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Allegra (Fexofenadine)

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Generic Allegra is a strong-active remedy which is taken in treatment and termination of bothersome outdoor allergy and its symptoms such as sneeze, itching, stuffy, runny nose and red, itchy, watery eyes. Generic Allegra also makes great progress in treatment of chronic idiopathic urticaria. Generic Allegra is safety both for adults and children. Generic Allegra controls, wards off, terminates allergy.

Other names for this medication:

Similar Products:
Periactin, Phenergan, Flonase, Clarinex, Zyrtec, Claritin


Also known as:  Fexofenadine.


Generic Allegra is developed by medical scientists to combat troublesome symptoms of outdoor allergy. Target of Generic Allegra is to control, ward off, terminate outdoor allergy. Generic Allegra acts as an anti-allergy remedy. Generic Allegra operates by making the level of natural chemical histamine lower to ward off outdoor (seasonal) allergy symptoms. Generic Allegra is antihistamine.

Generic name of Generic Allegra is Fexofenadine.

Allegra is also known as Fexofenadine, Telfast, Fastofen, Fexo-120, Fexigra.

Brand names of Generic Allegra are Allegra, Allegra-D 12 Hour, Allegra Oral Suspension, Allegra-D 24 Hour.


Generic Allegra can be taken in tablets, liquid forms, and capsules. You should take it by mouth.

It is better to take Generic Allegra 2 times a day (in the morning and evening).

It is better to take Generic Allegra every day at the same time with meals.

Liquid form can be given to children of 2-12 years. Tablets and capsules can be given to children to 6 years.

If you want to achieve most effective results do not stop taking Generic Allegra suddenly.


If you overdose Generic Allegra and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 20 and 25 degrees C (68 and 77degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Allegra are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Allegra if you are allergic to Generic Allegra components.

Try to be careful with Generic Allegra if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Allegra can harm your baby.

Do not use Generic Allegra in case of taking MAO inhibitors as phenelzine (Nardil), isocarboxazid (Marplan), selegiline (Eldepryl), tranylcypromine (Parnate); antacid which contains magnesium or aluminum as Milk of Magnesia, Pepcid Complete, Rolaids, Mylanta, Maalox.

Try to be careful with Generic Allegra usage in case of having heart, kidney or liver disease, urination problems, angina, glaucoma, coronary artery disease, diabetes, high blood pressure.

Try to be careful with Generic Allegra usage in case of taking erythromycin as Erythrocin, E.E.S., E-Mycin, ketoconazole as Nizoral, digoxin as Lanoxin, Lanoxicaps, Digitek, methyldopa as Aldomet, asthma medicines, reserpine as Serpalan, Serpasil, Serpatabs, diet medicines.

Try to avoid liquids which contain caffeine.

Generic Allegra liquid form can be given to children of 2-12 years. Generic Allegra tablets and capsules can be given to children to 6 years.

In case you drink fruit juice, remember that Generic Allegra in combination with fruit juice becomes less effective.

It can be dangerous to stop Generic Allegra taking suddenly.

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After the dosing of an extended-release (ER) formulation, compounds may exist in solutions at various concentrations in the colon because the drugs are released at various speeds from the ER dosage form. The aim of this study was to investigate the relationship between the drug concentration profiles in plasma and the drug doses in the colon. Several drug solutions of different concentrations were directly administered into the ascending colon of dogs using a lubricated endoscope, and the effects of the drug dose on colonic absorption were estimated. As a result, dose-dependency of colonic absorption varied from compound to compound. Although the relative bioavailability of colonic administration of diclofenac, metformin and cevimeline compared to oral administration was similar regardless of the drug doses in the colon, colonic absorption of diltiazem varied according to the doses. From the results of the co-administration of verapamil and fexofenadine, it was clear that diltiazem underwent extensive hepatic and gastrointestinal first-pass metabolism, resulting in a low area under the curves (AUC) at a low drug dose. During the design of oral ER delivery systems, a colonic absorption study of candidate compounds should be carried out at several solutions of different drug concentrations and assessed carefully.

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Of the 2622659 visits in the database, 8216 (0.3%) were for TIA. Females comprised 57%. There was a statistically significant increase in the annual admission rates for TIA patients from 2000 to 2010, from 70% to 91%, respectively (difference, 22%; 95% confidence interval, 18%-26% [P < .001]). Separate analysis by sex showed similar increased admission rates for females and males.

