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)

The use of beta-adrenergic antagonists for primary prevention of gastrointestinal hemorrhage in patients with cirrhosis and esophageal varices is discussed. In five controlled trials, patients with cirrhosis and endoscopically proven esophageal varices were treated with either propranolol or nadolol in doses to reduce heart rate by 20-25% or in doses to decrease hepatic vein pressure by 25% of basal levels or to a level of less than 12 mm Hg. In two of three studies, investigators found that propranolol significantly reduced frequency of initial bleeding in patients with esophageal varices. In one of two studies, nadolol significantly decreased the risk of variceal bleeding in patients with cirrhosis; in the other study, a significant difference in the frequency of initial bleeding was found only among patients who were compliant with therapy. Only one of the five studies showed a significant difference in survival between the treatment group and the placebo group. Adverse effects of therapy included dizziness, fatigue, cardiac insufficiency, Raynaud's phenomenon, and risk of bleeding associated with propranolol withdrawal. Therapy with a nonselective beta-adrenergic antagonist should be considered for primary prevention of gastrointestinal hemorrhage in patients with cirrhosis and suspected or documented large varices; however, abrupt discontinuation of the medication is associated with risk of bleeding.
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PMID:Beta-adrenergic antagonists for primary prevention of gastrointestinal hemorrhage in patients with cirrhosis and esophageal varices. 156 29

Nifedipine antagonises influx of calcium through cell membrane slow channels, and sustained release formulations of the calcium channel blocker have been shown to be effective in the treatment of mild to moderate hypertension and both stable and variant angina pectoris. Preliminary findings also indicate that these formulations are effective in the treatment of Raynaud's phenomenon and hypertension in pregnancy, and that they reduce the frequency of ischaemic episodes in some patients with silent myocardial ischaemia. The exact mechanism of action of nifedipine in all of these disorders has not been defined. However, its potent peripheral and coronary arterial dilator properties, together with improvements in oxygen supply/demand, are of particular importance. A major goal of sustained release therapy is to permit reductions in the frequency of nifedipine administration, preferably to once daily, and thus improve patient compliance. Two new once-daily formulations--the nifedipine gastrointestinal therapeutic system (GITS) and a fixed combination capsule comprising sustained release nifedipine 20 mg and atenolol 50 mg--have exhibited marked antihypertensive efficacy. The GITS preparation has also been used effectively in the treatment of stable angina pectoris, and both formulations appear to be well tolerated. Sustained release nifedipine formulations are generally better tolerated than their conventionally formulated counterparts, particularly with regard to reflex tachycardia. Adverse effects seem to be dose related, are mainly associated with the drug's potent vasodilatory action, and include headache, flushing and dizziness. Generally, these effects are mild to moderate in severity and transient, usually diminishing with continued treatment. Thus, sustained release nifedipine formulations are useful and established cardiovascular therapeutic agents which have demonstrable efficacy in various forms of angina, mild to moderate hypertension and Raynaud's phenomenon. Further, promising results shown by the nifedipine GITS formulation, with its advantage of once daily administration suggest that it is likely to become one of the preferred nifedipine formulations for the treatment of hypertension and the various forms of angina.
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PMID:Sustained release nifedipine formulations. An appraisal of their current uses and prospective roles in the treatment of hypertension, ischaemic heart disease and peripheral vascular disorders. 171 8

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

Ketanserin was used in a randomized double-blind trial in 15 patients with Raynaud's phenomenon in progressive systemic sclerosis (PSS). Its effect on Raynaud's phenomenon was evaluated by IR-radiometry, Doppler ultrasound, nailfold capillaroscopy, frequency of finger ulcerations and patient complaints before and after a 3-month course of treatment with oral ketanserin in the dosage of 60 mg daily in the first month and 120 mg in the second and third months. Of the 8 patients treated with ketanserin, 5 showed improvement. In the other 2 patients with progression of skin sclerosis and multiorgan involvement, the peripheral vascular disorder was unchanged. Ketanserin treatment was discontinued in one patient owing to dizziness and anxiety. In one patient ketanserin was reduced to 60 mg daily because of fluid retention. There were no other adverse effects. In 7 control patients on placebo there was no significant improvement in Raynaud's phenomenon. Ketanserin, a selective, specific and pure antagonist of 5-hydroxytryptamine (serotonin) appears to be an effective agent in the treatment of Raynaud's phenomenon and digital ischaemic ulcers in PSS. Moreover, ketanserin could contribute to the understanding of the role of 5-hydroxytryptamine in PSS pathogenesis.
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PMID:Effect of ketanserin on Raynaud's phenomenon in progressive systemic sclerosis: a double-blind trial. 391 37

