Academic literature on the topic 'Sumatriptana'

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Journal articles on the topic "Sumatriptana"

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Vincent, Maurice B., Linda R. White, Inger Johanne Bakken, and Ottar Sjaastad. "Sumatriptan Relaxes Isolated Porcine Ophthalmic Artery, But Inhibits VIP-Induced Relaxation." Cephalalgia 13, no. 6 (December 1993): 378–82. http://dx.doi.org/10.1046/j.1468-2982.1993.1306378.x.

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Sumatriptan, a 5-hydroxytryptamine (5HT)1-like receptor agonist, is a new antimigraine drug which is also effective in cluster headache (CH), a disorder with marked ocular circulatory abnormalities. Sumatriptan could putatively exert a therapeutic effect in this vascular bed. The present study is an attempt to assess sumatriptan's vasoactivity in isolated porcine ophthalmic artery (POA) and to verify whether it has similar activity to 5HT, and whether it interferes with the vasodilation induced by calcitonin gene-related peptide (CGRP) and vasoactive intestinal peptide (VIP). In contrast to 5HT, sumatriptan induced only slight contraction in POA at high concentrations. However, in some artery segments pre-contracted with PGF22a, sumatriptan induced a slight and short-lasting but marked relaxation. In addition, relaxations induced by VIP were inhibited significantly by sumatriptan, whereas CGRP effects were not influenced by the drug. Such reactions suggest that sumatriptan's effect in CH is probably unrelated to direct ocular arterial vasoconstriction.
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Mandema, JW, E. Cox, and J. Alderman. "Therapeutic Benefit of Eletriptan Compared to Sumatriptan for the Acute Relief of Migraine Pain — Results of a Model-Based Meta-Analysis that Accounts for Encapsulation." Cephalalgia 25, no. 9 (September 2005): 715–25. http://dx.doi.org/10.1111/j.1468-2982.2004.00939.x.

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A novel model-based meta-analysis was used to quantify the dose-response relationship of sumatriptan and eletriptan for the proportion of patients that achieve migraine pain relief up to 4h after treatment. The proportion of patients that became pain free was also evaluated. This analysis includes some unique features, allowing comparison of sumatriptan and eletriptan doses that have not been directly compared in a head to head study and also permitting comparison between the two drugs at multiple time points up to 4 h after treatment. Because the analysis allows comparison of response to blinded sumatriptan with that to marketed sumatriptan and contains timepoints as early as 0.5 h, it is especially suited to detection of possible effects of encapsulation on sumatriptan's therapeutic effectiveness and thus was employed to assess this also. Data from 19 randomized placebo controlled clinical trials were jointly analysed using a random-effects logistic regression model. The results of this analysis show a significant clinical benefit of eletriptan 40 mg compared to sumatriptan 100 mg at any point in time up to 4 h after treatment. The benefit of eletriptan 40 mg is greatest around 1.5-2 h after treatment with an absolute difference at 2 h of 9.1% (7.4-11.5%) more patients achieving pain relief and 7.3% (5.8-8.6%) more patient achieving pain free when compared to sumatriptan 100 mg. An absolute benefit of more than 5% of patients is maintained from 45 min up to 4 h after treatment for pain relief and from 1.5 h up to 4 h for pain free. Eletriptan 20 mg was superior to sumatriptan 50 mg and similar to sumatriptan 100 mg for pain relief while it was similar to sumatriptan 50 mg for pain free. The benefit of eletriptan 20 mg when compared to sumatriptan 50 mg is greatest around 1.5-2 h after treatment with an absolute difference at 2 h of 5.0% (2.9-8.1%) more patients achieving pain relief. An absolute benefit of more than 3% of patients was maintained from 1 h up to 3 h after treatment. No significant difference was found between eletriptan 20 mg and sumatriptan 50 mg for the fraction of patients that became pain free. No significant effect of encapsulation of sumatriptan was found on the time course of response up to 4 h after treatment when compared to commercial sumatriptan.
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Visser, W. Hester, Michel D. Ferrari, Evelyn M. Bayliss, Susan Ludlow, and Alison J. Pilgrim. "Treatment of Migraine Attacks with Subcutaneous Sumatriptan: First Placebo-Controlled Study." Cephalalgia 12, no. 5 (October 1992): 308–13. http://dx.doi.org/10.1046/j.1468-2982.1992.1205308.x.

