dinoprost and Emergencies

dinoprost has been researched along with Emergencies* in 2 studies

Trials

1 trial(s) available for dinoprost and Emergencies

ArticleYear
Serum tryptase level is a better predictor of systemic side effects than prostaglandin D2 metabolites during venom immunotherapy in children.
    Journal of investigational allergology & clinical immunology, 2011, Volume: 21, Issue:4

    We performed a prospective study to analyze mast cell mediators as predictors of systemic adverse reactions during rush venom-specific immunotherapy (VIT) in children.. Nineteen children aged 5-17 years received VIT with Venomenhal (HALAllergy). We analyzed serum tryptase (CAP, Phadia), plasma prostaglandin (PG) D2 metabolites (9alpha, 11beta-PGF2), and urine PGD2 metabolites (9alpha, 11beta-PGF2, tetranor-PGD-M) using gas chromatography mass spectrometry before and after the rush protocol.. Three boys with high baseline serum tryptase values (>7.76 g/L) (P < .001) and low 9alpha, 11beta-PGF2 concentrations developed grade III systemic adverse reactions during VIT. Baseline serum tryptase was lowest in children who had a Mueller grade II reaction (1.93 [0.36]) before VIT and highest in children with a Mueller grade III reaction (6.31 [4.80]) (P = .029). Repeated measures analysis of variance confirmed that, in children who developed systemic adverse reactions during VIT, serum tryptase was higher both before and after desensitization and increased significantly following the procedure. Analysis of PGD2 metabolites in the prediction of systemic adverse reactions during VIT was inadequate (sensitivity 67% and specificity 0.53%), whilst prediction based on serum tryptase was accurate.. In children with severe systemic adverse reactions to Hymenoptera sting, the evaluation of baseline tryptase levels should be a standard procedure. Children with Apis mellifera venom allergy and baseline tryptase levels higher than 7.75 g/L are at risk of anaphylaxis during buildup. Lower baseline values of plasma and urinary PGD2 metabolite concentration in patients with systemic adverse reaction during VIT suggest that prostaglandin catabolism is altered.

    Topics: Adolescent; Bee Venoms; Biomarkers; Child; Child, Preschool; Desensitization, Immunologic; Dinoprost; Emergencies; Female; Humans; Hypersensitivity, Immediate; Male; Mast Cells; Peak Expiratory Flow Rate; Prospective Studies; Prostaglandin D2; Tryptases; Wasp Venoms

2011

Other Studies

1 other study(ies) available for dinoprost and Emergencies

ArticleYear
Dysfunctional uterine bleeding.
    Canadian journal of surgery. Journal canadien de chirurgie, 1986, Volume: 29, Issue:5

    Dysfunctional uterine bleeding is defined as abnormal uterine bleeding in the absence of organic disease. It is the result of anovulation or the abnormal local production of prostaglandins, and in each case the primary fault is inappropriate hormone formation. There are two approaches to diagnosis. The traditional one is primarily concerned with the exclusion of cancer of the endometrium; this concern results in the frequent resort to uterine curettage. The second approach is to limit curettage to patients whose symptoms are not ameliorated by medical therapy. The aim of medical treatment is either to produce secretory change in the endometrium or to decrease the formation of uterine prostaglandins. Intermittent progesterone treatment is used to cause secretory changes in the endometrium. Decreased production of the prostaglandins is achieved indirectly by causing atrophy of the endometrium or directly through the use of prostaglandin synthetase inhibitors. Surgery in the form of dilatation and curettage has no long-term therapeutic effect; hysterectomy is definitive therapy.. Dysfunctional uterine bleeding is defined as abnormal uterine bleeding in the absence of organic disease. It is the result of anovulation or the abnormal local production of prostaglandins (PGs), and in each case, the primary fault is inappropriate hormone formation. There are 2 approaches to diagnosis. The traditional one is primarily concerned with the exclusion of cancer of the endometrium; this concern results in the frequent resort to uterine curettage. The 2nd approach is to limit curettage to patients whose symptoms are not ameliorated by medical therapy. The aim of the medical treatment is either to produce secretory change in the endometrium or to decrease the formation of uterine PGs. Intermittent progesterone treatment is used to cause secretory changes in the endometrium. Decreased production of the PGs is achieved indirectly by causing strophy of the endometrium or directly through the use of PG synthetase inhibitors. Surgery in the form of dilatation and curettage has no longterm therapeutic effect; hysterectomy is definitive therapy. (author's)

    Topics: Adult; Contraceptives, Oral; Cyclooxygenase Inhibitors; Dilatation and Curettage; Dinoprost; Dinoprostone; Emergencies; Estrogens, Conjugated (USP); Female; Humans; Hysterectomy; Medroxyprogesterone; Medroxyprogesterone Acetate; Mefenamic Acid; Menorrhagia; Norethindrone; Progesterone; Prostaglandins E; Prostaglandins F

1986