Labetalol is a combined alpha- and beta-adrenoceptor blocking agent for oral and intravenous use in the treatment of hypertension. It is a nonselective antagonist at beta-adrenoceptors and a competitive antagonist of postsynaptic alpha 1-adrenoceptors. Labetalol is more potent at beta that at alpha 1 adrenoceptors in man; the ratio of beta-alpha antagonism is 3:1 after oral and 6.9:1 after intravenous administration. Labetalol is readily absorbed in man after oral administration, but the drug, which is lipid soluble, undergoes considerable hepatic first-pass metabolism and has an absolute bioavailability of approximately 25%. There are no active metabolites, and the elimination half-life of the drug is approximately 6 hours. Unlike conventional beta-adrenoceptor blocking drugs without intrinsic sympathomimetic activity, labetalol, when given acutely, produces a decrease in peripheral vascular resistance and blood pressure with little alteration in heart rate or cardiac output. However, like conventional beta-blockers, labetalol may influence the renin-angiotensin-aldosterone system and respiratory function. Clinical studies have shown that the antihypertensive efficacy of labetalol is superior to placebo and to diuretic therapy and is at least comparable to that of conventional beta-blockers, methyldopa, clonidine and various adrenergic neuronal blockers. Labetalol administered alone or with a diuretic is often effective when other antihypertensive regimens have failed. Studies have shown that labetalol is effective in the treatment of essential hypertension, renal hypertension, pheochromocytoma, pregnancy hypertension and hypertensive emergencies. In addition, preliminary studies indicate that labetalol may be of value in the management of ischemic heart disease. The most troublesome side effect of labetalol therapy is posture-related dizziness. Other reported side effects of the drug include gastrointestinal disturbances, tiredness, headache, scalp tingling, skin rashes, urinary retention and impotence. Side effects related to the beta-adrenoceptor blocking effect of labetalol, including asthma, heart failure and Raynaud's phenomenon, have been reported in rare instances.
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PMID:Labetalol: a review of its pharmacology, pharmacokinetics, clinical uses and adverse effects. 631 May 29

Verapamil hydrochloride, a prototype calcium antagonist, is now marketed in the United States for the acute treatment of supraventricular tachyarrhythmias and for chronic management of vasospastic and chronic stable angina. It inhibits the slow inward channel in in the heart and blocks calcium influx in smooth muscle. Its intrinsic negative inotropic action, which is apparent in isolated tissues, is offset in vivo by peripheral vasodilation. It has a mild, noncompetitive sympathetic antagonist effect; its most important electrophysiologic action is a depression of AV nodal conduction, accounting for its effect in supraventricular tachyarrhythmias. Its hemodynamic actions are characterized by a complex interplay of changes in preload, afterload, contractility, heart rate, and coronary blood flow. It does not depress cardiac function, except in severe heart failure. The drug has a mild dilator action on coronary arteries and reverses ergonovine-induced vasoconstriction. Controlled trials have established its role in Prinzmetal's variant angina, unstable angina, and chronic stable angina. It has also been found to be effective in obstructive cardiomyopathies. The potential role of verapamil in such conditions as hypertension, cardioprotection, and Raynaud's phenomenon needs further evaluation; at present these indications have not been approved by the Food and Drug Administration. The most common side effects include constipation, skin rash, and dizziness; AV block, heart failure, and sinus arrest may occasionally be encountered, especially when ventricular function is compromised or conduction system disease is present.
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PMID:Verapamil hydrochloride: pharmacological properties and role in cardiovascular therapeutics. 676 30

A 19-year-old woman with long-standing mixed connective tissue disease was admitted for dizziness. We examined cerebral blood flow quantitation using 99mTc-hexamethylpropyleneamine oxime (HMPAO) and single photon emission computed tomography (SPECT) at rest and after cold pressor test. Mean cerebral blood flow reduced remarkably when she complained dizziness and showed peripheral Raynaud's phenomenon after cold exposure. We concluded cold-induced reversible brain ischemia was the reason of dizziness. Our finding suggests brain Raynaud's phenomenon. Further studies are necessary to clarify this phenomenon.
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PMID:[Cold-induced reversible brain ischemia in mixed connective tissue disease, a case report]. 1112 68

