dinoprost and Dermatitis--Atopic

Airway inflammation may be present in subjects affected by atopic dermatitis (AD) but still without asthma symptoms. Exhaled breath condensate (EBC) reflects the composition of bronchoalveolar extracellular lining fluid that contains a large number of mediators of airway inflammation and oxidative damage..   We assessed inflammatory markers in the EBC of patients with AD. Fifty-six children (34 girls and 22 boys) were enrolled: 33 affected by AD and 23 healthy controls..   EBC was collected using a condenser device. We measured EBC pH and concentrations of leukotriene B4 (LTB4), 8-isoprostane, H(2) O(2) , malondialdehyde and 4-hydroxynoneal. Respiratory resistance was also evaluated..   EBC pH in patients with AD was significantly lower than in healthy children, median (range) being 8·02 (7·94-8·12) in AD vs. 8·11 (8·05-8·16) (P = 0·02). The values of exhaled 8-isoprostane and LTB4 were significantly increased in subjects with AD compared with normal controls (P < 0·01 and P < 0·001, respectively). There was increased 4-hydroxynoneal in patients with AD but this did not reach statistical significance. Evaluating respiratory resistance, no bronchoreversibility was demonstrated in the children with AD.. pH, LTB4 and 8-isoprostane in EBC could be sensitive markers of airway inflammation in children with AD. Prospective studies would be of interest to evaluate if airway inflammation, not yet clinically evident, could predict the development of asthma later in life in children with AD.

Topics: Airway Resistance; Aldehydes; Biomarkers; Breath Tests; Case-Control Studies; Child; Child, Preschool; Dermatitis, Atopic; Dinoprost; Female; Humans; Hydrogen-Ion Concentration; Leukotriene B4; Male; Malondialdehyde; Oxidative Stress

Children with atopic eczema (AE) are at risk of developing asthma. Airway inflammation has been shown to be present before the onset of clinical asthma. Increased exhalation (forced expiration; FE) of nitric oxide (FE(NO)) and 8-isoprostane seems to be a feature of bronchial inflammation in people with asthma.. To determine whether the exhalation of these two molecules is increased in children with eczema, even in the absence of overt asthma.. In total, 21 children with AE were recruited and compared with healthy controls. A questionnaire was completed to identify respiratory symptoms compatible with asthma. The severity of AE was graded clinically. Spirometry, FE(NO) measurements and exhaled breath condensate collection for 8-isoprostane were performed.. The mean level of 8-isoprostane was similar for children with AE (2.33 +/- 4.76 pg/mL) and controls (3.37 +/- 3.43). FE(NO) was increased in children with AE (mean 64.97 parts per billion) compared with the normal range, even in the absence of respiratory symptoms and in the presence of normal lung function.. FE(NO) but not 8-isoprostane levels in exhaled breath condensate are higher in children with AE without asthma. Our finding may indicate a predictive role for FE(NO) for the development of asthma.

Topics: Adolescent; Asthma; Biomarkers; Breath Tests; Child; Dermatitis, Atopic; Dinoprost; Female; Humans; Male; Nitric Oxide; Predictive Value of Tests; Pulmonary Ventilation

To evaluate the role of Chlamydia pneumoniae respiratory tract infection on pediatric asthma, allergic rhinitis or atopic eczema initiation, children of three age groups (n=1211) were prospectively studied for a C. pneumoniae infection using throat swabs and polymerase chain reaction (PCR) with enzyme immunoassay (EIA) detection. Infected children (study group, SG) were examined monthly until the agent could not be detected, quantifying persistent infection. They were compared with randomly selected, non-infected children without asthma matched for age, gender and origin (control group, CG) regarding lung function and inflammatory parameters as well as initiation of allergic diseases judged by family doctor diagnosis after, in median, 22 months. At the first follow-up examination, SG children revealed a higher leukotriene B4 (median 36 pg/ml vs. 19, p=0.04) and 8-isoprostane (median 15 pg/ml vs. 12, p=0.04) in breath condensate characterizing neutrophil, agent-related inflammation and oxidative stress in the lower airways. Cysteinyl leukotrienes, important in acute allergic inflammation, were without difference. Local, anti C. pneumoniae secretory immunoglobulin A antibodies were higher in children after C. pneumoniae infection (optical density median 0.7 vs. 0.4, p=0.001) confirming PCR-EIA results. At the final examination, there was no difference in pathological lung function tests, parameters of exhaled breath condensate or eosinophilia of the nasal mucosa. Incidence of asthma (0/55 vs. 5/54, p=0.03) and allergic rhinitis [3/53 vs. 10/52, p=0.04, odds ratio and 95% confidence interval-OR 0.25 (0.06;0.98)] as well as prevalence of asthma [1/56 vs. 9/58, p=0.02, OR 0.1 (0.01;0.81)] and allergic rhinitis [6/56 vs. 16/58, p=0.03, OR 0.32 (0.11;0.88)] were lower in the SG children. There was no association in atopic eczema. Three children with persistent infection revealed a slightly higher incidence in allergic rhinitis without significance than those with single C. pneumoniae detection (1/3 vs. 2/50), however, not to the CG. In conclusion a C. pneumoniae upper respiratory tract infection may be regarded as a protective factor for childhood asthma or allergic rhinitis in a population of kindergarten and school-age children.

