A 56-year-old man who underwent a tooth extraction in the previous year presented with weakness of the right upper extremity. Brain CT and MRI scans showed subcortical hemorrhage in the left frontal lobe. His body temperature was 37.5°C. Blood examination revealed anemia, elevated levels of C-reactive protein, and a positive result for PR3-ANCA. Aggregatibacter segnis was identified in the incubated blood cultures, and transesophageal echocardiograms showed infectious growth in the anterior mitral leaflet. He was diagnosed with infectious endocarditis. After treatment with ceftriaxione, the clinical symptoms were improved. We concluded that infectious endocarditis caused cerebral hemorrhage and that the positive result for PR3-ANCA was a false positive. Infectious endocarditis can mimic ANCA-associated vasculitis. When ANCA-associated vasculitis is suspected, infectious endocarditis must be ruled out.
The patient was a 61-year-old woman with thyroid enlargement since her 20s. She began to fall down repeatedly towards the end of June 2015. She was admitted to our hospital in the middle of August because of difficulty in walking. Upon admission, she presented with neck tremor and was unable to maintain a sitting position due to ataxia of the trunk and limbs. We studied serum anti-neuronal antibodies and obtained a positive result for anti-amphiphysin antibody (AMPH-Ab). Cerebrospinal fluid analysis revealed elevated protein levels and IgG index. Other than the thyroid mass, a tumor was not detected. The resected thyroid specimen showed follicular adenoma. After performing immunotherapies, the cerebrospinal fluid protein levels and IgG index decreased, and her ataxia did not progress. When subacute cerebellar ataxia is suspected, studying AMPH-Ab should be considered.
A 56‐year‐old woman, who was treated with golimumab for rheumatoid arthritis, presented with myalgia and rash. She had proximal limbs weakness, and erythematous papules were evident on her hands and face. Her serum creatine kinase levels were elevated, and anti‐Mi‐2 antibody was detected. Magnetic resonance imaging of muscles revealed inflammatory lesions in muscles and soft tissues. She was diagnosed with inflammatory myopathy. A drug‐induced mechanism was suspected; therefore, we stopped treating her with golimumab and instead treated her with prednisolone. Subsequently, her symptoms gradually improved. This case suggests that tumor necrosis factor‐alpha inhibitors may induce anti‐Mi‐2 antibody‐positive inflammatory myopathies.
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