title: Muscle involvement in juvenile idiopathic arthritis.
abstract: OBJECTIVE
  An observational study of changes in muscle structure and the relation to muscle strength in juvenile idiopathic arthritis (JIA).
  
  
  METHODS
  Fifteen children and teenagers (eight girls and seven boys) with JIA, aged 9-19 yr (mean age 16.1), were studied. Muscle biopsies were obtained from the anterior tibial muscle and were examined using histopathological and immunohistochemical methods. Muscle fibre types were classified and fibre areas measured. As markers of inflammation, the major histocompatibility complex (MHC) class I and class II and the membrane attack complex (MAC) were analysed. Results were compared with biopsies from the gastrocnemius muscle in 33 young (19-23 yr) healthy controls. Isometric and isokinetic muscle strengths were measured in ankle dorsiflexion. Strength was compared with reference values for healthy age-matched controls. Nerve conduction velocities were recorded in the peroneal and sural nerves.
  
  
  RESULTS
  Four of the 15 muscle biopsies were morphologically normal. Eleven biopsies showed minor unspecific changes. Two of these also showed minor signs of inflammation. MHC class II expression was found in 4/15 patients, which was significantly more than in the healthy controls (P = 0.0143). The expression of MHC class I and MAC did not differ from that in the controls. The mean area of type I fibres was lower than that of type IIA fibres in 12/13 biopsies. Muscle strength was significantly reduced in the patient group. There was a significant positive correlation between muscle fibre area and muscle strength. Nerve conduction studies were normal in all cases.
  
  
  CONCLUSIONS
  Changes in leg muscle biopsies appear to be common in children and teenagers with JIA. The presence of inflammatory cells in the muscle and expression of MHC class II on muscle fibres may be a sign of inflammatory myopathy. There are no findings of type II muscle fibre hypotrophy or neuropathy, as in adults with RA.
authors.affiliation: Department of Clinical Neurophysiology, University Hospital, SE-581 85 Linköping, Sweden. hans.lindehammar@lio.se
authors.forename: H
authors.initials: H
authors.lastname: Lindehammar
authors.forename: B
authors.initials: B
authors.lastname: Lindvall
mesh_terms: D000293:Adolescent; D000328:Adult; D001171:Arthritis, Juvenile / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D015415:Biomarkers / Q000378:metabolism; D001706:Biopsy; D002648:Child; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D006801:Humans; D008297:Male; D009119:Muscle Contraction; D018485:Muscle Fibers, Skeletal / Q000473:pathology; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology; D009220:Myositis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D009431:Neural Conduction
chemical_list: D015415:Biomarkers; D000949:Histocompatibility Antigens Class II