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Generic Periactin is used to relieve cold- and allergy-related symptoms such as hay fever, nasal inflammation, stuffy nose, red and inflamed eyes, hives, and swelling. Generic Periactin is approved by FDA. Generic Periactin blocks the effects of the naturally occurring chemical histamine in your body.

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Also known as:  Cyproheptadine.


Generic Periactin is used to treat fever, nasal inflammation, stuffy nose, red and inflamed eyes, hives, swelling and other symptoms of cold and allergy.

Generic Periactin blocks the effects of the naturally occurring chemical histamine in your body.

Periactin is also known as Cyproheptadine, Ciplactin, Periactine, Ciproral.

Generic name of Generic Periactin is Cyproheptadine.

Brand name of Generic Periactin is Periactin.


Generic Periactin can be taken in tablets (4mg) and syrup. You should take it by mouth.

Take Generic Periactin by mouth with or without food.

Measure the syrup form of Generic Periactin with a special dose-measuring spoon or cup.

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


If you overdose Generic Periactin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Periactin overdosage: extreme sleepiness, confusion, weakness, ringing in the ears, blurred vision, large pupils, dry mouth, flushing, fever, shaking, insomnia, hallucinations, seizure.


Store at room temperature between 15 to 30 degrees C (59 to 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

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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 Periactin if you are allergic to Generic Periactin components.

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

Do not take cyproheptadine if you have taken a monoamine oxidase inhibitor (MAOI) such as isocarboxazid (Marplan), phenelzine (Nardil), or tranylcypromine (Parnate) in the last 14 days.

Be careful in taking Generic Periactin if you have glaucoma or pressure in the eye, stomach ulcer, enlarged prostate, bladder problems, difficulty urinating, hyperthyroidism, hypertension, any problems with heart, asthma.

Be careful with taking Generic Periactin if you use anxiety or sleep medicines such as alprazolam (Xanax), diazepam (Valium), chlordiazepoxide (Librium), temazepam (Restoril), or triazolam (Halcion); anti-depression medications such as amitriptyline (Elavil), doxepin (Sinequan), nortriptyline (Pamelor), fluoxetine (Prozac), sertraline (Zoloft), or paroxetine (Paxil); any other medications that make you feel drowsy, sleepy, or relaxed.

Avoid machine driving while taking Generic Periactin.

Avoid alcohol.

Do not stop taking Generic Periactin suddenly.

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Eleven patients (seven females, four males, age range: 5-60 years) with a clinical history suggestive of SU, verified by photo-provocation tests to ultraviolet A (UVA), visible light, and/or UVB, were treated with various combinations of antihistamines and leukotriene receptor antagonist.

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Many antidepressants reverse arylpiperazine-induced hypothermia after acute treatment by a mechanism that does not seem to implicate monoamine uptake inhibition. Activity is found in reversing 1-(m-trifluoromethylphenyl)piperazine (TFMPP)-induced hypothermia by desipiramine 5 and 10 mg/kg and not by maprotiline 10 and 20 mg/kg. Clomipramine and fluoxetine with comparable serotonin uptake blocking potential do not have comparable TFMPP-reversing effects. A dibenzothiadiazepine compound (IM/P/3/4), hypothesized to have antidepressant activity though devoid of uptake blocking properties, was active at 10 and 20 mg/kg. Other classes of tricyclics such as neuroleptics (clozapine 5 and 10 mg/kg) and chlorpromazine (2 and 10 mg/kg) and the H1 antihistamines, promethazine (20 mg/kg) and cyproheptadine (10 mg/kg) are active, as well as the calcium antagonists nifedipine (10 mg/kg) and verapamil (10 mg/kg). We hypothesize that properties other than monoamine-uptake block which these compounds share (such as calcium-uptake inhibition) could be involved. Activity was also seen with the 5-HT1A agonists 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, at 0.05 and 0.25 mg/kg), and 5-methoxy-N,N-dimethyltryptamine (5-MeODMT at 3 mg/kg) as well as with the muscarinic agonist oxotremorine (0.1 mg/kg).

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This study compares the potency, consistency, onset, and duration of action of levocetirizine with other popular antihistamines.

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To compare the efficacy and safety of histamine H1 receptor antagonist loratadine with Leukotriene receptor antagonist Ibudilast in steroid resistant allergic rhinitis in a randomized controlled clinical trial.

