Statin-associated autoimmune myopathy

This theory is supported by the higher prevalence of statin-naive SAAM patients in Asian cohorts, who have statin-rich diets.

[3] Severe weakness of the proximal muscles (shoulders, upper arms, thighs) on both sides of the body, very high blood levels of the enzyme creatine kinase (CK) being released by broken down skeletal muscle, and persistent symptoms and CK elevation despite stopping the offending statin medication are the hallmarks of SAAM.

[3] In people affected by SAAM, the median duration of statin therapy was 38 months before the onset of muscular symptoms.

[4] A differentiating feature between this and more benign statin side effects is SAAM typically has a late onset.

[1] There are likely other unidentified genetic and environmental risk factors associated with SAAM, given the prevalence of the DRB1 allele and the low incidence of autoimmunity in that group.

SAAM hypothetically triggers this increase in the production of HMG-CoA reductase and associated 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.

Such findings include the presence of endothelial cell membrane attack complex in non-necrotic muscle fibers and MHC class I expression.

Thus, the presence of anti-HMG CoA reductase antibodies in someone who uses a statin and has myopathy strongly supports the diagnosis.

Suitable candidates for first-line intravenous immunoglobulin include people who have diabetes mellitus or who wish to avoid corticosteroid therapy.

[3] An affected person is more likely to experience permanent muscle damage if they do not receive adequate treatment for a long time.