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Allergic rhinitis (AR) is a common chronic condition in children and may impact a child's quality of life. Increasing treatment compliance may improve quality of life. An oral suspension of fexofenadine hydrochloride (HCl) has been developed to ease administration to children and may, therefore, improve treatment compliance. The purpose of this study was to assess the pharmacokinetic behavior, safety, and tolerability of a single dose of fexofenadine HCl oral suspension administered to children aged 2-5 years with allergic rhinitis. Children (aged 2-5 years) with AR were recruited in a multicenter, open-label, single-dose study. Fexofenadine HCl (30 mg) was administered as a 6-mg/mL suspension (5 mL). Plasma samples were collected up to 24 hours postdose. Adverse events (AEs); electrocardiograms (ECGs); vital signs; and clinical laboratory tests for hematology, blood chemistry, and urinalysis were analyzed to evaluate safety and tolerability. Fifty subjects completed the study. Mean maximum plasma concentration of fexofenadine was 224 ng/mL, and mean area under the plasma concentration curve was 898 ng . hour/mL. Treatment-emergent AEs were mild in intensity and reported in a total of seven subjects. No trends or clinically meaningful changes in mean ECG, vital sign, or clinical laboratory test data occurred during the study. In children aged 2-5 years, the exposure after a 30-mg dose of fexofenadine HCl suspension was similar to the exposures previously seen after a 30- and 60-mg dose of fexofenadine HCl in children aged 6-11 years and in adults, respectively. The suspension was also well tolerated.

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One hundred fifty-two patients were enrolled; 78 were randomized to the intervention group. Nearly 70% of patients (103) were available for telephone follow-up. The study groups were statistically similar with regard to baseline demographic characteristics and the prevalence of moderate or severe nicotine addiction. None of the patients (0%) in the intervention group contacted or attended the smoking cessation program during the study period (95% CI = 0-4%). The percentages of patients who stopped smoking after three months were similar in the two groups [10.4% (5/48) control vs 10.9% (6/55) intervention; p = 1].

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To construct reference limits for gestation of umbilical vein blood flow (UVBF) in normal singleton pregnancies between 14 and 40 weeks of gestation using quantile regression.

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Previous studies revealed fewer visits for congestive heart failure (CHF) to emergency departments (EDs) in New Jersey, USA and fewer admissions for CHF to a Southern Indian and an Israeli hospital during warmer months. Using hospital admission rate for CHF as a marker for illness severity, we hypothesized that CHF would also be less severe in warmer months.

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The authors found no difference in the smoking cessation rates between ED patients who received written material and those who were counseled by emergency physicians. Referral of patients who smoked to a cessation program was unsuccessful.

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83 papers were analyzed, including 72 RCTs or meta-analyses. Experts determined the level of EBM of each drug, according to the literature and personal experience, using 3 levels of recommendation, A, B and C (from large RCTs to non-randomized trials).

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The oral administration of fexofenadine 120 mg daily is a common treatment of seasonal allergic rhinitis (SAR). It reduces the H1 receptor-mediated symptoms, such as sneezing, pruritus, and nasal secretion as well as non-nasal symptoms such as conjunctivitis. The objective was to assess the effect of fexofenadine on nasal symptoms (such as nasal obstruction) in seasonal allergic rhinitis. A placebo-controlled, double-blind, randomized, cross-over study was performed which yielded evidence that two-week therapy with fexofenadine 120 mg daily in patients with SAR also relieves nasal obstruction and congestion. The parameters of nasal obstruction were evaluated by means of rhinoscopy, a subjective symptom score, and active anterior rhinomanometry. The subjective evaluation of nasal obstruction/congestion as recorded by the patient every 15 minutes for 4.5 hours after nasal allergen provocation showed a significant difference of the AUC (p = 0.025) between fexofenadine and placebo with a 12.8% lower obstruction after fexofenadine. The swelling of the nasal mucosa, which was assessed by rhinoscopy for 4.5 hours after nasal allergen provocation, was 21% lower after treatment with fexofenadine (p = 0.041). In this double-blind, placebo-controlled trial, subjective patient ratings as well as objective investigator assessments demonstrate the anti-obstructive effect of fexofenadine in nasal allergen challenge.

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To assess the effects of the association of positive end-expiratory pressure (PEEP) with different inflation volumes (V(T)'s) on passive lung deflation and alveolar recruitment in ARDS patients.

