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The symptom and medication scores of BCG-PSN group were significantly lower than that of control group (P < 0.01) after BCG-PSN treatment. There was no significant difference in symptom score between the two groups at 6 months after BCG-PSN treatment (P > 0.05), while the medication score of BCG-PSN group was still much lower than that of control group (P < 0.01). No serious adverse events were reported in BCG-PSN group except for local pain on the injection place in one patient.
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The effects of variety of drugs on metabolic burst and phospholipase A2 in polymorphonuclear leukocytes (PMNs) were investigated. The stimulation of PMNs by n-formyl-methionyl-leucyl-phenylalanine (FMLP) causes arachidonic acid (AA) to be released in the cells concomitantly with the generation of superoxide anion. These variables were effectively diminished with some clinically employed drugs including chlorpromazine, trifluoperazine, azelastine, clemastine and mepacrine at the lower concentration of 20 microM. In contrast, indomethacin and procaine were ineffective even at the higher concentration of 100 microM. Subcellular fractionation of PMNs revealed that phospholipase A2 activity was located both in the plasma membrane-rich fraction as well as the granule-microsome-rich fraction, and the potency of inhibition of membrane-bound phospholipase A2 by the above mentioned drugs was: indomethacin (IC50 = 3 microM) less than chlorpromazine less than azelastine and clemastine (IC50 greater than 100 microM). The low potency of antipsychotropic drugs and antihistaminic drugs in inhibiting the fractionated phospholipase A2 contrast with the high efficiency with which they inhibit the superoxide generation and the AA release from stimulated PMNs. The AA releases from the PMNs stimulated by FMLP or calcium ionophore (A23187) were almost equally diminished by various drugs at the lower concentration. From these observations, it appeared likely that these drugs might inhibit the metabolic stimulations of PMNs at the sites of the Ca2+-dependent activation processes of the enzymes responsible for the AA release and the superoxide generation.
In an attempt to elucidate the effect of lipoxygenase inhibitors on hepatic injury, we investigated D-galactosamine (GalN)-treated C57BL/6 mice receiving an intravenous (i.v.) injection of lipopolysaccharide (LPS)-activated autologous spleen cells. As compared with control spleen cells, the number of monocytes in the spleen cells isolated from LPS-treated mice and their oxidative free radical production increased markedly. Oxygen radical production by the dish-adherent cells (macrophage-rich population) was enhanced a further 4-fold. Although hepatotoxicity was not demonstrated in mice treated with 20 mg GalN alone, marked hepatic injury was found in the GalN-treated mice with a supplementation of LPS-activated spleen cells. The dish-adherent cells aggravated this hepatic injury, in contrast to minor hepatotoxicity by the nonadherent cells. Oxygen radical production by LPS-activated spleen cells was markedly reduced by the lipoxygenase inhibitors (azelastine, ketotifen and AA861). Hepatotoxicity was scarcely detected in the GalN-treated mice with a supplementation of the LPS-activated spleen cells which had been previously treated with lipoxygenase inhibitors. From these results, LPS-activated spleen macrophages contributed to hepatic injury induced by GalN, and lipoxygenase inhibitors which reduced oxygen radical production by the activated cells, protected against macrophage-induced hepatic injury in mice.
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The greatest inhibition of mediator release was seen with 24 microM azelastine; this level of inhibition was matched with the use of 133 microM olopatadine. At this concentration, these drugs inhibited IL-6 release by 83% and 74%, tryptase release by 55% and 79%, and histamine release by 41% and 45%, respectively. Activated CHMCs were characterized by numerous filopodia that were inhibited by both drugs as shown by electron microscopy.
A once-daily dose of 256 microg of intranasal budesonide aqueous suspension is significantly more effective at relieving the symptoms of perennial allergic rhinitis compared with a twice daily dose of 280 microg of azelastine nasal spray.
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Effect of azelastine hydrochloride (azelastine) on release and production of platelet-activating factor (PAF) in neutrophils obtained from asthmatic and non-asthmatic patients was investigated. Neutrophils were preincubated with or without azelastine and stimulated with f-Met-Leu-Phe (fMLP, 10 microM) for 15 min. PAF-like activity was detected by aggregation of washed guinea pig platelets. PAF-like activity released from asthmatic neutrophils without preincubation of azelastine was 5.67[0.89] (mean[SD], ng/10(7) cells) in supernatants and 21.8[0.76] in cell pellets. After preincubation with 10(-8), 10(-6), and 10(-4) M of azelastine, PAF-like activity reduced to 5.96[0.97] (mean[SD], ng/10(7) cells), 3.49[0.63], and 1.89[0.09] (n = 15) in the supernatants, and 20.7[0.97], 13.9[0.29], and 8.91 [0.99] (n = 15) in the cell pellets, respectively. PAF-like activity in non-asthmatic neutrophils without preincubation of azelastine was 4.67[0.19] (mean[SD], ng/10(7) cells) in supernatants and 18.5[0.34] in cell pellets. After preincubation with 10(-8), 10(-6), and 10(-4) M of azelastine, PAF-like activity reduced to 4.39[0.51] (mean[SD], ng/10(7) cells), 2.77[0.22], and 1.75[0.07] (n = 15) in the supernatants, and 17.9[0.54], 10.8[0.25], and 5.97 [0.59] (n = 15) in the cell pellets, respectively. Our results showed that preincubation with azelastine caused a dose-dependent inhibition of intra and extracellular PAF-like activity from asthmatic and non-asthmatic neutrophils in the same manner.
