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PubMed2000

Permeation of sumatriptan through human vaginal and buccal mucosa.

Continued interest in the various routes by which sumatriptan may be administered prompted us to investigate its passage through buccal mucosa. Because human buccal mucosa is scarce, we proposed using the relatively abundant vaginal mucosa, which has been shown to have comparable diffusion rates for a number of widely varying molecules, as a model of buccal mucosa. In addition, by comparing these two tissues with respect to their permeability to sumatriptan, the human vaginal/buccal mucosa model could be further evaluated. Clinically healthy human vaginal and buccal mucosa specimens were used in the permeability studies. Permeability to sumatriptan was determined using a continuous flow-through diffusion system in the presence and absence of permeation enhancers. No statistically significant differences in permeability could be demonstrated for both mucosae toward sumatriptan. Flux values obtained in the absence and presence of glycodeoxycholate and lauric acid (1:1 molar ratio) to sumatriptan of buccal and vaginal mucosa, respectively, were not significantly different. The results obtained further support the hypothesis of the vaginal/buccal mucosal in vitro permeability model and suggest that this model may be used in conjunction with various absorption enhancers. Further studies on the buccal route of absorption of sumatriptan are thus warranted.

Administration, Buccal↗
PubMed2001

Sumatriptan nasal spray and cognitive function during migraine: results of an open-label study.

OBJECTIVE: To examine measures of cognitive function during acute migraine, before and after treatment with sumatriptan nasal spray, 20 mg. BACKGROUND: Migraineurs frequently report symptoms of cognitive impairment during migraine. The efficacy of sumatriptan for treatment of migraine-related cognitive impairment is undocumented. METHODS: This open-label, single-attack study of 28 subjects used the Headache Care Center-Automated Neuropsychological Assessment Metrics, a computerized neuropsychological assessment battery, to measure cognitive function under three patient conditions: migraine-free, untreated migraine, and following sumatriptan (primary outcome). Headache response and pain-free response, percent effectiveness, and clinical disability were measured. RESULTS: Cognitive function (simple reaction time, sustained attention/concentration, working memory, visual-spatial processing) and alertness/fatigue were adversely affected during migraine compared with migraine-free performance (P<.05), and rapidly restored following sumatriptan nasal spray, 20 mg (P<.05). Headache and pain-free response were 86% and 68%, respectively, at 135 minutes postdose. Changes in migraine pain severity, clinical disability, and percent effectiveness following treatment with sumatriptan nasal spray, 20 mg, were significantly correlated with cognitive function measures across all subtests (P<.001). CONCLUSIONS: Sumatriptan nasal spray, 20 mg, restored migraine-related cognitive function and clinical disability.

Acute Disease↗
PubMed2002

Impact of chest pain on cost of migraine treatment with almotriptan and sumatriptan.

Chest-related symptoms occur with all triptans; up to 41% of patients with migraine who receive sumatriptan experience chest symptoms, and 10% of patients discontinue treatment. Thus, the cost of chest pain-related care was estimated in migraineurs receiving almotriptan 12.5 mg versus sumatriptan 50 mg. A population-based, retrospective cohort study used data to quantify the incidence and costs of chest pain-related diagnoses and procedures. An economic model was constructed to estimate annual cost savings per 1000 patients receiving almotriptan versus sumatriptan based on the reported rates of chest pain. Annual direct medical cost avoided was calculated for a hypothetical health plan covering 1 million lives. Among a cohort of 1390 patients, the incidence of chest pain-related diagnoses increased significantly by 43.6% with sumatriptan (P=.003). Aggregate costs for chest pain-related diagnoses and procedures increased from $22,713 to $30,234. Payments for inpatient hospital services, costs for primary care visits, and costs for outpatient hospital visits increased by over 100%, 53.1%, and 14.4%, respectively. The model predicted $11,215 in direct medical cost savings annually per 1000 patients treated with almotriptan versus sumatriptan. Annual direct medical costs avoided totaled $194,358, and when applied to recent estimates of 86 million lives currently covered by almotriptan treatment, translates into an annual cost savings of just under $17 million for chest pain and associated care. Thus, using almotriptan in place of sumatriptan will likely reduce the cost of chest pain-related care.

