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)

Sulindac (cis-5-fluoro-2-methyl-l-[(p-methyl sulfinyl)-benzylidene]-indene-3-acetic acid) is a new nonsteroidal antirheumatic drug recently evaluated in a double-blind trial of 91 patients with hip osteoarthritis. Consecutive patients with documented flare following previous drug withdrawal were randomly assigned to one of 3 treatment groups: (1) sulindac given twice daily, (2) sulindac given 4 times daily, and (3) placebo. The dosage of sulindac, 100 to 300 mg daily, was adjusted according to patient global response and tolerance at 3- to 7-day intervals over 3 wk. Of 15 efficacy measurements evalulated, there was no difference between sulindac given 2 or 4 times daily, but differences were disclosed between one or both sulindac treatment groups and placebo in 11 of the 15 efficacy measurements (p less than 0.05, less than 0.01). The frequency of adverse reactions was of the same order for each treatment group. These included gastrointestinal upset, rash, and dizziness, usually transient and mild to moderate in severity. Serial laboratory studies revealed no evidence of renal, hepatic, or hematopoietic toxicity.
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PMID:A multicenter trial of sulindac in osteoarthritis of the hip. 33 80

Rilmenidine is an oxazoline derivative with antihypertensive activity which was developed to enhance the dissociation between the hypotensive and adverse effect profile of centrally acting agents. Experimental studies have indicated that rilmenidine is selective for both alpha 2-adrenoceptors (v alpha 1) and newly discovered nonadrenergic imidazoline receptors in the brain and in the periphery. In experimental studies, rilmenidine differs from clonidine in that it is more selective for imidazoline receptors than for alpha 2-adrenoceptors; at equihypotensive doses, rilmenidine causes less bradycardia and reduction in cardiac output, less sedation, and little or no antinociceptive action compared to clonidine. The hypotensive effects of rilmenidine are antagonised by idazoxan and yohimbine, but idazoxan (imidazoline structure) is six times more potent than yohimbine (a selective alpha 2-antagonist). In isolated renal proximal tubule cells, where imidazoline binding has also been shown, rilmenidine inhibits reabsorption of sodium. Clinical studies comparing 1 mg rilmenidine with placebo demonstrated significant reductions in blood pressure (BP) (61% rilmenidine v 23% placebo normalized to 160/90 mm Hg). The reduction in BP was not associated with classical alpha 2 side effects such as dry mouth or daytime drowsiness. Compared with clonidine (0.15 to 0.3 mg), equihypotensive doses of rilmenidine (1 to 2 mg) induced two to three times less dry mouth, daytime drowsiness, and constipation; no orthostatic hypotension was reported. Methyldopa (0.5 to 1 mg) v rilmenidine (1 to 2 mg) indicated a comparable reduction of BP with significantly less weakness, drowsiness, orthostatic dizziness, and dry mouth on rilmenidine; there was no evidence of the "clonidine withdrawal syndrome" on drug withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Distinctive features of rilmenidine possibly related to its selectivity for imidazoline receptors. 135 Jul 32

Felodipine is a dihydropyridine that blocks the slow entry channel for calcium. It is highly vascular selective and reduces blood pressure (BP) by dilatation of peripheral arterioles. It reduces BP in mild, moderate, and severe hypertension, and the fall in BP depends upon the initial level. It has been compared with a variety of other drugs as monotherapy or as add-on therapy. In these studies, felodipine (10-40 mg/day) has caused a similar or greater fall in BP and a similar or greater percentage of patients have achieved a diastolic BP less than or equal to 90 mm Hg. The plain tablet of felodipine needs to be given twice a day but an extended-release form can be given once daily. Some patients respond to 5 mg/day and most patients respond to a daily dose of 20 mg or less. The adverse effects are few except for a constellation of symptoms related to the vasodilator ability of the drug. These include palpitations, flushing, fatigue, dizziness, and headaches. These occur, if at all, usually within the first 2 weeks and diminish as the drug is continued. They can be limited by starting on a small dose of felodipine (5 mg/day). People who have these adverse effects usually have a good response to the drug. Another adverse effect, which is the most frequent reason for drug withdrawal, is ankle edema. This is more common on the higher doses of the drug. It is due to dilatation of the precapillary resistance vessels rather than sodium and water retention. Felodipine is a useful and effective antihypertensive drug and can be used as monotherapy or added to other antihypertensive drugs. It is effective in people with all grades of hypertension.
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PMID:A review of the antihypertensive effects of felodipine alone or in combination. 169 35

