To see the other types of publications on this topic, follow the link: Serotonin Antihistamines.
Journal articles on the topic 'Serotonin Antihistamines'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 26 journal articles for your research on the topic 'Serotonin Antihistamines.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Dukhanin, Alexander S. "Pharmacological profile of antihistamines: focus on unwanted drug interactions." Russian Journal of Allergy 17, no. 4 (January 29, 2021): 46–56. http://dx.doi.org/10.36691/rja1407.
Full textAbstract:
Differences between individual antihistamines are determined by such pharmacokinetic properties as the rate and completeness of absorption, half-life, the participation of hepatic and renal mechanisms of elimination from the body. Pharmacodynamic features of the antihistamine include selectivity and affinity for histamine H1-receptors and the presence of central effects. The mechanisms of the development of unwanted drug interactions with second-generation antihistamines are analyzed in detail. Three levels of interaction have been identified: 1) hepatic enzymes of the P450 system; 2) membrane carriers of organic anions (OATP) transport proteins on the sinusoidal membrane of hepatocytes and the luminal membrane of the epithelium of the proximal nephron tubule; 3) P-glycoprotein (Pgp, ABCB1-protein) of epithelial cells of the small intestine the area of absorption of oral forms of antihistamines, the epithelium of the proximal tubule and the BBB (blood-brain barrier). The emphasis is made on the description of the dependence of the pharmacological profile of antihistamines on its chemical structure. The elasticity of the bilastine molecule, the ability to induce a change in conformation underlies the high complementarity of bilastine to the recognition site of the H1-receptor which is a high affinity. Experimental evaluation confirms this conclusion: the dissociation constant (Dс) of the bilastin-receptor complex is in the nM concentration range. The bilastine molecule, as a representative of antihistamines with zwitterionic properties, carries both a positive and a negative charge at a physiological pH, making it difficult for its penetration into the brain. The peculiarities of the chemical nature of the bilastine molecule are reflected in the specific pharmacological profile of AGP. In vitro studies have shown a high specific affinity of bilastine for H1-receptors with a very low affinity for other histamine receptors (H2, H3, H4), serotonin, bradykinin, muscarinic and adrenergic receptors). According to this indicator, bilastine is 3 times higher than cetirizine and 5 times higher than fexofenadine. Bilastine is practically not metabolized in the body and is excreted mainly unchanged, and also does not have a cardiotoxic effect. Bilastine is well tolerated; as a therapeutic dose it has a less pronounced sedative potential compared to other second-generation antihistamines.
2
Winters, Tammy A., and Barbara L. Slifer. "Discriminative stimulus properties of antihistamines may involve mediation by serotonin." Pharmacology Biochemistry and Behavior 32, no. 4 (April 1989): 1087. http://dx.doi.org/10.1016/0091-3057(89)90127-5.
Full text
3
Yeh, S. Y., C. Dersch, R. Rothman, and J. L. Cadet. "Effects of antihistamines on 3,4-methylenedioxymethamphetamine-induced depletion of serotonin in rats." Synapse 33, no. 3 (September 1, 1999): 207–17. http://dx.doi.org/10.1002/(sici)1098-2396(19990901)33:3%3c207::aid-syn5%3e3.0.co;2-8.
Full text
4
Yeh, S. Y., C. Dersch, R. Rothman, and J. L. Cadet. "Effects of antihistamines on 3,4-methylenedioxymethamphetamine-induced depletion of serotonin in rats." Synapse 33, no. 3 (September 1, 1999): 207–17. http://dx.doi.org/10.1002/(sici)1098-2396(19990901)33:3<207::aid-syn5>3.0.co;2-8.
Full text
5
Tobback, Els, Olivier Desmet, Ignace Hanoulle, Liesbeth Delesie, Dirk Pevernagie, Dirk Vogelaers, and An Mariman. "Retrospective Analysis of Risk Factors for Periodic Limb Movements in a Large Cohort of Insomnia and Chronic Fatigue Patients." Pharmacopsychiatry 53, no. 02 (August 27, 2019): 71–77. http://dx.doi.org/10.1055/a-0991-0498.