Adolescent↗
PubMed2006

Concomitant variations of gastric tone and duodenal motility in humans: results of a placebo-controlled study assessing octreotide and sumatriptan.

OBJECTIVE: To describe the concomitant effects of octreotide and sumatriptan on fundic tone and duodenal phase III activity. MATERIAL AND METHODS: A double-blind study was performed in nine volunteers, studied for 2 h after receiving 50 microg octreotide, 6 mg sumatriptan or placebo. Fundic tone variations were assessed by barostat while antroduodenal motility was studied concomitantly using manometry. RESULTS: A rapid increase in intrabag volume was observed in all but one subject after both sumatriptan and octreotide administration, while only two subjects exhibited a volume variation after placebo, p<0.01. A significant decrease in the number of phasic contractions was observed after octreotide, while sumatriptan reduced only wave amplitudes (p<0.05). A total of 13 concomitant duodenal phase III-like activities were observed in the duodenum after octreotide, 3 after sumatriptan and 4 after placebo, all followed by spontaneous fundic relaxation with disappearance of phasic contractions, p<0.05. Spontaneous phase III activities were different from phases III-like activities after octreotide in velocity and duration (p<0.05). CONCLUSIONS: Octreotide induced concomitant fundic relaxation, disappearance of phasic contractions and duodenal phase III-like activity. Sumatriptan relaxed the proximal stomach and reduced the amplitude of fundic phasic contractions without affecting concomitant antroduodenal phase III activity.

Adult↗
PubMed1995

The safety of concomitant use of sumatriptan and antidepressant treatments.

It is presently contraindicated to use the antimigraine drug sumatriptan with selective serotonin reuptake inhibitors, monoamine oxidase inhibitors, or lithium. Consequently, many patients undergoing these pharmacotherapies for psychiatric disorders may not benefit from the therapeutic effect of sumatriptan in acute migraine attacks. Because sumatriptan does not appear to cross the blood-brain barrier and has a short half-life, it was deemed relatively safe to prescribe sumatriptan with antidepressant treatments. Fourteen patients receiving fluoxetine, fluvoxamine, sertraline, moclobemide, lithium, or buspirone did not experience significant side effects when they took oral sumatriptan for the relief of migraine on a total of 103 episodes. It is concluded that the combined use of sumatriptan with the above-mentioned antidepressant treatments may be safe.

Administration, Oral↗
PubMed1997

Comparison of the cardiovascular effects of the novel 5-HT(1B/1D) receptor agonist, SB 209509 (VML251), and sumatriptan in dogs.

The systemic cardiovascular effects of a novel 5-hydroxtryptamine (5-HT)(1B/1D)-receptor agonist were investigated in the anaesthetised dog. SB 209509 (VML 251) was more potent than sumatriptan in producing increases in carotid vascular resistance after intravenous administration and was similar in potency to sumatriptan after sequential intraduodenal administration at 30-min intervals. In open-chest dogs, sequential intravenous administration of SB 209509 or sumatriptan produced marked increases in carotid vascular resistance without changing coronary vascular resistance. In contrast to sumatriptan, after administration of high doses of SB 209509 (>790 nmol/kg), a reduction in coronary vascular resistance was observed. After a single bolus intraduodenal dose of SB 209509 (260, 520, or 790 nmol/kg), increases in carotid vascular resistance could be detected over a 5-h period. Sumatriptan (i.d.), 2.4 micromol/kg but not 700 nmol/kg, produced a sustained effect similar to the effects of SB 209509 (790 nmol/kg). In all experiments, SB 209509 and sumatriptan had minimal effects on arterial blood pressure or heart rate but produced marked changes in carotid vascular resistance over the same concentration range. SB 209509 was rapidly absorbed after intraduodenal administration in conscious dogs and had good bioavailability. These data indicate that SB 209509 is a potent 5-HT(1B/1D)-receptor agonist that is rapidly absorbed from the duodenum. The effects of SB 209509 are long lasting and selective for the carotid vascular bed.

Animals↗
PubMed1998

Effects of sumatriptan on coronary flow and left ventricular function in the isolated perfused guinea pig heart.

