"Mizolastine"

Adverse effects of mizolastine, dextromethorphan, desloratadine and loratadine Prescrire IN ENGLISH - Spotlight ''In the September issue of Prescrire International: adverse effects of mizolastine, dextromethorphan, desloratadine and loratadine'', 1 September 2016 {1}##LOC[OK]## {1} ##LOC[OK]## ##LOC[Cancel]## {1}##LOC[OK]####LOC[Cancel]## Register online| Log in| My Prescrire Issue contents events * A global network Offers * Subscribe now * Solidarity Subscription Rate * Subscribers: register online * Prescrire's other products * Free Special Edition * Sign up to receive the newsletter english.prescrire.org > Spotlight > 100 most recent > In the September issue of Prescrire International: adverse effects of mizolastine, dextromethorphan, desloratadine and loratadine

Effects of combination of mizolastine and proteoglycan on chronic urticaria: a randomized controlled trial. The present study aimed to observe the therapeutic effect of combined mizolastine and proteoglycan in chronic urticaria. The patients were randomly divided into the treatment group (n = 56) and the control group (n = 44). The treatment group was medicated with calcium gluconate (10 mg/ time , 1 time/day), vitamin D3 (intramuscular 10 mg/time, 1 time/week), mizolastine (10 mg/time, 1 time/day), and proteoglycan (1.2 g/time, 3 times/day), while the control group was administered with the same drugs except proteoglycan for 4 weeks. After treatment with combined mizolastine and proteoglycan, therapeutic effect with symptoms decline index (SDI) more than 60% was significant different (44 vs

C reactive protein (CRP) rs3093059C predicts poor mizolastine response in chronic spontaneous urticaria patients with elevated serum CRP level. Chronic spontaneous urticaria (CSU) is a frequent disorder with recurrent itchy wheals and/or angioedema, and nearly 35% patients respond poorly to non-sedating H1 antihistamine treatment. CRP gene encodes the C-reactive protein, which is involved of patients were determined by Sequenom MassARRAY. Functional studies including relative luciferase assay and β-hexosaminidase assay were conducted in HEK293T cells or RBL-2H3 cells to explore the function of variants. Forty (62.50%) CSU patients were effective when treated with mizolastine, and 55 (72.4%) patients were effective in the desloratadine group. We found that the patients carried

, mizolastine, or amisulpride is contraindicated.Most manufacturers advise avoiding the use of two or more drugs that are associated with QT prolongation.Increasing age, female sex, cardiac disease, and some metabolic disturbances (notably hypokalaemia) predispose to QT prolongation.Drugs that cause hypokalaemia (such as diuretics) — concurrent use with erythromycin can predispose to QT prolongation.Monitor

line * Cetirizine and loratadine are considered first choice oral antihistamines in pregnancy. * Levocetirizine is an isomer of cetirizine and desloratadine is the active metabolite of loratadine. Both may also be considered.Second line * Chlorphenamine is recommended if a first generation sedating antihistamine is needed.Other options * Safety data on the use of acrivastine, bilastine or mizolastine

Antihistamines Antihistamine, hydroxyzine, chlorophenamine, acrivastine, blastine, cetirizine, fexofenadine, levocetirizine, loratidine, mizolastine, desloratidine, alimemazine, clemastine, cinnarizine REFERENCES 1. Kritas SK, Ronconi G, Caraffa A, Gallenga CE, Ross R, Conti P. Mast cells contribute to coronavirus-induced inflammation

that patients who received QZLX showed considerable improvements in their Scoring Atopic Dermatitis (SCORAD) and Dermatology Life Quality Index (DLQI) scores compared with those who received mizolastine at week 4. Network pharmacological analysis identified GRα as a key target for QZLX in AD treatment. QZLX administration increased the serum GRα expression in AD patients, alleviated AD symptoms in mice

of rights (https://www.nice.org.uk/terms-and-conditions#notice-of-rights).Page 15 of19Acrivastine 8 mg 3 times a day £20.62 Bilastine 20 mg daily £15.09 Cetirizine 10 mg daily £1.06c Desloratadine 5 mg daily £1.35 Fexofenadine 180 mg daily £3.70 Levocetirizine 5 mg daily £3.94 Loratadine 10 mg daily £1.00 Mizolastine 10 mg daily £6.92 Rupatadine 10 mg daily £5.00 a Doses taken from the summaries

significant difference for complete suppression of urticaria (RR 0.91, 95% CI 0.78 to 1.06) or for 'good or excellent response' (RR 1.04, 95% CI 0.64 to 1.71). For loratadine(10 mg) versus mizolastine (10 mg) (intermediate-term), no statistically significant difference was seen for complete suppression of urticaria (RR 0.86, 95% CI 0.64 to 1.16) or for 'good or excellent response' (RR 0.88, 95% CI 0.55 not significantly different in the following comparisons: cetirizine versus placebo at 10 mg and 20 mg (RR 3.00, 95% CI 0.68 to 13.22); desloratadine 5 mg versus placebo (RR 1.46, 95% CI 0.42 to 5.10); loratadine 10 mg versus mizolastine 10 mg (RR 0.38, 95% CI 0.04 to 3.60); loratadine 10mg versus emedastine 2mg (RR 1.09, 95%CI 0.07 to 17.14);cetirizine 10 mg versus hydroxyzine 25 mg (RR 0.78, 95% CI 0.25 to 2.45

to diminish over time.Paradoxical stimulation may also occur and this is a particular problem for some children. Use of a test dose prior to using the drug in a given situation is advisable to avoid this idiosyncratic reaction.Arrhythmias - second-generation antihistamines mizolastine and terfenadine are particularly prone to cause ventricular arrhythmias (predominantly ventricular tachycardia and torsades