Full textAbstract:
Abstract Introduction Although the pathophysiology of periodic limb movements in sleep (PLMS) is not well understood, there is increasing belief that management of PLMS can modulate humans’ general health. The aim of this study is to investigate the associations between risk factors including the use of antidepressants, hypnotics, and antihistamines as well as of caffeine, alcohol, and nicotine and the occurrence of PLMS and periodic limb movement disorder (PLMD). Methods Patients with either chronic fatigue or insomnia who underwent polysomnography as standardized clinical assessment were included in a retrospective study. Associations were calculated between substance use and sleep variables. Results Tricyclic antidepressants and serotonin and norepinephrine reuptake inhibitor (SNRI) are significantly associated with higher rates of PLMS. Additionally, SNRI is significantly positive associated with PLMD, as also seen for selective serotonin reuptake inhibitors (SSRI). The most frequently used SSRI escitalopram was significantly positively associated with PLMS and PLMD. A significantly negative association was found between paroxetine and PLMS. Benzodiazepines are negatively associated with PLMS and PLMD. Sedative antidepressants, antihistamines, and substance use are not associated with PLMS nor PLMD in this study. Discussion This retrospective study adds supportive evidence to the association of drug classes with PLMS and PLMD. These findings may impact on clinical management of patients with a combined anxiety or mood disorder in need for these drug classes on the one hand and a significant sleep architecture disturbance through PLMS, potentially contributing to daytime symptoms, on the other hand.
6
Wauwe, J. P., and J. G. Goossens. "Arabinogalactan- and dextran-induced ear inflammation in mice: Differential inhibition by H1-antihistamines, 5-HT-serotonin antagonists and lipoxygenase blockers." Agents and Actions 28, no. 1-2 (August 1989): 78–82. http://dx.doi.org/10.1007/bf02022984.
Full text
7
Lader, Malcolm. "Fluoxetine Efficacy vs Comparative Drugs: An Overview." British Journal of Psychiatry 153, S3 (September 1988): 51–58. http://dx.doi.org/10.1192/s0007125000297298.
Full textAbstract:
The tricyclic antidepressants (TCAs) were discovered accidentally by pharmaceutical chemists seeking first, better antihistamines and then antipsychotic agents. Careful clinical assessment revealed the antidepressant properties and suggested that the closer the patient resembled the classical textbook description of ‘endogenous’ depression, the more likely was an adequate clinical response to occur (Kuhn, 1958). However, it was quickly realised that the TCAs possess a plethora of side-effects, particularly sedation and symptoms related to their anticholinergic effects.Despite much research over the past 25 years, it is unclear how TCAs effect clinical improvement. The two main neurotransmitters involved in some way are noradrenaline (Schildkraut, 1965) and 5-hydroxytryptamine (5-HT; serotonin; Van Praag, 1977). It was proposed that TCAs acted by blocking the reuptake of one or other or both of these neurotransmitters, thereby increasing their concentration in the synaptic cleft. However, as well as these acute effects, chronic effects, such as a decrease in the number of central beta-adrenoceptors (‘down-regulation’) occur, and these are probably more relevant to the clinical action.
8
Zamergrad, M. V., and S. V. Morozova. "Modern approaches to drug treatment for vestibular vertigo." Neurology, Neuropsychiatry, Psychosomatics 13, no. 1 (February 18, 2021): 101–6. http://dx.doi.org/10.14412/2074-2711-2021-1-101-106.
Full textAbstract:
In recent years, some progress has been achieved in elaborating the algorithms and standards for the treatment of many conditions accompanied by vertigo. The current possibilities of treating vestibular vertigo consist of a gradually expanding arsenal of symptomatic and pathogenetic drugs. Among the drugs used for the symptomatic treatment of vestibular vertigo, there are vestibular suppressants (antihistamines, benzodiazepines, and calcium antagonists) and antiemetics (dopamine antagonists and serotonin 5-HT3 receptor antagonists). The paper discusses the possibilities of using betahistine and vitamin D as pathogenetic agents for recurrent benign paroxysmal positional vertigo; diuretics, betahistine (including the new prolonged release formulation Betaserc® Long), glucocorticoids, and gentamicin for Meniere's disease; triptans, beta-blockers, tricyclic antidepressants, and anticonvulsants for vestibular migraine; glucocorticoids, antiviral agents, and drugs that accelerate vestibular compensation for acute unilateral peripheral vestibulopathy (vestibular neuritis and Ramsey Hunt syndrome).The emergence of new drugs, as well as the design of new dosage forms that enhance patient adherence to the prescribed treatment, can improve quality of life in patients suffering from diseases that have recently led to long-term disability or even incapacitation.
9
Leslie, R. A., Y. Shah, M. Thejomayen, K. M. Murphy, and H. A. Robertson. "The neuropharmacology of emesis: the role of receptors in neuromodulation of nausea and vomiting." Canadian Journal of Physiology and Pharmacology 68, no. 2 (February 1, 1990): 279–88. http://dx.doi.org/10.1139/y90-042.
