ABSTRACT
Statin-induced immune-mediated necrotizing myopathy (IMNM) is a subtype of IMNM linked to exposure to statins and is characterized by positive anti-hydroxymethylglutaryl (HMG) coenzyme A reductase (HMGCR) antibodies. Although rare, this entity has become increasingly recognized as a cause of proximal muscle weakness, especially with the widespread use of statin therapy. Unlike typical statin-associated muscle symptoms, IMNM myopathy often causes severe muscle injury, and muscle weakness persists or sometimes worsens following the withdrawal of statin therapy. Medical practitioners need to keep a high index of clinical suspicion for statin-induced IMNM in patients taking statins who present with muscle weakness. The disease can be debilitating, and treatment strategies are not well established despite the advances that have been made in the diagnosis. Here we present the clinical characteristics and disease course of two cases of statin-induced IMNM. Both patients presented with progressive proximal muscle weakness and myalgias while on long-term statin therapy without significant improvement in their symptoms following the withdrawal of statin therapy. IMNM was suspected, and both patients were found to have high titers of anti-HMG coenzyme A reductase antibodies and demonstrated microscopic features consistent with a diagnosis of IMNM on muscle biopsy. The patients experienced significant disability due to muscle weakness and required a protracted course of escalated immunosuppressive therapy. Although rare, IMNM should be suspected in patients taking statins who present with muscle weakness that fails to improve or worsens when statins were stopped. Early diagnosis and institution of immunosuppressive therapy are important to prevent the progression of the disease.
ABSTRACT
OBJECTIVE: To determine whether or not elevated titers of antinuclear antibodies (ANA) and/or rheumatoid factor (RF) are associated with patients with advanced peripheral arterial disease (PAD). SUBJECTS AND METHODS: A cross-sectional study was done between September 2005 and December 2006. Fifty-eight patients with clinical and angiographic evidence of PAD and 41 controls were studied. Controls had no documented history of peripheral, coronary or cerebral vascular disease. All subjects were screened for metabolic syndrome and C-reactive protein (CRP) as risk factors for peripheral vascular disease. Additionally, all were tested for anti-mitochondrial, anti-neutrophil cytoplasmic and anti-smooth muscle antibodies; those with positive results were excluded. ANA and RF were measured in sera from cases and controls. RESULTS: One case and 3 controls had positive anti-smooth muscle antibodies and were therefore excluded from statistical analysis. Metabolic syndrome was significantly more prevalent in patients than controls (p<0.05). Mean CRP level was 4.78+/-7.70 and 2.65+/-3.86 mg/dl in cases and controls, respectively (p=0.021). ANA were detected at a titer of >or=1:40 in 6 (10.5%) of the advanced PAD patients but none of the controls; the difference was not statistically significant. RF was less prevalent in cases than controls (p<0.05). CONCLUSION: RF and ANA do not appear to be associated with PAD in a Kuwaiti population.