Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ketanserin is a 5-HT2 receptor antagonist without partial agonist properties which also possesses weak alpha 1-adrenoceptor antagonistic activity, which may explain its antihypertensive mechanism of action in patients with essential hypertension. It also inhibits the effects of serotonin on platelets in cardiovascular disease, inhibits vasoconstriction caused by the amine, and when administered intravenously improves some haemorheological indices in patients with ischaemic diseases. The antihypertensive effect of oral ketanserin 40 mg twice daily is comparable with that of total daily doses of metoprolol 200 mg, propranolol 160 mg, captopril 100 mg, enalapril 20 mg, hydrochlorothiazide 50 mg, or alpha-methyldopa 1000 mg and is achieved without adverse effect on plasma lipoproteins or carbohydrate metabolism in patients with concomitant diabetes mellitus. Evidence from prospective studies suggests a greater antihypertensive efficacy in the elderly than in younger patients. In patients with intermittent claudication, results have been inconsistent in small studies, while a large study showed no improvement in pain-free walking distance but fewer amputations compared to placebo. In Raynaud's phenomenon symptomatic improvement relative to placebo was achieved in larger trials. Its role in preventing atherosclerotic complications requires further investigation. Ketanserin is reasonably well tolerated, the frequency of adverse effects being comparable with that of other antihypertensive drugs in controlled trials. Dizziness, tiredness, oedema, dry mouth and weight gain are the most commonly reported effects. Ketanserin prolongs QT interval in a dose-related manner, and when given in certain predisposing circumstances ventricular arrhythmias and syncope may occur. Administered intravenously, ketanserin 10mg followed by an infusion of 2 to 4 mg/h controls moderate to severe pre- and postoperative hypertension in most patients, acting as a balanced vasodilator, lowering cardiac pre- and afterload. Although the arrhythmogenic potential of ketanserin in patients receiving potassium-depleting diuretics requires suitable precautions, it appears that its antihypertensive activity is suited to the elderly provided plasma potassium concentrations are normal at the start of treatment and are maintained within the normal range.
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PMID:Ketanserin. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in hypertension and peripheral vascular disease. 207 1

The effects of pentoxifylline on intermittent claudication were evaluated at a dose of 1200 mg/day in an open-label twelve-week study on geriatric patients with chronic occlusive arterial disease (COAD). Standardized treadmill testing and clinical signs and symptoms of COAD were followed up before and during drug administration. Twenty-four subjects with a mean age of 73.5 years, capable of walking between 20 and 200 meters on the treadmill, were entered into the trial; 22 participated for eight weeks and 19 completed the study in terms of treadmill walking distance measurements at 12 weeks. The mean walking distance for all patients was increased 111% over baseline at week 12. Thirteen subjects were considered drug responders (greater than or equal to 50% increase in treadmill walking distance) and 9 were considered nonresponders (less than 50% increase). Improvements in clinical signs and symptoms of COAD were noted. Decreases in elevated systemic systolic pressures (but not diastolic) were unexpectedly observed in many drug responders. Seven of 19 males reported sexual function improvements while receiving pentoxifylline. Fourteen (58%) of the 24 subjects reported mild side effects of dyspepsia, nausea, vomiting, dizziness, headache, or insomnia; no subjects were withdrawn from the study because of side effects. In summary, pentoxifylline improved function and symptoms in 13 of 22 geriatric patients with intermittent claudication; the drug was safe and well tolerated at the usual dosage in this geriatric patient population.
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PMID:Efficacy and safety of pentoxifylline in geriatric patients with intermittent claudication. 266 64

Twenty patients underwent axilloaxillary bypass at Tufts-New England Medical Center, Boston, between 1973 and 1983, all for tight stenosis or occlusion of the subclavian artery. Review of records was possible for 19 cases. Symptoms included intermittent claudication and numbness of the upper extremity, as well as dizziness, vertigo, and ataxia due to episodes of vertebrobasilar insufficiency. Dacron, reversed saphenous vein, and polytetrafluoroethylene grafts were inserted, with all but one occupying a subcutaneous tunnel across the sternum. There were no operative deaths, and morbidity was minimal. The median follow-up was 83 months. The early patency rate was 94%, with a cumulative patency rate of 89% at ten years of follow-up, as determined by the life-table method. Our experience supports axilloaxillary bypass as a safe and effective treatment for symptomatic subclavian artery insufficiency.
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PMID:Subclavian artery insufficiency. Treatment with axilloaxillary bypass. 363 38