Full textAbstract:
The basic pharmacological mechanisms involved in mediating nausea and vomiting are still poorly understood. Several classes of drags have been identified that alleviate the symptoms of nausea and vomiting, either prophylactically or acutely. None of these is completely effective in all cases. They include antihistamines, dopamine antagonists, steroids, cannabinoids, benzodiazepines, serotonin antagonists, and anticholinergics. This paper examines the evidence that links each of these classes of drugs with the distribution of specific neurotransmitter receptor sites on which they may be acting. Studies on the central nervous system distribution of binding sites for one of these classes of drugs, the anticholinergics, are described. Binding sites for the muscarinic cholinergic radioligand [3H]quinuclidinyibenzilate occur in different concentrations throughout the dorsal vagal complex of the rabbit medulla oblongata. The distribution of such sites in this nonvomiting experimental animal is markedly different from that in the cat, an animal that has been used for many physiological and pharmacological studies of emesis. A previous study has suggested that muscarinic binding sites may occur presynaptically on vagal afferent terminals that synapse in the dorsal vagal complex of the cat; this appears not to be the case in the rabbit. Possible implications of these findings for the identification of the site of action of anticholinergic, antiemetic drags are discussed.Key words: neuromodulation, nausea, vomiting, receptors.
10
Bartley, Jim. "Nasal Congestion and Hyperventilation Syndrome." American Journal of Rhinology 19, no. 6 (November 2005): 607–11. http://dx.doi.org/10.1177/194589240501900614.
Full textAbstract:
Background This article evaluates the prevalence of hyperventilation syndrome (HVS) in patients who continue to complain of ongoing nasal congestion, despite an apparently adequate surgical result and appropriate medical management. Methods Prospective case series of 14 patients from June 2002 to October 2003 was performed. Patients, who presented complaining of nasal congestion after previous nasal surgery and who appeared to have an adequate nasal airway with no evidence of nasal valve collapse, were evaluated for HVS. When appropriate, nasal steroids and oral antihistamines also had been tested without success. Three patients had end-tidal PCO2 levels measured and five patients underwent breathing reeducation. Results All patients had an elevated respiratory rate (>18 breaths/minute) with an upper thoracic breathing pattern. Twelve of the 14 patients complaining of nasal obstruction had an elevated Nijmegen score indicative of HVS. An average number of 2.5 procedures had been performed on each patient. End-tidal PCO2 levels were ≤35 mmHg in the three patients who had expired PCO2 levels measured. Breathing retraining was successful in correcting the nasal congestion in two of five patients. Conclusion HVS should be included in the differential diagnosis of patients presenting with nasal congestion, particularly after failed nasal surgery. One possible explanation is increased nasal resistance secondary to low arterial PCO2 levels. Another possible explanation is reduced alae nasae muscle activity secondary to the reduced activity of serotonin-containing raphe neurons. Additional surgery may not necessarily be the answer in HVS patients complaining of nasal congestion.
11
Stewart, David J. "Cancer therapy, vomiting, and antiemetics." Canadian Journal of Physiology and Pharmacology 68, no. 2 (February 1, 1990): 304–13. http://dx.doi.org/10.1139/y90-045.
Full textAbstract:
Both radiotherapy and chemotherapy for cancer are capable of causing nausea and vomiting. With both treatment modalities, the nausea and vomiting is thought to be a second-order process rather than being due to direct stimulation of neuromechanisms that control vomiting. Both a peripheral (gastrointestinal tract) and central (chemoreceptor trigger zone) effect may be operating with both radiotherapy- and chemotherapy-induced vomiting. With radiotherapy, gastrointestinal toxicity is affected by the type of radiation, radiation dose and field size, fractionation schedule, individual patient factors, and the part of the patient that is radiated. Many different factors also influence the frequency and severity of nausea and vomiting following chemotherapy. With both radiotherapy and chemotherapy, the frequency and severity of nausea and vomiting is probably mediated by a reduction in breakdown of various neurotransmitters. It is presumed that as the levels of neurotransmitters increase, nausea and vomiting develop. Antagonists of these neurotransmitters may afford some antiemetic protection. Nausea and vomiting may be so severe in patients with cancer that they may refuse potentially curative therapy because of it. Anticipatory nausea and vomiting may develop in patients who have become quite sick after receiving treatment. Exposure to stimuli associated with the emetogenic agent is then sufficient to trigger nausea and vomiting. Standard antiemetics do not help anticipatory nausea and vomiting, although behavioural training may. A variety of different drugs have proven useful as antiemetics, including dopamine antagonists such as phenothiazines, metoclopramide, corticosteroids (dexamethasone and methylprednisolone), cannabinoids, and benzodiazapines. Antihistamines and anticholinergics are of value in some situations. New serotonin antagonists appear to be very promising and are currently undergoing clinical studies. Multiagent antiemetic regimens appear to be more effective than single agent regimens in some situations.Key words: nausea/vomiting, cancer, chemotherapy, radiotherapy, antiemetics.
