IgE antibodies specific for staphylococcal superantigens (SAg) have been implicated in the pathology of several allergic diseases such as rhinosinusitis, nasal polyposis, asthma, and aspirin intolerance. We sought to determine whether SAg-specific IgE levels associate with clinical parameters in patients with aspirin-intolerant asthma (AIA), as compared with patients with aspirin-tolerant asthma (ATA) and nonatopic controls. Eighty patients with AIA, 62 patients with ATA, and 52 normal controls were enrolled in this study. Total serum IgE and IgE specific for staphylococcal enterotoxin A, staphylococcal enterotoxin B, and staphylococcal toxic shock syndrome toxin 1 (TSST-1) were measured using the CAP system (Pharmacia, Uppsala, Sweden). The prevalence of staphylococcal enterotoxin B-specific IgE and TSST-1-specific IgE was significantly higher in the asthma patients than in the healthy controls. The prevalence of SEB-specific IgE was slightly higher in patients with AIA than in those with ATA (22.5% versus 14.5%), although this difference was not statistically significant. No significant difference in staphylococcal enterotoxin A-specific or TSST-1-specific IgE was found between AIA and ATA subjects. Total serum IgE levels were higher in asthma patients with detectable SAg-specific serum IgE than in those without. Airway hyperresponsiveness, as measured by PC20 methacholine, was significantly increased in asthma patients with detectable SAg-specific IgE than in asthma patients without (p = 0.038). There were no significant differences in other clinical parameters between AIA and ATA patients with and without detectable SAg-specific antibody responses. These findings suggest that the staphylococcal SAg may contribute to airway inflammation and the development of airway hyperresponsiveness in asthma.

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Background: Chronic cough is associated with increased sensitivity to inhaled capsaicin, and both tachykinins and their receptors play important roles in the cough reflex. However, associations between polymorphisms of the tachykinin receptor genes and cough sensitivity in patients with non-productive chronic cough have not been reported. Methods: Direct sequencing was used to identify single nucleotide polymorphisms (SNPs) in the genes for the neurokinin-1 and neurokinin-2 receptors (NK-1R and NK-2R, respectively). Informative nonsynonymous SNPs were scored using the single base extension method for 312 patients with chronic cough and for 100 age matched healthy controls. The cough response to capsaicin was recorded for 312 patients with chronic cough, and the potential genetic association between cough sensitivity to capsaicin and the NK-1R and NK-2R genotypes was evaluated. Results: Two informative SNPs were identified in NK-2R (Gly231Glu and Arg375His), whereas no informative SNP was found in NK-1R. After adjusting for atopy, sex, age, and smoking, the prevalence of enhanced cough sensitivity to capsaicin was higher in the chronic cough patients with the 231Glu allele (p = 0.004; OR 1.69 (95% CI 1.18 to 2.42)) and the 231Glu_375Arg haplotype (p = 0.003; OR 1.71 (95% CI 1.20 to 2.24)]. Moreover, the lowest capsaicin concentration to cause five consecutive coughs (C5) was significantly lower in patients with 231Glu (mean (SD) 44.1 (53.2) v 60.9 (55.8) mM/l, p = 0.04) and those with 231Glu_375Arg (43.2 (52.7) v 69.6 (52.0) mM/l, p = 0.03). Conclusions:The results of this study suggest that NK-2R gene polymorphisms are involved in the enhanced cough sensitivity to capsaicin of patients with chronic cough.

This is the first reported detection of serum IgE antibody to piperacillin-human serum albumin (HSA) conjugate in a patient presenting with anaphylaxis that developed after occupational exposure. A 24-yr-old nurse, who had worked at a University Hospital for 2 yr, experienced chest tightness, dizziness, generalized urticaria, abdominal pain, and diarrhea 10 min after administering a piperacillin injection. She had previously suffered from atopic dermatitis. A skin prick test for common inhalant allergens was entirely negative; in contrast, her serum total IgE was elevated (283 IU/mL). A high level of piperacillin-specific serum IgE was detected by ELISA using piperacillin-HSA conjugate. Significant inhibition upon addition of both free piperacillin and piperacillin-HSA conjugate was detected by inhibition ELISA. These data suggest that piperacillin exposure in the workplace can induce occupational anaphylaxis and urticaria mediated by an interaction of IgE with the hapten of piperacillin.

Pulmonary infection by capsule-deficient Cryptococcus neoformans (CDCN) is a very rare form of pneumonia and it is seldom seen in the immunocompetent host. The authors experienced a case of pulmonary cryptococcosis by CDCN in 25-year-old woman who was without any significant underlying disease. The diagnosis was made from the percutaneous lung biopsy and special tissue staining, including Fontana-Masson silver (FMS) staining. Fungal culture confirmed the diagnosis afterward. Her clinical and radiologic features improved under treatment with fluconazol. It's known that CDCN is not so readily confirmed because fungal culture does not always result in growth of the organism and the empirical fungal stain is not helpful for the differentiation between CDCN and the other infections that are caused by the nonencapsulated yeast-like organisms. In this report, we emphasize the diagnostic value of performing FMS staining for differentiating a CDCN infection from the other confusing nonencapsulated yeast-like organisms.