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Thirty-two adult Sprague-Dawley rats were used in the study. The rats were divided into the 4 following groups: the control group (C group); the AR group; an antihistamine-treated group (AH group); and an AR plus antihistamine-treated group (AR+AH group). The AR and AR+AH groups were sensitized using ovalbumin. The AR+AH and AH groups received desloratadine. The histopathological effects of AR and desloratadine treatment on the submandibular glands (SMGs) and the values of the oxidative and antioxidative serum parameters were evaluated.
In the desloratadine plus montelukast arm, the mean (SEM) quality of life score before treatment was 3.1 (0.41). After placebo, this score was 2.16 (0.43), after desloratadine it was 1.79 (0.38), after montelukast it was 1.48 (0.37), and after montelukast plus desloratadine it was 1.59 (0.37). In the montelukast plus levocetirizine arm, the mean quality of life score before treatment was 2.58 (0.49). After placebo it was 1.78 (0.46), after levocetirizine it was 1.38 (0.42), after montelukast it was 1.36 (0.37), and after montelukast plus levocetirizine it was 1.26 (0.39).
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To study the potentiation of chloroquine activity and mechanism by ketotifen and cyproheptadine in in vitro cultured Plasmodium falciparum Fcc SM1/yN strain.
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With Ze 339, the patient's time to recovery (5.4 ± 1.6 hours) from nasal obstruction after allergen challenge (time for return to 90% of baseline value ± SEM) was significantly shorter than with placebo (9.1 ± 2.3 hours, P = .035) and desloratadine (10.7 ± 2.5 hours, P = .022). Likewise, Ze 339's standardized symptom assessment for nasal obstruction (3.2 ± 1.3 hours) showed significantly faster relief (time for return to baseline value ± SEM compared with placebo, 8.3 ± 2.4 hours; P = .027) and desloratadine (4.5 ± 1.2 hours, P = .030). One interesting finding was that Ze 339 significantly reduced IL-8 and leukotriene B(4) levels in nasal secretions before challenge.
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Patients who had been diagnosed as having allergic rhinitis and had at least 1 prescription claim were identified from a database containing patient-level medical and pharmacy-related claims. The treatment patterns of patients with allergic rhinitis who met the study criteria were documented for a 12-month period in which the use of nonsedating antihistamines was described and the associated costs of various medications were assessed. Subanalyses of patients categorized by comorbidity status were also performed.
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The results of this study indicate that concomitant intake of food with a single 20-mg oral dose of rupatadine exhibits a significant increase in rupatadine bioavailability. Despite the absence of bioequivalence, the drug was well tolerated under fed and fasting conditions, and no major changes in severity and/or prevalence of AEs were reported.
We review the results of more than 120 studies of the treatment of tardive dyskinesia with noncatecholaminergic agents. The disorder is thought to arise from dopamine receptor supersensitivity brought on by long term neuroleptic-induced receptor blockade. Ironically, neuroleptics are the most consistently effective treatment of tardive dyskinesia. Nevertheless, it would be desirable to treat it with other compounds. The most intensively studied drugs are the cholinergics, including physostigmine, deanol, choline, and lecithin, but their efficacy has been equivocal. Anticholinergics, opiates, and tryptophan appear to worsen the syndrome or have no effect. Trials of gamma-aminobutyric acid agonists, lithium, and amantadine also produced mixed results. Effectiveness has been claimed for benzodiazepines, estrogens, and pyridoxine,, but the evidence is scant. A small number of preliminary reports on other treatments are also summarized. We discuss briefly the implications of these studies, but methodological problems limit interpretation.
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Six-seven adult patients completed mizolastine 10 mg (34/67) and loratadine 10 mg (33/67) once daily for 14 days. Other 5 patients withdrew or dropped out from the trial.
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To assess the effect of desloratadine on quality of life (QOL) in patients with seasonal allergic rhinitis.
