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Antifungals/corticosteroids/ibrutinib

Cerebral aspergillosis and decreased plasma concentration of voriconazole and isavuconazole: case report A 69-year-old man developed cerebral aspergillosis during treatment with ibrutinib for chronic lymphocytic leukaemia. Additionally, he experienced a decrease in the plasma concentrations of voriconazole and isavuconazole following concomitant administration of voriconazole and isavuconazole with an unspecified corticosteroid [routes, dosages, durationsof treatments to reaction onsets not stated; not all outcomes stated]. The man, who had been diagnosed with chronic lymphocytic leukaemia stage-A in 2012, further progressed to leukaemia stage-C along with autoimmune haemolytic anaemia and thrombocytopenia in September 2013. Therefore, he was started on unspecified corticosteroids. Later, the corticosteroids were discontinued, and he received 6 cycles of rituximab and bendamustin, which resulted in complete remission of his condition. In April 2016, he relapsed to Evans Syndrome and was treated with dexamethasone, rituximab and cyclophosphamide. In November 2016, he was found to have chronic lymphocytic leukaemia with 17p deletion. Therefore, he was started on ibrutinib along with immune globulin [immunoglobulin]. One year later, he experienced worsening of the breathing situation with feverish polypnea. The man’s treatment with ibrutinib was discontinued. Thereafter, he was diagnosed with acute respiratory distress syndrome Aspergillus fumigatus infection. He was treated with amphotericin-B liposomal [liposomal amphotericin-B]. This treatment was further replaced with voriconazole. During this therapy, clinical deterioration was noted along with the appearance of left miosis and balance disorder. An MRI of the brain revealed multiple abscesses significant with cerebral aspergillosis. It was concluded that cerebral aspergillosis was secondary to ibrutinib. Antifungal treatment with voriconazole was not changed as it had good penetration across the blood-brain barrier. Voriconazole therapeutic drug monitoring was performed once weekly. Subsequently, he was started on unspecified corticosteroids to control the cerebral oedema. However, due to interaction between voriconazole and corticosteroids led to decreased plasma levels of voriconazole. Therefore, voriconazole was replaced with isavuconazole, in spite of limited experience in cerebral aspergillosis. It was concluded that isavuconazole therapy was sufficient to reduce cerebral lesions without surgical resection as progressive decrease in the size of the fungal brain lesions was noted on MRI after 7 and 24 weeks after isavuconazole. Thereafter, therapeutic drug monitoring showed decreased plasma levels of isavuconazole than initially targeted on the first week of treatment. As a result, higher doses (300mg daily) of isavuconazole were given to maintain the plasma level above 2.8 mg/L. At follow-up visit, his condition was found to be stable without any adverse effects or laboratory abnormalities. There were no signs of