TY - JOUR T1 - Another Consequence of Severe Lupus: Invasive Fungal Disease JF - The Journal of Rheumatology JO - J Rheumatol SP - 1772 LP - 1774 DO - 10.3899/jrheum.120707 VL - 39 IS - 9 AU - CLAIRE E. BARBER AU - CHERYL BARNABE Y1 - 2012/09/01 UR - http://www.jrheum.org/content/39/9/1772.abstract N2 - Infections are a substantial cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE), accounting for one-quarter of all deaths1,2. The mechanisms for increased susceptibility to infections in patients with SLE are classically attributed to disease- and treatment-related factors. Polymorphisms in the mannose-binding lectin3 protein, which helps in host defense by activating the complement cascade, have been reported as a risk factor primarily for bacterial infections in SLE3. Patients with SLE may also have acquired hypogammaglobulinemia (as reviewed by Yong, et al4) or hyposplenism, which leads to increased susceptibility to infections with encapsulated organisms. Acquired neutropenia has also been cited as a risk factor for infections in SLE5 and for fungal infections in other populations6. Corticosteroids are frequently necessary in the treatment of SLE, resulting in diminished cellular immunity. Immunosuppressant therapy also clearly increases the risk of bacterial infection7.Invasive fungal infections were initially defined in 20028, with revisions occurring in 2008, including a change in terminology to “invasive fungal disease” (IFD)9 by the European Organization for Research and Treatment of Cancer/Invasive Fungal Infections Cooperative Group and the National Institute of Allergy and Infectious Diseases Mycoses Study Group (EORTC/MSG) Consensus Group. Proven IFD are subdivided into molds (Aspergillus) and yeasts (Candida species and Cryptococcus) and depend on culture or microscopic analysis from sterile anatomic sites, blood cultures, or cryptococcal antigen in cerebrospinal fluid. Separate criteria … Address correspondence to Dr. Barber; E-mail: cehbarbe{at}ucalgary.ca ER -