Pretreatment with an oral dose (45 mg/kg) of cyproheptadine (CPH), a drug that inhibits secretion and synthesis of insulin. 3 hr before alloxan (100 mg/kg, iv) protects mice from the permanent diabetes produced by alloxan. Pretreated animals at the time of alloxan administration were hyperglycemic. Therefore, the possibility that CPH-induced hyperglycemia protected mice from alloxan was investigated. This was accomplished by giving mannoheptulose (a glucose antagonist) or insulin (to lower blood glucose) after CPH and before alloxan. These interventions eliminated CPH-induced protection from alloxan, indicating a role for CPH-induced hyperglycemia in the protective effect. To confirm that CPH does not protect mice from alloxan-induced diabetes by a direct action, in vitro experiments using isolated pancreatic islets were conducted. Mouse islets were pretreated with CPH, its metabolite desmethylcyproheptadine (DMCPH), or an equal mixture of the two and/or various concentrations of glucose prior to an acute exposure to a toxic concentration of alloxan. Glucose-stimulated insulin release was used as a measure of pancreatic beta-cell function after alloxan exposure. CPH or DMCPH (alone or in combination) pretreatment did not provide protection against alloxan-induced inhibition of insulin release nor did pretreatments potentiate the protective action of glucose against in vitro alloxan toxicity. The results indicate that the protective action of CPH when given to mice before alloxan is due to drug-induced hyperglycemia and not to a direct effect of CPH or its metabolite.
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Before stimulation mast cell populations were treated with increasing concentrations of rupatadine, loratadine and SR-27417A. Histamine and TNF-alpha release were measured following 15-30 min and 3 h activation, respectively.
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We found 40 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
Poisoning with opioid analgesics including tramadol represents a challenge. Tramadol may induce respiratory depression, seizures and serotonin syndrome, possibly worsened when in combination to benzodiazepines. Our objectives were to investigate tramadol-related neurotoxicity, consequences of diazepam/tramadol combination, and mechanisms of drug-drug interactions in rats. Median lethal-doses were determined using Dixon-Bruce's up-and-down method. Sedation, seizures, electroencephalography and plethysmography parameters were studied. Concentrations of tramadol and its metabolites were measured using liquid-chromatography-high-resolution-mass-spectrometry. Plasma, platelet and brain monoamines were measured using liquid-chromatography coupled to fluorimetry. Median lethal-doses of tramadol and diazepam/tramadol combination did not significantly differ, although time-to-death was longer with combination (P=0.04). Tramadol induced dose-dependent sedation (P<0.05), early-onset seizures (P<0.001) and increase in inspiratory (P<0.01) and expiratory times (P<0.05). The diazepam/tramadol combination abolished seizures but significantly enhanced sedation (P<0.01) and respiratory depression (P<0.05) by reducing tidal volume (P<0.05) in addition to tramadol-related increase in respiratory times, suggesting a pharmacodynamic mechanism of interaction. Plasma M1 and M5 metabolites were mildly increased, contributing additionally to tramadol-related respiratory depression. Tramadol-induced early-onset increase in brain concentrations of serotonin and norepinephrine was not significantly altered by the diazepam/tramadol combination. Interestingly neither pretreatment with cyproheptadine (a serotonin-receptor antagonist) nor a benserazide/5-hydroxytryptophane combination (enhancing brain serotonin) reduced tramadol-induced seizures. Our study shows that diazepam/tramadol combination does not worsen tramadol-induced fatality risk but alters its toxicity pattern with enhanced respiratory depression but abolished seizures. Drug-drug interaction is mainly pharmacodynamic but increased plasma M1 and M5 metabolites may also contribute to enhancing respiratory depression. Tramadol-induced seizures are independent of brain serotonin.
The effects of serotonin and its related compounds on immunoreactive thyrotropin-releasing hormone (ir-TRH) concentrations of the rat stomach wall and gastric juice were studied. Either serotonin, cyproheptadine or GR38032F was injected intraperitoneally, and the rats were decapitated at various times after the injection. ir-TRH concentrations of the stomach wall and gastric juice were measured by radioimmunoassay, and gastric serotonin concentrations were measured by HPLC. ir-TRH concentrations of the stomach wall decreased, and ir-TRH concentrations of gastric juice increased significantly after serotonin injection. On the other hand, both cyproheptadine and GR38032F did not affect ir-TRH concentrations of the stomach. The effects of serotonin on ir-TRH concentrations of the stomach were significantly blocked by the pretreatment of cyproheptadine and GR38032F. The reciprocal changes of gastric ir-TRH and serotonin concentrations were observed without changes in gastric juice pH. These findings suggest that serotonin stimulates ir-TRH release from the stomach wall into gastric juice, and the effects of serotonin on ir-TRH release may be partly mediated via 5-HT2- and 5-HT3-receptors.
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This randomized, double-blind, placebo-controlled, parallel-group, multicentre, study was designed to assess primarily mean pruritus score (MPS) reduction with rupatadine, 10 and 20 mg, administered once daily for 4 weeks. Three hundred and thirty-three patients with active episodes of moderate-to-severe CIU were included.