. We considered in detail bilastine, cetirizine, levocetirizine, ebastine, fexofenadine, loratadine, desloratadine, mizolastine and rupatadine and concluded that all these drugs have an excellent safety profile with no evidence of cardiotoxicity even when updosed up to four times their standard licensed dose, provided that the prescribers carefully consider and rule out potential risk factors

of arachidonic acid (AA) levels in a rat model of collagen-induced arthritis. In the current study, the capacity of YNB to ameliorate inflammation was compared in carrageenan‑induced and AA‑induced acute inflammation of the rat paw with celecoxib and mizolastine, respectively (n=24 per group). The capacity of YNB to affect the phospholipase A2 (PLA2)/AA pathway (using reverse transcription‑quantitative polymerase chain reaction) and release of inflammatory lipid mediators (by ELISA) were investigated. Celecoxib ameliorated carrageenan‑induced paw edema, and mizolastine ameliorated AA‑induced rat paw edema. YNB alleviated paw edema and inhibited inflammatory cell infiltration in the two models. YNB inhibited production of 5‑LOX AA metabolite leukotriene B4 (LTB4), and suppressed expression of 5‑LOX

in our hospital from January 2013 to January 2015 were divided into study group and control group by random number table method. Patients in the study group with chloric thunder of citric acid treatment, the control group were treated with mizolastine in the treatment, the treatment time for 2 weeks. The difference of curative effect between the two groups and the changes of IL4, IL18, IL23, IL 33

) * antipsychotics (eg, phenothiazine derivatives, pimozide, haloperidol) * tricyclic antidepressants * some antimicrobial agents (eg, sparfloxacin, moxifloxacin, erythromycin IV, pentamidine, antimalaria treatment—particularly halofantrine) * some antihistamines (astemizole, mizolastine) * some antiretrovirals (eg, ritonavir, saquinavir, lopinavir)Use with drugs that increase escitalopram and citalopram

, cinnarizine, clemastine, cyclizine, cyproheptadine, desloratidine, diphenhydramine, diphenylpyraline, doxylamine, fexofenadine, hydroxyzine, levocetirizine, loratidine, mizolastine, promethazine, terfenadine and triproledene. Fourteen studies were found: one each related to cetirizine, doxylamine, and promethazine, and 11 related to diphenhydramine—none were relevant (search date 14 April 2006).Search

Differential modulation of mediator release from human basophils and mast cells by mizolastine. Basophils and mast cells play a major role in the pathogenesis of allergic disorders by releasing several proinflammatory mediators. Some histamine H1 receptor antagonists exert anti-inflammatory activities by modulating mediator release from basophils and mast cells. To study the in vitro effects of mizolastine, an H1 receptor antagonist, on the release of eicosanoids, histamine and IL-4 from human basophils and lung mast cells. Mizolastine (10(-7)-10(-5) M) concentration-dependently inhibited the release of cysteinyl leukotriene C4 from anti-IgE-stimulated basophils (IC(50): 3.85+/-0.28 microM) and mast cells (IC(50): 3.92+/-0.41 microM). The same concentrations of mizolastine did not affect anti-IgE

Inhibition of mediator and cytokine release from dispersed nasal polyp cells by mizolastine. Mizolastine is a potent and selective H1-receptor antagonist with antiallergic properties; in in-vitro animal models, mizolastine was shown to inhibit 5-lipoxygenase activity and to decrease the release of leukotrienes (LT) and tumor necrosis factor-alpha (TNF-alpha). This study investigated the effects of three concentrations of mizolastine (0.1, 1.0, 10 microM) on the release of LT (LTB4 and LTC4/D4) and prostaglandin D2 (PGD2) after stimulation by anti-IgE, and on the spontaneous release of cytokines (TNF-alpha and granulocyte/macrophage-colony-stimulating factor [GM-CSF]), from dispersed cells obtained from surgically resected nasal polyps of patients with nasal polyposis. Cells from nasal polyps

The effect of mizolastine on expression of vascular endothelial cell growth factor, tumour necrosis factor-alpha and keratinocyte-derived chemokine in murine mast cells, compared with dexamethasone and loratadine. It has been shown that many antihistamines may have anti-inflammatory activity in addition to being H1 antagonists. Mizolastine (MIZ), a novel antihistamine, might also have anti