12
Driban, Jeffrey B., Grace H. Lo, Charles B. Eaton, Kate L. Lapane, Michael Nevitt, William F. Harvey, Charles E. McCulloch, and Timothy E. McAlindon. "Exploratory analysis of osteoarthritis progression among medication users: data from the Osteoarthritis Initiative." Therapeutic Advances in Musculoskeletal Disease 8, no. 6 (September 16, 2016): 207–19. http://dx.doi.org/10.1177/1759720x16664323.
Full textAbstract:
Background: We conducted an exploratory analysis of osteoarthritis progression among medication users in the Osteoarthritis Initiative to identify interventions or pathways that may be associated with disease modification and therefore of interest for future clinical trials. Methods: We used participants from the Osteoarthritis Initiative with annual medication inventory data between the baseline and 36-month follow-up visit ( n = 2938). Consistent medication users were defined for each medication classification as a participant reporting at all four annual visits that they were regularly using an oral prescription medication at the time of the visit. The exploratory analysis focused on medication classes with 40 or more users. The primary outcome measures were medial tibiofemoral joint space width change and the Western Ontario and McMaster Universities Arthritis Index (WOMAC) knee pain score change (12–36-month visits). Within each knee, we explored eight comparisons between users and matched or unmatched nonusers (defined two ways). An effect size of each comparison was calculated. Medication classes had potential signals if (a) both knees had less progression among users compared with nonusers, or (b) there was less progression based on structure and symptoms in one knee. Results: We screened 28 medication classes. Six medication classes had signals for fewer structural changes and better knee pain changes: alpha-adrenergic blockers, antilipemic (excluding statins and fibric acid), anticoagulants, selective serotonin reuptake inhibitors, antihistamines, and antineoplastic agents. Four medication classes had signals for structural changes alone: anti-estrogen (median effect size = 0.28; range = −0.41–0.64), angiotensin-converting enzyme inhibitors (median effect size = 0.13; range = −0.08–0.28), beta-adrenergic blockers (median effect size = 0.09; range = 0.01–0.30), and thyroid agents (median effect size = 0.04; range = −0.05–0.14). Thiazide diuretics had evidence for symptom modification (median effect size = −0.12; range = −0.24–0.04). Conclusions: Users of neurovascular, antilipemic, or hormonal interventions may have less disease progression compared with nonusers.
13
Dainiak, Nicholas, Robert Nicolas Gent, Zhanat Carr, Rita Schneider, Judith Bader, Elena Buglova, Nelson Chao, et al. "Literature Review and Global Consensus on Management of Acute Radiation Syndrome Affecting Nonhematopoietic Organ Systems." Disaster Medicine and Public Health Preparedness 5, no. 3 (October 2011): 183–201. http://dx.doi.org/10.1001/dmp.2011.73.
Full textAbstract:
ABSTRACTObjectives:The World Health Organization convened a panel of experts to rank the evidence for medical countermeasures for management of acute radiation syndrome (ARS) in a hypothetical scenario involving the hospitalization of 100 to 200 victims. The goal of this panel was to achieve consensus on optimal management of ARS affecting nonhematopoietic organ systems based upon evidence in the published literature.Methods:English-language articles were identified in MEDLINE and PubMed. Reference lists of retrieved articles were distributed to conferees in advance of and updated during the meeting. Published case series and case reports of ARS, publications of randomized controlled trials of relevant interventions used to treat nonirradiated individuals, reports of studies in irradiated animals, and prior recommendations of subject matter experts were selected. Studies were extracted using the Grading of Recommendations Assessment Development and Evaluation system. In cases in which data were limited or incomplete, a narrative review of the observations was made.Results:No randomized controlled trials of medical countermeasures have been completed for individuals with ARS. Reports of countermeasures were often incompletely described, making it necessary to rely on data generated in nonirradiated humans and in experimental animals. A strong recommendation is made for the administration of a serotonin-receptor antagonist prophylactically when the suspected exposure is >2 Gy and topical steroids, antibiotics, and antihistamines for radiation burns, ulcers, or blisters; excision and grafting of radiation ulcers or necrosis with intractable pain; provision of supportive care to individuals with neurovascular syndrome; and administration of electrolyte replacement therapy and sedatives to individuals with significant burns, hypovolemia, and/or shock. A strong recommendation is made against the use of systemic steroids in the absence of a specific indication. A weak recommendation is made for the use of fluoroquinolones, bowel decontamination, loperamide, and enteral nutrition, and for selective oropharyngeal/digestive decontamination, blood glucose maintenance, and stress ulcer prophylaxis in critically ill patients.Conclusions:High-quality studies of therapeutic interventions in humans exposed to nontherapeutic radiation are not available, and because of ethical concerns regarding the conduct of controlled studies in humans, such studies are unlikely to emerge in the near future.(Disaster Med Public Health Preparedness. 2011;5:183–201)
14
Garnis-Jones, Sylvia, Stephen Collins, and Donald Rosenthal. "Treatment of Self-Mutilation with Olanzapine." Journal of Cutaneous Medicine and Surgery 4, no. 3 (July 2000): 160–62. http://dx.doi.org/10.1177/120347540000400310.