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The results of the very first large-scale placebo-controlled dose-response trial with the novel selective 5-hydroxytryptamine1-like (5HT 1-like) receptor agonist sumatriptan are presented. We studied the efficacy and tolerability of subcutaneous injections of 1 mg, 2 mg and 3 mg of sumatriptan in alleviating migraine attacks in a double-blind, placebo-controlled, parallel-group, multicentre clinical trial. Six-hundred and ninety patients were randomized and 685 received study medication. At 30 min, reduction of headache severity to mild or none (primary efficacy endpoint) was achieved in 22% (95% CI: 15-28%) of placebo-treated patients and in 39% (CI: 31-46%) of patients treated with 1 mg sumatriptan, 44% (CI: 36-51%) treated with 2 mg sumatriptan and 55% (CI: 48-63%) treated with 3 mg sumatriptan. Differences from placebo were 17% (CI: 8-27%) for 1 mg sumatriptan, 22% (CI: 13-32%) for 2 mg sumatriptan and 34% (CI: 24-44%) for 3 mg sumatriptan ( p < 0.001 for all three comparisons). Other migraine symptoms were also more effectively treated by sumatriptan than by placebo. Subsequently, an open-label 3 mg dose subcutaneous sumatriptan was given to partial or non-responders. Thirty minutes after this open dose the response rate to sumatriptan had improved to between 70 and 80%. Adverse events after sumatriptan were minor and short-lived. We conclude that subcutaneous sumatriptan is well tolerated in doses up to 3 + 3 mg and may rapidly abort migraine attacks.
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Tfelt-Hansen, P. "Efficacy and Adverse Events of Subcutaneous, Oral, and Intranasal Sumatriptan Used for Migraine Treatment: A Systematic Review Based on Number Needed To Treat." Cephalalgia 18, no. 8 (October 1998): 532–38. http://dx.doi.org/10.1046/j.1468-2982.1998.1808532.x.

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Objectives: To evaluate the efficacy, speed of onset, and adverse events of 6 mg subcutaneous, 100 mg oral, and 20 mg intranasal sumatriptan in the treatment of migraine attacks. Design: Systematic review of placebo-controlled randomized clinical trials. Data sources: Thirty trials up to April 1997 retrieved from a systematic literature search (Medline, review papers, handsearching of journals, congress proceedings, manufacturer's database); no restriction on language. Outcome parameters: Numbers needed to treat (NNT) were calculated for relief of headache and for adverse events (when data were available). Therapeutic gain was used to evaluate speed of onset of action. Results: Subcutaneous sumatriptan was more efficacious, combined number needed to treat 2.0 at 1 h, than oral (3.0 at 2 h) and intranasal sumatriptan (3.1 at 2 h). For adverse events, the NNT was 3.0 for subcutaneous and 8.3 for oral sumatriptan. Only limited data on adverse events for intranasal sumatriptan were available. Therapeutic gain analysis during the first 2 h showed that subcutaneous sumatriptan was the fastest-acting form of administration. Conclusions: Subcutaneous sumatriptan in a dose of 6 mg is significantly more efficacious than 100 mg of oral sumatriptan, but causes more adverse events than oral sumatriptan. Subcutaneous sumatriptan is the form with the quickest onset of action. Intranasal sumatriptan has the same efficacy as oral sumatriptan and a quicker onset of action than the oral form, but with a limited therapeutic effect for the first 30 min after administration.
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Coulie, B., J. Tack, B. Maes, B. Geypens, M. De Roo, and J. Janssens. "Sumatriptan, a selective 5-HT1 receptor agonist, induces a lag phase for gastric emptying of liquids in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 4 (April 1, 1997): G902—G908. http://dx.doi.org/10.1152/ajpgi.1997.272.4.g902.