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The records of 53 patients who underwent treatment after a diagnosis of abdominal migraine were retrospectively reviewed. Responses to treatment were graded as excellent (cessation of recurrent abdominal pain), fair (persistence of symptoms but milder and less frequent), or poor (no response). Follow-up data were available in 38 patients. Twenty-four patients were treated with propranolol and 12 with cyproheptadine. Four were not treated because of mild and infrequent symptoms.
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Cetirizine and loratadine-two new antihistaminic drugs were evaluated in 56 patients with seasonal rhinitis in cross-over open study. I our study, no difference between loratadine and cetirizine has been seen. Both evaluated drugs significantly inhibited the symptoms of allergic rhinitis and conjunctivitis. Adverse reaction and inhibition of histamine and codeine skin tests were similar.
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Some antihistamines, such as mizolastine and ebastine, can prolong the QT interval and provoke severe cardiac arrhythmias. This review examines the effects of two widely used antihistamines, cetirizine and loratadine, on the QT interval. As of mid 2009 very few clinical data had been published on the risk of QT prolongation with cetirizine or loratadine. The very rare reported cases of torsades de pointes linked to loratadine mainly appear to involve drug interactions, especially with amiodarone and enzyme inhibitors. We found no reports of QT prolongation attributed to desloratadine, the main metabolite of loratadine. Two cases of QT prolongation with cetirizine have been published, one of which involved overdose and renal failure. The reports are too vague to conclude that cetirizine was implicated. We found no reports of QT prolongation attributed to levocetirizine. Cetirizine is a metabolite of hydroxyzine, another antihistamine. In the 1960s, a study of patients with psychosis showed a risk of QT prolongation. A case of recurrent syncope with QT prolongation has since been reported, along with rare cases of cardiac arrhythmia. In practice, cetirizine and loratadine are first-line antihistamines. However, caution is needed in certain circumstances. In particular, it is best that patients who have risk factors for torsades de pointes or who are taking certain enzyme inhibitors avoid using loratadine. It is best to avoid using cetirizine in cases of renal failure.
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Cell-free preparations from superior and inferior colliculi of very young rats (1-3 days old) contained adenylate cyclase systems which were highly responsive to serotonin. The response to serotonin declined markedly during early development and was very low at maturity. Adenylate cyclase activity in the 10,000 times g particulate fraction from colliculi of newborn rats was significantly stimulated by 0.05 muM serotonin. Half-maximal activation was produced with less than 1 muM serotonin. Maximal stimulation of collicular adenylate cyclase was about 80% above basal enzyme activity and occurred with approximately 50 muM serotonin. Tryptamine and several derivatives of serotonin produced responses which were comparable to that obtained with serotonin; 5-methoxytryptamine was uniformly the most active compound tested. Norepinephrine or dopamine produced much smaller increases in adenylate cyclase activity. Stimulation of collicular adenylate cyclase by serotonin was significantly but incompletely blocked by serotonin antagonists, including d-lysergic acid diethylamide (d-LSD), 2-bromo-d-lysergic acid diethylamide, methysergide, 1-methyl-8 beta-carbobenzyloxy-aminomethyl-10 alpha-ergoline and cyproheptadine. Chlorpromazine also produced partial blockade. In contrast, l-lysergic acid diethylamide, haloperidol, propranolol, phenoxybenzamine and morphine were ineffective as serotonin blocking agents. Of the compounds which produced a partial blockage of serotonin action, d-LSD, cyproheptadine and chlorpromazine were themselves capable of stimulating adenylate cyclase activity. These results are consisent with the existence of multiple receptors in rat brain which are capable of interacting with indoleamines.
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One-day RIT with IFA WBE for IFA hypersensitivity is efficacious. Although there was a trend with premedications to reduce SRRs during the RIT, safety data with premedication require confirmation in a larger trial.
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We examined the effect of trazodone (TR), a non-tricyclic antidepressant drug with an unknown mechanism of action, as well as its supposed metabolites beta-(3-oxo-s-triazolo-[4, 3 a]-pyridin-2-yl-propionic acid (OTPA) and 1-(m-chlorophenyl)-piperazine (CPP) on the serotonin (5-HT) -system in a model of the hind limb flexor reflex of the spinal rat. When given alone at low doses (1 mg/kg) TR does not change the flexor reflex but counteracts its serotonergic stimulation induced by LSD, quipazine or fenfluramine. At higher doses (6--8 mg/kg), after a period of latency, it enhances the reflex; this effect is antagonized by the 5-HT receptor blockers (cyproheptadine, WA-335 and metergoline) but not by imipramine. From the two TR metabolites studied only CPP exerts an effect in the flexor reflex model. It considerably enhances (0.05--1 mg/kg) the reflex, this effect being antagonized by cyproheptadine, WA-335 and metergoline, but not by imipramine. Our findings indicate that TR has a double effect on the central 5-HT system: at low doses it acts as a 5-HT antagonist, whereas at higher ones--as a 5-HT agonist. The latter effect may be connected with formation of a metabolite, CPP, or a compound chemically related to CPP.