Full textAbstract:
Background: Self-mutilation or dermatitis artefacta is a facet of a much broader spectrum of factitial disease. Three nonpsychotic patients with self-mutilation are presented in this article who were successfully treated with low dose olanzapine when all other modalities of therapy had failed, including trials with numerous antidepressants and antipsychotics. Objective: The patients were simultaneously evaluated and treated by a dermatologist and a psychiatrist who run the psychodermatology or consultation-liaison clinic based at McMaster University. After dermatologic conditions had been excluded as a cause of the clinical findings, olanzapine was prescribed on a trial basis due to its low risk of parkinsonian side-effects and its antihistaminic properties. Conclusions: The excellent clinical response of the patients can be attributed to the low side-effect profile of the drug but also to the anti-impulsive effect which stems not only from antihistaminic properties but also from its anti-dopamine and serotonin-blocking action.
15
Lodise, T. P., N. Patel, A. Rivera, L. Tristani, V. Lazariu, H. Vandewall, and L. A. McNutt. "Comparative Evaluation of Serotonin Toxicity among Veterans Affairs Patients Receiving Linezolid and Vancomycin." Antimicrobial Agents and Chemotherapy 57, no. 12 (September 16, 2013): 5901–11. http://dx.doi.org/10.1128/aac.00921-13.
Full textAbstract:
ABSTRACTDespite the theoretical risk of serotonin toxicity (ST) with linezolid, “real-world” clinical evaluations of the risk of ST in patients receiving linezolid have been limited to case reports and noncomparator studies. An observational, matched-cohort study was conducted to evaluate the risk of ST among hospitalized patients who received linezolid or vancomycin at the Upstate New York Veterans Affairs Healthcare Network (Veterans Integrated Service Network 2 [VISN-2]). Matching criteria included VISN-2 hospital, hospital ward, prior hospital length of stay, age, and baseline platelet counts. The patients' electronic medical records were evaluated for symptoms consistent with ST and the Hunter serotonin toxicity criteria (HSTC) using an intensive, natural word search algorithm. The study included 251 matched pairs. Demographics and comorbidities were similar between groups. Over half of the study population received at least one concurrent medication with serotonergic activity. Receipt of agents with serotonergic activity was more pronounced in the vancomycin group, and the higher frequency was due to concomitant antihistamine and antiemetic use. Antidepressant use, including selective serotonin reuptake inhibitors (SSRIs), was similar between groups. No patients in either group were found to meet the criteria using the word search algorithm for ST. Fewer linezolid patients than vancomycin patients met the HSTC overall (3.2% versus 8.8%) and when stratified by receipt of a concurrent serotonergic agent (4.3% versus 12.4%). Of the patients meeting the HSTC, most had past or present comorbidities that may have contributed to or overlapped the HSTC. This study of hospitalized patients revealed comparably low frequencies of adverse events potentially related to ST among patients who received linezolid or vancomycin.
16
Ho, C. L., and L. L. Hwang. "Structure and biological activities of a new mastoparan isolated from the venom of the hornet Vespa basalis." Biochemical Journal 274, no. 2 (March 1, 1991): 453–56. http://dx.doi.org/10.1042/bj2740453.
Full textAbstract:
By gel filtration on a Fractogel TSK HW 50 column followed by cation-exchange chromatography on CM-Trisacryl M, a tetradecapeptide amide, designated ‘mastoparan B’, was purified from the venom of the hornet Vespa basalis. Its amino acid sequence was determined as: Leu-Lys-Leu-Lys-Ser-Ile-Val-Ser-Trp-Ala-Lys-Lys-Val-Leu-NH2 and its molecular mass was measured to be 1611 Da by fast-atom-bombardment mass spectrometry. In addition to having a common structure of vespid mastoparans, the peptide shows a less hydrophobic sequence at positions 1, 2, 5, 8 and 9. The peptide caused liberation of histamine from rat peritoneal mast cells and induced oedema in the rat paw. However, the latter effect was inhibited by ‘anti-serotonin’ (anti-5-hydroxytryptamine) (cyproheptadine), but not by antihistamine (chlorpheniramine). The peptide also possesses a potent haemolytic activity which acts in synergy with the lethal protein of the venom, suggesting the possible involvement of mastoparan B in the lethal effect of Vespa basalis venom.