A simultaneous approach to revascularization for combined coronary and carotid disease today is well accepted. The discussion about combined procedures of carotid and aortoiliac occlusive disease is still going on. We operated upon 3 patients, aged 63,56 and 65 years, who suffered from carotid, aortoiliac and renal artery disease. Main symptoms were hypertensive crisis with pulmonary edema and intermittent claudication. Dizziness, transient ischemic attacks and slight renal insufficiency were present in two, one and two patients respectively. After recompensation a simultaneous operation was performed: carotid endarterectomy with inlying shunt, reconstruction and patch-plasty of the renal arteries and implantation of a aortofemoral artery bypass graft. Postoperative complications: hypertensive crisis, low output syndrome and oliguria (1 pt.) and deep vein thrombosis (1 pt.) could be treated conservatively. 10 and 12 months later the patients are symptom-free except one, who suffers from angina NYHA II. In conclusion we recommend carotid endarterectomy simultaneously with any major vascular procedure, if a critical stenosis is visualized to improve long-term survival in addition to reducing operative mortality.
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PMID:[Simultaneous intervention on the carotid artery, abdominal aorta and their branches]. 400 9

Cilostazol is an antiplatelet agent with vasodilating properties that has been used in the treatment of patients with peripheral ischaemia such as intermittent claudication. The drug inhibits platelet aggregation induced by ADP, collagen and arachidonic acid. Unlike aspirin (acetylsalicylic acid), cilostazol inhibits both primary and secondary aggregation. It also acts as a vascular vasodilator by inhibiting calcium-induced contractions while having no direct effect on contractile proteins. In double-blind randomised trials, patients with intermittent claudication receiving cilostazol showed significant improvements versus placebo in terms of time to initial pain and maximal walking or absolute claudication distance; these findings were confirmed by cilostazol patients' positive responses on subscales measuring physical functioning and quality of life. In a 24-week randomised double-blind trial in patients with intermittent claudication, cilostazol 100mg twice daily produced significant improvements in pain-free and maximum walking distances, compared with pentoxifylline (oxpentifylline) 400mg 3 times daily and placebo. Cilostazol has been well tolerated, with the most common adverse events being headache, diarrhoea, abnormal stools and dizziness.
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PMID:Cilostazol. 1006 9

EGb 761 is a standardized extract of dried leaves of Ginkgo biloba containing 24% ginkgo-flavonol glycosides, 6% terpene lactones such as ginkgolides A, B, C, J and bilobalide. Its broad spectrum of pharmacological activities allows it to be in adequacy to the numerous pathological requirements--hemodynamic, hemorheological, metabolic--which occur in cerebral, retinal, cochleovestibular, cardiac or peripheral ischemia. Moreover, EGb 761 has direct effects against necrosis and apoptosis of neurons and improves neural plasticity as evidenced in vestibular compensation. At the molecular and the cellular levels, some evidence obtained with animal models indicates that EGb 761 can interact as a free radical-scavenger and a inhibitor of lipid peroxidation with all, or nearly all reactive oxygen species; maintains ATP content by a protection of mitochondrial respiration and preservation of oxidative phosphorylations; exerts arterial and venous vasoregulator effects involving the release of endothelial factors and the catecholaminergic system. Moreover, EGb 761 regulates ionic balance in damaged cells and exerts a specific and potent Platelet-activating factor antagonist activity. Numerous well-controlled clinical studies, realized in Europe and in USA, have revealed that EGb 761 is an effective therapy for a wide variety of disturbances of cerebral function, ranging from cerebral impairment of ischemic vascular origins (i.e. multi infarct dementia), early cognitive decline to mild-to-moderate cases of the more severe types of senile dementias (including Alzheimer's disease) or mixed origins (i.e. psychoorganic origin). Improvement of signs and symptoms have been demonstrated for cognitive functions, particularly for memory loss, attention, alertness, vigilance, arousal and mental fluidity. Some clinical studies have showed that EGb 761 treatment may improve the capacity of geriatric patients to cope with the stressful demands of daily life. The explanation is a dual stress-alleviating action of EGb 761: its facilitates behavioral adaptation to stress and may decrease the excess of cortisol release to stress. Moreover, EGb 761 shows a specific neuroprotective effects to hippocampic cells. Regarding the visual system, experimental studies have shown that EGb 761 can inhibit or reduce the functional retinal impairments resulting from ischemia-reperfusion, photo-degeneration, diabetic or proliferative retinopathy. Clinical studies have revealed that EGb 761 may be useful in treating visual activity impairments and damages to the visual field associated with chronic cerebrovascular insufficiency, senile macular degeneration and diabete mellitus. Regarding the vestibular and auditory systems, experimental and clinical studies have shown the efficacy of EGb 761 in treating hypoacusis, tinnitus, vertigo, dizziness and other symptoms of vestibulocochlear disorders. At least, adequatly controlled studies in patients with peripheral arterial occlusive disease have provided good evidence for therapeutic efficacy in intermittent claudication. The future of EGb 761 is undoubtedly in the promise in slowing the progression of Alzheimer's disease. Indeed, two recent american clinical studies have shown the efficacy and safety of EGb 761 in patients with mild to severe Alzheimer's disease and multi-infarct dementia. In clinical terms, progression of symptoms was delayed by approximately 6 months. Actually new clinical studies are undertaken in USA and Europe. At the dawn of the third millenium (the Sixth for Ginkgo biloba) we propose a state of art about it.
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PMID:[Ginkgo biloba extract (EGb 761). State of knowledge in the dawn of the year 2000]. 1048 50

