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All authors read and approved the final manuscript

All authors read and approved the final manuscript. Acknowledgements None. [1]. Autoimmune myasthenia gravis, often in association with thymus hyperplasia or thymoma, can affect young adults. However, it is now acknowledged that myasthenia gravis is actually more prevalent in middle-aged and older groups than more youthful age groups [2]. In elderly patients, bulbar presentation RGS13 is usually common [3] and often mislabeled as a stroke [4] leading to poorer rates of survival [5]. Statins (inhibitors of 3-hydroxy-3-methyl-glutaryl-CoA reductase) lower the incidence of cerebrovascular disease and coronary heart disease. Statin use has increased dramatically over the last decade, with a four-fold increase from 1996 to 1998 [6]. Although generally well-tolerated, statins may have primary care discontinuation rates of up to 30% [7] due to their side effects such as headache, myalgia, paraesthesia, and abdominal discomfort. Here, we report a case of acute myasthenia gravis presenting in a 60-year-old Caucasian man whose condition deteriorated until immunosuppressive therapy was commenced and statin therapy was withdrawn. Case presentation A 60-year-old Caucasian man of British origin was admitted to our hospital in September 2007 following acute onset of dysarthria and dysphagia. He was diagnosed with diabetes mellitus and hyperlipidaemia three months prior to presentation. He had no visual disturbance or sensorimotor symptoms in his limbs or torso on presentation. He was commenced on gliclazide, ramipril and aspirin when he was diagnosed with diabetes and hyperlipidemia 3 months earlier. He was also started on simvastatin at that time, but this was stopped following the development of proximal muscle weakness, myalgia, and an elevated creatine kinase (CK) of 2599 (normal: 200), which all resolved upon the termination of this medication. Gliclazide, ramipril and aspirin, however, were continued. Aside from the finding of mild dysarthria, examination revealed that our patient had no remarkable conditions. Results of routine haematology, biochemistry, thyroid function tests, and creatine kinase were also unremarkable. His serum cholesterol was 6.1 mmol/L and his random blood glucose was 11.2 mmol/L. An initial diagnosis of a brain stem stroke was considered, so dipyridamole and atorvastatin were added to his medication four days Trimipramine after his admission to our hospital. Meanwhile, a computed tomography (CT) brain scan showed that he had no obvious infarct. Our patient remained stable over the next few days with a mild dysarthria and dysphagia (tolerating soft food), but no other symptoms or signs were noted. One week after his admission to our hospital, his dysarthria and dysphagia worsened. Bilateral fatigable ptosis, diplopia, fatigable weakness of his neck flexion, and shoulder abduction were noted for the first time. A previously planned cranial magnetic resonance brain scan was thus cancelled. Edrophonium testing demonstrated a dramatic transient improvement in his dysarthria, and a diagnosis of myasthenia gravis with high titre anti-acetylcholine receptor antibodies was confirmed. A serum immunoglobulin assay revealed an IgA level of 0.05 g/L. He was noted to have normal IgG and IgM, and no paraprotein band. Our patient was then commenced on treatment with pyridostigmine. He was also started on incrementally increasing prednisolone every other day. Regular monitoring of his respiratory function was also initiated. His respiratory function worsened over the next 3 days. His spirometry also deteriorated. He developed a new fatigable diplopia and an inability to stand from a low squat position, together with increasing neck and proximal limb weakness. In view of his deteriorating state, intravenous immunoglobulin therapy (IVIg) was commenced. Following immunological advice regarding his low IgA titre, it was decided to use Vigam Immunoglobulin (2 g/kg over the next 4 days), which did not result in any adverse effect. No objective gains were noted over the subsequent week, and a repeat CK yielded a result of 842 mmol/L. His atorvastatin medication was then stopped two weeks after it had been introduced. Following this, our patient showed significant improvement in ptosis, a resolution of diplopia, and improved neck, shoulder, and elbow power. His ability to stand from a low squat Trimipramine position returned, Trimipramine and significant spirometric improvements were also seen. His CK readings fell over this period and returned to normal levels one week after the cessation of his statin medication (Figure ?(Figure11). Open in a separate window Figure 1 This image of a graph shows creatinine kinase.

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