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Immune reconstitution inflammatory syndrome and lack of efficacy: case report A 45-year-old man developed immune reconstitution inflammatory syndrome (IRIS) during treatment with abacavir, dolutegravir and lamivudine for HIV. Additionally, the patient exhibited lack of efficacy during treatment with amphotericin B liposomal, flucytosine, fluconazole and voriconazole for Cryptococcus gattii Meningitis [not all routes and dosages stated; durations of treatments to reaction onsets not stated]. The man, who was diagnosed with HIV disease at another institution, had been receiving antiretroviral therapy with abacavir, dolutegravir and lamivudine since June 2017. He was non-adherent to the antiretroviral therapy. One month following the diagnosis, he presented to the institution (current presentation) with vomiting and a severe headache for 2 days. He was diagnosed with Cryptococcal meningitis with pulmonary cryptococcoma. He was admitted and initiated on induction therapy with oral flucytosine and IV amphotericin B liposomal in July 2017. Following a 14-day course, he was discharged home on consolidation therapy with antiretroviral therapy and fluconazole. Fungal isolates from CSF and blood were demonstrated to be Cryptococcus gattii. He was hospitalised 9 times over a period of 12 months due to recurrence of fever, elevated intracranial pressure (ICP) and headache. Therapeutic lumbar punctures with CSF removal were intermittently required. In the fourth hospitalisation (October 2017), a follow-up brain MRI demonstrated the development of cryptococcomas in the left temporal region and right posterior cerebellum. He was considered a therapeutic failure on fluconazole. Induction therapy with amphotericin B liposomal and flucytosine was recommenced for 6 weeks. Subsequently, he was initiated on consolidation therapy with voriconazole 450mg two times a day (at calculated dosing 6 mg/kg). Salvage therapy with voriconazole did not improve his headache, fever or elevated ICP, reduce the CSF or blood CrAg titers or prevent hospitalisations. He was adherent to therapy, but therapeutic levels could not be achieved. Following 3 months on voriconazole, he developed dysphagia, which drew concern for worsening CNS cryptococcosis or possible onset of IRIS. Within 2 months, his dysphagia self-resolved, not requiring further workup. On the ninth hospitalisation (August 2018), and one year into treatment, an MRI of the head, showed a new cryptococcoma and evidence of cerebral venous thrombosis (CVT). Magnetic resonance venography of the brain showed a superior sagittal sinus thrombosis, for which he received unspecified anticoagulation therapy. He was received multiple rounds of antifungal induction therapy, having regiment durations of 2 weeks or 6 weeks. Typically, he ended up in the emergency room with hospitalisation for increased ICP. Consolidation therapies consisted of voriconazole and fluconazole, both of which failed, in spite of patient adherence. Therapeutic levels were achieved consistently with fluconazole treatment; ho