Cilostazol (Pletal), a quinolinone derivative, has been approved in the U.S. for the treatment of symptoms of intermittent claudication (IC) since 1999 and for related indications since 1988 in Japan and other Asian countries. The vasodilatory and antiplatelet actions of cilostazol are due mainly to the inhibition of phosphodiesterase 3 (PDE3) and subsequent elevation of intracellular cAMP levels. Recent preclinical studies have demonstrated that cilostazol also possesses the ability to inhibit adenosine uptake, a property that may distinguish it from other PDE3 inhibitors, such as milrinone. Elevation of interstitial and circulating adenosine levels by cilostazol has been found to potentiate the cAMP-elevating effect of PDE3 inhibition in platelets and smooth muscle, thereby augmenting antiplatelet and vasodilatory effects of the drug. In contrast, elevation of interstitial adenosine by cilostazol in the heart has been shown to reduce increases in cAMP caused by the PDE3-inhibitory action of cilostazol, thus attenuating the cardiotonic effects. Cilostazol has also been reported to inhibit smooth muscle cell proliferation in vitro and has been demonstrated in a clinical study to favorably alter plasma lipids: to decrease triglyceride and to increase HDL-cholesterol levels. One, or a combination of several of these effects may contribute to the clinical benefits and safety of this drug in IC and other disease conditions secondary to atherosclerosis. In eight double-blind randomized placebo-controlled trials, cilostazol significantly increased maximal walking distance, or absolute claudication distance on a treadmill. In addition, cilostazol improved quality of life indices as assessed by patient questionnaire. One large randomized, double-blinded, placebo-controlled, multicenter competitor trial demonstrated the superiority of cilostazol over pentoxifylline, the only other drug approved for IC. Cilostazol has been generally well-tolerated, with the most common adverse events being headache, diarrhea, abnormal stools and dizziness. Studies involving off-label use of cilostazol for prevention of coronary thrombosis/restenosis and stroke recurrence have also recently been reported.
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PMID:Cilostazol (pletal): a dual inhibitor of cyclic nucleotide phosphodiesterase type 3 and adenosine uptake. 1183 Jul 53