Topics: Adolescent; Animals; Asthma; Child; Child, Preschool; Chlamydophila Infections; Chlamydophila pneumoniae; Cohort Studies; Dermatitis, Atopic; Dinoprost; Female; Humans; Immunoenzyme Techniques; Immunoglobulin A; Leukotriene B4; Male; Pneumonia, Bacterial; Polymerase Chain Reaction; Respiratory Function Tests; Rhinitis

To study the role of mast cell activation in children with atopic eczema/dermatitis syndrome (AEDS), we measured levels of urinary 9alpha,11beta-prostaglandin F(2) (U-9alpha,11beta-PGF(2)) by enzyme-linked immunoassay in 88 children (mean age 44 months, range 3-135) with mild (n=32), moderate (n=34) or severe (n=22) AEDS, as well as in 72 non-atopic healthy controls. Fifty-eight of the children with AEDS were sensitized to common allergens (atopics) and 30 were not (non-atopics). Levels of U-9alpha,11beta-PGF(2) were higher in children with severe AEDS (median 324 microg/mmol creatinine, quartiles 220-593) than in controls (198, 102-389, p<0.001), whereas levels of U-9alpha,11beta-PGF(2) in moderate and mild disease were similar to controls. U-9alpha,11beta-PGF(2) levels were similar in atopic and non-atopic children, but in severe AEDS those with atopy had higher levels than those without atopy (p<0.05). The results suggest a role for mast cell activation in children with severe AEDS. Exacerbation of AEDS caused by allergen triggering may involve mast cell activation, and U-9alpha,11beta-PGF(2) may serve as a marker of this process.

Topics: Child; Child, Preschool; Dermatitis, Atopic; Dinoprost; Female; Humans; Infant; Male; Mast Cells; Severity of Illness Index

NC/Nga mice have similar pathological and behavioral features of human atopic dermatitis and are used as a model of the disease. Under conventional circumstances, spontaneous and persistent scratching is frequent and can lead to the onset of skin inflammation. We examined the effects of several prostanoids and their related compounds on the scratching behavior of NC/Nga mice. Among them, topically applied prostaglandin D2, prostaglandin E1, prostaglandin E2 and prostaglandin I2 significantly suppressed the scratching, the order of inhibitory activities being prostaglandin D2>>prostaglandin I2>prostaglandin E1=prostaglandin E2. Prostaglandin D2 metabolite, prostaglandin J2 also significantly suppressed the scratching but not so 13,14-dihydro-15-keto-prostaglandin D2, and 15-deoxy-Delta12,14-prostaglandin J2. The order of the inhibitory activities of these prostaglandin D2 metabolites depended on affinity of the prostanoid DP1 receptor but not on the DP2 receptor (chemoattractant receptor-homologous molecule expressed on T helper2 cells, CRTH2) and PPAR-gamma receptors. Likewise, topically applied arachidonic acid significantly suppressed the scratching while indomethacin enhanced it. Pretreatment of arachidonic acid increased the skin prostaglandins (prostaglandin D2, prostaglandin E2, prostaglandin F2alpha and 6-keto-prostaglandin F1alpha) contents, but indomethacin decreased the prostaglandin D2 and prostaglandin E2 contents. On the other hand, prostaglandin D2 and indomethacin had no apparent effects on histamine-induced scratching of ICR mice. These results suggested that prostaglandin D2 plays a physiological role in inhibiting pruritus of NC/Nga mice via their specific prostanoid DP1 receptors, and that prostaglandin D2 and/or a prostanoid DP1 receptor agonist may have therapeutic effects for cases of consecutive skin inflammation.

Topics: 6-Ketoprostaglandin F1 alpha; Alprostadil; Animals; Anti-Inflammatory Agents, Non-Steroidal; Arachidonic Acid; Behavior, Animal; Dermatitis, Atopic; Dinoprost; Dinoprostone; Dose-Response Relationship, Drug; Epoprostenol; Histamine; Indomethacin; Male; Mice; Mice, Inbred ICR; Mice, Inbred Strains; Prostaglandin D2; Prostaglandins; Pruritus; Receptors, Prostaglandin; Skin; Time Factors

Column chromatography followed by RIA was used to measure the blood plasma content of arachidonic acid metabolites (leukotrienes C4, B4, C4/D4/E4, prostaglandins F2 alpha, E2, 6-keto-prostaglandin F1 alpha, thromboxane B2) in 146 children aged 6 months to 14 years with atopic dermatitis. The data obtained were compared to the healthy children's parameters. The majority of the patients manifested activation of the system of arachidonic acid metabolism. The intensity of changes in the content of eicosanoids was found to depend on the clinical pattern and spreading of skin lesions.

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Arachidonic Acids; Child; Child, Preschool; Dermatitis, Atopic; Dinoprost; Dinoprostone; Humans; Infant; Leukotriene B4; SRS-A; Thromboxane B2

Topics: Adolescent; Adult; Autoantibodies; Chronic Disease; Dermatitis, Atopic; Dinoprost; Female; Histamine; Humans; Immunoglobulin G; Immunoglobulin M; Male