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Azelastine hydrochloride nasal spray is available worldwide for the treatment of seasonal allergic rhinitis (SAR) and perennial allergic rhinitis. One spray per nostril twice daily is the most commonly recommended dose.
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Evaluation of the number of microflora revealed increased bacterial reproduction after treatment, but this difference was not statistically significant. The use of azelastine nasal spray decreased the reproduction of three potentially pathogenic bacteria; however, it did not affect the reproduction of other potentially pathogenic bacteria.
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Since azelastine ocular drops are now available, the aim of the present study was the evaluation of the anti-allergic activity in the model of allergen specific conjunctival challenge (ASCC).
The influence of orally administered azelastine and selected H1-receptor antagonists on aeroallergen-induced acute lung anaphylactic responses in actively sensitized guinea pigs (experimental asthma model) was studied. Azelastine (1 mg/kg, PO, two hours) exerted significant inhibition of the aeroallergen-induced decline in dynamic lung compliance and an elevation in pulmonary airway resistance. Terfenadine, pyrilamine, and diphenhydramine given as oral doses of 1 mg/kg two hours before aeroallergen challenge exerted weak or no inhibition of acute lung anaphylactic responses. In conclusion, the data obtained in this study showed that azelastine administered orally is capable of exerting antiasthmatic effects in both the central and peripheral airways of guinea pigs. This effect may be attributed to its ability to inhibit the formation or secretion of pharmacologic mediators (ie, histamine, LTC4/D4, .O2-) from inflammatory cells.
MC9 mast cells, sensitized with monoclonal IgE antibody specific for 2,4-dinitrophenyl (DNP) group, were exposed to DNP-BSA and the pH and cytosolic calcium signals were recorded by using the fluorescent probes BCECF and Fura-2 respectively. DNP-BSA induced cell alkalinization was fully inhibited by azelastine with IC50 (1.6 +/- 0.5 mumol/l, mean +/- SEM, n = 5) similar to that required to inhibit histamine release (1.4 mumol/l). Conversely, high azelastine concentrations (> 100 mumol/l) were required to inhibit DNP-BSA-dependent cell calcium mobilization (IC50 approximately 200 mumol/l, n = 3). Amiloride, but not the H1 histamine antagonist pyrilamine, was able to inhibit the DNP-BSA induced pH signal. In acidified mast cells, azelastine potently inhibited Na+:H+ exchange activity (IC50 = 7.7 +/- 3.6 x 10(-6) M, mean +/- SEM, n = 3). Conversely, in mouse spleen lymphocytes azelastine was unable to inhibit the amiloride-sensitive pH signal induced by concanavalin A. In conclusion, the inhibition of histamine release by azelastine is not due to an interference with the cytosolic calcium signal. Conversely, azelastine potently antagonized the allergen-dependent Na+:H+ exchange activation, suggesting an action on the protein kinase C signaling pathway.
Sixty-three patients (29 male, 29 female; 34 in the age range of 6 to 65 years) with allergic conjunctivitis were enrolled in this study. The patients were randomly assigned to receive topical azelastine 0.02% (n = 31) or topical MMC (0.2 mg/10 mL) (n = 31) four times daily for 3 months. Follow-up examinations were done at 2 weeks to examine side effects of the medications and again at 4 weeks to assess the outcome of treatment. The eyes were examined for relief of symptoms, cure of signs, and the appearance of side effects with use of these drugs.
Allergic rhinitis (AR) can be challenging to treat. For many patients, current therapies (including multiple therapies) provide insufficient symptom relief. There is, therefore, a clear unmet medical need for a new and more effective AR treatment option. MP29-02 ( Dymista ) is a novel intranasal formulation of azelastine hydrochloride and fluticasone propionate in an advanced delivery system.
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clinicaltrials.gov Identifier: NCT00660517.
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The efficacy of these medications at improving subjective sleep quality has been established through multiple randomized, double-blind, placebo-controlled clinical trials.