Pharmacotherapy is limited for the relief of intermittent claudication (IC), a common manifestation of peripheral arterial disease (PAD). Pentoxyfylline, the only current pharmacological therapy for IC, has been shown to have similar efficacy as placebo. Cilostazol, a new phosphodiesterase III (PDE III) inhibitor, is a potent inhibitor of platelet aggregation with vasodilatory, antithrombotic, antiproliferative and positive lipid-altering effects. To evaluate the efficacy and safety of cilostazol for the treatment of IC in Indian patients, 123 patients were selected from 6 centres in India. The patients, aged 58-73 years, with the diagnosis of stable moderate-to-severe IC received cilostazol 100/50 mg twice daily for a period of 12 weeks. Primary efficacy measures included initial claudication distance (ICD) and absolute walking distance (ACD) by treadmill testing and ankle-brachial index (ABI) using Doppler ultrasonography-measured systolic pressures. Secondary efficacy outcomes included subjective assessment of symptom improvement by patient and investigator and estimation of lipid values. Adverse events were monitored throughout the study. Laboratory investigations were carried out at baseline and end of study. At the end of week 12 of cilostazol therapy, there was a significant improvement in the raw walking distances (ICD and ACD). Percentage change in ICD and ACD was 46.77% and 64.5%, respectively, at the end of study. There was a significant increase (32.7%) in the ABI by the end of study period. According to patient and investigator assessment of symptoms, 58-60% of the subjects showed significant improvement to complete resolution of claudication symptoms by the end of 12 weeks of therapy. In addition, there was a significant increase of 20.24% in the mean plasma HDL-cholesterol levels and a decrease of 29.55% in the mean plasma triglyceride concentrations by the end of study period. Headache, diarrhoea, palpitation and dizziness were the commonly reported adverse effects during the study. No adverse effect led to discontinuation of therapy. The present study suggests that cilostazol is an effective therapeutic option with an acceptable tolerability profile for the treatment of IC in patients with PAD.
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PMID:Efficacy and safety of cilostazol, a novel phosphodiesterase inhibitor in patients with intermittent claudication. 1516 99

Ginkgo is probably one of the most widely used medicinal herbs in Europe. In Norway products of ginkgo leaf extract have been approved by the Norwegian Medicines Agency for the following indication: traditionally used to improve blood circulation, for example, cold hands and feet. Elsewhere, ginkgo is used for cognitive impairment and dementia, acute ischaemic stroke, intermittent claudication, tinnitus and age-related macular degeneration. Evidence of the efficacy of ginkgo for these indications has previously been studied by the Cochrane Collaboration. In this update we have repeated all the searches in Medline and EMBASE exactly as described in the five Cochrane Systematic Reviews (last search date: 16.02.2011). We identified two new randomised and placebo-controlled studies on cognitive impairment and dementia (3187 patients) and one study on acute ischaemic stroke (3069 patients). The results of these studies gave no reason to change the conclusions of earlier reviews by the Cochrane Collaboration. There is no convincing evidence that ginkgo is effective for cognitive impairment or dementia, acute ischaemic stroke, intermittent claudication or tinnitus. There is still a lack of conclusive evidence for the effect on age-related macular degeneration. Ginkgo leaf extract appears to be safe to use, with no excess side effects compared with placebo. It can cause some minor side effects such as stomach upset, headache, dizziness, constipation, forceful heartbeat, and allergic skin reactions. There is some concern that ginkgo leaf extract might increase the risk of bruising and bleeding, and interactions with anticoagulants/antiplatelet drugs cannot be ruled out. As a general precaution, it is recommended withdrawing ginkgo two weeks before elective surgery.
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PMID:[Ginkgo biloba--effect, adverse events and drug interaction]. 2256 27

We investigated the efficacy of pregabalin (PGB) for neuropathic leg pain in lumbar spinal stenosis (LSS) patients with disturbed activities of daily living (ADL)/quality of life (QOL) in a prospective observational study. Subjects were a total of 104 LSS patients with neuropathic pain (NeP) in leg and neurological intermittent claudication (IMC) refractory to nonsteroidal anti-inflammatory drugs (NSAIDs) for at least a month. NeP was identified using screening tool, Pain DETECT questionnaire. Visual analog scale (VAS) scores and responses to the Japanese Orthopaedic Association Back Pain Evaluation Questionnaire (JOABPEQ) were assessed before and 6 weeks after PGB treatment initiation. Changes in IMC distance and adverse events were also recorded. PGB significantly improved their VAS scores for pain and sleep quality (P < 0.001). With respect to JOABPEQ, significant improvements were observed with regard to the following dimensions: pain-related disorders (P < 0.01), lumbar spine dysfunction (P = 0.031), gait disturbance (P = 0.028), and psychological disorders (P = 0.014). The IMC distance showed an improvement tendency after PGB treatment, albeit with no significance (P = 0.063). Minor adverse events such as dizziness were observed. PGB can be effective for neuropathic leg pain refractory to NSAIDs in LSS patients, resulting in not only pain control but also improving lower back pain-related ADL/QOL scores.
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PMID:Pregabalin for Refractory Radicular Leg Pain due to Lumbar Spinal Stenosis: A Preliminary Prospective Study. 2744 15


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