Remedial steps

Cutting Edge



Polymyositis is generally considered an auto-immunedisease. However, there are several other theories, and may well be different triggers for the auto-immune response.

Polymyositis is traditionally seen as an inflammatory myopathy mediated by cytotoxic T cells. (Hengstman December 2004)[1]

Interestingly, this destruction by t-cells is not as a normal part of cell apoptosis. "In the inflammatory myopathies, T cell inflammation is not cleared by apoptosis and affected muscle fibers do not die by apoptosis." (Schneider, Gold, Dalakas et al. 1996)[2] I take this to mean that cells do not die by normal programmed cell death, nor does the body deliberately kill them as a way of stopping the disease. As there are only two basic ways cells die.


There have been suggestions that auto-immune diseases including polymyositis may be a response to a virus that has not yet been detected. Certainly it is true that there are viruses that are uniformly found in conjuction with polymyositis. Notable amongst these is cytomegalovirus, which is detected in some 98% of patients. Although prevalent, cytomegalovirus does not appear to cause polymyositis, nor is any other virus known to do so.

While it does not cause polymyositis, its prevalence in patients and the numerous complications it can cause make it worthy of treatment. Cytomegalovirus is a type of virus with a lipid coating that protects it, often called an "enveloped RNA and DNA" virus. Others of this type include EBV Epstein Barre, HPV, Rubella, Herpes simples 1&2, HIV 1 and 6, and many others. In fact these viruses are all notable by their tendency to go chronic or dormant and hide in tissues for years, and for their difficulty in treatment.

Fortunately there is evidence that this type of viral infection (though not the polymyositis itself) can be treated with a natural substance with no side effects. Really. Read the paragraph on Lauricidin the remedies section. Read more about Lauricidin.


Statins as a cause of inflammatory myopathy. (Padala, Thompson. Nov. 2011) [3]

A reaction to statins has been linked to 3 cases of polymyositis. (TakagiShiio. 2004)[4]


Polymyositis can be a symptom of HIV infection. (Kaye. July 1989) [5]

Upregulation of MHC1

MHC-1 as a predictive or diagnostic determinant for inflammatory myopathy. (Salaroli, Baldin, Papa, Rinaldi, Tarantino, Badiali De Giorgi, Fusconi, Malavolta, Meliconi, D'Alessandro, Cenacchi. Nov. 2011) [6]

Here is a very informative article showing how conditional up-regulation of MHC class 1 in skeletal muscle leads to self-sustaining autoimmune myositis. (Nagaraju, Raben, Loeffler et al.. Aug. 2000) [7] It is interesting that this article shows that the upregulation of the MHC 1 appears at least occasionally to predate the presence of proinflammatory cytokines and the lymphocytic infiltration, thus implying that there may be another cause of the underlying MHC1 upregulation, which may in fact be different in different cases - truly ideopathic. I also understand him to say that this upregulation may be a result not only of the type of tissue injury that occurs, but also of the duration of that injury (my emphasis). Note also the article below on humoral response to tissue injury.

Here is a detailed article on how the auto-immune malfunction happens in PM. Explaines the MHC-1 and the CD*+ interaction, etc. together with the latest advances in diagnosis. (Dalakas 2004) [8]

Antigens, cytokines, interleukin, and cellular biology

These studies get deep fast, unless you know the language. Cellular mechanisms and anomolies of growth, genetic code manufacture and replication, and expression of cytokines and other chemicals that control cullular functions and interactions is a whole universe of knowledge, wonder, and unanswered questions.

The role of myositis specific Antigens. (Suzuki. Nov. 2011) [9] Also found here. [10]

The role of SMN1 (survival motor neuron) as a new target in Polymyositis. (Satoh, Ceribelli, Chan. Feb. 2011) [11]

The role of cytokines and TNF (De Paepe, Creus,De Bleecker. Aug. 2011) [12]

IFN-gamma is involved in the aberrant expression of major histocompatibility complex molecules in the affected muscles of patients with polymyositis-dermatomyositis.(Kalovidouris 1992) [13]

B7-H1 is expressed in PM (Xiaoyu, Yunxia, Qi, Dapeng, Xiuying, Jianhua, Hongxia. Jan. 2011) [14]

An artical showing the expression of Fas (tumor necrosis factor) on both cd4+ and CD8+ T cells in PM and DM. (Sugiura, Murakawa, Nagai, Kondo,Kobayash. Feb. 1999)[15]

