPM or CVSM, or postmortem diagnosis of EPM, CVSM, or other neurologic disease, and availability of serological results and archived samples for testing. RESULTS: Serum SAA and serum CRP levels were generally undetectable or low in horses with EPM (median CRP ≤0.1 mg/L, ≤0.1‐14.4 mg/L; median SAA ≤0.1 mg/L, ≤0.1‐6.11 mg/L) and CVSM (median CRP ≤0.1, ≤0.1‐2.41 mg/L; median SAA ≤0.1mg/L, ≤0.1‐13.88 mg/L). CSF CRP and SAA for horses with EPM (median CRP 3.35 mg/l, 0.19‐13.43 mg/l; median SAA ≤0.1 mg/L, ≤0.1‐2.4 mg/L) and CVSM (median CRP 4.015 mg/L, 0.16‐9.62 mg/L; median SAA 0.62 mg/L, ≤0.1‐2.91 mg/L) were also undetectable or low. Kruskal–Wallis test showed no statistically significant differences between serum CRP (P = .14), serum SAA (P = .79), spinal fluid CRP (P = .65), or spinal fluid SAA between horses with EPM and CVSM (P = .52). CONCLUSION: Neither SAA nor CRP in serum or CSF aid diagnosis of EPM. John Wiley & Sons, Inc. 2018-09-14 2018 /pmc/articles/PMC6189384/ /pubmed/30216559 http://dx.doi.org/10.1111/jvim.15254 Text en © 2018 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle EQUID
Mittelman, Neil S.
Stefanovski, Darko
Johnson, Amy L.
Utility of C‐reactive protein and serum amyloid A in the diagnosis of equine protozoal myeloencephalitis
title Utility of C‐reactive protein and serum amyloid A in the diagnosis of equine protozoal myeloencephalitis
title_full Utility of C‐reactive protein and serum amyloid A in the diagnosis of equine protozoal myeloencephalitis
title_fullStr Utility of C‐reactive protein and serum amyloid A in the diagnosis of equine protozoal myeloencephalitis
title_full_unstemmed Utility of C‐reactive protein and serum amyloid A in the diagnosis of equine protozoal myeloencephalitis
title_short Utility of C‐reactive protein and serum amyloid A in the diagnosis of equine protozoal myeloencephalitis
title_sort utility of c‐reactive protein and serum amyloid a in the diagnosis of equine protozoal myeloencephalitis
topic EQUID
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6189384/
https://www.ncbi.nlm.nih.gov/pubmed/30216559
http://dx.doi.org/10.1111/jvim.15254
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