Contact allergy in relation to hand eczema and atopic diseases in north Norwegian schoolchildren

Dotterud LK, Falk ES. Contact allergy in relation to hand eczema and atopic diseases in north Norwegian schoolchildren. Acta Psediatr 1995;84:402–6. Stockholm. ISSN 0803–5253
Patch testing was carried out in 424 schoolchildren (223M, 201F), aged 7–12 years, in northern Norway. In 99 (23.3%) of these children, one or more allergic patch test reactions were demonstrated; 30 children reacted to two and 6 to three or more substances; 53 irritant reactions were recorded in 33 (7.8%) of those tested. From a total of 144 positive tests, the most common allergen was nickel (14.9%), followed by cobalt (5.7%), kathon CG (5.2%), lanolin (1.7%) and neomycin (1.4%). Both allergic and irritant reactions were found twice as frequently in girls as in boys. Positive patch tests were significantly more frequent in atopic (28.8%) than in non–atopic (17.9%) children, being most pronounced in atopic girls (37.4%). Hand eczema was reported to have occurred or to be present in 6.5% of cases. Twenty–nine of 36 children reporting hand eczema participated in the clinical examination. Altogether 15 (3.5%) children had hand eczema at the time of the clinical examination but 12 of these children had no previous history of hand eczema. In 14 of these 15 subjects, the eczema was localized to the back of the hands, with 13 having atopic dermatitis. In 4 of these 15 children, an allergic patch test reaction was found; however, in only 2 of these 4 was the test considered to be clinically relevant for the diagnosis allergic hand eczema. In conclusion, irritant hand eczema may occur in early childhood and is most prevalent in children with atopic dermatitis     

Migraine preventive medications: a reappraisal

Newer acute care migraine medications demonstrate improved rapidity of action, consistent effectiveness, excellent safety profiles, and rarely cause rebound headaches. Their use could decrease the need for migraine-preventive medication. The present analysis derives a formula that can be used by practitioners to determine the cost-effectiveness of various migraine-preventive medications relative to selected acute-care medications. We propose a measure called the cost-equivalent number (CEN), the number of headaches per month at which the cost of the preventive medication equals the cost savings in acute-care treatment realized by using the preventive medication. The use of the CEN individualizes the decision of whether to use a migraine-preventive medication, weighing both the efficacy and cost of the preventive medication against the cost of the acute-care medication. A CEN lower than the migraine frequency suggests that use of a preventive medication will be cost-effective.     

No association between serum eosinophil cationic protein and atopic dermatitis or allergic rhinitis in an unselected population of children

Background In order to obtain background references when dealing with serum eosinophil cationic protein (s‐ECP) measurements in children with allergic diseases, population‐based studies are important. The objectives of our study were to explore the strength of associations between the s‐ECP level and atopic dermatitis (AD), allergic rhinitis (AR) and asthma in an unselected northern Norwegian schoolchildren population. Methods s‐ECP was sampled from 396 schoolchildren aged 7–12 years from Sør‐Varanger community, northern Norway as a part of a population‐based study of allergy. In advance, anamnestic information concerning a history of AD, AR and asthma were obtained. The children underwent a clinical investigation, including skin prick tests and peak expiratory flow measurements, where the presence of AD, AR and asthma were evaluated. The associations of these diseases to the s‐ECP values were examined in bivariate statistical analysis. Results No statistical significant associations were detected in bivariate analysis between s‐ECP and AD, AR or asthma: the mean s‐ECP in children without self‐reported AD/AR/asthma was 4.6 µg/L [95% confidence interval (CI) 4.0–5.2]. The mean s‐ECP in children with self‐reported AD or AR or asthma was 5.2 µg/L (95% CI 4.1–6.2), 4.6 µg/L (95% CI 3.5–5.7) and 6.4 µg/L (95% CI 4.4–8.3), respectively. The highest mean s‐ECP level was measured in children with clinically diagnosed asthma; 7.1 µg/L (95% CI 4.0–10.3). Above the 75‐percentile level of s‐ECP, only 17.2% of the children had a history of asthma. Conclusions In this unselected children population, the occurrence of AD or AR was not reflected by an increase in the s‐ECP level. The s‐ECP was increased in children with asthma, but was not statistically significant. Furthermore, the majority of children with high s‐ECP values were not asthmatics. We conclude that the associations between s‐ECP and allergic diseases are weak in an unselected population of children.     

Anandamide modulates the neuroendocrine responses induced by extracellular volume expansion

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Selective induction of a glycoprotein IIIa ligand-induced binding site by fibrinogen and von Willebrand factor

Ligand-induced binding sites (LIBS) are neoantigenic regions of glycoprotein (GP)IIb-IIIa that are exposed upon interaction of the receptor with the ligand fibrinogen or the ligand recognition sequence (RGDS). LIBS have been suggested to contribute to postreceptor occupancy events such as full-scale platelet aggregation, adhesion to collagen, and clot retraction. This study examined the induction requirements of a GPIIIa LIBS with regard to ligand specificity. Through the use of the anti-LIBS D3, we report that this complex- activating antibody induces fibrinogen- and von Willebrand factor- binding to GPIIb-IIIa on intact platelets. Bound ligand was detected by flow cytometric analysis and platelet aggregation assays. These bound ligands increased the number of D3-binding sites and altered the affinity of D3 for GPIIb-IIIa on platelets. In contrast, activation of platelet GPIIb-IIIa by D3 did not increase the binding of another RGD- containing ligand, vitronectin. Furthermore, bound vitronectin on thrombin-stimulated platelets did not cause the expression of the D3 LIBS epitope. We conclude direct activation of GPIIb-IIIa in the absence of platelet activation results in selective ligand interaction and that D3 LIBS induction requires the binding of the multivalent ligands, fibrinogen or von Willebrand factor. Thus, the region of GPIIIa recognized by D3 may be an important regulatory domain in ligand- receptor interactions that directly mediate platelet aggregation.