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Periactin (Cyproheptadine)

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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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Over a 15-yr time span, a 30-yr-old female chimpanzee (Pan troglodytes) exhibited recurrent upper respiratory disease that was suspected to be allergen induced. Until 1993, symptomatic therapy with several different antibiotics and antihistamines yielded variable results. In early 1993, the chimpanzee was consistently observed to be open-mouth breathing despite medication. Nasal polyposis was diagnosed using rigid endoscopy in September 1993, and the polyps were removed by loop excision. A fluorescent allergosorbent test was performed to differentiate hypersensitivity to specific regional allergens causing chronic inhalant allergic rhinitis. Oral immunotherapy was then instituted using standard human treatment for Sacramento Valley pollens. This combination of polyp removal and immunotherapy resulted in a marked reduction of clinical signs, and continuous oral immunotherapy has controlled these signs. Hyposensitization therapy will continue for at least 2-3 yr. The chimpanzee continues to breath normally following occasional antihistamine treatment.

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Some etiologic possibilities which must be considered are foods, drugs, infection, inhalant sensitivity, psychic factors, physical agents, underlying connective tissue disease or neoplasm, insect bite or stings and genetic abnormalities. A painstaking history and a complete physical examination are, of course, mandatory. These are followed by appropriate studies for whatever etiologic factors are suggested by the history and physical examination. Certain routine or more sophisticated studies might be indicated including a complete blood count, urinalysis, stools for ova and parasites, antinuclear antibody titer, complete complement, sedimentation rate, sinus, chest and dental X rays and any other specified test depending on where the clues lead. O'Loughlin described a practical approach in the use of laboratory studies for the diagnosis of chronic urticaria. Skin tests can be helpful especially for inhalants, but food tests are usually not reliable in the diagnosis of chronic urticaria. The acute urticaria reaction to a food is clinically obvious and this type of patient does not usually seek medical attention or need extensive investigation. Treatment includes a few basic medications. Hydroxyzine (Atarax, Vistaril), which combines tranquilizer and antihistamine action, is frequently effective. Cyproheptadine HCL (Periactin) both a serotonin and histamine antagonist with anticholinergic effect, is also helpful--especially in combination with hydroxyzine. Antihistamines, ephedrine, epinephrine, aminophyllin and occasionally corticosteroids are helpful. Immunotherapy with inhalants is occasionally indicated. Eliminating possible offending foods, dyes or drugs has been previously discussed. Anti-candidal therapy and low yeast diet is effective when indicated. The final aspect of the investigation and treatment process might best be described as "patient support"--patience on the part of the physician. It should be realized that in 75% of the cases of chronic urticaria, no convincing etiology is found. It should also be realized that urticaria all too frequently "settles down" due as much to the natural course as to the careful ministrations of the physician.

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These results allow the conclusion that cetirizine at its recommended therapeutic dose of 10 mg is demonstrably free from disruptive effects on aspects of psychomotor and cognitive function in a study where the psychometric assessments have been shown to be sensitive to impairment, as evidenced by the effects of the positive control, promethazine 25 mg.

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Diphenhydramine, 50 mg, given for 1 week provided statistically significant and clinically superior improvements in symptoms compared with 5 mg of desloratadine in patients with moderate-to-severe SAR. Somnolence occurred more frequently with diphenhydramine (22.1%) compared with desloratadine (4.5%) and placebo (3.4%).

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Rupatadine is a new second-generation antihistamine with H(1) receptor antagonist activity and platelet-activating factor antagonist properties. This study aimed to investigate the effect of rupatadine on histologic changes in the lungs in a murine model of chronic asthma.