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A prospective study design.

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Forty-nine patients were enrolled in the study; 25 received diclofenac and 24 received control vehicle drops. Both groups were similar in gender, age, pretreatment pain duration, NPIS score, and analgesic use. There was significantly greater improvement in the 2-hour NPIS score in the diclofenac group (3.1; 95% confidence interval [CI] 2.3 to 4) compared with the control group (1.0; 95% CI 0.1 to 2.0). The difference between the 2 groups was 2.1+/-1.3 (95% CI 0.8 to 3.4). There was a trend toward fewer patients taking rescue oxycodone-acetaminophen in the diclofenac group (20%; 95% CI 4% to 36%) versus the control group (42%; 95% CI 22% to 62%). Other than transient mild stinging, there were no complications associated with diclofenac use.

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Mitral valve diseases (MVD)s, comprising congenital and acquired forms, are characterized by a diverse etiology, pathophysiology, prevalence, and incidence. In industrialized countries, the acquired forms represent 2.5% of all cardiovascular diseases, with a marked augmentation after the age of 65 years. In addition, all forms of MVDs (i.e., degenerative forms) have a difficult clinical management. The major challenge is 'the early diagnosis', and echocardiographic analysis has been shown inappropriate for diagnosing MVD in moderate forms. Thus, there is a strong need to identify more appropriate biomarker tools to diagnose MVDs at early clinical stage before complications occur and worsen the prognosis. Innovative biomarker tools may particularly be appropriate for the complex treatment of elderly patients, the clinical management of which is very difficult due to the high risk of surgical interventions and no clear benefits in terms of life expectancy or quality of life compared to younger patients. These biomarker tools may be identified as genetic factors and/or components of cellular and molecular pathways related to the mechanisms of MDV pathophysiology. In this review, emphasis is placed on the possibility of proposing matrix metalloproteinase (MMP) pathways, their genetic variants and microRNA as promising predictive, diagnostic and prognostic biomarkers and targets for personalized treatments. Evidence is also provided of the lack of any consistent evidence which actually hampers their clinical application. Thus, criticisms and concerns are underlined, as well as suggestions to close the existing gaps.

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Sixty house dust mite (HDM) allergic children (23 girls and 37 boys) with allergic rhinitis and/or asthma completed the study. Mean age was 8.3 ± 2.0 years. In the fexofenadine group, a significant suppression was observed in post-treatment values when compared to baseline values in SPT with D. farinae (p = 0.019). In the montelukast group, no significant suppression was observed in SPT with D. farinae at all time points when compared to baseline.

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E-4031 produced a dose-dependent prolongation of cardiac action potential and blocked the hERG/IKr current with an IC50 of 17nM. At 3nM, dofetilide significantly increased APD90. Astemizole significantly increased APD60 and APD90 at 30nM. Terfenadine significantly increased APD90 at concentrations greater than 10nM. Fexofenadine, a metabolite of terfenadine, did not produce any electrophysiologic changes in cardiac action potentials. Flecainide produced a dose-dependent prolongation of the cardiac action potential at 1 and 3μM. Acute exposure to nifedipine significantly decreased APD60 and APD90 and produced a dose-dependent block of calcium current with an IC50 of 0.039μM. Verapamil first shortened APD60 and APD90 in a dose-dependent manner, until a compensating increase in APD90, presumably via hERG blockade, was observed at 1 and 3μM. Following a chronic exposure (20-24h) to clinically relevant levels of pentamidine, a significant increase in action potential duration was accompanied by early afterdepolarizations (EADs).

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buy allegra d 2016-05-24

The nonsedating histamine H1 receptor antagonist fexofenadine is the active metabolite of terfenadine. It reduced the allergic response in animal models of allergy and did not prolong the allegra buy QT interval (QTc) in dogs or rabbits at plasma concentrations many times higher than those seen after administration of therapeutic dosages. Similarly, relative to placebo, fexofenadine did not affect mean QTc in patients given dosages of up to 480 mg/day for 2 weeks or in volunteers who received up to 800 mg/day for 6 days or 240 mg/day for 12 months. In a double-blind clinical trial, oral fexofenadine 120 or 180mg once daily controlled symptoms in patients with seasonal allergic rhinitis as effectively as cetirizine. Other double-blind clinical trials showed that fexofenadine 40 to 240mg twice daily was significantly more effective than placebo. Fexofenadine 180 or 240mg once daily was significantly more effective than placebo in patients with chronic idiopathic urticaria. The drug was well tolerated in these clinical trials, with an adverse event profile similar to that seen with placebo. The most common adverse events were headache, throat irritation, viral infection, nausea, dysmenorrhoea, drowsiness, dyspepsia and fatigue.

