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Risk factors for fungal exposure in inner city homes
Leukotriene receptor antagonists ineffective as add-on therapy for chronic idiopathic urticaria Although antihistamines are the first-line treatment of chronic idiopathic urticaria (CIU), the response is often incomplete. Anecdotal accounts and some controlled studies have suggested that leukotriene receptor antagonists (LTRAs) might have a role in the treatment of CIU. In this issue of the Journal, Di Lorenzo and coworkers (p 619) report the results of a placebo-controlled, doubleblind examination of desloratadine, montelukast, both, or neither in 160 patients with moderate CIU. They specifically excluded those patients with allergic or physical urticaria, those with positive skin test results to autologous
Risk factors for fungal exposure in inner city homes The Inner City Asthma Study provides data on indoor mold exposure for 414 mold-sensitive children with moderate to severe asthma from 7 low-income suburban communities across the United States. In this issue of the Journal, O’Connor and coworkers (p 599) analyze these indoor concentrations of airborne fungi in relation to outdoor fungal levels and characteristics of the home. In keeping with previous reports, counts of Alternaria and Cladosporium were higher in outdoor air, whereas those of Penicillium and Aspergillus were higher in the samples from indoor air. For those 4 genera of fungi, indoor
Omalizumab reduces skin mast cell IgE receptors and function Infusions of omalizumab (anti-IgE) in allergic subjects are known to cause rapid declines in circulating free IgE levels as well as reductions in surface bound IgE and IgE receptors on blood basophils. This shift in basophil surface phenotype is directly linked to a decline in allergen-triggered basophil mediator release. However, the effects of omalizumab on tissue mast cell IgE receptor expression and allergen-triggered responses are less clearly understood. In a study by Beck et al (p 527), skin biopsy specimens were obtained from subjects undergoing
Page 464 September 2004
serum, and those with positive results to challenge with aspirin, nonsteroidal anti-inflammatory drug (NSAIDs), or food additives. Desloratadine was clearly the most effective treatment. All of the 80 subjects who received desloratadine completed the study. There was no additional benefit for any outcome with the addition of montelukast to desloratadine. Monotherapy was more effective with montelukast than with placebo, but montelukast was consistently less effective than desloratadine. Furthermore, 27 of the 40 subjects on montelukast monotherapy failed to complete the 6-week study, as did 35 of the 40 subjects receiving placebo. The results of this study do not support the use of LTRAs as either monotherapy or add-on therapy in moderate CIU in patients with negative autologous serum skin tests whose urticaria is not worse when challenged with aspirin or NSAIDs.
concentrations were moderately correlated with outdoor concentrations measured the same day, suggesting that the outdoor concentration is an important determinant of the indoor concentration. The fungal level for each home was expressed as the excess of the indoor concentration over the outdoor concentration (I – O) on a particular day; any home above the 75th percentile for this I – O difference was considered to have a high concentration of indoor molds. Those high mold levels were more likely in homes with evidence of dampness, cockroach infestation, or a cat living in the home and less likely in homes with forced air heating. The authors suggest that the I – O difference in the concentration of airborne fungi might be a valuable measure for assessing fugal exposure in future investigations.
omalizumab infusions over 6 months and examined for mast cell expression of IgE receptors and the size of allergen-induced acute wheals. The results support that a reduction occurs in skin mast cell receptor number and function similar to that observed in the subjects’ blood basophils; however, the onset of reduction is much slower (several weeks) than the rate (days) observed for blood basophils. There is also evidence that the late-phase cellular response to allergen challenge in the skin is reduced in omalizumab recipients. The authors conclude that the longer time interval required for modification of mast cell phenotype and function might hold implications for the onset of clinical response in allergic hosts.
J ALLERGY CLIN IMMUNOL
Risk factors for fungal exposure in inner city homes The Inner City Asthma Study provides data on indoor mold exposure for 414 mold-sensitive children with moderate to severe asthma from 7 low-income suburban communities across the United States. In this issue of the Journal, O’Connor and coworkers (p 599) analyze these indoor concentrations of airborne fungi in relation to outdoor fungal levels and characteristics of the home. In keeping with previous reports, counts of Alternaria and Cladosporium were higher in outdoor air, whereas those of Penicillium and Aspergillus were higher in the samples from indoor air. For those 4 genera of fungi, indoor
Omalizumab reduces skin mast cell IgE receptors and function Infusions of omalizumab (anti-IgE) in allergic subjects are known to cause rapid declines in circulating free IgE levels as well as reductions in surface bound IgE and IgE receptors on blood basophils. This shift in basophil surface phenotype is directly linked to a decline in allergen-triggered basophil mediator release. However, the effects of omalizumab on tissue mast cell IgE receptor expression and allergen-triggered responses are less clearly understood. In a study by Beck et al (p 527), skin biopsy specimens were obtained from subjects undergoing
Page 464 September 2004
serum, and those with positive results to challenge with aspirin, nonsteroidal anti-inflammatory drug (NSAIDs), or food additives. Desloratadine was clearly the most effective treatment. All of the 80 subjects who received desloratadine completed the study. There was no additional benefit for any outcome with the addition of montelukast to desloratadine. Monotherapy was more effective with montelukast than with placebo, but montelukast was consistently less effective than desloratadine. Furthermore, 27 of the 40 subjects on montelukast monotherapy failed to complete the 6-week study, as did 35 of the 40 subjects receiving placebo. The results of this study do not support the use of LTRAs as either monotherapy or add-on therapy in moderate CIU in patients with negative autologous serum skin tests whose urticaria is not worse when challenged with aspirin or NSAIDs.
concentrations were moderately correlated with outdoor concentrations measured the same day, suggesting that the outdoor concentration is an important determinant of the indoor concentration. The fungal level for each home was expressed as the excess of the indoor concentration over the outdoor concentration (I – O) on a particular day; any home above the 75th percentile for this I – O difference was considered to have a high concentration of indoor molds. Those high mold levels were more likely in homes with evidence of dampness, cockroach infestation, or a cat living in the home and less likely in homes with forced air heating. The authors suggest that the I – O difference in the concentration of airborne fungi might be a valuable measure for assessing fugal exposure in future investigations.
omalizumab infusions over 6 months and examined for mast cell expression of IgE receptors and the size of allergen-induced acute wheals. The results support that a reduction occurs in skin mast cell receptor number and function similar to that observed in the subjects’ blood basophils; however, the onset of reduction is much slower (several weeks) than the rate (days) observed for blood basophils. There is also evidence that the late-phase cellular response to allergen challenge in the skin is reduced in omalizumab recipients. The authors conclude that the longer time interval required for modification of mast cell phenotype and function might hold implications for the onset of clinical response in allergic hosts.
J ALLERGY CLIN IMMUNOL