Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For clarification of possible platelet activation in migraine and chronic muscle contraction headache (MCH) under stress, plasma platelet factor 4 (PF4), norepinephrine (NE), and free fatty acids (FFA) were investigated during the cold pressor test. Both PF4 and NE increased significantly, whereas FFA showed no remarkable changes. The increases of PF4 in MCH and migraine during this test were significantly greater than in healthy controls. The increase of PF4, however, was independent of NE increase and FFA changes. On the other hand, we observed decreased NE levels in both MCH and migraine, which might suggest peripheral sympathetic hypofunction. The platelets of MCH or migraine patients seem to be impaired, and the impairment may be caused by continuous sympathetic hypofunction. The behaviour of the above three substances in MCH was similar to that in migraine throughout the present study.
Cephalalgia 1989 Mar
PMID:Muscle contraction headache and migraine. Platelet activation and plasma norepinephrine during the cold pressor test. 270 77

In migraine, the role of platelets is regarded as an important factor. We investigated plasma beta-thromboglobulin (BTG), platelet factor 4 (PF4), and 5-hydroxytryptamine (5-HT) in migraine patients and muscle contraction headache (MCH) patients during headache-free periods. The mean values of the plasma BTG, PF4, and 5-HT concentrations in the migraine group and the MCH group were significantly higher than those in healthy controls. The mean value of the plasma BTG concentration was significantly higher in the migraine group than in the MCH group, but the differences in the mean plasma PF4 and 5-HT concentrations between the two groups were not significant. Continuous platelet activation exists in both MCH patients and migraine patients. From the biochemical point of view, we have provided evidence for a similarity between migraine and MCH.
Cephalalgia 1987 Dec
PMID:Platelet activation in muscle contraction headache and migraine. 296 39

In order to study the role of platelets in migraine and cerebrovascular disease, beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) plasma levels, indices of in vivo platelet activation, were assayed in two groups of patients suffering from migraine (common/classic and classic/complicated migraine, respectively) and in one group suffering from transitory ischemic attacks (TIAs). Plasma determinations were carried out in the absence of treatment and during the administration of aspirin (50 mg/daily) and flunarizine (10 mg/daily). Platelet activation was found in patients suffering from TIA; patients affected by classic and complicated migraine showed a high incidence of activation, in comparison with common migraine sufferers, also in headache-free periods. Administration of aspirin (ASA) was more effective than flunarizine in inducing a decrease in beta-TG and PF4 plasma levels in migraineurs. Aspirin, however, did not affect platelet activation in subjects suffering from ischemic attack even though we did not observe any relapse after one year of treatment. The different effect of ASA in TIAs and migraine indicates that the platelet activation in TIA patients is due not only to cyclo-oxygenase pathway but also to other in vivo pathways.
Cephalalgia 1985 May
PMID:Drugs and platelet activation in migraine and transient ischemic attacks. 316 Apr 72

Twenty-three patients with essential hypertension and diabetes mellitus type II were treated with the calcium antagonist diltiazem (120 to 180 mg twice daily). The mean dose was 307 mg/day. The study was a double-blind, placebo-controlled, crossover design. All measurements were performed 12 to 14 hours after drug intake. Blood pressure, heart rate and forearm blood flow were measured noninvasively. Platelet function was studied by measuring adenosine diphosphate-induced platelet aggregation and the platelet specific proteins, beta thromboglobulin and platelet factor 4. Thromboxane B2 formation in serum and the plasma concentration of diltiazem and its metabolites N-demethyldiltiazem, deacetyldiltiazem and N-demethyldeacetyldiltiazem were measured both during placebo and diltiazem treatment. Diabetic control was evaluated by following HbA1C, fasting blood glucose and urinary glucose. Diltiazem reduced both systolic and diastolic (supine and standing) blood pressure significantly. Forearm blood flow was significantly increased by 32%, p less than 0.05. Supine heart rate decreased significantly, while no such change was seen in the standing position. No significant changes were observed in platelet function during diltiazem treatment. There was no relation between the observed blood pressure reduction and the plasma concentration of diltiazem or its metabolites. A positive correlation between the change in heart rate and the metabolite N-demethyldeacetyldiltiazem was observed (r = 0.647, p = 0.005). Three patients were excluded during diltiazem treatment (skin exanthema, headache and atrial fibrillation) and 1 during placebo treatment (angina pectoris). No negative effect on diabetes control was observed. Thus, diltiazem could be used for treatment of hypertension in diabetic patients.
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PMID:Diltiazem in hypertensive patients with type II diabetes mellitus. 317 28

