We studied the relationship between parental smoking habits and atopy and bronchial responsiveness (BR) in 9-year-old, non-selected schoolchildren. A questionnaire on respiratory disease and maternal and paternal smoking habits was administered to one parent. Skin prick tests using the most common allergens present in central Italy, a flow-volume spirometric test, and a bronchial provocation test using carbachol in increasing doses were performed. Male children with smoking parents had significantly increased BR when compared to those whose parents did not smoke (Odds Ratio (OR) = 4.3, p = 0.009). No such significant increase in BR was found in female children of smoking parents (OR = 1.5, p = 0.4). The relationship between BR in children and smoking in parents was stronger in asthmatics (p = 0.02), but was still significant after controlling for asthma and atopy. Bronchial responsiveness was significantly correlated with atopy (p = 0.001). This was also true for nonasthmatic children and for both males and females separately. Male children of smoking parents had increased reactivity to allergens as assessed by the skin prick test index (p = 0.001). It is hypothesized that passive smoking, by increasing the frequency of BR and of atopy, may increase the risk of asthma in childhood and particularly in boys.
The objective of this study was to assess the role of parental smoking in changes, after a four year interval , in the prevalence and severity of the atopic state in 166 preadolescent children. Allergy skin prick tests were related to parental smoking habits and their changes during this same interval.The total number of cigarettes smoked by parents decreased in 56 families while it increased in only 16. Boys had significantly more persistently positive skin tests and changed more frequently from negative to positive. The skin test index did not show significant changes in girls. This index did not change in children of persistent non-smokers or those starting to smoke during this period, while it increased among sons of those that quit smoking and of persistent smokers. This was not only due to those boys who became skin test positive during foliow up. When analysis was restricted to 14 boys who had been skin test positive in 1983 and whose parents were persistent smokers, the index increased in eight, remained unchanged in four, and decreased in only two.This report supports the hypothesis that parental smoking is a factor that, together with specific allergenic exposure, may enhance allergic sensitisation in children.ing, by increasing the risk of atopy, may increase the risk of asthma, particularly in their sons.2Little is known about longitudinal changes occurring in skin prick test reactivity during the preadolescent years. Barbee et al reported that, out of 70 subjects aged 6-14 years, 15 (21-4%) had converted from initial negative to positive after a mean of 8-1 years of follow up, while 27 (38-6%) remained consistently positive, and 28 (40%) remained consistently negative. No subject became skin test negative during this age interval.4 These investigators also reported that, paradoxically, total IgE concentrations decreased both in consistent atopic and consistent non-atopic subjects in this same age interval.5 Factors other than the direct genetic control of IgE concentrations may play a significant part in atopic sensitisation during this crucial period of life.The objective of this present study was to assess the role of parental smoking in changes of prevalence and severity of the atopic state in children originally enrolled at the age of 9 years. For this purpose we recalled, after a four year interval, the group of 166 subjects in whom these relationships had already been studied in 1983.2 Allergy skin prick tests were repeated and results were related to parental smoking habits during this same interval. When we studied a random sample of 166 children aged 9 years, we showed that the prevalence of atopy was significantly higher in the sons of smoking parents than in the sons of non-smoking parents. We also showed, again in boys, that a prick skin test index, calculated from the combined diameters of the weals elicited by the allergens, was correlated with the total number of cigarettes smoked by their parents. We hypothesised that parental smok-
ABSTRACX. Samples of nasopharyngeal secretions from a group of 73 infants with bronchiolitis or upper respiratory illness alone during infection with respiratory syncytial virus were analyzed for leukotriene C4 (LTC4) content using a reverse-phase high-pressure liquid chromatography assay with confirmation by radioimmunoassay. Titers of respiratory syncytial virus (RSV)-specific IgE in nasopharyngeal secretion (NPS) specimens were determined using an enzyme-linked immunosorbent assay. The highest concentrations of L T C were found in the first 3 to 8 days after the onset of illness, and LTC4 was detectable in progressively lower concentrations in samples obtained up to 28 days after the onset of illness. LTC4 was detected in samples of NPS obtained in the acute phase of illness from 67% of infants with bronchiolitis due to RSV and in 33% of samples of NPS obtained during the same interval from infants with upper respiratory illness alone ( p < 0.025).Concentrations of LTC4 in children with bronchiolitis were 5-fold higher (1271 pg/ml) than the mean concentration of LTC4 in children with upper respiratory illness (224 pg/ ml, p < 0.02). LTC4 was detected in 83% of the children developing an RSV-IgE response and in 24% of subjects not developing an RSV-IgE response (p < 0.001). Quantities of L T C measured in NPS were directly correlated with the magnitude of the RSV-IgE response in secretions (r = 0 . 3 3 ,~ < 0.02). These studies lend support to previous investigations suggesting that severe bronchiolitis due to RSV results from IgE-mediated hypersensitivity reactions to viral antigens, with release of chemical mediators of airway obstruction. Their implications should be considered in new approaches to therapy of RSV bronchiolitis. (Pediatr Res 24: 504-507, 1988 Infection with RSV is the most common cause of bronchiolitis in infancy (1). Previous studies have indicated that infants with RSV bronchiolitis exhibit increased levels of virus-specific IgE and histamine in respiratory tract secretions in comparison to individuals with URI alone due to RSV (2, 3). In addition to histamine, other mast cell products, especially L T C and LTD4, have been shown to be potent mediators of bronchoconstriction and increased airway mucus secretion (4-6). However, their role in wheezing associated with respiratory infection in infancy has not been determined. Bronchoactive and vasoactive mediators may also be released by other effector cells that are present in the respiratory tract during acute viral infection (7, 8). Our study was designed to determine the presence of LT in the nasopharyngeal mucosa during RSV infection and to evaluate their potential role in RSV-induced wheezing in infancy and childhood. MATERIALS AND METHODS Subjects.A total of 73 children with RSV infection hospitalized during the winters of 1986 and 1987 was enrolled in this study. A diagnosis of bronchiolitis with or without pneumonia was made in 48 children on the basis of physical examination by a single member of the study team and a careful review of...
Celiac disease (CD) is an intestinal inflammatory disease that manifests in genetically susceptible individuals when exposed to dietary gluten. It is a common chronic disorder, with a prevalence of 1% in Europe and North America. Although the disease primarily affects the gut, the clinical spectrum of CD is remarkably varied, and the disease can affect many extraintestinal organs and systems, including the liver. The hepatic dysfunction presenting in CD ranges from asymptomatic liver enzyme elevations or nonspecific reactive hepatitis (cryptogenic liver disorders), to chronic liver disease. In this article, we review the clinical presentations and possible mechanisms of CD-related liver injury to identify strategies for the diagnosis and treatment of these disorders in childhood.
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