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Sumatriptan, a 5-hydroxytryptamine1 (5-HT1) receptor agonist at enteric neuronal 5-HT receptors, causes a relaxation of the gastric fundus and inhibition of antral contractile activity. The present study examined the effect of sumatriptan on gastric emptying of solids and liquids in humans. In eight healthy subjects the gastric emptying rate for liquids and solids was measured using the carbon-labeled glycine and octanoic acid breath test after subcutaneous administration of placebo or sumatriptan. Sumatriptan increased the gastric half-emptying time of liquids (P < 0.0005) and induced a prolonged lag phase for liquids (P < 0.0005) in all subjects. Sumatriptan increased gastric half-emptying time (P < 0.005) and the lag phase of solids (P < 0.05) in all subjects. In two healthy subjects gastric emptying of liquids and solids after subcutaneous administration of sumatriptan was studied by radioscintigraphy. Radioscintigraphy confirmed the delayed emptying and the prolonged lag phases after sumatriptan. In conclusion, sumatriptan delays gastric emptying of solids and liquids in healthy subjects. Moreover, sumatriptan induces a lag phase for liquids. The mechanism by which sumatriptan alters gastric emptying remains to be studied.
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Caro, G., D. Getsios, JJ Caro, G. Raggio, M. Burrows, and L. Black. "Sumatriptan: Economic Evidence for Its Use in the Treatment of Migraine, the Canadian Comparative Economic Analysis." Cephalalgia 21, no. 1 (February 2001): 12–19. http://dx.doi.org/10.1046/j.1468-2982.2001.00130.x.

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The objective of this study was to evaluate economic and health effects of sumatriptan relative to customary therapy in Canada. The relationship between treatment and functionality was established based on analysis of existing data from a multinational study. A Monte Carlo model was developed to simulate 1 year for each of customary therapy and six sumatriptan formulations. Costs are expressed in 1998 Canadian dollars. Sumatriptan is expected to reduce the time spent with migraine symptoms and resulting time lost. Under customary therapy, the annual cost of lost time is estimated at £908 ($1973). With sumatriptan, these costs ranged from £406 ($882) with subcutaneous sumatriptan to £577 ($1254) with nasal sumatriptan 10 mg, saving £331–502 ($719–1091) in the annual cost of time lost. All these benefits are expected to be obtained at an additional drug cost ranging from £869 ($1889) for subcutaneous sumatriptan to £278 ($605) for sumatriptan suppository. The cost of sumatriptan treatment is significantly offset by a substantial reduction of costs associated with time lost due to migraine symptoms.
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Depré, M., C. MacLeod, J. Palcza, MO Behm, I. de Lepeleire, T. Han, D. Panebianco, et al. "Lack of hemodynamic interaction between CGRP-receptor antagonist telcagepant (MK-0974) and sumatriptan: Results from a randomized study in patients with migraine." Cephalalgia 33, no. 16 (June 24, 2013): 1292–301. http://dx.doi.org/10.1177/0333102413494272.

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Objective The objective of this article is to assess the effects of sumatriptan monotherapy, telcagepant monotherapy, and their combination on blood pressure (BP) in migraine patients during a headache-free period. Methods A double-blind, placebo-controlled, four-period, single-dose, randomized crossover study in 24 migraine patients was conducted. In each period, patients received a single oral dose of sumatriptan 100 mg alone, telcagepant 600 mg alone, sumatriptan 100 mg coadministered with telcagepant 600 mg, or placebo. Semi-recumbent BP was measured pre-dose and at seven post-dose timepoints over a period of six hours. Individual time-weighted averages in mean arterial pressure (MAP) were evaluated using a linear mixed-effects model. The pharmacokinetics of sumatriptan alone and in the presence of telcagepant were also evaluated using limited sampling times. Results The mean difference in time-weighted (0–2.5 h) MAP (90% confidence interval) was 1.2 mmHg (−0.2, 2.7) between telcagepant and placebo, 4.0 mmHg (2.5, 5.5) between sumatriptan and placebo, and 1.5 mmHg (0.0, 3.0) between telcagepant with sumatriptan vs sumatriptan alone. When coadministered with telcagepant, the AUC0–6h and Cmax of sumatriptan were increased by 23% and 24%, respectively. The small MAP increases observed after coadministration could possibly be associated with the slight elevations in sumatriptan levels. Conclusion Telcagepant does not elevate mean MAP, and coadministration of telcagepant with sumatriptan results in elevations in MAP similar to those observed following administration of sumatriptan alone in migraineurs during the interictal period. When coadministered, telcagepant slightly increases the plasma levels of sumatriptan, but without an apparent clinically meaningful effect.
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de Hoon, Jan, Anne Van Hecken, Corinne Vandermeulen, Marissa Herbots, Yumi Kubo, Ed Lee, Osa Eisele, Gabriel Vargas, and Kristin Gabriel. "Phase 1, randomized, parallel-group, double-blind, placebo-controlled trial to evaluate the effects of erenumab (AMG 334) and concomitant sumatriptan on blood pressure in healthy volunteers." Cephalalgia 39, no. 1 (May 21, 2018): 100–110. http://dx.doi.org/10.1177/0333102418776017.

