Juvenile dermatomyositis

Recognition and treatment

A. M. Reed, M. Lopez

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Juvenile dermatomyositis (JDM) is a multisystem disease characterized by acute and chronic lymphocytic inflammation of the skeletal muscle and skin. The disease is marked early in its course by the presence of a vasculopathy or vasculitis, and later by the development of calcinosis. Research has focused on the epidemiology, etiology, and pathogenesis of the disease with, until more recently, limited therapeutic interventions. This article highlights treatment regimens, both traditional and more recent interventions. Traditional treatment for JDM includes high dose corticosteroid treatment with additional agents used in resistant disease or children with unwarranted adverse effects. Traditional therapy begins with daily oral corticosteroids, with intravenous corticosteroids utilized in severe disease; however, recent data suggests that short-term use of intravenous cortcosteroids will allow a short-term improvement in strength, with no long-term change in outcome. More recent investigations suggest that early intervention with additional immunomodulatory agents will allow for a faster recovery, with less medication and disease sequelae. Use of methotrexate as an agent early in the disease course is becoming common place. Methotrexate, in conjunction with oral corticosteroids, allows a rapid improvement in symptoms, and allows for a more rapid reduction in corticosteroid dose. Methotrexate is considered as a steroid sparing agent, whether oral or intravenous corticosteroids are used. Additional immunomodulatory agents include the use of cyclosporine with or without methotrexate. Intravenous immunoglobulin has been reported to have benefit in resistant disease. There are exciting new agents which have great potential in treating JDM. Many of these agents are termed biologics and are being tested in adult myositis and juvenile arthritis. These include tumor necrosis factor (TNF)-α inhibitors, such as a chimeric monoclonal antibody to TNF-α, and a recombinant soluble human TNF receptor (p75)-Fc fusion protein. Many other new biological agents are also being tested in myositis.

Original languageEnglish (US)
Pages (from-to)315-321
Number of pages7
JournalPediatric Drugs
Volume4
Issue number5
StatePublished - 2002

Fingerprint

Adrenal Cortex Hormones
Methotrexate
Myositis
Biological Factors
Therapeutics
Tumor Necrosis Factor-alpha
Calcinosis
Juvenile Arthritis
Tumor Necrosis Factor Receptors
Intravenous Immunoglobulins
Acute Disease
Vasculitis
Juvenile dermatomyositis
Cyclosporine
Epidemiology
Skeletal Muscle
Chronic Disease
Steroids
Monoclonal Antibodies
Inflammation

ASJC Scopus subject areas

  • Pharmacology
  • Pediatrics, Perinatology, and Child Health

Cite this

Reed, A. M., & Lopez, M. (2002). Juvenile dermatomyositis: Recognition and treatment. Pediatric Drugs, 4(5), 315-321.

Juvenile dermatomyositis : Recognition and treatment. / Reed, A. M.; Lopez, M.

In: Pediatric Drugs, Vol. 4, No. 5, 2002, p. 315-321.

Research output: Contribution to journalArticle

Reed, AM & Lopez, M 2002, 'Juvenile dermatomyositis: Recognition and treatment', Pediatric Drugs, vol. 4, no. 5, pp. 315-321.
Reed, A. M. ; Lopez, M. / Juvenile dermatomyositis : Recognition and treatment. In: Pediatric Drugs. 2002 ; Vol. 4, No. 5. pp. 315-321.
@article{8663978b5c2442039913d2d22b65dc5b,
title = "Juvenile dermatomyositis: Recognition and treatment",
abstract = "Juvenile dermatomyositis (JDM) is a multisystem disease characterized by acute and chronic lymphocytic inflammation of the skeletal muscle and skin. The disease is marked early in its course by the presence of a vasculopathy or vasculitis, and later by the development of calcinosis. Research has focused on the epidemiology, etiology, and pathogenesis of the disease with, until more recently, limited therapeutic interventions. This article highlights treatment regimens, both traditional and more recent interventions. Traditional treatment for JDM includes high dose corticosteroid treatment with additional agents used in resistant disease or children with unwarranted adverse effects. Traditional therapy begins with daily oral corticosteroids, with intravenous corticosteroids utilized in severe disease; however, recent data suggests that short-term use of intravenous cortcosteroids will allow a short-term improvement in strength, with no long-term change in outcome. More recent investigations suggest that early intervention with additional immunomodulatory agents will allow for a faster recovery, with less medication and disease sequelae. Use of methotrexate as an agent early in the disease course is becoming common place. Methotrexate, in conjunction with oral corticosteroids, allows a rapid improvement in symptoms, and allows for a more rapid reduction in corticosteroid dose. Methotrexate is considered as a steroid sparing agent, whether oral or intravenous corticosteroids are used. Additional immunomodulatory agents include the use of cyclosporine with or without methotrexate. Intravenous immunoglobulin has been reported to have benefit in resistant disease. There are exciting new agents which have great potential in treating JDM. Many of these agents are termed biologics and are being tested in adult myositis and juvenile arthritis. These include tumor necrosis factor (TNF)-α inhibitors, such as a chimeric monoclonal antibody to TNF-α, and a recombinant soluble human TNF receptor (p75)-Fc fusion protein. Many other new biological agents are also being tested in myositis.",
author = "Reed, {A. M.} and M. Lopez",
year = "2002",
language = "English (US)",
volume = "4",
pages = "315--321",
journal = "Paediatric Drugs",
issn = "1174-5878",
publisher = "Adis International Ltd",
number = "5",