The effects of the 5-HT1B/D receptor agonist, sumatriptan, on coronary flow (CF) and left ventricular function in the isolated perfused guinea pig heart were investigated in the presence and absence of coronary endothelial dysfunction induced by nitric oxide (NO) synthase inhibition with Nomega-nitro-L-arginine methyl ester (L-NAME; 10 microM). Hearts were perfused under constant pressure (80 cm H2O) with oxygenated (95% O2/5% CO2) Krebs bicarbonate buffer (pH 7.4) and were driven at 4 Hz. In the absence of L-NAME (n=37), sumatriptan (0.1-32 microM) failed statistically significantly to affect left ventricular developed pressure (LVDP; maximal change, -8.1+/-1.8%; NS vs. vehicle), left ventricular end-diastolic pressure (LVEDP; +10.4+/-9.8%, NS), or CF (-12.2+/-1.4%; NS compared with vehicle). L-NAME per se significantly reduced coronary flow (CF; -26.3+/-2.9%; p < 0.001), thereby increasing coronary vascular tone, and decreased LVDP (-17.1+/-1.8%; p < 0.01). In hearts perfused with L-NAME (10 microM; n=61), sumatriptan (0.1-32 microM) still failed significantly to affect CF (maximal change, 0.2+/-5.7%, NS) but concentration-dependently increased LVEDP [maximal increase, 89.0+/-30.3%; p < 0.05; geometric mean EC50 3.6 (2.9-5.7) microM], which was not prevented by the 5-HT1B/D receptor antagonist, GR 127935 (0.1 microM; maximal increase, 51.8+/-11.1%; n=48, NS compared with sumatriptan alone). In conclusion, sumatriptan failed significantly to affect CF even in the presence of endothelial dysfunction. LV function similarly remained unaffected in normal hearts, but sumatriptan produced diastolic contracture in the presence of coronary endothelial dysfunction by a mechanism apparently not involving 5-HT1B/D receptors. Collectively the data indicate that 5-HT1B/D receptor expression or effector coupling or both are absent or low in the guinea pig heart, because no detectable functional responses were observed.

Animals↗
PubMed1997

Cost benefit of sumatriptan to an employer.

Benefit and occupational health managers need information on whether new treatments, such as sumatriptan, for migraine headache improve organizational or individual performance. A work productivity outcomes assessment was conducted among sumatriptan-using employees of an Independent Practice Association-health maintenance organization population. Of the 164 sumatriptan users, 101 full-time employees were surveyed by telephone once in an open-label, before-after design. The results revealed that lost labor costs, a function of days missed from work and reduced productivity at work as a result of migraine, were decreased after sumatriptan treatment initiation. Incremental benefit of this reduction in lost productivity is valued at $435/month per employee. The sumatriptan cost associated with this benefit is $43.78/month. The benefit-to-cost ratio is 10:1. Other costs and benefits were excluded. In conclusion, the availability of sumatriptan for migraine headache treatments in this IPA-HMO resulted in improved work productivity and had a net benefit for the employer.

Absenteeism↗
PubMed1996

Sumatriptan-induced cerebral vasoconstriction as treatment of experimental intracranial hypertension.

BACKGROUND: Increased intracranial pressure (ICP) is a major cause of mortality in severe head injuries and pharmacologically induced cerebral vasoconstriction has been suggested as a possible treatment. In the present study a porcine model of increased ICP was utilized to study the changes in cerebral haemodynamics and energy metabolism induced by a selective 5-hydroxytryptamine1 agonist (sumatriptan). METHODS: ICP was raised by inflation of two balloons covering both parieto-occipital regions extradurally. The animals were randomized into four groups receiving sumatriptan. 0.01 mg.kg-1 (A), 0.03 mg.kg-1 (B), 0.1 mg.kg-1 (C), and 0.5 mg.kg-1 (D) intravenously over 10 min. Measurements of cerebral blood flow (CBF), arterio-venous oxygen content difference (CavO2), and jugular venous pH (vpH) were performed 5, 20, 40, 60, and 75 min after start of the infusion. ICP, mean arterial pressure, and EEG were recorded continuously. Direct effects of sumatriptan were also compared in cortical arteries and veins in vitro. RESULTS: Significant decreases in ICP were obtained in groups A, B, and C while group D exhibited a progressive increase in ICP. Significant reductions in CBF, increase in CavO2, and slowing of EEG were observed in groups B, C, and D. Sumatriptan caused moderate constriction of the arteries and a more pronounced dilatation of veins in vitro. CONCLUSION: The results indicate that a low dose of sumatriptan has the potential to reduce a raised ICP. High doses of sumatriptan cause a further increase of ICP possibly by dilatation of intracerebral veins.