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Objectives The aim of this study was to assess the effects of concomitant administration of erenumab and sumatriptan on resting blood pressure, pharmacokinetics, safety, and tolerability in healthy subjects. Methods In this phase 1, parallel-group, one-way crossover, double-blind, placebo-controlled study, healthy adult subjects were randomized (1:2) to receive either intravenous placebo and subcutaneous sumatriptan 12 mg (i.e. two 6-mg injections separated by 1 hour) or intravenous erenumab 140 mg and subcutaneous sumatriptan 12 mg. Blood pressure was measured pre-dose and at prespecified times post-dose. The primary endpoint was individual time-weighted averages of mean arterial pressure, measured from 0 hours to 2.5 hours after the first dose of sumatriptan. Pharmacokinetic parameters for sumatriptan were evaluated by calculating geometric mean ratios (erenumab and sumatriptan/placebo and sumatriptan). Adverse events and anti-erenumab antibodies were also evaluated. Results A total of 34 subjects were randomized and included in the analysis. Least squares mean (standard error) time-weighted averages of mean arterial pressure were 87.4 (1.0) mmHg for the placebo and sumatriptan group and 87.4 (1.2) mmHg for the erenumab and sumatriptan group. Mean difference in mean arterial pressure between groups was −0.04 mmHg (90% confidence interval: −2.2, 2.1). Geometric mean ratio estimates for maximum plasma concentration of sumatriptan was 0.95 (90% confidence interval: 0.82, 1.09), area under the plasma concentration–time curve (AUC) from time 0 to 6 hours was 0.98 (90% confidence interval: 0.93, 1.03), and AUC from time 0 to infinity was 1.00 (90% confidence interval: 0.96, 1.05). No clinically relevant safety findings for co-administration of sumatriptan and erenumab were identified. Conclusion Co-administration of erenumab and sumatriptan had no additional effect on resting blood pressure or on pharmacokinetics of sumatriptan. Trial registration: ClinicalTrials.gov, NCT02741310.
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Vachharajani, NN, W.-C. Shyu, PS Nichola, and DW Boulton. "A Pharmacokinetic Interaction Study Between Butorphanol and Sumatriptan Nasal Sprays in Healthy Subjects: Importance of the Timing of Butorphanol Administration." Cephalalgia 22, no. 4 (May 2002): 282–87. http://dx.doi.org/10.1046/j.1468-2982.2002.00359.x.

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Sumatriptan and butorphanol nasal sprays are commonly used agents for the management of migraine headaches. Under certain circumstances, these two agents may be administered closely in time. However, the possibility of a pharmacokinetic interaction and the safety of this regime have not been examined. In this crossover design study, 24 healthy subjects received the following four treatments, each separated by at least 7 days: 1 mg butorphanol (Stadol NS7®); 20 mg sumatriptan (Imitrex® Nasal Spray); or both formulations together with butorphanol administered either 1 or 30 min after sumatriptan. Serial plasma samples were collected for 24 h post-dose and analysed for butorphanol and/or sumatriptan by HPLC-MS/MS. Butorphanol plasma concentrations were reduced when it was administered 1 min (mean 28.6% decrease in AUC0-∞) , but not 30 min, after sumatriptan. The pharmacokinetics of sumatriptan were not substantially altered by butorphanol. The combination of nasally administered sumatriptan and butorphanol appeared safe. However, if butorphanol nasal spray is administered < 30 min after sumatriptan nasal spray, the analgesic effect of butorphanol may be diminished due to reduced nasal absorption resulting from probable transient vasoconstriction of nasal blood vessels by sumatriptan.
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Babes, Alexandru, Cristian Neacsu, Michael JM Fischer, and Karl Messlinger. "Sumatriptan activates TRPA1." Cephalalgia Reports 2 (January 1, 2019): 251581631984715. http://dx.doi.org/10.1177/2515816319847155.