17
Tanaka, Satoshi, Katsuya Deai, Mariko Inagaki, and Atsushi Ichikawa. "Uptake of histamine by mouse peritoneal macrophages and a macrophage cell line, RAW264.7." American Journal of Physiology-Cell Physiology 285, no. 3 (September 2003): C592—C598. http://dx.doi.org/10.1152/ajpcell.00470.2002.
Full textAbstract:
We have previously demonstrated that dietary histamine is accumulated in the spleens of l-histidine decarboxylase (HDC)-deficient mice, which lack endogenous histamine synthesis. To characterize the clearance system for dietary histamine in mice, we investigated the cell type and mechanism responsible for histamine uptake in the spleens of HDC-deficient mice. Immunohistochemical analyses using an antihistamine antibody indicated that a portion of the CD14+cells in the spleen is involved in histamine storage. Peritoneal macrophages obtained from Balb/c mice and a mouse macrophage cell line, RAW264.7, had potential for histamine uptake, which was characterized by a low affinity and high capacity for histamine. The histamine uptake by RAW264.7 cells was observed at physiological temperature and was potently inhibited by pyrilamine, chlorpromazine, quinidine, and chloroquine, moderately inhibited by Nα-methylhistamine, dopamine, and serotonin, and not affected by tetraethylammonium and 1-methyl-4-phenylpyridinium. Intracellular histamine was not metabolized in RAW264.7 cells and was released at physiological temperature in the absence of extracellular histamine. These results suggest that histamine uptake by macrophages may be involved in the clearance of histamine in the local histamine-enriched environment.
18
Varsha, Ahirwar, Khushwant S. Yadav, and Shailendra Bindaiya. "Formulation Development and Evaluation of Fast Dissolving Films of Oloptadine HCl." Asian Journal of Research in Pharmaceutical Sciences 11, no. 2 (May 10, 2021): 103–8. http://dx.doi.org/10.52711/2231-5659.2021-11-2-2.
Full textAbstract:
Our studies on the performance of formulation development and evaluation of fast dissolving films of Oloptadine HCL its anti-allergic drug. Prepare mouth dissolving film of Oloptadine HCl by solvent casting method. To characterize the prepared mouth dissolving film of Oloptadine HCL in terms of— Thickness, percent elongation, tack test, swelling index, in-vitro disintegration time and dissolution test. Oloptadine OLO), 11-[{z}-3-(Dimethlamino) propylidene]-6-11-dihydrobenz [b, e] oxepin-2-acetic acid hydrochloride, is widely used as an antihistaminic. Oloptadine HCL is a relatively selective histamine H1-receptor antagonist that inhibits the release of histamine from mast cells. Oloptadine does not affect alpha-adrenergic dopamine, muscarinic type 1 and 2 or serotonin receptor. They are hydrophobic in nature and non-polar, sparingly soluble in water and freely soluble methanol, ethanol. Olopatadine HCl is a mouth dissolving film. We is trying to sort out the problem of allergic. They are rapidly onset of action, when placed upon the tongue that it is disperse rapidly swallowing within 3-5 seconds without need of water or chewing.
19
Mao, Xinliang, Sheng-ben Liang, Rose Hurren, Marcela Gronda, Sue Chow, G. Wei Xu, Xiaoming Wang, et al. "Cyproheptadine displays preclinical activity in myeloma and leukemia." Blood 112, no. 3 (August 1, 2008): 760–69. http://dx.doi.org/10.1182/blood-2008-02-142687.
Full textAbstract:
Abstract D-cyclins are regulators of cell division that act in a complex with cyclin-dependent kinases to commit cells to a program of DNA replication. D-cyclins are overexpressed in many tumors, including multiple myeloma and leukemia, and contribute to disease progression and chemoresistance. To better understand the role and impact of D-cyclins in hematologic malignancies, we conducted a high throughput screen for inhibitors of the cyclin D2 promoter and identified the drug cyproheptadine. In myeloma and leukemia cells, cyproheptadine decreased expression of cyclins D1, D2, and D3 and arrested these cells in the G0/G1 phase. After D-cyclin suppression, cyproheptadine induced apoptosis in myeloma and leukemia cell lines and primary patient samples preferentially over normal hematopoietic cells. In mouse models of myeloma and leukemia, cyproheptadine inhibited tumor growth without significant toxicity. Cyproheptadine-induced apoptosis was preceded by activation of the mitochondrial pathway of caspase activation and was independent of the drug's known activity as an H1 histamine and serotonin receptor antagonist. Thus, cyproheptadine represents a lead for a novel therapeutic agent for the treatment of malignancy. Because the drug is well tolerated and already approved in multiple countries for clinical use as an antihistamine and appetite stimulant, it could be moved directly into clinical trials for cancer.
