Our mechanistic study is the first to show that MHC class II alleles influence not only quantitative aPL production but also the pathogenic capacity of induced aPL.

Systemic lupus erythematosus (SLE) is a heterogeneous, chronic, inflammatory, autoimmune disease characterised by multiorgan involvement and the production of multiple autoantibodies. Neurological manifestations in SLE patients are frequently reported—the prevalence is 37%–90%. We present a unique case where the patient presented with bilateral wrist and foot drop for 4 days, which later led to the diagnosis of SLE-related vasculitic polyneuropathy. During the course of treatment, the patient received prednisone, rituximab and hydroxychloroquine. At 6-month follow-up, patient had reported significant improvement in her weakness with increased mobility in upper and lower extremities. Prompt diagnosis and treatment are necessary in these cases to prevent disease progression and morbidity.

Statins are one of the most widely prescribed drugs in the world. One of the common side effects of statin use is myopathy. We report a case of statin-induced autoimmune myopathy, which is a variant of statin-induced myopathy. A 56-year-old female with a history of hypertension, hyperlipidemia, cerebral aneurysm status post clipping, and seizure disorder presented with progressive muscle weakness. Her initial laboratory results demonstrated an elevated creatine phosphokinase (CPK) of 17,144 IU/L. The patient’s atorvastatin was discontinued and she was placed on high-rate intravenous fluids; however, despite this, her CPK remained elevated. Patient underwent further blood testing for specific autoimmune etiologies. As there was high concern for autoimmune myositis, she was started on high-dose steroids. Anti-3-hydroxy-3-methylglutaryl-coenzyme A (anti-HMG-CoA) reductase antibody returned strongly positive. While the patient was on steroids, her muscle weakness and CPK level gradually improved. She was discharged on oral steroids. Statin-induced autoimmune myopathy should be considered with high suspicion when there is a significantly elevated CPK level. Discontinuation of statin therapy does not lead to muscle recovery or improvement in the CPK level. Diagnosis is confirmed by positive anti-HMG-CoA reductase autoantibody and a muscle biopsy.

Adult-onset Still's disease (AOSD) is a rare systemic inflammatory disorder. The exact pathogenesis is unknown but believed to have multiple etiologies. The Yamaguchi criteria are used to aid in the diagnosis of AOSD. Typical characteristics are spiking fevers, febrile rash, arthritis, and the absence of other serologic markers of rheumatic diseases. We present a case of a 31-year-old Hispanic female who presented with fevers, arthritis, febrile rash, high ferritin levels, and cervical and axillary lymphadenopathies. The unique feature of our case is that the patient was positive for antinuclear antibody (ANA) titers of greater than 1:640 and anti-Ro antibody. She responded with the pulse dose steroids and later prescribed methotrexate and tapered off prednisone with improvement in her symptoms.