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Background: Migraine therapy with sumatriptan may cause adverse side effects like pain at the injection site, muscle pain, and transient aggravation of headaches. In animal experiments, sumatriptan excited or sensitized slowly conducting meningeal afferents. We hypothesized that sumatriptan may activate transduction channels of the “irritant receptor,” the transient receptor potential ankyrin type (TRPA1) expressed in nociceptive neurons. Methods: Calcium microfluorometry was performed in HEK293t cells transfected with human TRPA1 (hTRPA1) or a mutated channel (TRPA1-3C) and in dissociated trigeminal ganglion neurons. Membrane currents were recorded in the whole-cell patch clamp configuration. Results: Sumatriptan (10 and 400 µM) evoked calcium transients in hTRPA1-expressing HEK293t cells also activated by the TRPA1 agonist carvacrol (100 µM). In TRPA1-3C-expressing HEK293t cells, sumatriptan had hardly any effect. In rat trigeminal ganglion neurons, sumatriptan, carvacrol, and the transient receptor potential vanillod type 1 agonist capsaicin (1 µM) generated robust calcium signals. All sumatriptan-sensitive neurons (8% of the sample) were also activated by carvacrol (14%) and capsaicin (48%). In HEK293-hTRPA1 cells, sumatriptan (100 µM) evoked outwardly rectifying currents, which were almost completely inhibited by the TRPA1 antagonist HC-030031 (10 µM). Conclusion: Sumatriptan activates TRPA1 channels inducing calcium inflow and membrane currents. TRPA1-dependent activation of primary afferents may explain the painful side effects of sumatriptan.
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Dissertations / Theses on the topic "Sumatriptana"

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Oshiro, Alisson. "Preparação e caracterização de sistemas carreadores para liberação modificada de succinato de sumatriptano destinado ao tratamento de migrânea." reponame:Repositório Institucional da UFABC, 2013.

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Finniss, Mathew Christopher MD, Nimrat MD Bains, and Shelby DO Shamas. "Sumatriptan Induced Coronary Vasospasm." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/179.

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Migraines are recurrent debilitating headaches that predominately afflict young women. The pathophysiology of migraines is still not well understood but is related to neurovascular dysfunction. Meningeal blood vessel dilation, extravasation of pro-inflammatory cytokines and activation of trigeminal afferent neurons promote migraine generation. Serotonin (5-HT) is an endogenous vasoactive peptide with diverse physiology. In meningeal blood vessels, serotonin causes vasoconstriction, however in coronary arteries, serotonin causes both vasodilation and vasoconstriction. In diseased coronary arteries, with impaired endothelial function, vasoconstriction predominates. Selective meningeal blood vessel serotonin agonists, termed ‘triptans’, have become the therapy of choice for migraine headaches. However, due to their constrictive effects on the coronary vasculature, triptans are not recommend in patients with known coronary artery disease, patients with greater than one coronary artery risk factor or patients with atherosclerotic cardiovascular disease risk (ASCVD) greater than ten percent. Triptan associated chest pain is a well-known phenomenon. Age, hypertension, dyspepsia, and Raynauds phenomenon are associated with triptan associated chest pain. Hypertension is the strongest risk factor for triptan associated chest pain in males. Although triptan associated chest pain is assumed to be cardiovascular due to its constrictive effect on the coronary vasculature, only a few cases of myocardial infarction, with documented ST elevation and/or troponin elevation, have been reported. Herein we report the case of a male patient with inferolateral ST elevation myocardial infarction, within minutes of receiving subcutaneous sumatriptan for migraine headache. The patient had a normal echocardiogram and electrocardiogram prior to sumatriptan use, and a normal cardiac catheterization afterwards.
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Marion, Cécile. "Données pharmacologiques du sumatriptan." Paris 5, 1993. http://www.theses.fr/1993PA05P051.

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Drapier, Céline. "La maladie migraineuse : intérêt du sumatriptan dans le traitement des crises." Bordeaux 2, 1995. http://www.theses.fr/1995BOR2P062.

