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Acetaminophen (AcAP), a widely-used antipyretic and analgesic drug, has been considered to exert its effects via central mechanisms, and many studies have demonstrated that the analgesic action of AcAP involves activation of the serotonergic system. Although the serotonergic system also plays an important role in thermoregulation, the contribution of serotonergic activity to the hypothermic effect of AcAP has remained unclear. In the present study, we examined whether the serotonergic system is involved in AcAP-induced hypothermia. In normal mice, AcAP (300 mg/kg, intraperitoneally (i.p.)) induced marked hypothermia (ca. -4°C). The same dose of AcAP reduced pain response behavior in the formalin test. Pretreatment with the serotonin synthesis inhibitor DL-p-chlorophenylalanine (PCPA, 300 mg/kg/d, i.p., 5 consecutive days) substantially decreased serotonin in the brain by 70% and significantly inhibited the analgesic, but not the hypothermic action of AcAP. The same PCPA treatment significantly inhibited the hypothermia induced by the selective serotonin reuptake inhibitor fluoxetine hydrochloride (20 mg/kg, i.p.) and the serotonin 5-HT2 receptor antagonist cyproheptadine hydrochloride (3 mg/kg, i.p.). The lower doses of fluoxetine hydrochloride (3 mg/kg, i.p.) and cyproheptadine hydrochloride (0.3 mg/kg, i.p.) did not affect the AcAP-induced hypothermia. These results suggest that, in comparison with its analgesic effect, the hypothermic effect of AcAP is not mediated by the serotonergic system.
The aim of this study was to identify the dose of desloratadine in children aged > or =6 months- < or =2 years that would yield a single-dose target exposure (AUC) comparable with that in adults taking 5 mg desloratadine as syrup.
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A 44-year-old female with Cushing's disease associated with a pituitary macroadenoma was treated with cyproheptadine, 24 mg per day, after partial surgical resection of the tumor. A large residual tumor remained. There was no clear suppression of serum and urinary cortisol during therapy, but both levels rose markedly to beyond pre cyproheptadine levels, on withdrawal of the drug. This is the first report on the use of cyproheptadine in Cushing's disease associated with a pituitary macroadenoma. The response in this patient indicates an influence of cyproheptadine on ACTH secretion by the macroadenoma.
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The development of subsensitivity to first-generation H1 blockers often occurs within days or weeks of treatment. It is manifested by a decrease in efficacy and a waning of the inhibition of skin reactivity to allergen or histamine. Subsensitivity to loratadine was investigated in a double-blind, placebo-controlled parallel group study in 20 allergic subjects (22 to 35 years) who received either placebo or loratadine (10 mg one daily) for 12 weeks. Skin prick tests were done with six threefold increasing concentrations of standardized allergen extracts (orchard grass or mite) and histamine-coated Phazet. Skin tests were done before any treatment and after 7, 28, 56, and 84 days. Wheals and flares were measured. Compliance was monitored strictly during the study. Statistical analysis was done by parallel line bioassay and Wilcoxon W test. Skin test reactivity to histamine or allergen did not change throughout the trial in the placebo-treated group. Patients treated by loratadine had a significantly smaller wheal-and-flare reaction after 7 days. This effect was greater at 28 days and lasted throughout the treatment period. This study demonstrates that subsensitivity to loratadine measured by histamine and allergen skin tests does not develop during a 12-week period.
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Histamine and cysteinyl leukotrienes are pivotal mast cell mediators which contribute considerably and likely complementary to the symptoms of allergic rhinitis. Currently, we sought to explore the direct actions of histamine and leukotriene D(4) (LTD(4)), a cysteinyl leukotriene, on porcine nasal arteries and veins. We also studied combined blocks of histamine and cysteinyl leukotrienes using loratadine and montelukast in an in vivo model of allergy-mediated nasal inflammation.
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Desloratadine (descarboethoxyloratadine, CAS 100643-71-8) is an active metabolite of loratadine (CAS 79794-75-5) that exhibits qualitatively similar pharmacodynamic activity with a relative oral potency in animals 2.5-4 times greater than loratadine. Its antihistaminic effect lasts 24 h. Desloratadine was shown to be a selective H1 antagonist with more potent antihistaminic activity in vitro than either loratadine or terfenadine (CAS 50679-08-8), as indicated by its displacement of 3H-mepyramine from H1 receptors in rat brain, guinea pig brain, and guinea pig lung, and by its antagonism of histamine-induced contractions of guinea pig ileum. Antihistaminic activity and anitallergic effects also were observed in vivo. After oral administration, desloratadine was 2.5 to 4 times more potent than loratadine in protecting against histamine-induced lethality in the guinea pig and paw edema in the mouse; after topical administration, it was almost 10 times more potent in antagonizing histamine-induced increases in nasal microvascular permeability in the guinea pig. Histamine-induced changes in pulmonary resistance and compliance were also prevented by oral administration of desloratadine and loratadine in the monkey. An oral antiallergic effect was demonstrated by important reductions of acute bronchospasm in the allergic monkey and potent inhibition of allergic cough in the guinea pig. These preclinical studies provide evidence that desloratadine is an antihistaminic agent with a greater potency than loratadine and, together with results from numerous published studies, suggest an antiallergic effect of desloratadine.