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This was a randomized (gender-balanced), parallel-group study involving 160 healthy volunteers. Rupatadine, 10 and 100 mg day(-1), and placebo were administered single-blind for 5 days, whilst moxifloxacin 400 mg day(-1) was given on days 1 and 5 in open-label fashion. ECGs were recorded over a 23-h period by continuous Holter monitoring at baseline and on treatment days 1 and 5. Three 10-s ECG samples were downloaded at regular intervals and were analysed independently. The primary analysis of QTc was based on individually corrected QT (QTcI). Treatment effects on QTcI were assessed using the largest time-matched mean difference between the drug and placebo (baseline-subtracted) for the QTcI interval. A negative 'thorough QT/QTc study' is one where the main variable is around < or =5 ms, with a one-sided 95% confidence interval that excludes an effect >10 ms.

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Basal and post-glucose growth hormone (GH) responses were evaluated in 10 acromegalics receiving cyproheptadine (cypro) 4 mg 6 hourly at 2 and 21 days after initiating therapy. Of the 10 patients, six had macroadenomas with varying degree of suprasellar extensions, one a microadenoma and three had persistent hypersomatotropism despite pituitary adenomectomy due to residual tumour. The basal and post-glucose GH showed no significant change in all, except one with a pituitary microadenoma. His GH was reduced from 680 to 108 mU/L on the second and 82 mU/l on the 21st day of cypro therapy. These data do not suggest any therapeutic role of cypro in the management of acromegaly.

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The development of IDDM results from the destruction of pancreatic beta cells. Genetic factors, various immune system alterations, and environmental factors have been studied as the possible causes of IDDM. The concordance rate for developing IDDM between monozygotic twins approaches 50%, suggesting that genetic factors are necessary, but nongenetic factors such as various immune system alterations and environmental factors also influence the clinical expression of genetic susceptibility. Environmental factors (e.g., viruses, chemicals, and diet) affecting the induction of diabetes may act as primary injurious agents which damage pancreatic beta cells or as triggering agents of autoimmunity. Certain viruses including EMC-D and Mengo virus 2T can directly infect pancreatic beta cells and replicate in the cells. The replication of viruses in the beta cells results in the destruction of the cells within 3 days, and the infected mice develop a diabeteslike syndrome in 3-4 days without the involvement of autoimmunity. In contrast, rubella virus appears to be somewhat weakly associated with autoimmune IDDM in hamsters. In addition, endogenous retrovirus expressed in pancreatic beta cells is clearly associated with the development of insulitis and diabetes in NOD mice. In man, there appears to be no correlation between the detection of islet cell autoantibodies and anti-Coxsackie B viral antibodies in newly diagnosed IDDM. In contrast, persistent infection of CMV and rubella virus appears to be associated with the presence of autoantibodies in newly diagnosed IDDM patients. It is particularly noteworthy that human CMV can induce islet cell autoantibodies that react specifically with a 38 kDa islet cell protein which may represent islet cell-specific antigens in a proportion of CMV-associated IDDM cases. These observations suggest that the association of diabetes with Coxsackie B viruses might be due to cytolytic infection of the beta cells with no link to autoimmunity, while both rubella virus and CMV are probably associated with autoimmune IDDM. A number of structurally diverse chemicals including alloxan, streptozotocin, chlorozotocin, Vacor, and cyproheptadine are diabetogenic mainly in rodents and sometimes in man. Possible mechanisms for beta cell destruction by these chemicals include (a) generation of oxygen free radicals and alteration of endogenous scavengers of these reactive species; (b) breakage of DNA and a consequent increase in the activity of poly-ADP-ribose synthetase, an enzyme depleting nicotinamide adenine dinucleotide in beta cells; and (c) inhibition of active calcium transport and calmodulin-activated protein kinase activity. (ABSTRACT TRUNCATED AT 400 WORDS)

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The present study was undertaken to investigate the pathological role of substance P in allergic nasal symptoms in rats. The topical application of substance P caused an increase in the incidence of sneezing and nasal rubbing in a dose-dependent fashion, and at a dose of 30 nM/site it showed a significant effect. L-732,138, a tachykinin NK(1) receptor antagonist, at doses of 3 and 10 mg/kg showed a significant inhibition of the nasal signs induced by exogenous substance P in rats. In addition, L-732,138 also showed a significant inhibition of nasal behavior induced by antigen in actively sensitized rats at the same dose. On the other hand, histamine H(1) receptor antagonists, such as cyproheptadine, epinastine and olopatadine had no effect on the nasal behaviors induced by exogenous substance P, even at higher doses, indicating that exogenous substance P does not cause the degranulation of mucosal mast cells in the rat. Moreover, all the histamine H(1) receptor antagonists showed the dose-dependent inhibition of the nasal signs induced by antigen in actively sensitized rats, which revealed that the inhibition of these drugs was exhibited through the antagonistic effect on histamine H(1) receptors. Therefore, from these results, it is reasonable to conclude that substance P released from the nasal mucosa through the activation of tachykinin NK(1) receptors during the antigen antibody reaction plays an important role in allergic nasal symptoms.