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Gisbert, Sophie. "Modélisation des cinétiques du sumatriptan et de son métabolite principal (GR49336) par des techniques de pharmacocinétique de population." Paris 5, 2001. http://www.theses.fr/2001PA05P042.

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Vignol, Léonor. "Influence des variabilités pharmacocinétique et pharmacodynamique sur l'efficacité du sumatriptan en spray nasal." Paris 5, 2001. http://www.theses.fr/2001PA05P043.

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Tabet, John Kennedy. "Traitement de la crise de migraine : apport du sumatriptan et de quelques analogues." Paris 5, 1995. http://www.theses.fr/1995PA05P071.

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Sällberg, Lina. "Hur effektiv är kombinationen av naproxen och sumatriptan vid behandling av migrän jämfört med monoterapi och/eller placebo?" Thesis, Linnéuniversitetet, Institutionen för naturvetenskap, NV, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-18562.

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Syftet med denna studie var att undersöka hur stor effekt kombinationsbehandling med naproxen och sumatriptan har vid migrän hos vuxna människor jämfört med monoterapi med naproxen eller sumatriptan samt placebo. Studien utformades som en litteraturstudie och sökningar skedde i PubMed via Linnéuniversitetets bibliotek med sökorden ”migraine AND triptan* AND NSAID AND efficacy”, ”migraine AND sumatriptan AND naproxen AND combination AND efficacy” samt ”naproxen AND sumatriptan”. Sökningarna ledde till granskning av 6 studier.     Sammanfattningsvis hade kombinationsbehandlingen statistiskt signifikanta fördelar gällande flera effektmått vid behandling av migrän, bland annat smärtfrihet 2 timmar efter behandling och ihållande smärtfrihet upp till 24 timmar efter behandling, jämfört med såväl monoterapierna som placebo, medan biverkningsrisken inte ökade statistiskt signifikant med kombinationsterapin. Tidigt insättande av behandling, när migränen fortfarande är mild, gav bäst resultat, och effekten kvarstod under flera behandlingstillfällen. Patienter, som behandlades med kombinationsterapin, kunde statistiskt signifikant snabbare återgå till normal funktion i vardagsliv och på arbete, med minskat produktionsbortfall som följd, och de var också nöjdare med kombinationsbehandlingen än med monoterapierna och placebo. Trots dessa resultat blir långt ifrån alla bra. Knappt varannan patient, som behandlas med sumatriptan och naproxen vid mild migrän, är smärtfria efter 2 timmar. Vid måttlig till svår migrän är det ungefär 1 av 3 som är smärtfria 2 timmar efter kombinationsbehandling. Effektivare läkemedel mot migrän är önskvärt.
The purpose of this study was to analyse the efficacy of the combination of naproxen and sumatriptan when used for migraine in adults, and compare with monotherapy with naproxen or sumatriptan and placebo. The study was a literature study and searches were carried out in PubMed via the Linnaeus University library with the keywords ”migraine AND triptan* AND NSAID AND efficacy”, ”migraine AND sumatriptan AND naproxen AND combination AND efficacy” and also ”naproxen AND sumatriptan”. The searches resulted in 6 studies that were reviewed.     In summary, the combination therapy resulted in statistically significant improvements for multiple endpoints in the treatment of migraine, including patients being free of pain 2 hours after treatment and sustained pain-free response up to 24 hours after treatment, compared with both monotherapies and placebo, while the potential for adverse events did not increase statistically significantly with the combination therapy. Early intervention, when migraine was still mild, gave best results, and the effect persisted for several treatment sessions. Patients treated with combination therapy returned statistically significantly faster to normal function in everyday life and at work, with reduced downtime, and they were also more satisfied with the combination therapy than with mono therapy or placebo. Despite this, far from everybody gets well with treatment. Hardly every second patient treated for mild migraine with sumatriptan and naproxen is free from pain after 2 hours and when treating more severe forms of migraine only about 1 in 3 is free from pain after 2 hours. More effective treatments of migraine are needed.
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Koch, Andreas. "Untersuchungen zum Einflu von Sumatriptan auf die Perzeption intrarektaler Dehnungsreize." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=964956969.