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We aimed to evaluate the influence of genetic polymorphisms involved in deferasirox metabolism and transport allegra buy on its pharmacokinetics and treatment toxicity, in a cohort of β-thalassaemic children.

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In this study of rifampicin 450 mg, the interactive magnitude of Feldene Melt Tablets the mean AUC values of fexofenadine enantiomers was higher than that observed in the previous study of rifampicin 600 mg, and no dose-dependent inhibitory effects of rifampicin were observed. These effects may be clinically significant in patients receiving fexofenadine and rifampicin.

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In patients with recurrence of stage III colon cancer, deficient MMR was significantly associated with better SAR, and this benefit was limited to primary Cytoxan High Dose tumors of the proximal colon. Mutations in BRAFV600E were significantly associated with worse SAR, and worse SAR for BRAFV600E or KRAS mutant tumors was more strongly associated with distal cancers. These biomarkers have implications for patient management at recurrence.

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A MEDLINE search (1966-2002) Anafranil Reviews was performed to obtain studies examining the use of antihistamines in the treatment of atopic dermatitis. Search terms included: atopic dermatitis; eczema; antihistamines; azatadine; brompheniramine; cetirizine; chlorpheniramine; clemastine; cyclizine; cyproheptadine; desloratadine; diphenhydramine; fexofenadine; hydroxyzine; loratadine; meclizine; promethazine; trimeprazine. Further references were gathered from these publications.

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First- and second-generation antihistamines may significantly impair driving performance. In the context of driving safety but also taking into account the cardiotoxic properties of some of the second-generation antihistamines, we advise treating patients with third-generation antihistamines Generic Deltasone Online such as fexofenadine and levocetirizine.

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We measured plasma concentrations of tri-iodothyronine (T3), reverse T3 (rT3), thyroxine (T4), free T3 (fT3) and free T4 (fT4) estimates Duricef Generic Name , TSH, and TGF-beta1 in 48 elderly NTI patients consecutively admitted in our Division of Internal Medicine and Metabolic Diseases, and in 11 healthy age- and sex-matched controls.

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To investigate the effects and the mechanisms of the first-generation histamine H(1)-antagonist diphenhydramine and the second-generation Anafranil 225 Mg histamine H(1)- antagonist fexofenadine on seizure development of pentylenetetrazole (PTZ)-induced kindling in rats.

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Human thymidylate synthase (TS) protein specifically binds to its own TS mRNA and functions as a translational repressor. In the presence of reducing agents, the RNA binding activity of TS protein is significantly enhanced. In contrast, treatment of TS protein with the oxidizing agent diamide inhibits RNA binding. Scatchard analysis reveals that in the presence of the reducing agent 2-mercaptoethanol, the TS protein/TS mRNA interaction changes from low (Kd = 66 nM) to high (Kd = 2.6 nM) apparent affinity. The catalytic activity of TS is increased by up to 6.5-fold in the presence of 2-mercaptoethanol. These studies demonstrate that the interaction between TS protein and its target TS mRNA is sensitive Allegra 360 Mg to the presence of reducing reagents and is dependent upon a reversible sulfhydryl switch mechanism.

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Berberine (BBR), an isoquinoline alkaloid mainly isolated from plants of Berberidaceae family, is extensively used to treat gastrointestinal infections in clinics. It has been reported that BBR can block human ether-a-go-go-related gene (hERG) potassium channel and inhibit its membrane expression. The hERG channel plays crucial role in cardiac repolarization and is the target of diverse proarrhythmic drugs. Dysfunction of hERG channel can cause long QT syndrome. However, the regulatory mechanisms of BBR effects on hERG at cell membrane level remain unknown. This study was designed to investigate in detail how BBR decreased hERG expression on cell surface and further explore its pharmacological rescue strategies. In this study, BBR decreases caveolin-1 expression in a concentration-dependent manner in human embryonic kidney 293 (HEK293) cells stably expressing hERG channel. Knocking down the basal expression of caveolin-1 alleviates BBR-induced hERG reduction. In addition, we found that aromatic tyrosine (Tyr652) and phenylalanine (Phe656) in S6 domain mediate the long-term effect of BBR on hERG by using mutation techniques. Considering both our previous and present work, we propose that BBR reduces hERG membrane stability with multiple mechanisms. Furthermore, we found that fexofenadine and resveratrol Suprax Reviews shorten action potential duration prolongated by BBR, thus having the potential effects of alleviating the cardiotoxicity of BBR.