}

TY - JOUR

T1 - Juvenile dermatomyositis

T2 - Recognition and treatment

AU - Reed, A. M.

AU - Lopez, M.

PY - 2002

Y1 - 2002

N2 - Juvenile dermatomyositis (JDM) is a multisystem disease characterized by acute and chronic lymphocytic inflammation of the skeletal muscle and skin. The disease is marked early in its course by the presence of a vasculopathy or vasculitis, and later by the development of calcinosis. Research has focused on the epidemiology, etiology, and pathogenesis of the disease with, until more recently, limited therapeutic interventions. This article highlights treatment regimens, both traditional and more recent interventions. Traditional treatment for JDM includes high dose corticosteroid treatment with additional agents used in resistant disease or children with unwarranted adverse effects. Traditional therapy begins with daily oral corticosteroids, with intravenous corticosteroids utilized in severe disease; however, recent data suggests that short-term use of intravenous cortcosteroids will allow a short-term improvement in strength, with no long-term change in outcome. More recent investigations suggest that early intervention with additional immunomodulatory agents will allow for a faster recovery, with less medication and disease sequelae. Use of methotrexate as an agent early in the disease course is becoming common place. Methotrexate, in conjunction with oral corticosteroids, allows a rapid improvement in symptoms, and allows for a more rapid reduction in corticosteroid dose. Methotrexate is considered as a steroid sparing agent, whether oral or intravenous corticosteroids are used. Additional immunomodulatory agents include the use of cyclosporine with or without methotrexate. Intravenous immunoglobulin has been reported to have benefit in resistant disease. There are exciting new agents which have great potential in treating JDM. Many of these agents are termed biologics and are being tested in adult myositis and juvenile arthritis. These include tumor necrosis factor (TNF)-α inhibitors, such as a chimeric monoclonal antibody to TNF-α, and a recombinant soluble human TNF receptor (p75)-Fc fusion protein. Many other new biological agents are also being tested in myositis.

AB - Juvenile dermatomyositis (JDM) is a multisystem disease characterized by acute and chronic lymphocytic inflammation of the skeletal muscle and skin. The disease is marked early in its course by the presence of a vasculopathy or vasculitis, and later by the development of calcinosis. Research has focused on the epidemiology, etiology, and pathogenesis of the disease with, until more recently, limited therapeutic interventions. This article highlights treatment regimens, both traditional and more recent interventions. Traditional treatment for JDM includes high dose corticosteroid treatment with additional agents used in resistant disease or children with unwarranted adverse effects. Traditional therapy begins with daily oral corticosteroids, with intravenous corticosteroids utilized in severe disease; however, recent data suggests that short-term use of intravenous cortcosteroids will allow a short-term improvement in strength, with no long-term change in outcome. More recent investigations suggest that early intervention with additional immunomodulatory agents will allow for a faster recovery, with less medication and disease sequelae. Use of methotrexate as an agent early in the disease course is becoming common place. Methotrexate, in conjunction with oral corticosteroids, allows a rapid improvement in symptoms, and allows for a more rapid reduction in corticosteroid dose. Methotrexate is considered as a steroid sparing agent, whether oral or intravenous corticosteroids are used. Additional immunomodulatory agents include the use of cyclosporine with or without methotrexate. Intravenous immunoglobulin has been reported to have benefit in resistant disease. There are exciting new agents which have great potential in treating JDM. Many of these agents are termed biologics and are being tested in adult myositis and juvenile arthritis. These include tumor necrosis factor (TNF)-α inhibitors, such as a chimeric monoclonal antibody to TNF-α, and a recombinant soluble human TNF receptor (p75)-Fc fusion protein. Many other new biological agents are also being tested in myositis.

UR - http://www.scopus.com/inward/record.url?scp=0036113910&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036113910&partnerID=8YFLogxK

M3 - Article

VL - 4

SP - 315

EP - 321

JO - Paediatric Drugs

JF - Paediatric Drugs

SN - 1174-5878

IS - 5

ER -