A detailed and interesting article covering many of the mechanisms involved in muscle disregulation in the IIM diseases. Can muscle regeneration fail in chronic inflammation: a weakness in inflammatory myopathies?(Loell, Lundberg. Jan. 2011) [16]

Interferon 1

Treatment with interferon 1 has been shown to induce polymyositis and other auto-immune diseases, and interferon 1 has been shown to be upregulated in a high percentage of cases of both polymyositis and dermatomyositis. Regulation of interferon 1 may be a target for therapy. (Wlash, Kong, Jellal et al. 2007)[17.] (also Lundbeg, Helmers 2010).)[18.]

Important study on interferon interaction with immature muscle cells is "Immature muscle precursors are a source of interferon-β in myositis: role of Toll-like receptor 3 activation and contribution to HLA class I up-regulation".(Tournadre , Lenief, Eljaafari et al 2012)[19.]

Humoral Response To Tissue Injury

A recent article concluding that a humoral response to tissue injury is important in this disorder, and that the idea that PM is exclusively a T cell mediated myopathy requires revision. (Cappelletti, Morandi, Mora, Salerno, Confalonieri, Mantegazza Bernasconi. Feb. 2012) [20]

[1]Gerald J D Hengstman., Polymyositis, invasion of non-necrotic muscle fibres, and the art of repetition. BMJ 2004;329:1464 as found at 10.1136/bmj.329.7480.1464

[2] Schneider C, Gold R, Dalakas MC et al. MHC class 1-midiated cytotoxicity does not induce apoptosiss in muscle fibres nor in inflammatory Tcells: studies in patients with polymyositis, dermatomyocitis, and inclusion body myositis. J Neuropathol Exp Neurol 1996 Dec;55(12): 1205-9

[3] Santosh Padala, Paul D., Statins as a possible cause of inflammatory and necrotizing myopathies. Thompson Department of Internal Medicine, University of Connecticut. BMJ 2004; 329 doi: 10.1136/bmj.329.7480.1464. 2011 Nov. as found at http://www.glyconutrientsreference.com/mannatech/medicalconditions/polymyositis.html

[4] Takagi AShiio Y. Pravastatin-associated polymyositis, a case report. Journal of Internal Medicine.  Department of Neurology, Toranomon Hospital. Clinical Neurology. 2004. as found at http://ukpmc.ac.uk/abstract/MED/15199734/reload=0;jsessionid=PitH2QRyzzqP5b83nCJM.4

[5] Brian R. Kaye. Rheumatologic Manifestations of Infection with Human Immunodeficiency Virus (HIV). Ann Intern Med. July 1989. as found at http://annals.org/article.aspx?volume=111&issue=2&page=158

[6] Roberta Salaroli, Elisa Baldin, Valentina Papa, Rita Rinaldi, Lucia Tarantino, Lucilla Badiali De Giorgi, Marco Fusconi,Nazzarena Malavolta, Riccardo Meliconi, Roberto D'Alessandro, Giovanna Cenacchi. Validity of internal expression of the major histocompatibility complex class I in the diagnosis of inflammatory myopathies. Dipartimento Clinico di Scienze Radiologiche e Istocitopatologiche, Alma Mater Studiorum, Università di Bologna. Journal of clinical pathology DOI:10.1136/jclinpath-2011-200138. 2011 Nov. as found at http://www.researchgate.net

[7] Kanneboyina Nagaraju, Nina Raben, Lisa Loeffler, Tomasina Parker, Paul J. Rochon, Eunice Le, Carol Danning, Ryuichi Wada, Cynthia Thompson, Gul Bahtiyar, Joseph Craft, Rob Hooft van Huijsduijnen, and Paul Plotz. Conditional up-regulation of MHC class I in skeletal muscle leads to self-sustaining autoimmune myositis and myositis-specific autoantibodies. PNAS doi:10.1073/pnas.97.16.9209.as found at http://www.pnas.org/content/97/16/9209.long

[8] Marinos C. Dalakas. Inflammatory disorders of muscle: progress in polymyositis,dermatomyositis and inclusion bodymyositis. Neuromuscular Diseases Section, National Institute of Neurological Disorders and
Stroke, National Institutes of Health. Curr Op in Neurol 17:561–567. Lippincott Williams & Wilkins 2004as found at http://edulife.com