Although platelet activation is known to occur during migraine attacks, the cause-effect relationship remains to be determined. This problem was approached by studying the possible occurrence of platelet activation in vivo in headache-free periods of subjects affected by common or classic migraine and, subsequently, by verifying the possibility of its pharmacological control through administration of a classic anti-aggregation drug such as aspirin (ASA). The plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4), indices of the occurrence of platelet activation in vivo, were therefore first assayed in both groups of migraine sufferers in the absence of therapy and then during the administration of aspirin (50 mg/daily). In the group of 15 patients affected by classic migraine, basal plasma levels of beta-TG and PF4 were significantly higher than control subjects. On the other hand, only beta-TG plasma levels were significantly higher in the group of 18 patients affected by common migraine. Patients suffering from classic migraine showed a high incidence of platelet activation (greater than 90%) in comparison with common migraine patients (approximately 33%). This suggests that platelet activation occurs in vivo in migrainous patients also during headache-free periods. Administration of aspirin to the patients affected by common and classic migraine caused a decrease in plasma beta-TG and PF4 concentration. Consequently, pharmacological treatment with aspirin in adequate dose may prove to be helpful in diminishing the vascular side-effects known to occur in migraine sufferers.
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PMID:Study of platelet activation in migraine: control by low doses of aspirin. 623 Jul 78

Several studies in vivo indicate platelet activation in migraine, as reflected by increased plasma concentrations of platelet secretory products. In vitro data on platelet secretion are scant, which prompted an investigation into agonist-induced platelet aggregation and secretion in platelets from patients with migraine. Sixty two patients with migraine with aura (MA) and 41 with migraine without aura (MwA) were studied during a headache-free phase, together with 26 healthy controls. Platelet aggregation and secretion in platelet-rich plasma were induced by collagen and platelet activating factor (PAF). Serotonin was measured by high performance liquid chromatography and platelet factor 4 (PF4) with an enzyme immunoassay kit. There were no significant aberrations in platelet aggregation in those with migraine compared with healthy controls. The platelet PF4 secretion induced by PAF (1.0 and 0.1 microM) was increased in MwA (p < 0.05, p < 0.0001) compared with controls, and there was a similar trend in MA (NS, p < 0.01). By contrast, the PF4 secretion induced by collagen (0.5 and 2.0 micrograms/ml) was reduced in MA (p < 0.01 and p < 0.05). Further, the MA group exhibited increased basal intraplatelet serotonin concentrations (p < 0.0001) and increased serotonin secretion induced by both concentrations of collagen (p < 0.0001) and PAF (p < 0.001). The data indicate an abnormal platelet a-granule secretion in those with migraine, and focus attention on PAF as a possible factor contributing to the platelet activation associated with migraine. The increased platelet content and secretion of serotonin was specific to MA, and may reflect different serotonin turnover in the two clinical migraine types.
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PMID:Platelet secretion from dense and alpha-granules in vitro in migraine with or without aura. 820 23

We investigated platelet aggregation and secretion from dense and alpha-granules in vitro in 28 tension-type headache (TH) patients and 26 healthy controls. We also measured basal platelet serotonin levels. Platelet aggregation was normal in TH, but the secretion of serotonin and platelet factor 4 (PF4) was significantly increased in response to 0.5 and 2.0 micrograms/ml collagen and to 1.0 mumol/l PAF. The basal platelet serotonin levels were also higher in patients than in controls. The mechanisms of platelet hypersecretion remain to be determined, but the increased secretion of serotonin is probably in part related to the increased basal levels. The increased platelet serotonin in TH patients may reflect an enhanced serotonin turnover.
Cephalalgia 1993 Oct
PMID:Increased platelet serotonin content and hypersecretion from dense and alpha-granules in vitro in tension-type headache. 824 29