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A single dose of rupatadine at four times the recommended dose is well tolerated, highly effective for up to 72 h against PAF- and histamine-induced dermal flares and has demonstrable PAF-receptor antagonism ex vivo.
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To compare the effects of 3 modem nsAHs with those of the fgAH hydroxyzine on histamine- and allergen-induced skin reactions in a controlled, double-blind, clinical trial.
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.
The inclusion criteria for all relevant randomised studies were that they should focus on people with schizophrenia or other chronic mental illnesses, with neuroleptic-induced TD and compare the use of the interventions listed above versus placebo or no intervention.
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The Kyung Hee University Hospital in Korea.
A 10-year-old Thoroughbred mare was presented with a 2.5-week history of headshaking. Based on a thorough physical examination, blood analysis, and a fine needle aspirate of an enlarged thyroid gland, a tentative diagnosis of seasonal idiopathic headshaking was made. Treatment with cyproheptadine was attempted.
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H1-receptor inhibiting drugs, namely loratadine and cetirizine, were frequently used in treatment of chronic urticaria. Urticarial weal and flare reactions, a neurogenic reflex due to neuropeptides, were reported to be more effectively inhibited by cetirizine than loratadine. The aim of this study was to determine and compare the effects of systemic loratadine and cetirizine treatments on serum levels of selected neuropeptides in chronic urticaria. Treatment groups of either systemic loratadine or cetirizine (10 mg/d), consisting of 16 and 22 patients, respectively, were included. Serum levels of stem cell factor (SCF), neuropeptide Y (NPY), calcitonin gene-related peptide (CGRP), nerve growth factor (NGF), vasoactive intestinal peptide (VIP), and substance P (SP) were detected before and after one week of treatment with antihistamines. Serum NPY and VIP levels were significantly decreased when compared before and after treatment with antihistamines (P < 0.001 and P < 0.01, respectively). SCF and NGF values were also decreased after antihistamine treatment (P < 0.05). Post-treatment levels of CGRP were significantly higher compared with pretreatment values, while no significant difference was detected between pre and post treatment levels of SP. Cetirizine was significantly more effective than loratadine on lowering serum levels of SCF among the other neuropeptides. Systemic loratadine and cetirizine treatments in patients with chronic urticaria precisely caused variations in serum levels of neuropeptides. The predominant effect of cetirizine compared to loratadine on reducing serum SCF levels might be explained with anti-inflammatory properties of cetirizine.
A gas chromatographic-mass spectrometric screening procedure is described for the identification and differentiation of the following alkylamine antihistamines and their metabolites in urine: azatadine, benzquinamide, brompheniramine, chlorphenamine, (clofedanol), cyproheptadine, dimetindene, ketotifen, mebhydroline, phenindamine, pheniramine, pyrrobutamine, terfenadine and tolpropamine. After acid hydrolysis of the conjugates, extraction and acetylation, the urine samples were analysed by computerized gas chromatography-mass spectrometry. Using ion chromatography with the selective ions m/z 58, 169, 203, 205, 230, 233, 262 and 337, the presence of alkylamine antihistamines and/or their metabolites was indicated. The identity of positive signals in the reconstructed ion chromatograms was confirmed by a visual or computerized comparison of the stored full mass spectra with the reference spectra. The ion chromatograms, reference mass spectra and gas chromatographic retention indices (OV-101) are documented. The procedure presented is integrated in a general screening procedure (general unknown analysis) for several groups of drugs.