[9] Shigeaki Suzuki., Myositis-specific Autoantibodies and Their Clinical Significance. Department of Neurology, Keio University School of Medicine. 2011 Nov. as found at http://www.biomedsearch.com/nih/Myositis-specific-Autoantibodies-Their-Clinical/22068472.html

10] Shigeaki Suzuki., Myositis-specific autoantibodies and their clinical significance. Department of Neurology, Keio University School of Medicine. 2011 Nov. as found at http://www.researchgate.net/

[11] Satoh M, Ceribelli A, Chan EK., Common pathways of autoimmune inflammatory myopathies and genetic neuromuscular disorders. Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Florida. Clin Rev Allergy Immunol. 2012 Feb as found at http://www.ncbi.nlm.nih.gov/pubmed/22083460

[12] Boel De Paepe, Kim K. Creus, and Jan L. De Bleecker., The Tumor Necrosis Factor Superfamily of Cytokines in the Inflammatory Myopathies: Potential Targets for Therapy. Laboratory for Myopathology, Department of Neurology and Neuromuscular Reference Center, Ghent University Hospital. Clinical and Developmental Immunology Volume 2012, doi:10.1155/2012/369432 2011 Aug. as found at http://www.hindawi.com/journals/cdi/2012/369432/

[13] Kalovidouris, AE. The role of cytokines in polymyositis: interferon-gamma induces class II and enhances class I major histocompatibility complex antigen expression on cultured human muscle cells. J Lab Clin Med. 1992 Aug;120(2):244-51, as found at http://www.ncbi.nlm.nih.gov/pubmed/1500823

[14] Duan Xiaoyu, Wang Yunxia, Fang Qi, Wang Dapeng, Cai Xiuying, Jiang Jianhua, Wang Hongxia., Expression of B7-homolog 1 in Polymyositis. Laboratory for Myopathology, Department of Neurology, The First Hospital of Soochow University. Annals of clinical and laboratory science 2011 Jan. as found at http://www.researchgate.net/publication/51574268_Expression_of_B7-homolog_1_in_Polymyositis

[15] Sugiura, T., Murakawa, Y., Nagai, A., Kondo, M. and Kobayash. Fas and Fas ligand interaction induces apoptosis in inflammatory myopathies: CD4+ T cells cause muscle cell injury directly in polymyositis. Arthritis & Rheumatism, 42: 291–298. doi: 10.1002/1529-0131(199902)42:2<291::AID-ANR11>3.0.CO;2-1. February 1999. as found at http://onlinelibrary.wiley.com/doi/10.1002/1529-0131(199902)42:2%3C291::AID-ANR11%3E3.0.CO;2-1/abstract

[16] I. Loell, I. E. Lundberg. Can muscle regeneration fail in chronic inflammation: a weakness in inflammatory myopathies?. Journal of Internal Medicine. 269: 243–257. doi: 10.1111/j.1365-2796.2010.02334.x. January 2011 as found at Can muscle regeneration fail in chronic inflammation: a weakness in inflammatory myopathies?

[17] Walsh RJ, Kong SW, Yao Y. et al, Type I interferon-inducible gene expression in blood is present and reflects disease activity in dermatomyositis and polymyositis. Arthritis Rheum. 2007 Nov;56(11):3784-92. as found at http://www.ncbi.nlm.nih.gov/pubmed/17968926.

[18] Jundberg IS, Helmers SB. The type I interferon system in idiopathic inflammatory myopathies. Autoimmunity. 2010 Apr;43(3):239-43. as found at http://www.ncbi.nlm.nih.gov/pubmed/20187702

[19]Tournadre A, Lenief V, Eljaafari A, et al. Immature muscle precursors are a source of interferon-β in myositis: role of Toll-like receptor 3 activation and contribution to HLA class I up-regulation. Arthritis Rheum. 2012 Feb; 64(2):533-41 found at http://f1000.com/13781957

[20] Cristina Cappelletti, Lucia Morandi, Marina Mora, Franco Salerno, Paolo Confalonieri, Renato Mantegazza and Pia Bernasconi. Idiopathic Inflammatory Myopathies: A Review of Immunopathological Features and Current Models of Pathogenesis. Department of Neurology IV. Neuromuscular Diseases and Neuroimmunology,
Fondazione Istituto Neurologico2012 Feb as found at http://cdn.intechweb.org/pdfs/20185.pdf