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Two experiments were conducted to determine whether serotoninergic pathways, which are implicated in the neuroendocrine regulation of luteininzing hormone (LH) secretion in domestic animals, have a similar action in red deer hinds. In the non-breeding season (August), ovariectomized (n = 5) and ovariectomized-thyroidectomized (n = 5) hinds received a vehicle solution followed 4 h later by either serotonin (66 microg kg(-1) i.v.) every 10 min for a further 4 h or the serotonin antagonist, cyproheptadine (3 mg kg(-1) i.v.) as a single injection. This procedure was repeated in the breeding season (June). In the non-breeding season serotonin was without effect, but cyproheptadine reduced LH pulse frequency and amplitude in ovariectomized-thyroidectomized hinds (P<0.01). During the breeding season, serotonin reduced LH pulse amplitude in ovariectomized hinds (P<0.05) and cyproheptadine reduced LH pulse frequency in both ovariectomized and ovariectomized-thyroidectomized hinds (P<0.05 and P<0.01, respectively). On each occasion, cyproheptadine increased (P<0.01) plasma prolactin concentration, whereas serotonin had no effect. These results indicate a stimulatory role for serotoninergic neurons on the hypothalamic GnRH pulse generator mechanism of red deer hinds during the breeding season. In a second experiment, the LH response to GnRH (5 microg i.v.) was examined in ovariectomized hinds (n = 5) following administration of a serotonin infusion (6.6 microg kg(-1) min(-1) i.v. for 15 min), cyproheptadine (3 mg kg(-1) i.v. as a single dose) or vehicle, in the breeding season (July) after induction of halothane anaesthesia and in the non-breeding season (December) without anaesthesia. Halothane anaesthesia eliminated endogenous pulses of LH. In comparison with the vehicle-treated controls, the response of plasma LH to exogenous GnRH was not altered by serotonin or cyproheptadine in either season, which shows that serotonin has no effect on LH release at the pituitary gland level in these animals. It was concluded that in the regulation of LH release in red deer hinds, serotoninergic pathways have a stimulatory role operating at the hypothalamic level.
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On day 14, the desloratadine group had a significantly greater percentage decrease in total nasal symptom score vs the placebo group (-40% vs. -30%; P < .04). Similarly, on day 14, there was a 47% and 37% respective decrease in total symptom score (P = .01). Mean peak nasal inspiratory flow scores showed numeric, albeit not statistically significant, improvements from baseline through day 14 with desloratadine. A significantly greater improvement in Rhinoconjunctivitis Quality of Life Questionnaire scores occurred with desloratadine vs placebo on day 14 (-1.4 vs. -0.9; P = .004). The mean global response to therapy was better with desloratadine vs placebo (3.4 vs. 3.9; P = .004). The adverse event rate was similar in both groups.
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The biochemical mechanisms of serotonergic and adrenergic action on skeletal muscle cyclic nucleotide, glycogen, and amino acid metabolism have been investigated in intact rat epitrochlaris skeletal muscle preparations. Endogenous catecholamine levels in these preparations were 28.6 +/- 2.1 pg/mg of muscle. Release of these catecholamines by tyramine produced a 25% inhibition of alanine and glutamine release. Pretreatment of animals in vivo with 6-hydroxydopamine depleted catecholamine content by 85%. On incubation, preparations from these pretreated animals showed no effect of tyramine on amino acid metabolism. Serotonin (10(-5) M) and epinephrine (10(-5) M) inhibited alanine and glutamine release equally in preparations from 6-hydroxydopamine-pretreated as compared to control rats. Adrenergic antagonists such as dl-propranolol (10(-8)-10(-6) M), oxprenolol (10(-8)-10(-6) M), and practolol (10(-6)-10(-4) M) blocked equally the inhibition of alanine and glutamine release, prevented the stimulations of muscle cAMP levels, phosphosphorylase a formation, and the depletion of muscle glycogen produced by either epinephrine or serotonin. In contrast, serotonergic antagonists such as methysergide (10(-8)-10(-6) M) and cyproheptadine (10(-8)-10(-6) M) blocked the inhibition of alanine and glutamine release, the stimulations of muscle cAMP levels and phosphorylase a formation, and the decreased muscle glycogen content effected by serotonin but not by epinephrine. Incubation of muscles with both epinephrine and serotonin together produced additive stimulation of muscle cAMP levels, but not of the inhibition of alanine and glutamine release. These data indicate that the action of these agonists on skeletal muscle protein and amino acid, glycogen, and cyclic nucleotide metabolism proceeds directly via separate and discrete serotonergic and adrenergic receptor-adenylyl cyclase mechanisms in skeletal muscle.
