Tacrolimus

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Antibody-negative autoimmune encephalitis: case report A 58-year-old man developed antibody-negative autoimmune encephalitis during immunosuppressive therapy with tacrolimus. The man presented with intermittent confusion, lethargy, dizziness and lightheadedness. His wife reported that he forgot how to turn the lights off and how to use a television remote, stating that such episodes had occurred during previous 5 nights. After sleeping, he returned to normal until the following evening. He had undergone liver transplant 14 years previously due to alcoholic cirrhosis. Following transplant, he had been receiving immunosuppressive therapy with tacrolimus [route and dosage not stated] for prevention of chronic rejection. He made dietary and lifestyle changes due to hyperlipidaemia. He also had a sinus infection, which was treated with amoxicillin 2 weeks previously. His other medical history was significant for a single episode of autoimmune haemolytic anaemia (AIHA) triggered by vaccination and a single episode of immune thrombocytopenic purpura (ITP) triggered by upper respiratory tract infection or unspecified antibacterial [antibiotic] use. Both the episodes were refractory to unspecified steroids and required rituximab therapy. Later, complete resolution was noted. At the current presentation, a physical examination showed that he was alert and oriented. He was noted to have psoriasis. After admission, he started experiencing intermittent episodes of confusion which progressed to complete disorientation, inability to follow commands and agitation. He was found to have an increased startle reflex and hyperreflexia. Laboratory examination showed mildly low albumin level (3.0) and bicarbonate level of 23.2. His tacrolimus level was 3.9 (goal 3–5) [unit not stated] and erythrocyte sedimentation rate (ESR) was increased to 30 mm/hour. During an episode of confusion, his blood glucose level was 96 mg/dL. A brain MRI showed mild, hyperintense white matter lesions on T2 imaging of the anterior right putamen and periventricular white matter. An electroencephalogram (EEG) showed mild, generalised, non-specific cerebral dysfunction without seizure tendencies and a slow, posterior dominant rhythm. Lumbar puncture returned colourless cerebrospinal fluid with increased protein, albumin quotient, glucose and IgG. An MRI of the abdomen showed a non-specific early-enhancing lesion of the right lobe of the liver suspicious for a portosystemic hunt. The Mayo clinic laboratories autoimmune encephalitis panel did not reveal antineuronal antibodies. CNS infection was highest on the differential list and he was empirically treated with valaciclovir [valacyclovir]. However, based on the clinical findings, he was diagnosed with antibody-negative autoimmune encephalitis [duration of treatment to reaction onset not stated]. His CSF IgG increased. Furthermore, his BBB was disrupted, which indicated by a high albumin quotient of 23. The man was treated with methylprednisolone. His tacrolimus was continued in hospital and at the time of d