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In both subject groups, C5 was not significantly different after fexofenadine compared to placebo. In subjects with URI, pulmonary function studies were also similar. In healthy volunteers, however, FEV1 and FEF(25-75), pulmonary function parameters reflecting the degree of airway dilatation, were significantly increased after fexofenadine. Mean (95% CI) values for FEV1(L) after fexofenadine and placebo were 3.16 (2.77, 3.55) and 3.08 (2.69, 3.47), respectively (P = 0.017). Mean Cymbalta Prescription Prices values for FEF(25-75)(L/s) were 3.49 (3.10, 3.88) and 3.26 (2.79, 3.72), respectively (P = 0.029).

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Self-evaluated symptom scores in all 3 active treatment groups showed significant improvements compared with the placebo group. Furthermore, the cetirizine group showed significant improvement in the domains of frequency of nose blowing and nasal obstruction compared with placebo. In addition, improvement in Japanese Rhinoconjunctivitis Quality of Life Questionnaire scores was higher in the cetirizine group than in the loratadine and placebo groups.

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Seven Italian infertility centres were invited to collect data on IVF cycles performed over the first 4 months of application of the new legislation. As a control, all centres provided data on cycles performed in the same solar period, 1 year before.

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2976 unrelated consecutive Italian patients with degenerative Parkinsonism were screened for mutations on exon 41 (G2019S, I2020T) and a subgroup of 1190 patients for mutations on exon 31 (R1441C/G/H). Demographic and clinical features were compared between LRRK2-carriers and non-carriers, and between male and female LRRK2 mutation carriers.

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Multivariable logistic regression models estimated odds ratios (ORs) and 95 % confidence intervals (CIs) for high versus low resilience in relation to HCU and SRH improvements over 2 years. Resilience indicators included: cumulative lifetime adversity, social support, global mastery and domain-specific mastery. Cumulative lifetime adversity was defined as 0, 1-2, 3-4 or 5+ events. HCU included hospitalization (any vs. none) and physician visits (< 20 vs. ≥ 20) over 2 years.

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To determine if a short course of oral corticosteroids benefits LBP ED patients.

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Tiotropium is an anticholinergic drug for Chronic Obstructive Pulmonary Disease (COPD) patients, with a peak bronchodilator effect observed after 1.5 to 2 hours and a long duration of action. The aim of our study was to quantify the early protection of a single dose of inhaled tiotropium against methacholine-induced bronchoconstriction in asthmatic patients with airway hyperresponsiveness. Ten subjects (7M, 3F), with history of asthma and a baseline FEV(1) (Forced Expiratory Volume 1 sec) > 80% of predicted, were enrolled in the study. Each subject performed three methacholine challenge tests, with a time of 72 hours between each challenge: Test A (methacholine challenge test), and successively, at random, Test B (methacholine 30 minutes after inhaled Tiotropium) and Test C (methacholine 30 minutes after inhaled Placebo). PD20 (Provocative Dose causing a 20% decrease in basal FEV(1) value) was reached to assess airways responsiveness. All the subjects showed in Test A and Test C a mild-moderate airway hyperresponsiveness. In Test B no PD20 was reached at the inhaled maximum dose of methacholine (1600 microg), FEV(1) before tiotropium was 88.6% +/- 4.4, beginning test FEV(1) 92.6% +/- 4.3, end test FEV(1) 85.7% +/- 4.6. Inhaled tiotropium bromide 18 microg has shown a protective effect against methacholine-induced bronchoconstriction in asthmatic patients, with mild-moderate airways hyperresponsiveness, already 30 minutes after its administration.