We investigated the in vitro effect of loratadine, a new nonsedating H1 histamine antagonist, on the eosinophil functions of chemotaxis, superoxide anion (O2-) generation and eosinophil cationic protein (ECP) release, using purified eosinophils obtained from allergic patients. Loratadine significantly attenuated platelet-activating factor (PAF)-induced eosinophil chemotaxis and O2- generation at therapeutic concentrations (equivalent to serum concentrations after single oral administration of 20 mg or 40 mg). Loratadine, however, had no effect on PAF-induced ECP release. These findings suggest that loratadine has a direct inhibitory effect on eosinophil activation and may be beneficial in the therapy of allergic disorders with its anti-allergic properties.
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This note reports the interaction of three currently used tricyclic antidepressant drugs (clomipramine, imipramine and amitriptyline) with delta, mu and kappa opioid binding sites in the bovine adrenal medulla. Clomipramine was the only drug interacting with delta and mu sites. On the contrary, all three drugs showed a significant interactions with subtypes of the kappa binding site. Clomipramine was the most active on the kappa 2 and kappa 3 subtypes while amitriptyline showed the highest interaction with the kappa 1 subtype. On the contrary the tricyclic cyproheptadine did not present any interaction with opioid binding sites in our system. This interaction between tricyclic antidepressants and opioid binding sites might be the origin of their analgesic action.
Constitutively active 5-HT2 receptors have been suggested to contribute to motoneuronal excitability, muscle spasms and spasticity. Accordingly, 5-HT2C receptor inverse agonists have been demonstrated in pilot experiments to reduce spasticity in animal model of spasticity and patients with spinal cord injuries. Thus, 5-HT2C receptor inverse agonists may represent a novel class of anti-spasticity agents justifying a search for compounds with robust 5-HT2C receptor inverse agonist activity either among the existing medications or via a dedicated drug discovery program. Morphine-induced Straub tail response in mice is regarded as a model of transient spasticity that may be suitable for supporting such drug discovery efforts. Subcutaneous injection of morphine (10-60mg/kg) induced a dose-dependent Straub tail reaction in male Swiss mice with maximum response obtained 15-30min after the morphine administration. When given prior to morphine, 5-HT2B/2C receptor inverse agonists cyproheptadine (1-10mg/kg, i.p.) and SB206553 (0.3-3mg/kg, i.p.) diminished Straub tail reaction dose-dependently without affecting spontaneous locomotor activity. In contrast, 5-HT2B/2C receptor antagonist methysergide (1-5.6mg/kg, i.p.) and 5-HT2C receptor antagonist SB242084 (1-5.6mg/kg, i.p.) as well as 5-HT2A receptor inverse agonist pimavanserin (1-10mg/kg, i.p.) had no appreciable effects on Straub tail response. Taken together, the findings indicate that constitutive activity of 5-HT2B/2C receptor may be involved in the mechanisms of morphine-induced spasticity. Thus, morphine-induced Straub tail response may be evaluated further as a candidate higher throughput test to identify 5-HT2C receptor inverse agonists with anti-spasticity effects in vivo.
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Cypro, a serotonin and histamine antagonist, has been shown to be a moderately potent reversible inhibitor of tissue monoamine oxidase (MAO) obtained from hamsters and rabbits. In the present study, Cypro inhibits MAO obtained from human platelets with the same potency as harmine (Ki = 5 x 10(-5) M). However, when ten normal volunteers received conventional therapeutic doses of Cypro (16 mg/day) for two days, there was no alteration in their urinary excretion of tryptamine, 5-hydroxyindoleacetic acid, 3-methoxy-4-hydroxymandelic acid, epinephrine, or norepinephrine. We conclude that, when used in conventional clinical doses, Cypro does not inhibit MAO in man.
