Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the dosing equivalency and the early and late antianginal efficacy of a gastrointestinal therapeutic system for once-daily, continuous-release nifedipine (N-GITS), 10 patients with stable angina pectoris, who were previously receiving chronic treatment with nifedipine, completed a 12-week trial comparing N-GITS with standard nifedipine. All patients (nine men and one woman; mean age 54 +/- 2 [SEM] years) who were receiving standard nifedipine (mean dose 40 +/- 5 mg/24 hr) for more than 2 weeks (mean 8 +/- 2 months, range 2 to 36 months) were switched to an equivalent once-daily dose (39 +/- 5 mg/24 hr) of N-GITS. Standard nifedipine and N-GITS were compared by symptom-limited exercise treadmill tests with a baseline test (A) performed 3 hours after a standard dose of nifedipine. Exercise tests were also performed after 2 weeks of treatment with N-GITS 3 hours (B) and 24 hours (C) after the drug was given, and after 12 weeks of treatment with N-GITS, 24 hours after dosing (D). Results of exercise tests showed no significant difference in mean exercise time--(A) 422 +/- 25 vs (B) 426 +/- 36 vs (C) 438 +/- 35 vs (D) 487 +/- 37 seconds. Likewise, there was no significant mean difference in peak double product, resting heart rate, peak exercise heart rate, or resting or maximal systolic blood pressure for any of the exercise test points. Furthermore, five patients (50%) reported side effects with standard nifedipine (all vasodilator-flushing, dizziness, or both), which resolved after treatment with N-GITS (p +/- 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative dosing and efficacy of continuous-release nifedipine versus standard nifedipine for angina pectoris: clinical response, exercise performance, and plasma nifedipine levels. 335 8

Two hundred patients clinically certified as suffering from anxiety state were investigated with a view to understanding the clinical manifestation of the condition in Nigeria. We found that 67 symptoms were manifested by those patients, but only 15 symptoms were presented by about 10% of the sample. These common symptoms were: frequent headaches, difficulty in falling asleep, flushing, difficulty in concentrating, rapid or irregular heart beating, weakness, hot flashes, dizziness, feeling of something crawling in the head, heaviness of the head, nervousness, poor appetite, poor sight, nightmares, and chest pain. The five major precipitating factors were physical ailments, studying and examinations, use of drugs, psychological phenomona, pregnancy and childbirth, in decreasing order of magnitude. The most vulnerable age group was between 18 and 23 years old. The first born children account for the highest number of anxiety patients, but as the number of siblings increases, the vulnerability of the last-born increases. Anxiety neurosis as seen here is predominantly a problem of single males and females with secondary school education.
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PMID:Clinical anxiety in Nigeria. 340 42

Formaldehyde is but one of many chemicals capable of causing the tight building syndrome or environmentally induced illness (EI). The spectrum of symptoms it may induce includes attacks of headache, flushing, laryngitis, dizziness, nausea, extreme weakness, arthralgia, unwarranted depression, dysphonia, exhaustion, inability to think clearly, arrhythmia or muscle spasms. The nonspecificity of such symptoms can baffle physicians from many specialties. Presented herein is a simple office method for demonstrating that formaldehyde is among the etiologic agents triggering these symptoms. The very symptoms that patients complain of can be provoked within minutes, and subsequently abolished, with an intradermal injection of the appropriate strength of formaldehyde. This injection aids in convincing the patient of the cause of the symptoms so he can initiate measures to bring his disease under control.
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PMID:Diagnosing the tight building syndrome. 344 98

A randomised, double-blind, placebo-controlled parallel study was conducted in adult females to evaluate the efficacy and safety of a combination of cimetidine 300 mg orally and metoclopramide 10 or 20 mg intravenously in reducing pre-operative residual gastric volume and raising gastric pH. The effect of preoperative metoclopramide on postoperative nausea and vomiting was also investigated. Oral cimetidine was given approximately 2-2.5 hours before, and intravenous metoclopramide either 15 or 30 minutes prior to induction of anaesthesia. The study showed that placebo-treated patients undergoing outpatient operations have an increased risk of acid aspiration because of high residual gastric volume and low pH and increased risk of serious pulmonary injury should acid aspiration occur. Metoclopramide 10 or 20 mg intravenously prior to induction of anaesthesia was effective in reducing the residual gastric volume significantly, but not in raising pH. The combination of cimetidine and metoclopramide, as well as cimetidine alone, reduced the risk factors of acid aspiration by raising gastric pH and reducing residual volume. No anti-emetic effect of metoclopramide was observed. Higher doses of metoclopramide (20 mg) produced significant side effects (flushing, dizziness, extrapyramidal side effects), but were only marginally more effective than 10 mg doses in reducing residual gastric volume.
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PMID:Premedication with cimetidine and metoclopramide. Effect on the risk factors of acid aspiration. 352 7

