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A 62 year old man had RA for five years that had been diagnosed according to the 1987 American Rheumatic Association criteria. His disease was well controlled with disease modifying antirheumatic agents (DMARDs). However, the DMARDs were discontinued in March 2000, and he entered a leflunomide clinical trial from April 2000 to August 2000. He improved during the trial. After the trial ended and the leflunomide was discontinued, his joint pain and swelling resumed, so DMARDs were started again.
In December 2000, he arrived in our emergency department with the sudden onset of a disturbance of consciousness, fever, chills, throbbing headache, and left limb weakness for a few days. On physical examination, his temperature was 38.3°C, and he had slurred speech, isochoric pupils, a supple neck, and muscle power in all four extremities grade 3/5. However he then had a seizure. Emergency computed tomographic (CT) scanning showed decreased lucency in the right mastoid air cells and a lesion suggestive of a focal infarct or cerebritis affecting the lower part of the right posterior frontal lobe (fig 1). A lumbar puncture was performed with an opening pressure of 240 cm H2O and a closing pressure of 210 cm H2O. The cerebrospinal fluid (CSF) was clear and he had a white blood cell (WBC) count of 8730/ml with 60% neutrophils and 37% lymphocytes.
The Pandy test was positive, protein 150 (10–45) mg/day. Microbiological investigations (antigens and/or culture) were all negative, as were blood cultures for bacteria and fungi. Penicillin and chloramphenicol were given but did not improve his condition. Phenytoin was also given for seizure control. Ten days after admission, magnetic resonance imaging (MRI) showed focal cerebritis with possible abscess formation in the right frontal and temporal lobes and the right insular cortex and a portion of the right basal ganglion (TR 2500/TE 100) (fig 2). A right frontotemporal craniotomy was performed to drain the abscess. The pathology report was consistent with an abscess, noting purulent exudate with granulation tissue, an accumulation of foamy cells, and reactive gliosis in adjacent brain tissue. No micro-organisms were identified. The antibiotics were changed to ceftriaxone, metronidazole, chloramphenicol, and vancomycin. The patient’s mental status became clear and he gradually regained muscle power.
Our case demonstrates that brain abscess should be suspected in immunocompromised patients, such as those with RA, who present with headache, fever, change in consciousness, and seizure. The diagnosis of cerebral abscess would have been delayed in our patient if a CT scan or MRI had not been done.
The non-specific symptoms and signs of brain abscess (fever, headache, focal neurological deficits) may lead to diagnostic delay, as was the case with our patient. We were unable to identify a micro-organism, either by bacteriology, serology, or pathology. This might have been due to the early use of empirical parenteral antibiotic treatment. The patient might have had impaired immunity secondary to his underlying RA or, possibly, the leflunomide trial he had previously participated in, or both. Leflunomide has a long half life of about two weeks,1 but he did not present with the brain abscess until four months after the end of the trial. We did not check the serum leflunomide level during the admission for the abscess. We have found no reported cases of patients with RA developing brain abscess while being treated with leflunomide, hydroxychloroquine, sulfasalazine, or methotrexate.
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