20
Weisshaar, E., N. Dunker, U. Domröse, K. H. Neumann, and H. Gollnick. "Plasma serotonin and histamine levels in hemodialysis-related pruritus are not significantly influenced by 5-HT3 receptor blocker and antihistaminic therapy." Clinical Nephrology 59, no. 02 (February 1, 2003): 124–29. http://dx.doi.org/10.5414/cnp59124.
Full text
21
Chandrashekar, Kodangala Subraya, Kodangala Subraya Prasanna, and Borthakur Abinash. "Anti-inflammatory effect of the methanol extract from Anthocephalus cadamba stem bark in animal models." International Journal of Plant Biology 1, no. 1 (February 17, 2010): 6. http://dx.doi.org/10.4081/pb.2010.e6.
Full textAbstract:
Background:<em> Anthocephalus cadamba </em>(Rebox)Miq. (Rubiaceae) is widely distributed throughout the greater part of India, especially at low levels in wet place. Traditionally the bark is used as tonic, febrifuge and to reduce the pain and inflammation. The anti-inflammatory effect of methanol extract obtained from <span style="font-style: italic;"> Anthocephalus cadamba </span> aerial parts, MEAC, were investigated in this study. Design and methods: The effects of MEAC on the acute and chronic phases of inflammation were studied in carrageenan, dextran and mediators (histamine and serotonin) induced paw edema and cotton pallet-induced granuloma, respectively. The anti-edema effect of MEAC was compared with 10 mg/kg of indomethacin orally. Results: The results suggested that MEAC possess potent anti-inflammatory activity. The acute inflammatory model showed that all the doses of MEAC effectively suppressed the edema produced by histamine, so it may be suggested that its anti-inflammatory activity is possibly backed by its antihistaminic activity. In chronic inflammatory model the effect may be due to the cellular migration to injured sites and accumulation of collagen and mucopolysaccharide. Conclusions: On the basis of these findings, it may be inferred that <span style="font-style: italic;"> Anthocephalus cadamba </span> is an anti-inflammatory agent and the results are in agreement with its traditional use.
22
Ananth, Jambur, Kamala Aduri, Sharath Parameswaran, and Sarath Gunatilake. "Neuroleptic malignant syndrome: risk factors, pathophysiology, and treatment." Acta Neuropsychiatrica 16, no. 4 (August 2004): 219–28. http://dx.doi.org/10.1111/j.0924-2708.2004.00085.x.
Full textAbstract:
Neuroleptic malignant syndrome (NMS) is associated with the administration of antipsychotic agents and other drugs such as l-dopa, antidepressants, and antihistaminic agents. Unexpected changes in mental status, new-onset catatonia, episodic tachycardia, tachypnea, hypertension, dysarthria, dysphagia, diaphoresis, sialorrhea, incontinence, low-grade temperature elevations, and rigidity should arouse suspicion. Several lines of evidence provide support for the involvement of dopamine. Most of the drugs implicated in NMS are D2 dopamine receptor antagonists. Central noradrenergic activity is also possibly related to the disorder, as sympathetic hyperactivity is associated with the active phase of NMS. Currently, the definitive role of GABA deficiency in NMS is yet to be established. Differential diagnosis should include malignant hyperthermia, lethal catatonia, lithium toxicity, serotonin syndrome, and heat stroke. A high degree of suspicion and the discontinuation of antipsychotic agents even if the diagnosis is not established are essential for the safety of the patient. Treatment of NMS should be individualized and be based empirically on the character, duration, and severity of the clinical signs and symptoms noted. The initial step in the treatment of NMS is the removal of the offending agent. Full-blown NMS is a serious condition and requires immediate supportive, nutritive, and electrolyte therapies. The administration of drugs that can improve NMS, such as IV dantrolene and/or oral bromocriptine, may also be taken into consideration, based on the severity and nature of the NMS.
23
Yoshikawa, Yoshito, Yoshinobu Matsuda, Sachiko Okayama, Juri Nimura, Minako Doi, and Shinobu Nagata. "A Case of Obstructive Jaundice-associated Pruritus Which Was not Improved by an Antihistamine and a Selective Serotonin Reuptake Inhibitor Treatment, but Was Responded to Nalfurafine Hydrochloride." Palliative Care Research 12, no. 1 (2017): 506–10. http://dx.doi.org/10.2512/jspm.12.506.
