Lysozyme levels in the nasal secretions of patients with perennial allergic rhinitis and recurrent sinusitis.

BACKGROUND: The association of perennial allergic rhinitis (PAR) with recurrent sinusitis (RS) is well recognized. Anatomic abnormalities at the osteomeatal complex or ciliary dysfunction may play a significant role in some patients. However, for most patients with allergy, the determinants of RS are unknown. OBJECTIVE: To determine whether altered concentrations of antimicrobial peptides and proteins, such as lysozyme, lactoferrin, human beta-defensin-2 (HBD-2), and human neutrophil peptides 1 to 3 (HNP-1 to 3), contribute to the development of RS in patients with PAR. METHODS: Nasal secretions were collected by vacuum aspiration from 15 individuals with PAR+RS, 16 with PAR alone, and 16 controls. Lysozyme and lactoferrin levels were determined in nasal secretions by using quantitative enzyme-linked immunosorbent assay, and HBD-2 and HNP-1 to 3 levels were determined in nasal secretions by using semiquantitative Western blot analysis. Eosinophil-derived neurotoxin (EDN) levels were measured by using enzyme-linked immunosorbent assay as a marker of nasal eosinophilia in all 3 groups. RESULTS: Levels of EDN were elevated significantly in patients with PAR+RS compared with controls. Lysozyme levels were decreased significantly in patients with PAR+RS compared with PAR alone or controls. Mean lysozyme levels were significantly lower in patients with EDN levels greater than 1,000 ng/mL vs those with levels of 1,000 ng/mL or less in the PAR+RS group. There were no statistically significant differences in lactoferrin, HBD-2, and HNP-1 to 3 levels among the 3 groups. CONCLUSIONS: The presence of eosinophils and their products and reduced lysozyme concentrations may be critical factors that predispose the airways of patients with PAR to RS.

The syndrome of chronic mucocutaneous candidiasis with selective antibody deficiency.

BACKGROUND: Most patients with chronic mucocutaneous candidiasis (CMC) have a selective defect of cell-mediated immunity against Candida albicans (as demonstrated by cutaneous anergy and decreased lymphoproliferative responses to Candida antigen) and intact antibody responses. Many CMC patients also develop infections with other organisms, suggesting a more extensive immunologic defect. OBJECTIVES: The aim of this study was to describe a patient with CMC and selective antibody deficiency and identify eight similar previously reported patients. DATA SOURCES: Relevant articles in the English language derived from searching the MEDLINE database were used. RESULTS: We describe an 18-year-old male patient who was identified with CMC as an infant and later developed immunoglobulin (Ig)G2, IgG4, and IgA deficiency at age 12 associated with poor antibody responses to vaccine antigens. We have identified eight other previously reported CMC patients with selective antibody deficiencies and bacterial infections. IgG2 deficiency was present in all nine patients, and was associated with IgG4 deficiency in 8 patients and IgA deficiency in 3 patients. Six patients had poor or absent antibody responses to pneumococcal polysaccharide vaccine, and all nine patients developed severe recurrent lung infections. CONCLUSIONS: We suggest that these cases represent a distinct phenotype of CMC and should be studied for common histocompatibility leukocyte antigen types and molecular defects.