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Cyproheptadine prevention of the neuropsychiatric adverse effects of an antiretroviral regimen including efavirenz has been evaluated in a randomized clinical trial. Twenty-five patients (16 males and 9 females with mean±SD ages of 36±9 years) in a cyproheptadine group, and 26 patients (17 males and 9 females with mean±SD ages of 34±7 years) in a control group completed the trial. Sexual contact and injection drug use were the main routs of HIV infection in both groups. The patients' neuropsychiatric adverse effects were evaluated based on the Hamilton Depression Rating Scale, Hamilton Anxiety Rating Scale, Positive and Negative Syndrome Scale, Beck Depression Scale, Pittsburgh Sleep Quality Inventory, Positive and Negative Suicide Ideation, and Somatization Subscale of Symptom Checklist 90 at baseline and 4 weeks after treatment. Cyproheptadine significantly decreased the scores of Hamilton Depression Rating Scale, Hamilton Anxiety Rating Scale, Positive and Negative Syndrome Scale, Beck Depression Scale, Pittsburgh Sleep Quality Inventory, Positive and Negative Suicide Ideation of the patients after 4 weeks in comparison with control group. All of the scores increased in control group following antiretroviral therapy. Although short duration of the patients' follow-up was a major limitation of the study, the results of the study showed that cyprohepradine is effective in prevention of depression, anxiety, hallucination, aggressive behaviors, emotional withdrawal, poor rapport, poor impulse control, active social avoidance, suicidal ideation, and improved sleep quality of HIV-positive patients after initiation of antiretroviral therapy including efavirenz.

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Levocetirizine suppressed the cutaneous allergic reactions with a higher potency than desloratadine, which correlated with its high receptor occupancy. Receptor occupancy rather than drug affinity or plasma half-life is more representative of antihistamine potency.

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In this work, a method for the determination of the antihistaminic drugs loratadine and pheniramine from human serum is presented. Serum samples are extracted under basic conditions with hexane-n-amyl alcohol (95:5, v/v), the analytes are reextracted into diluted hydrochloric acid and, after basification, are once again extracted into the organic phase. The samples are measured by GC-MS. The limits o detection of the assay are 0.5 ng/ml for loratadine and 2 ng/ml for pheniramine. The R.S.D.s in the day-to-day precision test for loratadine are 7.0% at 20 ng/ml and 12.4% at 2 ng/ml. for pheniramine, the R.S.D. are 6.4% at 300 ng/ml and 10.2% at 20 ng/ml.

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The data are presented on changes in the rat arcuate nuclear neuron ultrastructure after using cyproheptadine (peritol, Egyt Pharmaceutical Works, Hungary) in a water suspension at a dose of 20 mg/kg once daily during 7 successive days and twice a day within 10 days. It was shown that cyproheptadine decreases the functional activity of the arcuate nuclear neurons, depending on the total amount of the drug used. Cyproheptadine-induced inhibition of the forming neurohormone release from neurons is likely to be one of the mechanisms of its therapeutic effect in Itsenko-Cushing's disease.

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Canatoxin, a convulsant neurotoxin from the seeds of Canavalia ensiformis, induces lipoxygenase-dependent hypoxia in rats which is blocked by hexamethonium. The purpose of the present study was to examine the relationship between canatoxin-induced hypoxia and bronchoconstriction. Since several effects of the toxin are very similar to those described for morphine and opioid-like peptides, the effects of opioid antagonists were also investigated. Pretreatment of male, adult Wistar rats (200-250 g) with cyproheptadine (80 micrograms/kg, ip, N = 6) and isoproterenol (100 micrograms/kg, ip, N = 6) partially blocked (% variation of pO2: CNTX alone: -26.67 +/- 2.56, N = 6; with cyproheptadine: -16.15 +/- 2.97*, N = 6; with isoproterenol: -17.73 +/- 1.93*, N = 6; *P < 0.05 as compared to CNTX alone) the hypoxia but no effect was observed with diphenhydramine (2 mg/kg, ip, N = 6) or atropine (2 mg/kg, ip, N = 6). The hypoxemic effect of canatoxin (100 micrograms/kg, i.v., 20 min, N = 6) was also almost completely blocked with either naloxone (1 mg/kg, sc, N = 6) or naltrexone (5 mg/kg, sc, N = 6). The results presented here provide evidence suggesting that both opioid peptides and bronchoconstriction seem to play a role in the hypoxia caused by canatoxin.