Animals↗
PubMed2000

Tolerability of sumatriptan: clinical trials and post-marketing experience.

Through December 1998, sumatriptan had been used to treat more than 236 million migraine attacks world-wide. In clinical trials alone, more than 88000 migraine patients had treated more than 300000 migraine attacks with sumatriptan, and 2000 normal healthy volunteers had been exposed to the drug. This paper describes the safety and tolerability profile of sumatriptan in three sections: adverse events reported in clinical trials, special issues, and spontaneous post-marketing reports of adverse reactions. Data from the extensive clinical trials programme coupled with information from nearly 10 years of experience in clinical practice demonstrate that sumatriptan is generally well-tolerated, with an acceptable benefit-risk ratio when used properly. Significant cardiovascular and cerebrovascular events are rare but have been observed. This fact highlights the need for careful patient selection and vigilant adherence to the prescribing recommendations for sumatriptan. The wealth of clinical trials and post-marketing information for sumatriptan may be useful in guiding prescribing decisions for members of this class of drugs.

Cardiovascular Diseases↗
PubMed2006

Infrequent or non-response to oral sumatriptan does not predict response to other triptans--review of four trials.

A migraineur can claim to be an infrequent responder ('non-responder') to an oral triptan independent of which triptan he or she is presently using. Four trials of an alternative triptan (zolmitriptan/rizatriptan; eletriptan; naratriptan; almotriptan) in patients with a history of infrequent response to oral sumatriptan were compared and contrasted in terms of study design, patient characteristics, and efficacy and tolerability of the triptan under investigation. Unfortunately, none of the reported studies used an appropriate parallel design, which would have had the non-responding triptan (oral sumatriptan) in one arm and without encapsulation. While the four trials differed in terms of study design (open-label vs. placebo-controlled), definition of sumatriptan 'non-responder' (retrospective vs. prospective) and pain intensity at baseline (30% severe to 70% severe), all four demonstrated that lack of response to sumatriptan did not predict lack of response to an alternative triptan. Changing triptans resulted in 2-h pain-relief rates of 25-81% in patients with a history of poor response to sumatriptan. It can be concluded that migraine patients who respond infrequently to sumatriptan should be switched to a different triptan, as lack of response to one triptan does not predict likelihood of responsiveness to another. A review of the available evidence suggests that almotriptan may be one of the most appropriate choices for an alternative triptan.

Administration, Oral↗
PubMed1991

Role of 5-HT1-like receptors in the reduction of porcine cranial arteriovenous anastomotic shunting by sumatriptan.

1. The new tryptamine derivative sumatriptan (GR43175) is effective in the treatment of migraine. Since several antimigraine agents reduce cranial arteriovenous anastomotic blood flow in the anaesthetized pig, we have investigated the carotid haemodynamic effects of sumatriptan. 2. Sumatriptan (10, 30, 100 and 300 micrograms kg-1, i.v.) reduced total common carotid blood flow, exclusively by affecting its arteriovenous anastomotic fraction; the capillary fraction even increased with the highest doses. 3. These reductions in the carotid arteriovenous anastomotic ('shunt') blood flow were mediated by a 5-HT1-like receptor, as methiothepin, but not ketanserin, antagonized the responses to sumatriptan. 4. Sumatriptan increased the difference in oxygen saturation between arterial and jugular venous blood, which is likely to be a consequence of the reduction of the carotid shunt blood flow. 5. The selective reduction in arteriovenous anastomotic blood flow produced by sumatriptan may reflect its antimigraine action, thought to involve vasoconstriction of those cranial vessels, be they 'shunt' vessels or not, which are distended and inflamed during a migraine attack.

Animals↗
PubMed1994

Comparison between venoconstrictor effects of sumatriptan and ergotamine in migraine patients.