Full text
24
Werda, Ines, Jihene Feki, Souhir Khemiri, Wala Ben Kridis, and Afef Khanfir. "A case of severe paraneoplastic itch resistant to antihistamines and responding to serotonin reuptake inhibitors." Clinical Case Reports 9, no. 7 (July 2021). http://dx.doi.org/10.1002/ccr3.4279.
Full text
25
Garakani, Amir, James W. Murrough, Rafael C. Freire, Robyn P. Thom, Kaitlyn Larkin, Frank D. Buono, and Dan V. Iosifescu. "Pharmacotherapy of Anxiety Disorders: Current and Emerging Treatment Options." Frontiers in Psychiatry 11 (December 23, 2020). http://dx.doi.org/10.3389/fpsyt.2020.595584.
Full textAbstract:
Anxiety disorders are the most prevalent psychiatric disorders and a leading cause of disability. While there continues to be expansive research in posttraumatic stress disorder (PTSD), depression and schizophrenia, there is a relative dearth of novel medications under investigation for anxiety disorders. This review's first aim is to summarize current pharmacological treatments (both approved and off-label) for panic disorder (PD), generalized anxiety disorder (GAD), social anxiety disorder (SAD), and specific phobias (SP), including selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), azapirones (e.g., buspirone), mixed antidepressants (e.g., mirtazapine), antipsychotics, antihistamines (e.g., hydroxyzine), alpha- and beta-adrenergic medications (e.g., propranolol, clonidine), and GABAergic medications (benzodiazepines, pregabalin, and gabapentin). Posttraumatic stress disorder and obsessive-compulsive disorder are excluded from this review. Second, we will review novel pharmacotherapeutic agents under investigation for the treatment of anxiety disorders in adults. The pathways and neurotransmitters reviewed include serotonergic agents, glutamate modulators, GABAergic medications, neuropeptides, neurosteroids, alpha- and beta-adrenergic agents, cannabinoids, and natural remedies. The outcome of the review reveals a lack of randomized double-blind placebo- controlled trials for anxiety disorders and few studies comparing novel treatments to existing anxiolytic agents. Although there are some recent randomized controlled trials for novel agents including neuropeptides, glutamatergic agents (such as ketamine and d-cycloserine), and cannabinoids (including cannabidiol) primarily in GAD or SAD, these trials have largely been negative, with only some promise for kava and PH94B (an inhaled neurosteroid). Overall, the progression of current and future psychopharmacology research in anxiety disorders suggests that there needs to be further expansion in research of these novel pathways and larger-scale studies of promising agents with positive results from smaller trials.
26
Hu, B., Y. Kuang, Y. Jing, Y. Li, H. Zhao, and H. Ouyang. "Pediatric allergic rhinitis with functional gastrointestinal disease: Associations with the intestinal microbiota and gastrointestinal peptides and therapeutic effects of interventions." Human & Experimental Toxicology, May 21, 2021, 096032712110173. http://dx.doi.org/10.1177/09603271211017325.
Full textAbstract:
Children are susceptible to allergic rhinitis (caused by external allergens) accompanied by functional gastrointestinal disease, which seriously affects physical and mental health. Antihistamines and nasal spray hormones are commonly used in clinical treatment, but these drugs often have unsatisfactory efficacy and result in high recurrence rates. Therefore, understanding the pathogenesis of allergic rhinitis with functional gastrointestinal disease and seeking safer treatment and prevention methods is essential. Herein, molecular ecology and immunoassays were used to analyze correlations between pediatric allergic rhinitis with functional gastrointestinal disease and both the intestinal microbiota and gastrointestinal peptide levels. Fifty healthy children (healthy group) and 80 children with allergic rhinitis with functional gastrointestinal disease (case group: evenly divided into a control group (conventional drug therapy) and an intervention group (conventional drug therapy + glutamine+probiotics)), were enrolled. Bifidobacterium and Lactobacillus counts and the gastrin and motilin levels were lower in the case group than in the healthy group, whereas Enterobacter, yeast, and Enterococcus counts and the somatostatin, serotonin, and vasoactive intestinal peptide levels were higher. Post treatment, intestinal microbiota indices, gastrointestinal peptide levels, and intestinal barrier function were better in the intervention group than in the control group ( p < 0.05). The intervention group had a significantly higher total therapeutic response rate (95.00%) than the control group (77.50%). The intestinal microbiota was closely associated with gastrointestinal peptide levels. Treatment with glutamine and probiotics regulated these levels, re-established balance in the intestinal microbiota, and restored intestinal barrier function.