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A subanalysis of a longitudinal, observational, prospective, multicenter Spanish study was carried out in spring-summer 2007. Enrolled patients had a clinical diagnosis of AR of at least 2 years' evolution, a total nasal symptom score (TNSS) of at least 5, and had not received antihistamines in the previous week or ICSs in the previous 2 weeks. HRQoL (ESPRINT-15 questionnaire), disease severity (using both the original and modified Allergic Rhinitis and its Impact on Asthma [ARIA] classifications), and nasal symptoms (TNSS) were measured at baseline and after 4 weeks of rupatadine treatment.
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Preventia I was a randomized placebo-controlled study involving 22 countries worldwide. The children were 12-30 months of age at enrollment and had experienced at least five episodes of ENT infections, and no more than two episodes of wheezing during the previous 12 months. Phase I was a 12-month double-blind period during which the children were treated with loratadine 5 mg/day (2.5 mg/day for children=24 months of age) or placebo. Phase II was a double-blind follow-up period without study medication.
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Vasopressor response and release of eicosanoids following intravenous injection of arachidonic acid (AA) were examined in normotensive rats. AA administration caused a rapid initial fall of arterial pressure followed by a brief rise and a subsequent prolonged fall in anesthetized rats. Immediately after AA injection the blood levels of TXB2 and 6-keto-PGF1 alpha, the stable metabolites of TXA2 and prostacyclin, rose, from 1.52 +/- 0.23 ng/ml to 176.4 +/- 42.6 ng/ml and from 4.05 +/- 0.67 ng/ml to 171.4 +/- 31.2 ng/ml, respectively. Blood pressure behaviour and eicosanoid blood level were influenced by different inhibitors and antagonists of vasoactive mediators. The cyclooxygenase inhibitor acetylsalicylic acid completely eliminated the second blood pressure depression after AA injection and simultaneously diminished TXB2 and 6-keto-PGF1 alpha formation in murine blood, whereas the TXA2 receptor antagonist BM 13.177 prevented the return of the blood pressure to preinjection level after the initial brief fall in arterial pressure. Although the TXA2 synthase inhibitor HOE 944 markedly inhibited TXB2 formation, no influence on AA-induced blood pressure changes could be registered. The receptor antagonist of platelet activating factor BN 52021 and the serotonin and histamine receptor antagonist cyproheptadine also reduced TXB2 amounts, in murine blood without any effects on blood pressure behaviour.
A total of 360 patients were randomized to rupatadine (n = 180) or placebo (n = 180) treatment. Rupatadine showed statistically significant differences vs. placebo for the T4SS reduction both at 4 (-2.5 ± 1.9 vs. -3.1 ± 2.1; p = 0.018) and 6 wk (-2.7 ± 1.9 vs. -3.3 ± 2.1; p = 0.048). Rupatadine also showed a statistically better improvement in the children's quality of life compared with placebo. Adverse reactions were rare and non-serious in both treatment groups. No QTc or laboratory test abnormalities were reported.
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Inadequate stocking of essential antidotes in hospitals for the treatment of poisoned patients has been reported worldwide. Joint National Poisons Information Service (NPIS)/College of Emergency Medicine (CEM) guidelines for antidote stocking in UK emergency departments and acute hospitals were published in 2008.
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The clinical efficacy of the H1 receptor blocker loratadine was to be measured upon a wheal response subsequent to an intracutaneous injection of 0.1 ml histamine (0.1%).
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Patients' diagnoses included migraine with aura (n=49), migraine without aura (n=65), clinical migraine without aura not fulfilling International Classification of Headache Disorders-3 beta criteria (suspected migraine without aura; n=38), and hemiplegic migraine (n=2). Abortive medicine was effective in 74 of 97 patients, and preventive medicine was effective in 61 of 84 patients. Drugs with high efficacy were acetaminophen and ibuprofen for abortive therapy and cyproheptadine, amitriptyline, and propranolol for preventive therapy. Psychosocial problems were less common, and abnormalities on electroencephalography were more common in the suspected migraine without aura group. Otherwise, clinical features and drug responsibility were comparable among the migraine with aura, migraine without aura, and suspected migraine without aura groups. Retrospectively, experts clinically diagnosed childhood migraine without aura when the headache met at least one of the three criteria B, C, and D in International Classification of Headache Disorders-3 beta in addition to A and E. Abortive and preventive medication including paroxetine (n=2) benefited 10 and 15 of the 33 patients with daily headache, respectively. Psychotherapy/counseling (n=4), treatment for orthostatic dysregulation (n=4), and elimination of stressors (n=3) markedly alleviated headache in this group.