The vasoconstrictor activity of sumatriptan and ergotamine were compared by injecting these drugs in the hand vein of migraine subjects. We used the "venotest method", which permits the evaluation of the venoconstrictor effect of small doses of drugs, acting locally in the hand vein. Sumatriptan injected at increasing doses in the hand vein provoked contraction only at high doses (500 micrograms): venoconstriction lasted 5-15 minutes and was similar in intensity and duration to that induced by 0.5-1 micrograms of 5-hydroxytryptamine (5-HT). Likewise, ergotamine induced contraction only at a dose of 50 micrograms: this venoconstrictor effect was long lasting (at least 1 hour). Ergotamine-induced hand vein contraction, almost completely inhibited by ketanserin, seems mediated at least in part by 5-HT2 receptors, like the one induced by 5-HT and sumatriptan, already observed in a previous study. Clinical doses of ergotamine (0.25 mg intramuscular) and of sumatriptan (6 mg subcutaneous) do not provoke hand vein contraction for at least 1 hour: this could be due to a low activity of these drugs on the 5-HT2 vein receptors or a technique that is unsuitable to detect the vasoconstrictor effect of drugs given by the systemic route. The long lasting venoconstrictor effect of ergotamine may be due to a slow dissociation from receptor sites. The short vasoconstriction induced by sumatriptan could account for the recurrence of headache in many sumatriptan-treated migraine subjects.

Adult↗
PubMed2006

Subcutaneous sumatriptan for refractory trigeminal neuralgia.

BACKGROUND: Mechanical compression of the trigeminal root by an artery is thought to cause trigeminal neuralgia. The 5-HT(1B/1D) receptor agonist may inhibit neurogenic inflammation and vasodilation near the irritated trigeminal root. OBJECTIVE: To examine the effectiveness of a 5-HT(1B/1D) receptor agonist, sumatriptan, on a paroxysmal pain in trigeminal neuralgia. METHODS: Twenty-four patients with trigeminal neuralgia refractory to previous treatment were randomized to receive subcutaneously either 3 mg (1 mL) of sumatriptan or 1 mL of saline placebo. Following a 7-day period, patients crossed over to receive the alternative treatment. Paroxysmal pain triggered by touching or moving the face was assessed with VAS before and 15 minutes after the treatment. Patients used a descriptive scale to pain-grade outcome, and asked to note whether the pain returned and how long after therapy it recurred. RESULTS: Subcutaneous sumatriptan, but not placebo, significantly decreased VAS from 8.3 +/- 2.1 to 2.4 +/- 3.0 cm (mean +/- SD). The number of patients who described their pain as moderately or slightly better was 20 in the sumatriptan group and 1 in the placebo group. The effect of subcutaneous sumatriptan persisted for a median period of 7.9 hours (range: 1-20 hours). CONCLUSIONS: Subcutaneous sumatriptan produced prompt analgesia without serious adverse reactions in patients with trigeminal neuralgia refractory to previous treatment.

Adult↗
PubMed2002

Amplification of sumatriptan-induced contraction in rabbit saphenous vein but not in basilar artery.

The modulation of serotonin (5-HT(1B/1D)) receptor-induced vascular contractility by histamine and U-46619 was compared in the rabbit basilar artery and saphenous vein. In the saphenous vein, histamine (5 x 10(-7) M) significantly increased the potency (from pEC(50) of 6.0 to 6.8) and efficacy (from 52.3% to 88.2%) of sumatriptan. Likewise, U-46619 (5 x 10(-9) M) also increased the potency (from pEC(50) of 5.9 to 6.6) and efficacy (from 51.8% to 92.1%) of sumatriptan in the saphenous vein. In contrast, equieffective concentrations of histamine (10(-7) M) and U-46619 (3 x 10(-9) M) failed to amplify contraction to sumatriptan in the basilar artery. Contraction to sumatriptan was inhibited by nitrendipine (10(-7) M) in the basilar artery but not in the saphenous vein, suggesting that different contractile signaling mechanisms are operating in these tissues. Furthermore, U-46619- and thrombin-induced contractility in the basilar artery were also not amplified by histamine, suggesting that lack of amplification of contraction in the basilar artery was not restricted to sumatriptan but was rather a characteristic of this cerebral vessel. These data suggest that in the in vivo plasma milieu sumatriptan will more markedly contract the peripheral saphenous vein than the basilar artery, a cerebral blood vessel.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2002

Calcium-antagonistic activity of sumatriptan in the rat anococcygeus muscle.