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1. The human HERG gene encodes the cardiac repolarizing K(+) current I(Kr) and is genetically inactivated in inherited long QT syndrome 2 (LQTS2). The antihistamine terfenadine blocks HERG channels, and can cause QT prolongation and torsades de pointes, whereas its carboxylate fexofenadine lacks HERG blocking activity. 2. In the present study the ability of fexofenadine to block the K897T HERG channel variant was investigated. The underlying single nucleotide polymorphism (SNP) A2960C was identified in a patient reported to develop fexofenadine-associated LQTS. 3. K897T HERG channels produced wild-type-like currents in Xenopus oocytes. Even at a concentration of 100 micro M, fexofenadine did not inhibit wild-type or K897T HERG channels. Coexpression of wild-type and K897T HERG with the ss-subunit MiRP1, slightly changed current kinetics but did not change sensitivity to terfenadine and fexofenadine. 4. Western blot analysis and immunostaining of transiently transfected COS-7 cells demonstrated that overall expression level, glycosylation pattern and subcellular localization of K897T HERG is indistinguishable from wild-type HERG protein, and not altered in the presence of 1 micro M fexofenadine. 5. We provide the first functional characterization of the K897T HERG variant. We demonstrated that K897T HERG is similar to wild-type HERG, and is insensitive to fexofenadine. Although the polymorphism changes PKA and PKC phosphorylation sites, regulation of K897T HERG by these kinases is not altered. 6. Our results strongly indicate that QT lengthening and cardiac arrhythmia in the reported case of drug-induced LQT are not due to the K897T exchange or to an inhibitory effect of fexofenadine on cardiac I(Kr) currents. British Journal of

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High TS expression was associated with a significantly worse prognosis in node-positive but not in node-negative breast cancer patients. Twenty-seven percent of node-positive patients with high TS expression were disease-free at 10 years, compared with 44% of node-positive patients with low TS expression (P = .03). Forty-one percent of patients with node-positive high-TS-expressing tumors were alive after 10 years, compared with 49% of those with low TS expression (P = .06). The association between TS and disease-free survival (DFS) and overall survival (OS) was independent of other prognostic factors such as tumor size, tumor grade, nodal status, vessel invasion, estrogen receptor (ER)/ progestin receptor (PR) status, c-erb B-2, or Ki-67 expression. In node-positive patients, six cycles of standard adjuvant cyclophosphamide, methotrexate, and fluorouracil ([5-FU] CMF) CT improved DFS and OS compared with one cycle of perioperative CMF therapy. The magnitude of this benefit was greatest in patients whose tumors had high TS expression (P < .01 for DFS; P < .01 for OS). Node-negative patients demonstrated no difference in outcome to CT based on TS expression; however, the power to detect differences was limited by the small number of events in this group.

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Recent reports suggest an association between Chlamydia pneumoniae and Helicobacter pylori bacteria and atherosclerosis. We studied 51 patients (mean age, 68.3 years) who underwent abdominal aortic aneurysm surgery. For each patient we performed a microimmunofluorescence test for immunoglobulin G (IgG), IgA, and IgM antibodies to C. pneumoniae specific antigen (TW-183). Anti-H. pylori antibodies were determined by means of an EIA-G test. Each aortic aneurysm surgical specimen was sampled into multiple sections of 0.3 cm2 each and frozen at -20 degrees C. Two samples of each aneurysm were used for a nested PCR with two sets of C. pneumoniae and two sets of H. pylori specific primers. Specimens were treated with a solution containing 20 mM Tris-HCl, Tween 20-Nonidet P-40 (0.5% [vol/vol] each), and 100 micrograms of proteinase K per ml and incubated at 60 degrees C for 1 h and at 98 degrees C for 10 min. DNA was extracted twice with phenol-chloroform-isoamylic alcohol and precipitated with sodium acetate-ethanol by standard methods. Forty-one patients were seropositive for C. pneumoniae with past-infection patterns in 32 patients (16 < or = IgG < 512; 32 < or = IgA < 256) and high antibody titers in 9 patients (IgG > or = 512). In 26 of 51 patients, C. pneumoniae DNA was detected in aortic aneurysm plaque specimens. Of these patients, 23 had a serologic past-infection pattern, 2 had an acute reinfection pattern, and 1 was seronegative. Forty-seven of 51 patients were seropositive for H. pylori. In all cases PCR showed no evidence of H. pylori presence in plaque specimens. This study provides data on a possible C. pneumoniae involvement in the pathogenesis of aortic aneurysm and additional evidence for an association between this agent and atherosclerosis. Conversely, notwithstanding a high H. pylori seroprevalence observed, our results tend to rule out the possibility of a direct involvement of H. pylori in atherosclerosis.

buy allegra d 2015-11-09

The highest concentrations of antihistamines in STP wastewaters correlate with the outbreak of allergic reaction caused by high amounts of plant pollens in the air. The analysis results of the river water samples show that the antihistamines are carried far away from the effluent discharge points. They may account for a part of the mix of pharmaceuticals and of pharmaceutical metabolites that occur downstream of STPs.