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Wang, Yu-Chin Lily. "Postmarketing surveillance of sumatriptan : patient population, efficacy, and adverse effects." Scholarly Commons, 1994. https://scholarlycommons.pacific.edu/uop_etds/2273.

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A postmarketing surveillance survey of sumatriptan use comprised 32 questions including patient demographics, headache history, and sumatriptan experience. One hundred and forty-one questionnaires were sent out, and 109 patients responded; a total of 108 patients were included in the data analysis. When compared with the national migraine population, on a percentage basis, significantly more African-Americans, females, young patients (less 45 years of age), and patients with higher mean incomes (>$45,000) were found in the present study of those taking sumatriptan (p Males (N=8) and females (N=55) had a significantly different percentage of relief from the second dose of 94.7%±7.1 and 83.5%±24.4, respectively (p=0.01). An average percent of pain relief from the first dose in those weighing less or greater than 144 pounds was 76.5%±28.3 and 86.9%±16.4, respectively (p=0.023). The incidence of the adverse effects reported in this study was significantly greater than those reported in the literature (p<0.005).
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Books on the topic "Sumatriptana"

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Visser, Willemina Hester. 5-HT₁ receptor agonists in the acute treatment of migraine: Clinical, epidemiological and pharmacological aspects. [Delft: Eburon, 1996.

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Parker, Philip M., and James N. Parker. Imitrex: A medical dictionary, bibliography, and annotated research guide to Internet references. San Diego, CA: ICON Health Publications, 2004.

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John, Edmeads, ed. Advances in migraine therapy: Focus on oral sumatriptan. Cleveland, OH: Advanstar, 1995.

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Gibson, Barbara A. Fibromyalgia : Exploring the Possibilities, Vol. 1 : Sumatriptan: Exploring the Possibilities. Gemini Press (Clearwater, FL), 1994.

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1926-, Lance James W., Pfaffenrath V, and Migraine Trust International Symposium, eds. Sumatriptan: From molecule to man : an official session at the 8th Migraine Trust International Symposium, London, UK, 28th September, 1990. Basel: Karger, 1991.

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Patrick, Humphrey, Olesen Jes, and Ferrari M. D, eds. The triptans: Novel drugs for migraine. Oxford: Oxford University Press, 2001.

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(Editor), Patrick Humphrey, Michel Ferrari (Editor), and Jes Olesen (Editor), eds. The Triptans: Novel Drugs for Migraine (Frontiers in Headache Research). Oxford University Press, USA, 2001.

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Book chapters on the topic "Sumatriptana"

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Diener, H. C. "Sumatriptan - Therapy." In Drug Treatment of Migraine and Other Headaches, 93–109. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000061579.

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Connor, H. E. "Sumatriptan - Pharmacology." In Drug Treatment of Migraine and Other Headaches, 83–92. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000061609.

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Lohse, Martin J., and Franz Bernhard M. Ensink. "Pharmakologie von Sumatriptan." In Migräne, 391–415. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-93522-0_16.

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Ensink, Franz Bernhard M. "Ergänzende Sicherheitsaspekte und Ergebnisse erster Langzeitstudien mit Sumatriptan." In Migräne, 445–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-93522-0_19.

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Humphrey, P. P. A., W. Feniuk, M. Motevalian, A. A. Parsons, and E. T. Whalley. "The Vasoconstrictor Action of Sumatriptan on Human Isolated Dura Mater." In Serotonin: Molecular Biology, Receptors and Functional Effects, 421–29. Basel: Birkhäuser Basel, 1991. http://dx.doi.org/10.1007/978-3-0348-7259-1_42.

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Chevrel, Guillaume, and Virginie Dessus. "sumatriptan." In 300 médicaments injectables, 451–53. Elsevier, 2009. http://dx.doi.org/10.1016/b978-2-294-70698-1.50179-3.

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Moore, Joanne. "Sumatriptan." In xPharm: The Comprehensive Pharmacology Reference, 1–6. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.62704-7.

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"Sumatriptan." In Checkliste Arzneimittel A–Z, edited by Detlev Schneider and Frank Richling. Stuttgart: Georg Thieme Verlag, 2013. http://dx.doi.org/10.1055/b-0034-82767.

