Adalimumab
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Disseminated tuberculosis, and IRIS following drug withdrawal: case report A 17-year-old girl with SAPHO syndrome developed disseminated tuberculosis during treatment with adalimumab; after discontinuation of treatment, she developed immune reconstitution inflammatory syndrome (IRIS) manifesting as intracranial lesions and tuberculomas. The girl received adalimumab [dosage and route not stated] for 3 years before presenting with a 4-week history of a persistent dry cough, and a 5-day history of ataxia and speech disturbance. Cerebral CT scan at this point was normal and she was subsequently discharged. The next day, she presented with fever, somnolence and dyspnoea; she was confused, showed tonic extension of her lower limbs, and had abnormal deep tendon reflexes. She experienced a seizure upon admission, and her condition further deteriorated with tachycardia, respiratory decompensation and hypotension, consistent with septic shock. Laboratory findings included leucocytosis, elevated CRP, serum lactate and serum creatinine, and mildly elevated liver enzymes. Imaging studies showed pleural effusions, impaired cardiac function, and areas of T2 hyperintensity were observed upon cerebral MRI; CSF analysis confirmed meningitis. Further testing led to a diagnosis of disseminated tuberculosis. Adalimumab was withdrawn 4 weeks befire the girl was initially hospitalised and she received amoxicillin and clarithromycin. When she was admitted the second time, she received midazolam for her seizure, and then was intubated and treated with epinephrine [adrenaline], meropenem, vancomycin, ciprofloxacin and amphotericin B when her condition deteriorated. The M. tuberculosis infection and tubercular meningitis were treated with isoniazid, rifampicin, pyrazinamide, streptomycin and dexamethasone. Her circulation was stabilised and her renal and liver function improved. After 7 days, her cardiac function recovered. She exhibited confusion, tremor and weakness and flaccid paresis of her lower limbs, and experienced increasing headaches. Cerebral MRI on day 44 showed tuberculomas and ventricle distension, treated with CSF drainage and a ventriculo-peritoneal shunt. Due to her refractory disease course, streptomycin was substituted with ethambutol and moxifloxacin, and her steroid therapy was intensified. After 7 months, despite continued steroid and antitubercular treatment, she developed additional tuberculomas and tuberculous abscesses. Treatment with thalidomide was initiated. At last follow-up she was fully oriented; however, she had memory problems, panic attacks and continued weakness in her legs. Author comment: "In our patient, the history of TNF-α blockade and a typical radiographic image gave decisive clues [indicative of] . . . miliary or disseminated tuberculosis . . . immune reconstitution following discontinuation of adalimumab treatment may well have contributed to the development of new intracranial lesions." Hess S, et al. Life-threatening disseminated tuberculosis as a complication of TNFalpha blockade in an ad
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