Parenteral compounds present special drug delivery challenges. This open-label study evaluated a portable infusion pump as a means to deliver intravenous ciprostene, a stable prostacyclin analog. Ten patients with peripheral vascular disease and claudication received ciprostene (titrated to 120 ng/kg/min) infused over 8 hours 1 day per week for 4 consecutive weeks. Patients successfully maintained the pump strapped to the waist. The mean +/- standard deviation delivery error, with volumes of 6 to 10 mL over 8 hours, was -0.895 +/- 3.177%. Accordingly, the pump performed well with a potent drug under these clinical conditions. Headache, flushing, and infusion site irritation during infusion were the most frequent side effects. Blood pressure remained unchanged during infusion; however, heart rate increased significantly (P < .05, maximum increase was 13.9 +/- 2.1 beats per minute [mean +/- standard error of the mean]. Mean (+/- standard error of the mean) relative claudication times on treadmill remained unchanged; however, absolute claudication times increased (P < .05) from 6.6 +/- 1.8 to 10.0 +/- 2.2 minutes. Ciprostene inhibited adenosine diphosphate-induced platelet aggregation by 56.0 +/- 12.7% (mean +/- standard error of the mean). Mean template bleeding times and plasma concentrations of platelet-specific proteins (beta-thromboglobulin, platelet factor 4) did not change.
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PMID:Continuous intravenous dosing with ciprostene using a portable pump in ambulatory patients. 844 Jul 64

We analysed 22 patients suffering from migraine to evaluate the possible activation of platelet function utilizing the following methods: platelet factor 4, thromboxane B2 and 6 - keto prostaglandin F 1 alpha levels in platelet poor plasma. Laboratory tests were performed on all patients during headache-free period and the results obtained were compared with those of a normal healthy individuals. The mean results obtained in the patients group during pain-free period indicated a significant activation of platelet function when compared with the normal group.
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PMID:Migraine--a haematological disorder? 868 25

A 27-year-old woman was admitted to our hospital because of headache, fever and right neck pain. Neurological examination revealed mild meningeal signs, and hyper-reflexia in all extremities. In the laboratory tests, white-cell count was 13,000/mm3, rheumatoid factor(RF) and C-reactive protein(CRP) were positive. The cerebro-spinal fluid showed pleocytosis (56/mm3, neutorophils and lymphocytes were 26 and 28, respectively). Thus, she was diagnosed as aseptic meningitis. A few days later, she had weakness and dysesthesia of the right face and the left extremities. Pulse therapy with intravenous methylprednisolone was started. A magnetic resonance imaging (MRI) of the brain showed a hemorrhagic infarction in the right parietal lobe. In hemostatic markers, thrombin-antithrombin III complex(TAT; 106 ng/dl), D-dimer 1234 ng/dl, prothrombin fragment 1 + 2(F1 + 2; 2.36 nmol/L), beta-thromboglobulin (beta TG; 4,300 ng/dl) and platelet factor 4 (PF-4; 1,770 ng/dl) were extremely elevated. On duplex ultrasonography, a low echo lucent plaque was observed at the right internal carotid artery and the mean blood flow velocity in the right carotid artery was decreased. She was placed on oral prednisolone and warfarin for suspected stroke due to hypercoagulability associated with vasculitis. Afterwards, she discharged from our hospital. Two months later, she was readmitted to our hospital because of irregular menses and vaginal bleeding. Endometrial uterus biopsy was conducted, which revealed a grade I endometrioid adenocarcinoma. She was under total uterectomy without tumor recurrence. After the radical operation, white-cell count, RF, CRP, TAT, D-dimer, F1 + 2, and beta TG were normalized, and the mean flow velocity of the right common carotid artery was increased. Thereafter, she did not experience stroke recurrence. Therefore, we speculated that she had stroke due to hypercoagulability in association with malignancy, that is Trousseau's syndrome. We also assumed that aseptic meningitis, brainstem encephalitis associated with vasculitis in this patient are other clinical variants of paraneoplastic syndrome through immunological mechanisms associated with malignancy. We emphasize that patients with Trousseau's syndrome can be associated with other paraneoplastic manifestations such as vasculitis as seen in this patient.
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PMID:[A young patient with endometrioid adenocarcinoma who suffered Trousseau's syndrome associated with vasculitis]. 1247 93


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