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To provide supportive evidence for the European guidelines.

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Erythromelalgia is a rare poorly understood clinical condition characterized by intense burning pain, pronounced erythema, and increased skin temperature. Although there are many classifications of the disease, it can basically be divided into primary, which begins spontaneously at any age, and secondary, which is associated with myeloproliferative disorders-related thrombocythemia, polycythemia, collagen-vascular diseases, diabetes mellitus, peripheral neuropathy, autoimmune and infectious diseases, and use of certain medicaments. A wide variety of etiological conditions can cause erythromelalgia, all having a single common pathogenetic mechanism - microvascular arteriovenous shunting. The disease is characterized by severe pain associated with redness and hotness in extremities. The diagnosis is based on the medical history and clinical findings. The most useful oral medications for erythromelalgia seem to be aspirin, propranolol, clonazepam, cyproheptadine, drugs inhibiting serotonin re-uptake (venlafaxine and sertraline), tricyclic antidepressants (amitriptyline, imipramine), anticonvulsants (gabapentin), calcium antagonists (nifedipine, diltiazem), and prostaglandins (micoprostol). Erythromelalgia is usually chronic, sometimes progressive, and disabling disease, which can greatly affect the quality of life. Some patients have stable disease and get better, or even experience full resolution of the disease, with time. This review article presents the etiological basis, diagnostics, and therapy of erythromelalgia.

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The biological activity of a stable unknown material(s), generated by aortic rings (bioactive aortic substance = BAS) isolated from rats injected with a high dose of indomethacin, was explored on contractions of several smooth muscle preparations from normal rats and its effects compared with those elicited by prostacyclin (PGI2) or by 6-keto-prostaglandin F1 alpha (6-k-PGF1 alpha). The BAS evoked, as did PGI2 or 6-k-PGF1 alpha, positive inotropism in strips from rat stomach, ileum and urinary bladder, but failed to influence uterine contractions as did prostacyclin or its non-enzymatic metabolite. When tested in rat aortic strips both, PGI2 and the BAS produced relaxation, whereas 6-k-PGF1 alpha was not active. Moreover, lipid substances present in the incubates of aortic rings, were extracted and explored for effects on contractions of rat aortic strips and on arachidonate-evoked human platelet aggregation. These extracts were devoid of influence on both parameters. On the contrary, dried aqueous residues, after the lipid extraction of the supernatants of aortic ring incubates, exhibited human platelet antiaggregatory capacity as well as the ability to evoke positive and negative inotropism similar to those triggered by the BAS in different smooth muscle preparations. Experiments with BAS were also performed employing smooth muscle strips exposed to indomethacin, atropine, propranolol, phentolamine and cyproheptadine. The presence of these antagonists of several neuromodulators and of indomethacin failed to alter de BAS-induced inotropic capacity observed in controls. The findings suggest that the effects attributable to the BAS are not subserved by prostacyclin or other prostanoids, nor by acetylcholine, norepinephrine, histamine or 6-OH-tryptamine.

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Placebo, montelukast, desloratadine and levocetirizine significantly improved quality of life. Combining montelukast with either levocetirizine or desloratadine gave additional benefits in comparison to each agent alone and could be considered for patients whose quality of life is impaired by persistent allergic rhinitis.

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Hydrogen sulphide (H(2)S), considered as a novel gas transmitter, is produced endogenously in mammalian tissue from L-cysteine by two enzymes, cystathionine β-synthase and cystathionine γ-lyase. Recently, it has been reported that H(2)S contributes to the local and systemic inflammation in several experimental animal models. We conducted this study to investigate on the Comment Generic Leave Online Paxil signalling involved in H(2)S-induced inflammation.

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To Viagra Buy update a prior study evaluating the use and costs of new-generation antihistamines for the treatment of allergic rhinitis in a managed care population.

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Forty children (15 males; 25 females), aged 3-15 years, were included in this study. They were randomized to receive L + PS (0.2 mg kg[-1] body weight-2.4 mg kg[-1] body weight respectively) or placebo (PLA) for 14 days. After 7 days of washout, patients were shifted to the other treatment for a further 14 days. Nasal symptoms (sneezing/itching, Imitrex Mg congestion, nasal dripping) and signs (turbinal swelling, retronasal drainage), rated on a scale ranging from: 1. absent to 5. very intense, and their sum or mean total symptom score (MTSS) were used as efficacy measurement.