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Rats pretreated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 10 micrograms/kg) are supersensitive to the edemagenic effects of carrageenan and dextran as indicated by the increased potency of these irritants in TCDD-treated animals compared to controls. This effect of TCDD was characterized using indomethacin, dexamethasone and a combination of cyproheptadine and pyrilamine as inhibitors of edema formation. Because TCDD increases the potency of carrageenan and dextran, it was necessary to select appropriate doses of the edemagenic irritants in order to evaluate the effect of edema inhibitors properly. At low and moderate irritant doses, TCDD-treated and control rats exhibited similar responses to inhibitory agents, suggesting that the mechanisms by which carrageenan and dextran produce edema involve the same mediators in control and TCDD-treated animals. The effect of TCDD on edema induced by bradykinin, histamine, prostaglandin E2 and serotonin, substances which are postulated endogenous mediators of carrageenan-, dextran- and/or compound 48/80-induced edemas, was also examined. Inasmuch as TCDD increased the edemagenic potency of bradykinin and histamine, but not that of prostaglandin E2 or serotonin, it was concluded that TCDD enhances carrageenan-, dextran- and compound 48/80-induced edema formation by augmenting the edemagenic activities of bradykinin and histamine. It is postulated that the mechanism of enhancement may involve TCDD-induced potentiation of the ability of bradykinin and histamine to stimulate phospholipase activity in vascular endothelial cells.
In an attempt to delineate the mechanism and the site of action of cyproheptadine and dopaminergic agonists as well as hormones including thyrotropin-releasing hormone (TRH) and hydrocortisone, the effects of these substances on ACTH secretion from corticotroph adenoma cells in culture were examined. Dispersed cells of pituitary adenomas obtained at surgery from four patients with Nelson's syndrome and one subject with Cushing's disease formed a monolayer and actively secreted ACTH into the medium. When TRH (0.1 microM) was added to the medium, a significant increase in ACTH secretion was demonstrated by adenoma cells from two patients who responded to TRH preoperatively. Moreover, a dose-response relationship between TRH concentrations and ACTH secretion was observed. Incubation of cells with cyproheptadine (1 or 0.1 microM) resulted in a significant decrease in ACTH release, and inhibited stimulation produced by TRH in one experiment. This effect of cyproheptadine was blocked when equimolar concentrations of serotonin was coincubated, whereas serotonin by itself did not affect ACTH secretion. Dopamine (0.1 microM) lowered ACTH accumulation in the medium, which was blocked by the addition of haloperidol. When hydrocortisone was added to the culture, dose-dependent suppression of ACTH secretion was demonstrated. TRH at an equimolar concentration reversed this effect, but, failed to overcome the inhibition induced by a higher concentration of hydrocortisone in cells from one adenoma studied. Cultured normal corticotrophs obtained from a patient with metastatic breast cancer, on the other hand, did not show any response to these substances, except for hydrocortisone. We suggest that TRH, cyproheptadine, dopamine affect ACTH secretion in patients with ACTH-producing pituitary adenomas by their direct action on the adenoma.
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Treatment of manifestations: Supportive care to protect the skin from blistering; use of dressings that will not further damage the skin and will promote healing of open wounds. Lance and drain new blisters. Dressings involve three layers: a primary nonadherent contact layer; a secondary layer providing stability, adding padding, and absorbing drainage; and a tertiary layer with elastic properties. Prevention of primary manifestations: Aluminum chloride (20%) applied to palms and soles can reduce blister formation in some individuals with EBS. Cyproheptadine (Periactin(®)), tetracycline, erythromycin, or botulimun toxin can reduce blistering in some individuals. Keratolytics and softening agents for palmar plantar hyperkeratosis may prevent tissue thickening and cracking. Prevention of secondary complications: Monitor for wound infection; treatment with topical and/or systemic antibiotics or silver-impregnated dressings or gels can be helpful. Nutritional support and feeding therapy may be necessary for infants and children with oral manifestations of EBS. Management of fluid and electrolyte problems in severely affected infants. Appropriate footwear and physical therapy may preserve ambulation in children who have difficulty walking because of blistering and hyperkeratosis. Surveillance: For infection and proper wound healing. Agents/circumstances to avoid: Excessive heat may exacerbate blistering and infection. Avoid poorly fitting or coarse-textured clothing/footwear and activities that traumatize the skin. Avoid ordinary medical tape or Band-Aids(®).
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The benzodiazepine nitrazepam, which has a marked hypnotic effect in human subjects and a myorelaxating effect in mice with aggressive behaviour, was applied in non-isolated and isolated non-aggressive and aggressive mice. The observed weaker inhibition of exploration behaviour is isolated mice (mice with isolation syndrome) compared with non-isolated mice suggests the significance of the functional activity of the serotoninergic system in the brain for the manifestation of the effects of the drug, since in mice with isolation syndrome the serotonin turnover is changed. The results obtained by combined application of nitrazepam with cyproheptadine suggest that nitrazepam exercises its influence partly by stimulation of the postsynaptic serotonin receptors. Combined application of nitrazepam with fenfluramine shows that serotonin and to a lesser extent the remaining neurotransmitters affected by fenfluramine play a considerable role in the mechanism of action of this benzodiasepine.
