A review of the infection pathogenesis and prophylaxis recommendations in patients with chronic lymphocytic leukemia

ABSTRACT

Introduction: The majority of patients with CLL will suffer from infections during their disease, accounting for approximately 60% of deaths in CLL. Patients are predisposed to infection due to immune defects related to the primary disease, and as a result of therapy. The range of infectious complications has evolved alongside therapeutic advances in the treatment of CLL. More recently several novel therapeutic compounds have been introduced in CLL, whose unique safety profiles will probably have an impact on the prophylaxis and management of infections in these patients.

Areas covered: This review describes the pathogenesis of infections due to intrinsic CLL or therapy-related immunosuppression, and elightens the importance of proactive and reactive infection management as a key focus of patient care. Infections related to conventional chemotherapy, immunochemotherapy with monoclonal antibodies, target therapies with B-cell receptor pathway inhibitors and Bcl-2 antagonists are reviewed.

Expert commentary: Despite the importance of infection management and prevention in high-risk patients, there are only limited infection risk-assessment guidelines that can be easily used in clinical practice to guide more appropriate infection prophylaxis and its management. Here we provide an overview of suggested prophylaxis management of infection, and include key prophylactic interventions that we feel should be performed in CLL patients routinely.

KEYWORDS:

• Chronic lymphocytic leukemia/CLL
• infection pathogenesis
• prophylaxis infection management
• immunosuppression
• infection complications
• hypogammaglobulinemia

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Corrigendum

Declaration of interest

T Tadmore has received honoraria and travel grants from Takeda, Roche, Janssen, Gilead, Neopharm, Pfizer, and Mundipharma. M Welslau has received speaker honoraria from Janssen, Novartis, Roche, Celgene, Amgen, and Bristol-Myers Squibb. I Hus has received honoraria and travel grants from Roche, Janssen, Mundipharma, and Gilead. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. A peer reviewer on this manuscript has declared speakers’ bureau membership for Genentech, Celgene, Gilead, and Pharmacyclics but have no other relevant financial relationships to disclose

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Funding

This paper was not funded.