The relaxant effect of sumatriptan, a 5-HT(1B/1D) receptor agonist, on the rat anococcygeus muscle was investigated. Sumatriptan induced concentration-dependent relaxations of the phenylephrine-precontracted rat anococcygeus muscle. N(G)-nitro-L-arginine, methylene blue, glibenclamide, tetrodotoxin, indomethacin, GR 113808, GR 55562, methysergide, ketanserin, ICS 205930, clozapine, methiothepin, metergoline, mesulergine, and ritanserin did not inhibit the relaxations induced by sumatriptan. Sumatriptan converted calcium-induced contractions into relaxations in the preparations depolarized by a calcium-free, high-potassium solution. In membrane preparations obtained from the rat anococcygeus muscle, the basal rate of cAMP production by adenylate cyclase was 4.77 +/- 0.02 pmol/mg protein/min (n = 15). The enzyme activity was increased to 104 +/- 51.7 pmol/mg protein/min by forskolin (10(-4) mol/l), but did not change in the presence of sumatriptan. The mRNA expression of 5-HT(1B), 5-HT(1D), and 5-HT(7) receptors was not observed in the rat anococcygeus muscle. The results indicate that sumatriptan causes relaxation of the precontracted rat anococcygeus muscle by a calcium-antagonistic activity.

Adenylyl Cyclases↗
PubMed1991

Preclinical studies on the anti-migraine drug, sumatriptan.

Sumatriptan is believed to constrict selectively the cranial vessels that are distended and inflamed during migraine. The action is mediated by activation of a 5-HT1 receptor subtype which has been shown in animals to be localized in cranial vessels. Further studies to elaborate sumatriptan's precise clinical mode of action have focused on the human meningeal circulation and should lead to a better understanding of the pathogenesis of migraine. Administering [14C]sumatriptan, drug-related material was shown to be well absorbed. Following absorption there was some first-pass metabolism resulting in oral bioavailabilities of 37, 58 and 23% in rat, dog and rabbit, respectively. In all species, circulating sumatriptan was cleared rapidly by metabolic and renal clearance with a half-life of 1-2 h. The indoleacetic acid metabolite is the primary metabolic product; however, rats, mice and rabbits also N-demethylate the methylaminosulphonylmethyl side-chain. The passage of sumatriptan and its metabolites across the blood-brain barrier appeared to be very limited, although some drug could be detected in the cerebrospinal fluid after administration of high intravenous doses. Safety studies in various animal species showed that sumatriptan produced few adverse pharmacodynamic effects when administered acutely, except at high doses, although it was less well tolerated in dogs. No findings of toxicological significance were observed in rats and dogs after chronic dosing for 1 year or more.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Long-term experience with sumatriptan in the treatment of migraine.

Sumatriptan, a specific 5-hydroxytryptamine agonist, is a novel acute treatment for migraine. The efficacy and safety profiles of sumatriptan have previously been demonstrated in several controlled short-term studies. However, because migraine is a recurrent disorder which may persist throughout adult life, sustained efficacy and tolerability are essential if sumatriptan is to be of value in clinical practice. These aspects were therefore evaluated in a programme of three 12-month studies. Sustained efficacy with long-term use of single 100-mg oral doses has been demonstrated in an open study in which 288 patients treated 8,094 migraine attacks. The long-term safety profile of oral and subcutaneous sumatriptan has been evaluated in a total of 849 patients who treated 24,907 migraine attacks in studies lasting up to 1 year. Sumatriptan was well tolerated. Adverse events did not differ qualitatively or quantitatively from those in short-term studies, irrespective of the frequency of attacks or the number of doses used. Migraine attacks were effectively treated with doses less than the recommended maximum and there was no evidence of any adverse effect on attack frequency. In long-term studies the high efficacy of sumatriptan is maintained, and the adverse event profile is unchanged and unaffected by attack frequency.

Administration, Oral↗