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"Sumatriptan." In PharmacotherapyFirst Drug Information. 2215 Constitution Avenue, N.W. Washington, DC 20037-2985: The American Pharmacists Association, 2017. http://dx.doi.org/10.21019/pfdi.sumatriptan.

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"Sumatriptan." In Hale’s Medications & Mothers’ Milk™ 2019. New York, NY: Springer Publishing Company, 2018. http://dx.doi.org/10.1891/9780826150356.0968.

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Reports on the topic "Sumatriptana"

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Halker Singh, Rashmi B., Juliana H. VanderPluym, Allison S. Morrow, Meritxell Urtecho, Tarek Nayfeh, Victor D. Torres Roldan, Magdoleen H. Farah, et al. Acute Treatments for Episodic Migraine. Agency for Healthcare Research and Quality (AHRQ), December 2020. http://dx.doi.org/10.23970/ahrqepccer239.

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Abstract:
Objectives. To evaluate the effectiveness and comparative effectiveness of pharmacologic and nonpharmacologic therapies for the acute treatment of episodic migraine in adults. Data sources. MEDLINE®, Embase®, Cochrane Central Registrar of Controlled Trials, Cochrane Database of Systematic Reviews, PsycINFO®, Scopus, and various grey literature sources from database inception to July 24, 2020. Comparative effectiveness evidence about triptans and nonsteroidal anti-inflammatory drugs (NSAIDs) was extracted from existing systematic reviews. Review methods. We included randomized controlled trials (RCTs) and comparative observational studies that enrolled adults who received an intervention to acutely treat episodic migraine. Pairs of independent reviewers selected and appraised studies. Results. Data on triptans were derived from 186 RCTs summarized in nine systematic reviews (101,276 patients; most studied was sumatriptan, followed by zolmitriptan, eletriptan, naratriptan, almotriptan, rizatriptan, and frovatriptan). Compared with placebo, triptans resolved pain at 2 hours and 1 day, and increased the risk of mild and transient adverse events (high strength of the body of evidence [SOE]). Data on NSAIDs were derived from five systematic reviews (13,214 patients; most studied was ibuprofen, followed by diclofenac and ketorolac). Compared with placebo, NSAIDs probably resolved pain at 2 hours and 1 day, and increased the risk of mild and transient adverse events (moderate SOE). For other interventions, we included 135 RCTs and 6 comparative observational studies (37,653 patients). Compared with placebo, antiemetics (low SOE), dihydroergotamine (moderate to high SOE), ergotamine plus caffeine (moderate SOE), and acetaminophen (moderate SOE) reduced acute pain. Opioids were evaluated in 15 studies (2,208 patients).Butorphanol, meperidine, morphine, hydromorphone, and tramadol in combination with acetaminophen may reduce pain at 2 hours and 1 day, compared with placebo (low SOE). Some opioids may be less effective than some antiemetics or dexamethasone (low SOE). No studies evaluated instruments for predicting risk of opioid misuse, opioid use disorder, or overdose, or evaluated risk mitigation strategies to be used when prescribing opioids for the acute treatment of episodic migraine. Calcitonin gene-related peptide (CGRP) receptor antagonists improved headache relief at 2 hours and increased the likelihood of being headache-free at 2 hours, at 1 day, and at 1 week (low to high SOE). Lasmiditan (the first approved 5-HT1F receptor agonist) restored function at 2 hours and resolved pain at 2 hours, 1 day, and 1 week (moderate to high SOE). Sparse and low SOE suggested possible effectiveness of dexamethasone, dipyrone, magnesium sulfate, and octreotide. Compared with placebo, several nonpharmacologic treatments may improve various measures of pain, including remote electrical neuromodulation (moderate SOE), magnetic stimulation (low SOE), acupuncture (low SOE), chamomile oil (low SOE), external trigeminal nerve stimulation (low SOE), and eye movement desensitization re-processing (low SOE). However, these interventions, including the noninvasive neuromodulation devices, have been evaluated only by single or very few trials. Conclusions. A number of acute treatments for episodic migraine exist with varying degrees of evidence for effectiveness and harms. Use of triptans, NSAIDs, antiemetics, dihydroergotamine, CGRP antagonists, and lasmiditan is associated with improved pain and function. The evidence base for many other interventions for acute treatment, including opioids, remains limited.
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