Dear Editor,
Dorph et al. provided new additional data on muscle inflammation on
polymyositis (PM) and dermatomyositis (DM). [1] In particular, the Authors
found that symptomatic and asymptomatic muscles featured similar
histopathologic changes, numbers of T cells, macrophages, expression of IL
-1[alfa] in endothelial cells and expression of MHC-I and -II on muscle
fibres. The Authors conclude that "the inflammatory changes constitute a
general phenotype in skeletal muscle tissue from patients with PM or DM
and suggest that other factors are more important in causing the clinical
symptoms". [1]
PM and classical DM (CDM) are part of the idiopathic inflammatory
myopathies (IIM) spectrum, which also include amyopathic DM (ADM), a
subset characterized the presence of hallmark cutaneous manifestations of
DM for more than six months with no clinical or laboratory evidence of
muscle involvement and in absence of immunosuppressive therapy and/or use
of drugs capable of producing DM-like skin lesions. [2] Although
epidemiologic data are lacking, ADM may account for 10% to 50% of all DM
cases. [2,3] In some cases, ADM may evolve into CDM. It is evident that
ADM may represent a useful in vivo model for the study of sublinical
muscle alterations, although performing muscle biopsies may raise ethical
reserves, since muscle enzymes, electromyography and magnetic resonance
imaging have higher sensitivity to detect muscle changes. [2]
At muscle biopsy, PM and DM can be distinguished by well-known
histopathologic and immunopathologic differences. [4] In fact, PM muscle
specimens are characterized by strong infiltration of CD8+ T cells that
invade MHC-I-expressing muscle fibres. Instead, weak perifascicular,
perimysial or perivascular infiltrates of T CD4+ and B cells, endothelial
hyperplasia, reduction of capillary density and perifascicular atrophy
feature DM lesions.
Regrettably, apart from MHC, results from PM and DM specimens were
provided undivided by Dorph et al. [1] This appears to be either a failure
per se or a loss of useful information in the view of future research on
subclinical muscle damage in IIM, including ADM.
References
1. Dorph C, Englund P, Nennesmo I, Lundberg IE. Signs of inflammation in
both symptomatic and asymptomatic muscles from patients with polymyositis
and dermatomyositis. Ann Rheum Dis 2006;0:ard.2005.051086v1.
2. Gerami P, Schope JM, McDonald L, Walling HW, Sontheimer RD. A
systematic review of adult-onset clinically amyopathic dermatomyositis
(dermatomyositis siné myositis): A missing link within the spectrum of the
idiopathic inflammatory myopathies. J Am Acad Dermatol 2006;54:597-613.
3. Caproni M, Cardinali C, Parodi A, Giomi B, Papini M, Vaccaro M, et
al. Amyopathic dermatomyositis: A review by the Italian group of
immunodermatology. Arch Dermatol 2002;138:23-7.
4. Dalakas MC, Hohlfeld R. Polymyositis and dermatomyositis. Lancet
2003;362:971-82.
Dear Editor,
Dorph et al. provided new additional data on muscle inflammation on polymyositis (PM) and dermatomyositis (DM). [1] In particular, the Authors found that symptomatic and asymptomatic muscles featured similar histopathologic changes, numbers of T cells, macrophages, expression of IL -1[alfa] in endothelial cells and expression of MHC-I and -II on muscle fibres. The Authors conclude that "the inflammatory changes constitute a general phenotype in skeletal muscle tissue from patients with PM or DM and suggest that other factors are more important in causing the clinical symptoms". [1]
PM and classical DM (CDM) are part of the idiopathic inflammatory myopathies (IIM) spectrum, which also include amyopathic DM (ADM), a subset characterized the presence of hallmark cutaneous manifestations of DM for more than six months with no clinical or laboratory evidence of muscle involvement and in absence of immunosuppressive therapy and/or use of drugs capable of producing DM-like skin lesions. [2] Although epidemiologic data are lacking, ADM may account for 10% to 50% of all DM cases. [2,3] In some cases, ADM may evolve into CDM. It is evident that ADM may represent a useful in vivo model for the study of sublinical muscle alterations, although performing muscle biopsies may raise ethical reserves, since muscle enzymes, electromyography and magnetic resonance imaging have higher sensitivity to detect muscle changes. [2]
At muscle biopsy, PM and DM can be distinguished by well-known histopathologic and immunopathologic differences. [4] In fact, PM muscle specimens are characterized by strong infiltration of CD8+ T cells that invade MHC-I-expressing muscle fibres. Instead, weak perifascicular, perimysial or perivascular infiltrates of T CD4+ and B cells, endothelial hyperplasia, reduction of capillary density and perifascicular atrophy feature DM lesions. Regrettably, apart from MHC, results from PM and DM specimens were provided undivided by Dorph et al. [1] This appears to be either a failure per se or a loss of useful information in the view of future research on subclinical muscle damage in IIM, including ADM.
References
1. Dorph C, Englund P, Nennesmo I, Lundberg IE. Signs of inflammation in both symptomatic and asymptomatic muscles from patients with polymyositis and dermatomyositis. Ann Rheum Dis 2006;0:ard.2005.051086v1.
2. Gerami P, Schope JM, McDonald L, Walling HW, Sontheimer RD. A systematic review of adult-onset clinically amyopathic dermatomyositis (dermatomyositis siné myositis): A missing link within the spectrum of the idiopathic inflammatory myopathies. J Am Acad Dermatol 2006;54:597-613.
3. Caproni M, Cardinali C, Parodi A, Giomi B, Papini M, Vaccaro M, et al. Amyopathic dermatomyositis: A review by the Italian group of immunodermatology. Arch Dermatol 2002;138:23-7.
4. Dalakas MC, Hohlfeld R. Polymyositis and dermatomyositis. Lancet 2003;362:971-82.