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In patients with Cushing's syndrome of hypothalamischem Cushing-Syndrom wereden eine zentrale Störung und eine wichtige Rolle des Serotonins. Accordingly, in the present study a patient with hypothalamic-pituitary hypercorticism was treated with the seotonin antagonist cyproheptadine. Urinary free cortisol excretion was measured repeatedly before, during and after therapy. In addition, night-day rhythm of plasma cortisol was determined before and at the end of cyproheptadine medication. Within 2 months, therapy with 24 mg cyproheptadine resulted in a lowering of urinary cortisol excretion to normal values. Then, however, despite continuation of the therapy, urinary free cortisol excretion rates again rose to pathological levels. Due to the Cold Sore Zovirax Dose occurrence of severe psychosis, the drug had to be withdrawn. Before and under cyproheptadine no night-day rhythm of plasma cortisol could be observed.

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The disposition of loratadine, a new orally active histamine H1 receptor antagonist and its primary metabolite descarboethoxyloratadine were characterized in adult volunteers with normal renal function (group I), patients with chronic renal failure, i.e., creatinine clearance less than 30 mL/min (group II), as well as chronic hemodialysis patients (group III). The effect of hemodialysis on the disposition of loratadine and descarboethoxyloratadine was also assessed. Subjects in groups I and II were given a single oral 40 mg dose of loratadine while the patients in Group III received two single 40 mg doses of loratadine (during an interdialytic period and just prior to hemodialysis). Loratadine was rapidly absorbed and the decline of plasma concentrations after attainment of the Cmax was biexponential in all subjects. No significant differences in t1/2 beta were observed between the three groups (8.7 +/- 5.9, 7.6 +/- 6.9, 8.6 +/- 1.6 hrs: in groups I, II, and III, respectively). The apparent total body clearance and apparent volume of distribution of loratadine also did not differ significantly among the three groups. No significant differences in the Cmax or tmax of the metabolite were observed. The metabolite AUC infinity 0 however was significantly greater in group II subjects: (212.4 +/- 37.8, 469.5 +/- 95.4, 325.2 +/- 114.6; groups I, II, and III, respectively). No significant relationship was observed between the terminal elimination half-life of loratadine or descarboethoxyloratadine and creatinine clearance. Hemodialysis augmented endogenous clearance by less than 1%. The disposition of loratadine is not significantly altered in patients with severe renal Reglan 10 Mg Medication insufficiency nor is hemodialysis an effective means of removing loratadine or descarboethoxyloratadine from the body.

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To evaluate the Betnovate Ointment Storage effect of terfenadine and loratadine on the early nasal allergic response to challenge and the subsequent cellular influx and hyperresponsiveness.

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Mastoparan B is a cationic, amphiphilic tetradecaeptide (LKLKSIVSWAKKVL-CONH2) isolated from the venom of the hornet Vespa basalis. Intravenous injection of the peptide into rats caused a profound depression of blood pressure and cardiac function, which was inhibited by cyproheptadine, reserpine and multiple doses of compound 48/80, but not by diphenhydramine and cromolyn. Mastoparan from Paravespula lewisii showed little cardiovascular inhibitory activity. A synthetic mastoparan B analog in which lysine at position 2 was replaced by asparagine showed a marked decrease in the cardiovascular depressor effects, while replacing lysine at position 4, 11 or 12 with leucine did not cause a significant reduction in these effects. Replacing lysine at position 12 with leucine even caused a more sustained depressor effect. However, the analog in which lysines at positions 11 and 12 were replaced by leucine lost its cardiovascular inhibitory activity. Replacing tryptophan at position 9 with phenylalanine in mastoparan B did not affect its activity. It is concluded that mastoparan B is involved in the cardiovascular disturbances induced by the hornet venom. Lysine at position 2 is a critical residue for the cardiovascular effects of mastoparan B. Zofran 10 Mg A peptide molecule with two lysine residues, one located close to the amino terminus and the other near the carboxyl end of the peptide, appears to be the optimal structure for eliciting the cardiovascular depressor effects.