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The allergy cascade presents widespread inflammatory and proinflammatory activation, robust cytokine and chemokine signaling, and heterogeneous immune and endothelial responses that lead ultimately to the manifestations of allergic reaction. Histamine, a small peptide with inherent vasoactive properties, is released from granules contained within mast cells, basophils, lymphocytes, and other reservoirs and interacts with histamine receptors to regulate numerous cellular functions involved in allergic inflammation and immune modulation. Of the known histamine receptors, the H(1)-receptor is most clearly associated with potentiation of proinflammatory immune cell activity and enhanced effector function and is the prime focus of suppressive therapy. Second-generation oral H(1)-antihistamines, such as cetirizine, desloratadine, fexofenadine, levocetirizine, and loratadine, are mainstays of allergy treatment, acting as highly specific, long-acting H(1)-receptor agonists at its unique receptor. The ongoing identification of immune effector cells and mediators involved in the allergic cascade indicates that further research is necessary to define the role of antihistamines such as desloratadine in anti-inflammatory therapy.

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Chronic idiopathic urticaria (CIU) is a disabling affliction that considerably limits patients' daily activities and interferes with sleep. Clinical studies have shown that histamine H1-receptor antagonists (antihistamines) are highly effective for inhibiting the hives/wheals and pruritus associated with CIU, as well as improving patients' quality of life. Desloratadine is a rapid-acting, once-daily, nonsedating selective H1-receptor antagonist/inverse receptor agonist with proven clinical efficacy in patients with CIU. It has 10-20 times the in vivo H1 receptor-binding affinity of loratadine, its parent compound, and 52-194 times the H1 receptor-binding affinity of cetirizine, ebastine, loratadine, and fexofenadine. Desloratadine displays linear pharmacokinetics after oral administration. Age and sex have no apparent effect on the drug's metabolism and elimination, and food does not affect its bioavailability or absorption. Desloratadine also exerts anti-inflammatory effects via mechanisms that are independent of H1-receptor antagonism. Results from randomized, double-blind, placebo-controlled studies of 6 weeks' duration in adults and adolescents with moderate-to-severe CIU indicate that desloratadine significantly minimizes the severity of pruritus, reduces the number and size of hives, and improves disease-impaired sleep and daily activities. Improvements were noted after a single dose of desloratadine and were maintained over 6 weeks of treatment. Desloratadine was safe and well tolerated in clinical trials of patients with CIU. The adverse effect profile of desloratadine in adults, as well as in children aged from 6 months to 11 years, is comparable to that of placebo. Evaluations of cognitive and psychomotor performance in adults indicate no impairment of function with dosages of desloratadine 5 mg/day. In conclusion, desloratadine is an important therapeutic option for prompt and enduring symptom relief in patients with moderate-to-severe CIU. In addition to efficacy and safety, desloratadine affords a convenient administration regimen, rapid onset of action, and an absence of drug-drug or drug-food interactions. Other important prescribing considerations are that, unlike all first-generation and some second-generation antihistamines, desloratadine is nonsedating at its clinically approved dosage and does not impair psychomotor function.

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Complete resection was performed in all patients (44 adenocarcinoma, 17 squamous cell carcinoma), with no operative deaths. Multivariable analysis demonstrated a significant relationship between cancer-specific death and the following variables: low-level P-gp expression (p = 0.004), high-level expression of p53 (p = 0.04), and low-level expression of transforming growth factor-alpha (p = 0.03). In addition, the number of involved tumor markers present was strongly predictive of negative outcome (p = 0.0001).

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This prospective, randomized, double-blind, crossover, placebo-controlled study was conducted in 18 healthy adults. Subjects were exposed to Coriolis vestibular cross-coupling in the laboratory using the Staircase Profile Test for baseline susceptibility and when under the influence of cetizirine, fexofenadine, and placebo. Subjective evaluation of sickness symptoms was based on the Graybiel diagnostic criteria of acute motion sickness, Golding's scale, and the Coriolis Sickness Susceptibility Index.