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Summary: CPK-BB (CK-BB) isoenzyme is an intracellular enzyme released in various neurologic conditions, including central nervous system (CNS) infections. Activity of CK-BB in cerebrospinal fluid (CSF) was determined in 80 [...]

Background: Leukotrienes are bronchoactive mediators secreted by inflammatory cells in the respiratory mucosa on exposure to asthma triggers. Objective: We investigated the effect of montelukast, a leukotriene receptor antagonist, on the release of leukotrienes in the respiratory mucosa of children with persistent asthma. Method: Twenty-three children aged 6 to 11 years with moderately severe asthma were treated in a cross-over design starting, after a 2-week run in period, with either montelukast (n = 12) or cromolyn (n = 11) for 4 weeks with a 2-week washout period between treatments. Twelve of them were then treated with either montelukast or beclomethasone for 6 months. The use of @b"2-agonists was recorded on a diary card. The concentration of leukotriene C"4 (LTC"4) was measured by HPLC in nasal washes obtained before and at the end of each treatment period. Eosinophilic cationic protein (ECP) was measured in the nasal washes by RIA. Results: The LTC"4 concentration significantly decreased in the children treated for the first 4 weeks with montelukast, from 5.03 +/- 1.17 to 1.42 +/- 0.33 ng/mL (P < .005), and a nonsignificant increase was noted in children treated with cromolyn, from 3.37 +/- 1.11 to 5.88 +/- 2.17 ng/mL (P = .17). ECP concentration also decreased in the children receiving montelukast (P = .12). The concentration of LTC"4 remained low after 3 and 6 months of treatment with montelukast (0.8 +/- 0.7 and 1.0 +/- 0.3 @mg/mL) and was lower than with beclomethasone. Children treated with montelukast required significantly fewer @b"2-agonists (P < .04), Conclusion: Montelukast reduces the concentration of leukotrienes in the respiratory tract of children with persistent asthma parallel to reduction in ECP and clinical improvement. This effect was not observed when the same children were treated with cromolyn. (J Allergy Clin Immunol 1999;104:1162-7.)

Binding of secretory IgA (sIgA) to human milk macrophages was identified by rosette formation with sIgA-sensitized indicator cells and competitive inhibition binding studies with [125I]-sIgA. Macrophages formed rosettes with sIgA-sensitized sheep red blood cells that were inhibited by sIgA (87) but not IgG. Both IgA1and IgA2inhibited sIgA-sensitized sheep red blood cell rosette formation. Rosette formation was completely inhibited by galactose, partially inhibited by asialofetuin, and unaffected by mannose. [125I]-labeled sIgA binding to macrophages reached a plateau after 60 min, was dependent on the number of macrophages in culture, and was specifically inhibited by unlabeled sIgA. Incubation of macrophage monolayers with increasing concentrations of sIgA-anti-IgA immune complexes resulted in a progressive increase in the oxidative burst and increased secretion of prostaglandins. These studies indicate that human milk macrophages have a receptor for sIgA and that activation of these macrophages may occur via these receptors.

Background: Twenty-four-hour serum cortisol secretion is a sensitive parameter for the assessment of the pituitary-adrenal function of asthmatic children treated with inhaled corticosteroids. This study was undertaken to determine the effect of the long-term administration of inhaled budesonide on 24-hour cortisol production in young children with asthma. Methods: We studied 11 children, aged 7 to 12 years, with severe perennial asthma. All had been receiving 100 @mg of inhaled budesonide twice daily, administered with a spacer device, for 3 to 5 years. Serum cortisol concentration was measured at 8:00 AM, 60 minutes after intravenous administration of 0.25 mg of corticotropin, and every 30 minutes for 24 hours in an open-design study. Urinary cortisol secretion was measured by 24-hour urine collection. All determinations were made with a radioimmunoassay kit. Results: The individual morning serum cortisol concentration and the serum cortisol concentration at 60 minutes after corticotropin stimulation were within normal limits in all children. The 24-hour urinary cortisol excretion was also normal. The individual 24-hour serum cortisol concentration showed a normal pattern in all children, with no evidence of nocturnal suppression of serum cortisol concentration. Conclusion: Prolonged (3 to 5 years) administration of 200 @mg/day of inhaled budesonide in young children with severe asthma does not impair pituitary-adrenal function, even according to the sensitive test for 24-hour serum cortisol secretion. (J ALLERGY CLIN IMMUNOL 1995;96:874-8.)

Background: Inhaled corticosteroids have a greater antiinflammatory potency and fewer systemic effects than intravenous, intramuscular, or oral corticosteroids. However, their role in acute asthma has not been established. We prospectively investigated the efficacy and safety of inhaled corticosteroids in controlling moderately severe acute asthma attacks in children who were treated in the emergency department. Methods: Children who were treated in the emergency department with moderately severe asthma attacks after receiving treatment with inhaled terbutaline were allocated by double-blind design to receive 1 dose of either 1600 @mg budesonide turbohaler or 2 mg/kg prednisolone. The pulmonary index score and peak expiratory flow rate were measured hourly for the first 4 hours. After discharge the children were treated with the same initial doses given 4 times daily, followed by a 25% reduction in dose every second day for 1 week. Parents recorded asthma symptoms and use of @b-2 agonists on a daily diary card. Serum cortisol concentration was measured at the end of weeks 1 and 3. Results: Twenty-two children (11 in each group) with similar baseline parameters completed the study. There was a similar improvement in pulmonary index score and peak expiratory flow rate in the 2 groups. Children treated with budesonide showed an earlier clinical response than those given prednisolone, who also showed a decrease in serum cortisol concentration. Conclusion: In children with moderately severe asthma attacks who were treated in the emergency department, a short-term dose schedule of inhaled budesonide turbohaler, starting with a high dose and followed by a decrease over 1 week, is at least as effective as oral prednisolone, without suppressing serum cortisol concentration. (J Allergy Clin Immunol 1998;102:605-9.)

Abstract: Congenital syphilis is re-emerging in modern society. The pediatric radiologist may contribute to its early diagnosis. A case of unusual bone involvement with fracture of the olecranon and facial bone lesions is described; the condition had to be differentiated from the “battered child syndrome”. The problem of congenital syphilis as an infectious disease versus bone dystrophy is also discussed.

Six asthmatic children participated in an acute crossover randomized study. They received a single dose of aminophylline syrup 6 mg/kg after having received ketotifen syrup 1 mg b.i.d. or place-bo for 8 days. Ketotifen did not significantly affect the heart rate, pulse pressure or such pharmacokinetic parameters of theophylline as peak serum level, time to peak, half life and AUC. Thus, ketotifen had no significant effect on the disposition of theophylline.