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The selective pharmacology of the selective serotonin reuptake inhibitors (SSRIs) results in a lower potential for pharmacodynamic drug interactions relative to other antidepressants such as the tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs). However, the SSRIs have been implicated in the development of the serotonin syndrome--a potentially life-threatening complication of treatment with psychotropic drugs. The syndrome is produced most often by the concurrent use of two or more drugs that enhance central nervous system serotonin activity and often goes unrecognized because of the varied and nonspecific nature of its clinical features. The serotonin syndrome is characterized by alterations in cognition (disorientation, confusion), behavior (agitation, restlessness), autonomic nervous system function (fever, shivering, diaphoresis, diarrhea), and neuromuscular (ataxia, hyperreflexia, myoclonus) activity. The difference between this syndrome and the occurrence of adverse effects caused by serotonin reuptake inhibitors alone is the clustering of the signs and symptoms, their severity, and their duration. There are important pharmacokinetic interactions between SSRIs and other serotonergic drugs due principally to their effects on the cytochrome P450(CYP) isoenzymes, the potential for which varies widely amongst the SSRI group, which may increase the likelihood of a pharmacodynamic interaction. The exceptionally long washout period required after fluoxetine discontinuation may cause additional problems and/or inconvenience. Patients with serotonin syndrome usually respond to discontinuation of drug therapy and supportive care alone, but they may also require treatment with antiserotonergic agent such as cyproheptadine, methysergide, and/or propranolol. To reduce the occurrence, morbidity, and mortality of the serotonin syndrome, it must be both prevented by prudent pharmacotherapy and given prompt recognition when it is present.

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We compared the effects of 5 mg of desloratadine and placebo on nasal airflow and SAR symptoms, including nasal congestion, in response to grass pollen in an allergen-exposure unit.

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The efficacy and safety of loratadine, 40 mg once daily, were compared with terfenadine, 60 mg twice daily, and placebo in controlling symptoms of ragweed hay fever. The study was a randomized, multicentric, parallel-group, double-blind design involving 280 patients divided into three groups receiving either loratadine, terfenadine, or placebo for a period of 14 days in the autumn of 1984. Both loratadine and terfenadine demonstrated a statistically greater reduction in symptom score compared to placebo. They were not statistically different from each other, and there was no statistical difference in the incidence of side effects between the two drugs.

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A nasal lavage model and a new filter paper disk model have been used to measure biologic and physiologic responses to antigen challenge in patients with allergic rhinitis. Pretreatment of subjects with cetirizine reduced the number of sneezes induced by antigen challenge but did not significantly reduce levels of histamine or prostaglandin D2 in a double-blind, placebo-controlled trial with the lavage model. Pretreatment with 60 or 300 mg of terfenadine did significantly Ceftin Childrens Dosage reduce levels of histamine, kinin, albumin, and TAME-esterase activity in a double-blind, placebo-controlled study with this model. Again with the nasal lavage model, a double-blind, placebo-controlled comparison of pretreatment with 60 mg of terfenadine or 10 mg of loratadine showed that both agents significantly reduced sneezing. Both drugs also lowered levels of antigen-induced histamine and TAME-esterase, but only terfenadine did so significantly. In a double-blind, placebo-controlled study, the new disk method showed that terfenadine reduced sneezing but not nasal congestion in eight patients with allergic rhinitis. Terfenadine significantly reduced the weight of nasal secretions on both sides of the nose and significantly reduced histamine on the ipsilateral side.

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This study shows that the activity of levocetirizine in suppressing skin reactivity to histamine was clearly superior to that of desloratadine for 24 h after Detrol 4mg Prices a single dose. In addition, its activity was more consistent and lasted longer.

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Desloratadine and levocetirizine are histamine H(1) receptor antagonists (antihistamines) that were launched in the UK in 2001. Our objective was to compare the frequency with which drowsiness and sedation were reported for desloratadine and levocetirizine within the first 30 days Augmentin 250 Mg of observation, as monitored using the observational cohort technique of prescription-event monitoring (PEM).

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Eosinophil/basophil (Eo/B) progenitors fluctuate in the peripheral circulation during seasonal allergen exposure in atopic subjects. Several drugs have been shown to modulate Eo/B Effexor Standard Dose progenitor levels in the peripheral blood but, to date, the possible effect of antihistamines on Eo/B progenitors has not been explored. Our objective was to evaluate whether the antihistamine desloratadine (DL) can modulate peripheral blood Eo/B progenitors or other markers of allergic inflammation.

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Senenty patients with moderate and severe persistent allergic rhinitis were devided randomly study group (n = 35) and control group (n = 35). The study group were treated with montelukast sodium tablets combined with budesonide nasal spray and desloratadine citrate disodium tablets for 4 weeks, the control group received budesonide nasal spray and desloratadine citrate disodium tablets for 4 weeks. Comparing Parlodel Drug visual analogue scale (VAS) scores of nasal symptoms, rhino conjunctivitis quality of life questionnaire (RQLQ) scores and total effective rate in two groups at baseline and after treatment.