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5HT modulates the rhythmic locomotor output of most vertebrates by enhancing the duration and intensity of motor bursts in each cycle, but there is little clear evidence on the Celexa 40 Mg pharmacological profile of the 5HT receptor subtype(s) involved. In this study we extend our previous work on the role of 5HT in the development and modulation of locomotor behaviour in newly hatched Xenopus tadpoles by examining the 5HT receptor type responsible for enhancing the swimming activity in immobilized preparations. By applying a range of agonists and antagonists against different 5HT receptor subtypes, we conclude that serotonergic modulation of swimming activity is accomplished via the activation of just one receptor type with a pharmacological profile similar to the mammalian 5HT1a receptor. The effects of 5HT on burst duration (an increase) and on episode length (a decrease) are mimicked by the 5HT1a receptor agonists, 5-carboxamidotryptamine (5CT) and R(+)-8-OH-DPAT, and reversed by the 5HT1a receptor antagonist NAN-190. Agents acting at other 5HT1, as well as 5HT2 and 5HT3, receptor subtypes were without noticeable effect on the 5HT-enhanced swimming rhythm.

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A multicentre, open-label, phase IV study in patients recruited from 33 centres in Spain, from September 2002 to November 2005. The study enrolled 324 male and female patients (aged 12-70 years) with a medical history of PER for at least 12 months and a documented positive skin-prick test to an appropriate allergen. On 4 of the 7 days prior to start of treatment, the patients were required to have a minimum total nasal symptom score (TNSS [for sneezing, rhinorrhoea, nasal obstruction/congestion and nasal itching]) of >or=5. Of the 324 eligible patients starting Blood Pressure Medication And Viagra treatment, 120 needed to be treated for more than 6 months and were followed up until the end of 12 months. All patients received rupatadine 10 mg/day and were allowed to continue their normal concomitant medication for all conditions, other than rhinitis, for up to 6 or 12 months. Safety was assessed by means of adverse events (AEs) reported by patients or detected by investigators, scheduled centralized ECG with special attention to Bazzet corrected QT interval (QTcB) and standard laboratory investigations.

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The process of choosing and prescribing prescription drugs is complex. While the choice about which drug to prescribe is made by the physician, the physician may be influenced by patient demand, which, in turn, may be influenced by consumer advertisements. As a result, consumer advertisements for prescription Brahmi Capsule drugs need to provide information that gives consumers an understanding, not only of drug risks and efficacy but also of the notable limits on benefits claimed. This Article examines the drug-specific focus of consumer advertising for prescription drugs from two perspectives: the need to prevent confusion that could affect medical decisions about alternative treatments and the need to prevent misimpressions about the value of a drug that can create consumer demand on physicians and insurers for more expensive drugs than needed.

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An analysis is made of the effectiveness of terfenadine at dosages of 60 and 120 mg, of cetirizine at a dose of 10 mg, and of loratadine and ebastine at a dose of 10 mg in inhibiting the papule induced by 20 mcg of intradermal histamine. Although all produced significant inhibition, cetirizine and terfenadine 120 mg showed a significantly greater inhibition coefficient than loratadine.

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Injection of serotonin (5-HT) into the third ventricle of the rat resulted in a rapid increase of serum TSH; a significant effect was observed 5 min after injection, whereas the maximal effect appeared 10 min after the injection of 1 microgram 5-HT. This stimulating effect of 5-HT was completely prevented by pretreatment with cyproheptadine, a blocker of 5-HT receptors, whereas fluphenazine, a dopamine receptor blocker, was unable to block it. Third venticle injection of 5-HT in rats bearing anterior hypothalamic lesions (which did not affect the suprachiasmatic nucleus or the medio-basal hypothalamus) also induced an increase of serum TSH similar to that observed in normal rats despite the fact that these animals show a lower basal TSH. In vitro, the addition of 5-HT to an incubation medium containing one hemi-anterior pituitary did not modify medium TSH, whereas 5-HT addition induced an increase of medium TSH in the system containing one hemi-anterior pituitary and two hypothalami. We conclude that 5-HT acts on TSH function probably through a stimulation of TRH release.

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The most common sexual dysfunctions found in the literature were libido decrease, difficulties in achieving and maintaining erection, ejaculatory dysfunction, orgasmic dysfunction, and menstrual irregularities. Thirteen papers were found: eight of them were open-label studies, four were descriptions of cases, and only one was a randomized clinical trial. All of them were short-term and had small sample sizes. The agents used were: bromocriptine, cabergoline, cyproheptadine, amantadine, shakuyaku-kanzo-to, sildenafil and selegiline.

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Levocetirizine (5 mg) is a potent inhibitor of the effects of histamine in human skin with an efficacy that exceeded that of loratadine (10 mg) when single doses of the drugs were administered 4 h before the test.