TY - JOUR
T1 - Lack of detection of enteroviral rna or bacterial dna in magnetic resonance imaging–directed muscle biopsies from twenty children with active untreated juvenile dermatomyositis
AU - Pachman, Lauren M.
AU - Litt, Deborah L.
AU - Rowley, Anne H.
AU - Hayford, Jennifer R.
AU - Caliendo, Janice
AU - Heller, Scott
AU - Ticho, Baruch S.
AU - Christensen, Mary
AU - Patterson, Bruce
AU - Ytterberg, Steven R.
AU - Pallansch, Mark
PY - 1995/10
Y1 - 1995/10
N2 - Objective. To investigate for the presence of increased titers of circulating antibody to putative infectious agents and for detectable viral RNA or bacterial DNA in children with active recent‐onset juvenile der‐ matomyositis (DM). Methods. Magnetic resonance imaging–directed muscle biopsies were performed in 20 children with active, untreated, recent‐onset juvenile DM and in age‐matched children with neurologic disease. Sera were tested for complement‐fixing antibody to Coxsack‐ievirus B (CVB), influenza A and B, parainfluenza 1 and 3, Mycoplasma pneumoniae, mumps, respiratory syncytial virus, and Reovirus; and by immunofluorescence for IgG antibody to Toxoplasma gondii cytomegalovirus and IgM antibody to Epstein‐Barr virus. Muscle from juvenile DM patients and control children, CD‐1 Swiss mice with and without CVB1 infection, and viral stock positive for CVB1–6 were tested using reverse‐transcriptase polymerase chain reaction with 5 primer sets, 4 probes (1 Coxsackievirus, 3 Enterovirus), and universal primers for DNA. Results. No increased antibody, viral RNA, or bacterial DNA was present in the juvenile DM patients or the control children. Conclusion. Juvenile DM may be triggered by unidentified agent(s) in the genetically susceptible host.
AB - Objective. To investigate for the presence of increased titers of circulating antibody to putative infectious agents and for detectable viral RNA or bacterial DNA in children with active recent‐onset juvenile der‐ matomyositis (DM). Methods. Magnetic resonance imaging–directed muscle biopsies were performed in 20 children with active, untreated, recent‐onset juvenile DM and in age‐matched children with neurologic disease. Sera were tested for complement‐fixing antibody to Coxsack‐ievirus B (CVB), influenza A and B, parainfluenza 1 and 3, Mycoplasma pneumoniae, mumps, respiratory syncytial virus, and Reovirus; and by immunofluorescence for IgG antibody to Toxoplasma gondii cytomegalovirus and IgM antibody to Epstein‐Barr virus. Muscle from juvenile DM patients and control children, CD‐1 Swiss mice with and without CVB1 infection, and viral stock positive for CVB1–6 were tested using reverse‐transcriptase polymerase chain reaction with 5 primer sets, 4 probes (1 Coxsackievirus, 3 Enterovirus), and universal primers for DNA. Results. No increased antibody, viral RNA, or bacterial DNA was present in the juvenile DM patients or the control children. Conclusion. Juvenile DM may be triggered by unidentified agent(s) in the genetically susceptible host.
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U2 - 10.1002/art.1780381019
DO - 10.1002/art.1780381019
M3 - Article
C2 - 7575702
AN - SCOPUS:0028826336
SN - 2326-5191
VL - 38
SP - 1513
EP - 1518
JO - Arthritis and Rheumatology
JF - Arthritis and Rheumatology
IS - 10
ER -