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Retrospective study from 2004 Zyrtec Syrup Dosage to 2010.

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40 monosensitized House Dust Mite (HDM) mild-to-moderate allergic rhinitis patients were included in the study. During the study, twenty patients Himplasia Medicine randomly received 10 mg loratadine daily, the other twenty did not take any antihistamine. All patients were treated with nasal budesonide daily and sodium cromoglycate nasal spray when needed. Serum soluble ICAM-1 and VCAM-1 levels were determined by immunoenzimatic assay before and in the end of the study period.

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Sixteen healthy male and female volunteers took part in a 6-way, double-blind cross-over trial to compare the effects of single doses of cetirizine 10 mg, loratadine 10 mg and placebo, with and without alcohol (0.72, lean body mass). Performance was measured in two repetitions of a psychometric test battery, and a standard, over-the-road driving test. EEG was also measured during driving. Alcohol significantly affected almost every performance measure and altered the EEG energy spectrum during driving whilst the blood concentrations declined from 0.37 to 0.20 The effects of cetirizine of on driving performance resembled those of alcohol. It caused the subjects to operate with significantly greater variability in speed and lateral position ('weaving' motion). The effects of alcohol and cetirizine appeared to be additive. Certain cetirizine-placebo differences in subjective feelings and test battery performance were also significant Seroquel Recommended Dosage . Loratadine had no significant effect on any performance parameter. It was concluded that cetirizine, but not loratadine, generally caused mild impairment of performance after a single 10 mg dose.

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1 The effect of the putative 5-hydroxytryptamine (5-HT) receptor antagonists, methysergide, methergoline, mianserin, cyproheptadine, cinanserin (all at 10 mg/kg), methiothepin (5 mg/kg) and (-)-propranolol (20 mg/kg) on the behavioural responses to tranylcypromine (10 mg/kg) followed 30 min later by L-tryptophan (100 mg/kg) was examined.2 Methysergide, methergoline, methiothepin and (-)-propranolol inhibited head weaving, forepaw treading and hind-limb abduction. Methysergide and methergoline increased reactivity. In contrast, cypropheptadine, cinanserin and mianserin had no effects on the behaviour.3 Similar findings were obtained when the behaviours were elicited by administration of tranylcypromine (10 mg/kg) followed by the putative 5-HT receptor agonist, 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) (2 mg/kg).4 When the behaviours were elicited by the putative 5-HT receptor agonist, quipazine (50 mg/kg), all the drugs effectively inhibited head weaving and forepaw treading.5 When the dose of cypropheptadine was doubled to 20 mg/kg an inhibition of the tranylcypromine/L-tryptophan induced behaviours was seen.6 Methiothepin produced a marked inhibition of apomorphine-induced locomotor activity whilst all the others enhanced this response, suggesting that only methiothepin inhibits the 5-HT behaviours by dopamine antagonism and that the increased reactivity seen following tranylcypromine/L-tryptophan after pretreatment with methysergide or methergoline might be due to enhanced dopamine function.7 Pretreatment with p-chlorophenylalanine resulted in enhanced behavioural responses to both 5-MeODMT and quipazine.8 Both methergoline and methiothepin decreased the rate of 5-HT synthesis in whole brain but not spinal cord and methergoline decreased spinal cord 5-HIAA concentration. None of the other drugs had any significant effects on the concentration of 5-HT, 5-HIAA or 5-HT synthesis rate in brain or spinal cord.9 Experiments with compounds structurally related to quipazine and with molecular models suggested that quipazine produces behavioural changes probably by stimulating the 5-HT receptor in a similar way to 5-HT but that it would bind weakly, in agreement with ligand-receptor binding studies.10 It is suggested, therefore, that cyproheptadine, cinanserin and mianserin fail to inhibit 5-HT and 5-MeODMT-induced behaviours because they are weak antagonists whilst they are able to inhibit the same behaviours induced by quipazine because it is a weak agonist.11 These data indicate that extreme care should be taken in accepting or rejecting 5-HT as a mediator of behaviours or of other responses unless several antagonists or agonists have been examined.