Symptoms of simple allergic conjunctivitis (itching, tearing and photophobia) were significantly reduced at the end of 1(st) week. Signs such as conjunctival chemosis, congestion, tarsal papillae, and eyelid edema were effectively treated in all cases at the end of 1(st) week. At the end of 4(th) week, all cases were fully cured and none of the patient had any recurrences up to 7(th) week. Mean score at 1(st) day (9.6 ± 3.27) was significantly (P < 0.0001) reduced by 7(th) day (1.35 ± 1.19) of treatment.
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Small biopsies of the anterior portion of the lower nasal turbinate were collected with the help of a Hartmann forceps under direct visual inspection. The samples were processed for light microscopy and morphometric analysis. Inflammatory infiltration (neutrophils and lymphocytes) of the nasal mucosa was evaluated by a semiquantitative method. Unpaired t test and Bernoulli distribution were applied to evaluate statistical differences between data from the different groups of samples.
The most recent addition to intranasal sprays for the maintenance therapy of AR is MP-AzeFlu, a single formulation nasal spray of azelastine hydrochloride and fluticasone propionate in an advanced delivery system. Analysis of clinical data showed this to be the first new intranasal medication that provides greater clinical benefit than an INCS in treating AR.
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Twenty-eight male Wistar albino rats were randomly divided into four groups: a control group; a group in which allergic rhinitis was induced and no treatment given; a group in which allergic rhinitis was induced followed by treatment with azelastine hydrochloride on days 21-28; and a group in which allergic rhinitis was induced followed by treatment with curcumin on days 21-28. Allergy symptoms and histopathological features of the nasal mucosa were examined.
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Patients aged at least 12 (United States) or 16 years (Europe) with allergic rhinitis or nonallergic vasomotor rhinitis.
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Allergic rhinitis and other rhinitis subtypes are increasingly becoming some of the most prevalent and expensive medical conditions that affect the U.S.
We identified 30 trials with a total of 4344 participants randomised, with 17 different drugs or treatment comparisons. The following antihistamines and mast cell stabilisers were evaluated in at least one RCT: nedocromil sodium or sodium cromoglycate, olopatadine, ketotifen, azelastine, emedastine, levocabastine (or levocabastine), mequitazine, bepotastine besilate, combination of antazoline and tetryzoline, combination of levocabastine and pemirolast potassium. The most common comparison was azelastine versus placebo (nine studies).We observed a large variability in reporting outcomes. The quality of the studies and reporting was variable, but overall the risk of bias was low. Trials evaluated only short-term effects, with a range of treatment of one to eight weeks. Meta-analysis was only possible in one comparison (olopatadine versus ketotifen). There was some evidence to support that topical antihistamines and mast cell stabilisers reduce symptoms and signs of seasonal allergic conjunctivitis when compared with placebo. There were no reported serious adverse events related to the use of topical antihistamine and mast cell stabilisers treatment.
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The objective of the present study was to compare the efficacy and tolerability of azelastine nasal spray administered at the recommended dosage of 2 sprays per nostril twice daily with those of cetirizine in the treatment of moderate to severe SAR.
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Recently, we showed that leukotrienes (LTs) regulate ovarian cell function in vitro. The aim of this study was to examine the role of LTs in corpus luteum (CL) function during both the estrous cycle and early pregnancy in vivo. mRNA expression of LT receptors (BLT for LTB(4) and CYSLT for LTC(4)), and 5-lipoxygenase (5-LO) in CL tissue and their localization in the ovary were studied during the estrous cycle and early pregnancy. Moreover, concentrations of LTs (LTB(4) and C(4)) in the CL tissue and blood were measured. 5-LO and BLT mRNA expression increased on days 16-18 of the cycle, whereas CYSLT mRNA expression increased on days 16-18 of the pregnancy. The level of LTB(4) was evaluated during pregnancy compared with the level of LTC(4), which increased during CL regression. LT antagonists influenced the duration of the estrous cycle: the LTC(4) antagonist (azelastine) prolonged the luteal phase, whereas the LTB(4) antagonist (dapsone) caused earlier luteolysis in vivo. Dapsone decreased progesterone (P(4)) secretion and azelastine increased P(4) secretion during the estrous cycle. In summary, LT action in the bovine reproductive tract is dependent on LT type: LTB(4) is luteotropic during the estrous cycle and supports early pregnancy, whereas LTC(4) is luteolytic, regarded as undesirable in early pregnancy. LTs are produced/secreted in the CL tissue, influence prostaglandin function, and serve as important factors during the estrous cycle and early pregnancy in cattle.
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Azelastine nasal spray may be useful in decreasing adenoid pad size and the severity of symptoms related to adenoidal hypertrophy. Hippokratia 2014; 18 (4): 340-345.