Mucormycosis is an infection caused by fungi from the Mucoromycotina group. The clinical manifestations are dependent of the portal of entry and immune status of the human host. Patients with hematological malignancies on treatment causing immune suppression are at higher risk of mucormycosis. The number of medications to treat mucormycosis is very limited, in contrast with the development of medications with novel mechanisms of action against hematological malignancies.
A patient with chronic lymphocytic leukemia (CLL) receiving ibrutinib, a Bruton's tyrosine kinase (BTK) inhibitor, developed a skin lesion in left leg after local trauma. He developed progressive inflammation around trauma site, and fever. His lesion did not respoond to broad-spectrum antibiotic use. Biopsy of lesion revealed braching hyphae suggestive for mucormycosis. Liposomal amphotericin B (LAMB) was started empirically, with slow improvement in skin lesion. Brain, sinuses, and lungs were not compromised with invasive mold infection. Despite supportive measures, the patient did not tolerate LAMB, so he was switched to posaconazole. Ibrutinib was stopped while receiving posaconazole. Despite continuous improvement in skin infection, his overall function continued to decline. The patient elected withdrawal of medical care. His death was not attributed to invasive mucormycosis.
Despite the known drug-drug interaction between ibrutinib and posaconazole (elevation of serum ibrutinib due to CYP3A4 inhibition by posaconazole), data regarding the management of invasive mucormycosis by long-term posaconazole use in patients with CLL receiving BTK inhibitors is very limited, and it could impact the management of CLL. Effective communication between oncology, pharmacy, and infectious diseases is recommended. Invasive mucormycosis should be considered in patients receiving BTK inhibitors⇓.
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