Nabilone is a new orally active cannabinoid for the treatment of severe gastrointestinal toxicity associated with cancer chemotherapy. The pharmacological profile of nabilone suggests that it acts primarily by preventing emesis controlled by the medulla oblongata, although its secondary mild anxiolytic activity may contribute to the overall efficacy. Nabilone 2mg twice daily starting 12 hours prior to, and continued for the duration of, chemotherapy produces significant reduction in the severity and duration of nausea and the frequency of vomiting in about 50 to 70% of patients with severe symptoms refractory to conventional therapy. Nabilone has proven to be more effective in controlling symptoms and preferred by more patients than prochlorperazine 10mg 2 to 4 times daily in a limited number of studies, despite a higher incidence of side effects. Comparative trials against other new antiemetic agents, such as high dose metoclopramide, and use of nabilone in combination with other antiemetics remain to be undertaken. The incidence of side effects is high with nabilone; drowsiness, dizziness and/or vertigo occur in 60 to 70% of patients, but rarely lead to drug withdrawal, although more troublesome effects, such as postural hypotension, ataxia, vision disturbance and toxic psychoses, may cause discontinuation of therapy. Thus, nabilone offers an effective alternative to the treatment options available in a difficult therapeutic area - those patients with severe gastrointestinal side effects from cancer chemotherapy who are refractory to conventional therapy.
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PMID:Nabilone. A preliminary review of its pharmacological properties and therapeutic use. 286 27

Data on adverse reactions due to the quinolone antibacterial agents--ciprofloxacin, ofloxacin, pefloxacin, norfloxacin, and enoxacin--observed in a patient sample of approximately 30,000 are reviewed. Overall rates of adverse reactions were 4.0%-8.0%, and adverse reactions necessitated discontinuation of therapy in 1.0%-2.6% of patients. Patterns of organ-system involvement and of signs and symptoms were quite similar, with gastrointestinal effects predominating (nausea, vomiting, diarrhea, or abdominal pain in 1.0%-5.0% of the patients), followed by effects on the central nervous system (dizziness, headache, and/or insomnia in 0.1%-0.3% of the patients) and skin (0.5%-2.2% of the patients). Elevation in levels of hepatic enzymes occurred in 1.8%-2.5% of the patients, azotemia in 0.2%-1.3%, and eosinophilia in 0.2%-2.0%. These adverse effects were reversible after drug withdrawal and were generally not dose-dependent. Within the constraints of the relatively small number of well-documented patients and the unique mechanism of action of these antimicrobial agents, the safety profile of these drugs seems to make them acceptable for use when their administration is well directed and specific. In addition, close surveillance for new phenomena should be maintained.
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PMID:Adverse effects of the fluoroquinolones. 327 99

To establish long-term efficacy and the relation between drug plasma concentration and antiarrhythmic response, 12 patients with encainide-responsive frequent complex ventricular ectopic activity underwent 1 year of therapy with encainide. Twenty-four hour ambulatory electrocardiograms were obtained at baseline and every 2 months. Drug withdrawal with concomitant plasma sampling and electrocardiographic monitoring was performed at 6 and 12 months. Average group premature ventricular contraction (PVC) suppression during the year was 97 to 99%, with nearly total suppression of pairs and salvos. The most common adverse effects were transient visual disturbances and dizziness or lightheadedness. During a dose interval (6 to 12 hours) the concentration of encainide metabolites exceeded that of encainide by several-fold. The median time of arrhythmia return after drug withdrawal was 12 to 14 hours. At the time of arrhythmia return encainide was generally no longer detectable but the average concentration of O-demethylencainide and 3 methoxy-O-demethylencainide was 72 +/- 49 and 172 +/- 74 ng/ml, respectively. It is concluded that encainide therapy is extremely effective for continuous long-term suppression of complex ventricular arrhythmias and its metabolites contribute significantly to its antiarrhythmic action during chronic oral therapy.
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PMID:Possible contribution of encainide metabolites to the long-term antiarrhythmic efficacy of encainide. 640 50

In 26 patients with mild-to-moderate hypertension, 80.8% of whom had a history of concomitant diseases, the effect of moxonidine (0.2 mg b.i.d.) on the 24-h ambulatory blood pressure profile (ABPM) was compared with captopril (25 mg b.i.d.) in a double-blind, parallel-group study. After 4 weeks of treatment with placebo, ABPM was performed and the patients were treated with moxonidine (n = 14) or captopril (n = 12) for a further 4 weeks. ABPM was then repeated. Both moxonidine and captopril reduced systolic and diastolic blood pressure sufficiently and to the same extent. Mean 24-h pulse rate and standard laboratory parameters were not changed by active treatment. After drug withdrawal for 5 days, sitting blood pressure did not differ from baseline values in both groups. Serious adverse events did not occur, the most frequent complaints were nausea (2 of 14 patients receiving moxonidine) and dizziness (3 of 12 patients receiving captopril). We concluded that the blood pressure-lowering effects of moxonidine (0.2 mg b.i.d.) and captopril (25 mg b.i.d.) are comparable in patients with mild-to-moderate hypertension.
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PMID:Twenty-four-hour blood pressure profiles in patients with mild-to-moderate hypertension: moxonidine versus captopril. 753 24

