It is unclear precisely how<unk> s lead to<unk> . The disorder is positively<unk>  with HLA-DR11 and the DRB1*11:01 allele. There are likely other unidentified genetic and environmental risk factors<unk>  with SAAM, given the prevalence of the DRB1 allele and the low incidence of<unk> ty in that group.<unk> s inhibit HMG-CoA reductase activity and consequently lower cholesterol levels in the blood. However, by doing this, they also increase the production of the HMG-CoA reductase protein. SAAM hypothetically triggers this increase in the production of HMG-CoA reductase and<unk>  abnormal processing of this protein in genetically susceptible individuals. This abnormal processing theoretically triggers the generation of antibodies targeting the HMG-CoA reductase protein resulting in SAAM. Another theory postulates that the configuration of the HMG-CoA reductase protein may change when<unk>  medications bind to it causing the protein to expose certain antigens that the immune system is not tolerant to resulting in the production of antibodies against it.
Statin-associated autoimmune myopathy
Desmin-related myofibrillar myopathy
Acquired non-inflammatory myopathy
Dermatopolymyositis
Inclusion body myositis
Scleromyositis
Dermatomyositis
Hereditary inclusion body myopathy