Patients are at high risk of developing serotonin-toxicity syndrome (toxidrome) when they take multiple serotonergic drugs, particularly co-administered with monoamine oxidase inhibitors or 5-hydroxytryptamine (5-HT) reuptake blockers. The toxidrome can vary from mild to severe. The primary goal of the present study was to understand the relationship between behavioral signs and degrees of toxidrome induced by 5-hydroxy-l-tryptophan (5-HTP) in clorgylinized rats. The severity was obtained by scoring behavioral signs including head shakes, penile erection, forepaw treading, hind limb abduction, Straub tail and tremor. It was found that 5-HTP produced a dose-dependent increase in degrees of the toxidrome. Furthermore, correlation between the toxidrome and changes in body-core temperature (delta Tcor) was determined. There was hypothermia in the mild toxidrome (delta Tcor<-1 degrees C), high hyperthermia in the severe toxidrome (delta Tcor>+2 degrees C) and a small change in T(cor) in the moderate toxidrome (-1 degrees C
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The majority of patient with intentional overdose had no (42.1%) or mild (40.4%) sedative symptoms. Some 17% of patients developed anticholinergic symptoms, such as delirium, agitation, disorientation, and hallucination. The mean dose ingested was found to be significantly higher in patients who presented with delirium (188.6 mg) than those who were asymptomatic (49.8 mg) (p < 0.001). The time of symptom onset in all symptomatic patients was less than 6 h.
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Mizolastine provides effective symptom relief in PAR together with a satisfactory safety profile. Improvement with mizolastine was significantly greater than placebo throughout the study despite a large placebo effect. Also mizolastine's effects were greater those observed with loratadine after 2 weeks of treatment.
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Radioactivity was excreted in the urine and feces of rats, mice, and humans after a dose of 14C-cyproheptadine. The major metabolite in rat urine was unconjugated, but the majority of radioactive materials in mouse and human urine were conjugated with glucuronic acid. Identification of the rat urinary metabolite of cyproheptadine as an epoxide was accomplished with mass spectrometry and other methods. The rat metabolite was 10.11 -epoxydesmethylcyproheptadine and accounted for about 25% of a 45-mg dose of cyproheptadine per kg. Only a small amount of this epoxide was found in mouse urine, and none was apparent in the urine of two humans who received 5 mg of the drug. Dihydrodiols, which could arise by epoxide hydrase hydrolysis of possible 10.11-epoxy metabolites, were not found in the urine of any of the species studied. The spoxide found in rat urine appears to be unusually stable to in vivo hydrolysis. Possible implications of these results in the species-selective pancreotoxicity of cyproheptadine in the rat are presented.
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The interaction of mizolastine (CAS 108612-45-9, SL 85.0324) with histamine H1 receptors has been evaluated in the rodent. Mizolastine inhibited with high affinity (IC50 = 47 nmol/l) the binding of [3H]pyrilamine to histamine H1 receptors in guinea pig cerebellar membranes and sections. The order of potency of mizolastine and various H1 antagonists in this binding assay was the following: cyproheptadine > pyrilamine > mequitazine > mizolastine > astemizole > terfenadine > cetirizine > loratadine. Mizolastine also potently antagonized the contractile effects of histamine in the guinea pig ileum (pA2 = 8.5) and histamine-induced stimulation of phosphoinositide turnover in rat cortical slices (IC50 = 0.35 mumol/l). In contrast, this compound displayed very low affinity for serotonergic, noradrenergic and muscarinic cholinergic receptors as evidenced in both binding assays and functional tests. In guinea pig cerebellar membranes, [3H]mizolastine labelled in a saturable and reversible manner a single population of binding sites with Kd and Bmax values of 1.1 nmol/l and 635 fmol/mg protein, respectively. [3H]Mizolastine binding in guinea pig cerebellar membranes was inhibited by histamine (IC50 = 30 mumol/l) and by drugs that possess affinity for the H1 receptor such as pyrilamine (IC50 = 1 nmol/1), DL-chlorphenyramine (IC50 = 6.4 nmol/l) terfenadine (IC50 = 6 nmol/l) and loratadine (IC50 = 50 nmol/l). At concentrations lower than 10 mumol/l, the H2 receptor ligands dimaprit and cimetidine and the H3 receptor ligands burimamide and 4-methyl-histamine failed to displace [3H]mizolastine binding.(ABSTRACT TRUNCATED AT 250 WORDS)