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• W2065202046 abstract "Dear Editor, Etanercept can significantly improve clinical outcome in both methotrexate-naïve and -failure patients with rheumatoid arthritis (RA). Withdrawal of etanercept is mostly attributed to loss of efficacy or serious adverse effects, such as severe infection, congestive heart failure, malignancy, demyelinating or autoimmune disorders.1 Abducens nerve palsy (ANP) rarely occurs in RA during anti-tumor necrosis factor (TNF)-α treatment. Although the associations and mechanisms between ANP and anti-TNF-α agents are not fully understood, prompt recognition of this condition is important for practitioners. We report a case of RA presenting with ANP during etanercept treatment and spotlight the potential association in the management of RA. A 57-year-old woman with a 10-year history of erosive RA was admitted because of rapid-onset blurred vision, dizziness, proptosis, right eye tenderness and horizontal diplopia of 1-week duration (Fig. 1). She began using etanercept when all standard treatments for RA, including methotrexate and hydroxychloroquine, had failed and the Disease Activity Score (DAS)-28 remained high at 8.52. After receiving etanercept for 12 weeks, her DAS-28 declined from 8.52 to 3.76. However, visual impairment and abnormal eyeball movement developed at this time. Cerebral infarction and infectious disease were excluded. She had no clinical evidence of deep vein thrombosis or pulmonary thromboembolism, and her serum anti-cardiolipin antibody, functional assay of protein C and antithrombin III were all within normal ranges. She denied a previous history of trauma or surgery. Binocular intraocular pressure was normal. Other than the ANP, there were no other abnormal neurological manifestations. Magnetic resonance imaging (MRI) of the brain showed prominent right cavernous sinus with flow void signals; thus dural carotid-cavernous fistula (CCF) was considered. There was no evidence of cerebral demyelination in the brain MRI study (Fig. 2). Etanercept was terminated immediately and the patient received a course of intravenous pulse therapy with 750 mg of methylprednisolone daily for 3 consecutive days, and then was maintained on 20 mg/day of oral prednisolone with gradual tapering. Anti-platelet agents such as low-dose aspirin and ginkgoflavone were prescribed. The illness gradually subsided at 1 year. Isolated ANP in adults can be caused by craniofacial trauma, surgery, brain tumor, spontaneous intracranial hypotension, diabetic neuropathy, Tolosa-Hunt syndrome, CCF, subarachnoid hemorrhage,2 systemic lupus erythematosus,3 central nervous system infections4 or demyelinating disorders.5 In our case, there were no fever, headache or nausea; thus, spontaneous intracranial hypotension, meningitis, and encephalitis were not likely by the clinical manifestations. Brain MRI also excluded the possibility of subarachnoid hemorrhage or granulomatous inflammation of cavernous sinus. According to a large cohort study by Mohan et al.,6 the incidence of symptomatic demyelinating disorders in patients receiving TNF-α antagonist is higher than the general population (16 vs. 4–6/10 000 person-years of exposure). The patients with demyelination usually present with paresthesias, visual disturbances, confusion, gait disturbance, apraxia, facial palsy and Guillain-Barré syndrome. White matter lesions in brain MRI can be seen in most cases. However, the present case did not have the above clinical and neuroimaging characteristics. The most likely etiology of isolated ANP in this case is dural CCF, because flow void signal is a pathognomonic finding in this condition. CCF can be divided into direct (Barrow type A) and dural type (Barrow type B to D) by their anatomic structures.7 The majority of Barrow type A CCF results from head trauma. Compared to the direct type CCF, dural CCF in middle-aged women may be associated with a history of head trauma, hypertension, hypercoagulable state, or idiopathic causes, and exhibit less severe bruit, blurred vision, headache, ocular/orbital pain, proptosis and chemosis. Anterior-draining dural CCF tends to increase the intraocular pressure, chemosis and orbital congestions, whereas the posterior-draining type is associated with non-injected ophthalmoplegia and involvement of the oculomotor, abducens and trochlear nerves.8 According to the clinical manifestations of the present case, posterior-draining dural CCF is more likely. Venous thromboembolic event (TE) in the cavernous or petrosal sinus may precede the formation of dural CCF and is believed to be the inciting factor in the majority of cases. In the report of Petitpain et al., 9 venous TE could be elicited by TNF-α antagonist therapy; 4/43 venous TE were cerebral venous thromboses. The mean delay of TE onset after etanercept treatment initiation can be shorter, especially for venous TE (2.4 months). Dural CCF usually spontaneously obliterates. In our case, the onset of ANP after etanercept initiation was 2.8 months and the subsidence after termination of etanercept was 1 year. The putative explanation of dural CCF-related isolated ANP might be caused by TNF-α antagonist-induced cavernous sinus thrombosis. Although the direct causal relationship between TNF-α antagonist and ANP has not been clearly described in the literature, prompt avoidance of anti-TNF-α agents is suggested. This report highlights the association between etanercept and ANP, and the fog will be lifted when more cases are identified. The authors declared no conflict of interest." @default.
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• W2065202046 title "Etanercept-associated right abducens nerve palsy in rheumatoid arthritis" @default.
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• W2065202046 doi "https://doi.org/10.1111/j.1756-185x.2012.01742.x" @default.
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