Urticaria and, to a lesser extent, angioedema are common occurrences in the pediatric population. There are multiple causes of acute and chronic urticaria and angioedema. Most causes are benign, although they can be worrisome for patients and their parents. An allergist should evaluate acute urticaria and/or angioedema if there are concerns of an external cause, such as foods or medications. Chronic urticaria and angioedema can severely affect quality of life and should be managed aggressively with antihistamines and immunomodulators if poorly controlled. Chronic symptoms are unlikely to be due to an external cause. Anaphylaxis is a more serious allergic condition characterized by a systemic reaction involving at least 2 organ systems. Anaphylaxis should be initially managed with intramuscular epinephrine. Patients who experience anaphylaxis should be evaluated by an allergist for possible causes; if found, avoidance of the inciting antigen is the best management. All patients should also be given an epinephrine autoinjector and an action plan. Foods are a common cause of anaphylaxis in the pediatric population. New evidence suggests that the introduction of highly allergic foods is safe in infancy and should not be delayed. In addition, the early introduction of foods such as peanuts may help prevent the development of food allergies.
Background
Exposure to secondhand smoke (SHS) is associated morbidity in children. Alterations in immune responses may explain this relationship, but have not been well-studied in children. Our objective was to determine the association between SHS exposure and serum cytokine levels in healthy children.
Methods
We recruited 1–6 year old patients undergoing routine procedures. A parent interview assessed medical history and SHS exposure. Children with asthma were excluded. Blood was collected under anesthesia. We used Luminex to test for a panel of cytokines; cotinine was determined using an enzyme-linked immunosorbent assay. Children were categorized as no, intermediate, or high exposure. A mixed-effects model was fit to determine differences in cytokines by exposure level.
Results
Of the 40 children recruited, 65% (N=26) had SHS exposure; 16 intermediate, and 10 high. There were no differences by demographics. In bivariate analyses, children exposed to SHS had lower concentrations of IL-1β, IL-4, IL-5, and IFN- γ than those with no exposure. In the mixed-effects model, children with any SHS exposure had significantly lower concentrations of IL-1β (0.554 pg/mL vs. 0.249 pg/mL) and IFN- γ (4.193 pg/mL vs. 0.816 pg/mL), and children with high exposure had significantly lower mean concentrations of IL-4 (8.141 pg/mL vs. 0.135 pg/mL) than children with no exposure.
Conclusions
This study suggests that SHS exposure decreases expression of some pro-inflammatory cytokines in SHS exposed children, including IFN-γ. Further research to describe the acute and chronic effects of SHS on the immune systems of children is needed.
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