We report a case of systemic sclerosis complicated by Takayasu's arteritis. A 68-year-old woman had been treated for hypertension since 1984. She also had Raynaud's phenomenon and noticed vertigo and dizziness. In January 1992, she was diagnosed with back bruit. In April 1994, she was complicated by vertigo and diagnosed with asymmetrical blood pressure. In October 1998, she consulted our hospital because of neck bruit, abdominal bruit, back bruit and stenosis of descending aorta bifurcation on chest computed tomography. Her blood pressure was asymmetrical, being recorded as 190/101 on the right and 140/90 on the left. Scleroderma was observed from the finger to forehand, precordia, and face. Telangiectasia was observed on the precordia. Laboratory studies revealed the presence of anti-nuclear antibody (x 1280, discrete speckled.), anti-centromere antibody but anti-topoisomerasel antibody was negative. Skin biopsy from the left forehand detected proliferation of collgen fibers and perivascular inflammatory cell infiltration. A diagnosis of systemic sclerosis was made according to the American Rheumatism Association criteria. We suspected complication by Takayasu's arteritis because of asymmetrical blood pressure and bruit. Chest-abdominal angiography detected stenosis of the right brachiocephalic trunk, celiac artery, and left renal artery. We diagnosed Takayasu's arteritis. This is the second case report of a patient with systemic sclerosis complicated by Takayasu's arteritis.
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PMID:[A case of systemic sclerosis complicated by Takayasu's arteritis]. 1216 15

A 54-year-old recreational angler was stung in his right forefinger by Echiichthys draco. Within a few seconds he developed severe swelling with extreme pain sensation at the sting site, accompanied by dizziness and chill. Even under morphine therapy the pain symptoms were only slightly reduced. During the subsequent weeks, an erythema with marginate medium-sized scaling developed at the sting site and the patient experienced a approximately 50% reduced bending capacity of the forefinger and permanent numbness in this region. After 4 months, Raynaud phenomenon developed limited to the right forefinger. Great weever fishes (Echiichthys spp.) are the most venomous fishes in European waters. In humans, life-threatening sting reactions occur only in exceptional cases. As a commercial antiserum is not available, the therapy is mainly empiric (General measures of first aid and emergency medicine, the wound should be thoroughly washed). Patients should be informed that reduced motion ability, swelling or Raynaud's phenomenon can persist for several months.
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PMID:[Persistent skin reaction and Raynaud phenomenon after a sting by Echiichthys draco (great weever fish)]. 1283 65

The postural orthostatic tachycardia syndrome is a disease characterized by excessively increased heart rate during orthostatic challenge associated with symptoms of orthostatic intolerance including dizziness, exercise intolerance, headache, fatigue, memory problems, nausea, blurred vision, pallor, and sweating, which improve with recumbence. Postural orthostatic tachycardia syndrome patients may present with a multitude of additional symptoms that are attributable to vascular vasoconstriction. Observed signs and symptoms in a patient with postural orthostatic tachycardia syndrome include tachycardia at rest, exaggerated heart rate increase with upright position and exercise, crushing chest pain, tremor, syncope, loss of vision, confusion, migraines, fatigue, heat intolerance, parasthesia, dysesthesia, allodynia, altered traditional senses, and thermoregulatory abnormalities. There are a number of possible dermatological manifestations of postural orthostatic tachycardia syndrome easily explained by its recently discovered pathophysiology. The author reports the case of a 22-year-old woman with moderate-to-severe postural orthostatic tachycardia syndrome with numerous dermatological manifestations attributable to the disease process. The cutaneous manifestations observed in this patient are diverse and most noticeable during postural orthostatic tachycardia syndrome flares. The most distinct are evanescent, hyperemic, sharply demarcated, irregular patches on the chest and neck area that resolve upon diascopy. This distinct "evanescent hyperemia" disappears spontaneously after seconds to minutes and reappears unexpectedly. Other observed dermatological manifestations of this systemic disease include Raynaud's phenomenon, koilonychia, onychodystrophy, madarosis, dysesthesia, allodynia, telogen effluvium, increased capillary refill time, and livedo reticularis. The treatment of this disease poses a great challenge. The author reports the unprecedented use of an oral angiotensin II type 1 receptor antagonist resulting in remarkable improvement.
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PMID:Postural orthostatic tachycardia syndrome: a dermatologic perspective and successful treatment with losartan. 2516 60


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