We compared the response of blood pressure (BP) to either K-Canrenoate (K-Can) or hydrochlorothiazide (HCTZ) in 26 mild-to-moderate essential hypertensives in a double-blind, cross-over design over 2 months each. The dose was 12.5 mg o.d. for HCTZ and 50 mg o.d. for K-Can: dosing was doubled after 1 month if seated diastolic BP was > or = 95 mmHg. Eight pts were "selective responder" to the lowest dose of HCTZ (HCTZ-R), and 6 to K-Can (K-Can-R). Seven pts had their high blood pressure controlled by the highest dose of both drugs and 4 were insensitive to both. One pt dropped out during HCTZ for low plasma K+, and 3 during K-Can (nausea and dizziness: 2 pts; plasma creatinine rise: 1 pt). All these side effects were reverted after drug withdrawal. HCTZ-R and K-Can-R differed for PRA (1.4 +/- 0.6 vs 0.8 +/- 0.4 Ang I ng/ml/h, p < 0.05) and Na-K-Cl cotransport (230 +/- 39 vs 372 +/- 24 mumolNa/L RBC/h, p < 0.01). Our data suggest the existence of a subgroup of essential hypertensives surprisingly insensitive to HCTZ, characterized by a "low" PRA and by a Na(+)-K(+)-Cl- cotransport higher than the HCTZ-R. Their selective response to K-Can suggest a peculiar pathogenetic mechanism underlying their high blood pressure.
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PMID:Different sensitivity to hydrochlorothiazide and to potassium-canrenoate among essential hypertensive patients. 851 9

Torasemide is a lipophilic anilinopyridine sulphonylurea derivative that acts as a high ceiling loop diuretic and has been used for the treatment of both acute and chronic congestive heart failure (CHF) and hypertension. Torasemide is similar to other loop diuretics in terms of its mechanism of diuretic action; namely, blockade of Na+/K+/2Cl- cotransport in the thick ascending limb of the loop of Henle. It has high bioavailability (> 80%), as does bumetanide, but a longer elimination half-life (3 to 4 hours) than either bumetanide or furosemide (frusemide). In the treatment of chronic CHF, oral torasemide (5 to 20 mg/day) has been shown to be an effective diuretic. Patients treated with torasemide for up to 1 year have reduced bodyweight, improved pulmonary haemodynamics, and decreased CHF severity. Intravenous torasemide (20 to 60mg as a single dose) has been shown to be as effective as furosemide in the treatment of acute CHF, and resulted in significant diuresis, bodyweight loss, and improved pulmonary haemodynamics and exercise performance. 'Non-diuretic' dosages (2.5 to 5 mg/day) of oral torasemide have been used to treat essential hypertension, both as monotherapy and in combination with other antihypertensive agents. When used in these dosages, torasemide lowered diastolic blood pressure (DBP) to below 90mm Hg in 8 to 12 weeks in 70 to 80% of patients. With dose doubling, this level of efficacy occurred in more than 90% of hypertensive patients. Clinical trials have established that blood pressure can be maintained at this level for at least 1 year with low dose torasemide. Torasemide is well tolerated in dosages up to 20 mg/day for at least 1 year. The most commonly reported adverse effects are those associated with loop diuretics in general. These include transient hypokalaemia, hyperuricaemia, dizziness, headache, gastrointestinal disturbances, orthostatic hypotension and fatigue. Adverse effects are comparable with those of other diuretics and rarely necessitate drug withdrawal.
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PMID:Benefits and risks of torasemide in congestive heart failure and essential hypertension. 885 25

The objective of this paper was to evaluate the efficacy of diphenhydramine hydrochloride (DPH) in dystonic patients. In 1995, Truong et al reported encouraging results in five patients with idiopathic torsion dystonia (ITD) treated with DPH, an H1 antagonist with sedative and anticholinergic properties. Five patients with generalized ITD, one with secondary generalized dystonia and one with idiopathic segmental dystonia were included in the prospective study. Initially the response to intravenous administration of DPH versus placebo in two sessions a week apart was evaluated. Two weeks later all patients started oral DPH in increasing doses (range 100-300 mg, mean 164 mg). The degree of dystonia was determined by a modified University of Columbia Scale evaluating the baseline score, after placebo and DPH I.V. administration then at one and six months after starting oral treatment. The results were analyzed by Friedman's test for repeated measurements. On comparing scores for baseline severity, I.V. placebo and I.V. DPH presented a highly significant correlation (12.09; p = 0.00) as well as comparing baseline score with oral DPH at one and 6 months, treatment (12.78; p = 0.00). Functional score results were 9.5 p = 0.01 and 8.4 p = 0.02 at one and 6 months respectively. The most common side effects were somnolence and dizziness. It can be concluded that DPH proved effective in our patients with mild to moderate adverse effects not requiring drug withdrawal in any case. However, I.V. challenge was unable to predict the long-term response to oral medication perhaps due to the limited number of cases.
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PMID:Beneficial effects of diphenhydramine in dystonia. 1034 17


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