Excessive accumulation of intracellular calcium in Duchenne muscular dystrophy (DMD) may be a necessary step in the process that causes muscle damage in this disease. Because of this possibility, a controlled trial of the calcium channel blocking agent nifedipine was undertaken. One hundred and five patients were randomized and treated in a double-blind manner for 18 months. Muscle strength, contractures, functional ability, cardiopulmonary changes, and laboratory data were monitored. The dose of nifedipine was 0.75-1 mg/kg/day in the first 6 months and 1.5-2 mg/kg/day for the next 12 months. Satisfactory blood levels of nifedipine were attained. The study had a power greater than 0.99 to detect a slowing of the illness to 25% of its original rate of progression. No significant improvement was demonstrated in the treated group. One or more of the frequent mild side effects of flushing, dizziness, and leg edema, often associated with the use of nifedipine in adults, occurred transiently in approximately one-half of the patients in the nifedipine group and in 21% of the placebo group. Four patients died, two on nifedipine and two on placebo. This study demonstrates that nifedipine is safe to administer in children, but that it is without beneficial effect on the course of DMD.
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PMID:Clinical investigation in Duchenne dystrophy. VI. Double-blind controlled trial of nifedipine. 355 Apr 55

A case of intravenous labetalol in the treatment of a resistant hypertensive emergency is reported. Although there have been several reports of the use of oral labetalol in resistant hypertension, no intravenous administration in hypertensive emergency resistant to other drugs has been reported to date. A 36-year-old black female with BP of 270/160 mm Hg with complaints greater than one month's duration of dizziness, severe headaches, blurred vision, shortness of breath, vomiting, palpitations, flushing, agitation, diarrhea, weakness, and weight loss, was treated successfully with intravenous labetalol after she failed to respond to other established parenteral antihypertensive drugs. The patient received labetalol 20 mg iv bolus, and then 20 mg every ten minutes until a cumulative dose of 200 mg was attained. Labetalol produced a prompt but smooth reduction in BP without any reflex tachycardia or other adverse effects. Intravenous labetalol may be safe and effective for the management of rapid BP control in hypertensive emergencies resistant to other parenteral antihypertensive agents.
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PMID:Intravenous labetalol in the management of resistant hypertensive emergency. 360 97

The Oriental flushing reaction is an adverse response to alcohol that appears to be genetically determined. In this study, the Oriental flushing reaction that was produced with ingestion of small amounts of alcohol was antagonized by antihistamine administration. A group of 17 subjects was tested. Each subject received placebo, diphenhydramine 50 mg (H-1 receptor antagonist), and cimetidine 300 mg (H-2 receptor antagonist) singularly and in combination. Alcohol was then administered orally. Most subjects given placebo experienced the typical flushing reaction that included a cutaneous flush, increase in skin temperature, decrease in blood pressure, increase in pulse rate and subjective symptoms such as dizziness, sleepiness, anxiety, headache, generalized weakness, and nausea. The flush, temperature and systolic hypotension were significantly blocked by the combined antihistamine administration. Cimetidine given alone blocked the flush, temperature increase, and systolic hypotension significantly more than diphenhydramine but less than the combined antihistamines. Diphenhydramine was similar to placebo in its effect on the flushing reaction. The role of histamine in the expression of tolerance to alcohol is not known. Antihistamine antagonism of the adverse flushing reaction suggests that histamine receptors may participate in the intolerance to ethanol in Orientals. Histamine may be an important protective factor in the low prevalence of alcoholism in Orientals.
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PMID:Histamine receptor antagonism of intolerance to alcohol in the Oriental population. 368 Dec 77

The antihypertensive effect and safety of long-term therapy with nifedipine were evaluated in 132 hypertensive patients, including 100 aged patients who received nifedipine alone or with other antihypertensive agents for a mean duration of 28.6 months. A prompt hypotensive effect was observed 1 month after the initiation of nifedipine therapy. The hypotensive effect persisted for the entire follow-up period and was related to the pretreatment mean blood pressure level. Late drug tolerance was not observed. Dizziness, facial flushing and other unpleasant sensations were observed in 7.5% and ankle edema in 9.8% of the patients. The therapy did not significantly influence serum creatinine levels. Hypotension and side effects were the cause of discontinuation in 10.6% and 4.5% of patients, respectively. We conclude that long-term antihypertensive therapy with nifedipine is both effective and safe, not only in adult patients but also in the high-risk aged patient.
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PMID:The efficacy and safety of long-term antihypertensive therapy with nifedipine. 372 91

We reviewed clinical findings in 740 patients over age 65 who consulted the Otological Medical Group, Inc., during a one-year period for dizziness. A thorough neurotologic evaluation is indicated in every such case to determine the specific cause of dizziness. In 21 per cent of these patients, a specific cause of dizziness was found. In the remaining 79 per cent, the diagnosis of primary dysequilibrium of ageing (presbyastasis) was made. We classified dysequilibrium of ageing (presbyastasis) according to the character, time course, and precipitating factors of dizziness. Two clinical types were described: constant and episodic; episodic dizziness was subdivided into orthostatic, positional, and unclassified. The histological findings in the temporal bones of four cases with dysequilibrium of ageing were reviewed. Pathological changes other than those in the peripheral vestibular system seem to be responsible for dysequilibrium of ageing. In the present series, about three-fourths of the patients had a daily dose of nicotinic acid to produce flushing of the skin. In 16 per cent, the dizziness was minor, requiring no special treatment. In the remaining 9 per cent with incapacitating vertigo, a vasodilator regimen, antivertiginous drugs, and Cawthorne's vestibular exercises were prescribed.
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PMID:Dysequilibrium of ageing (presbyastasis). 376 Jun 85

This study evaluated 1 year the efficacy of therapy with nicardipine in patients with chronic stable angina pectoris. Twenty-five male patients were entered. After a placebo run-in phase, the patients received nicardipine 30 mg, nicardipine 40 mg, and placebo, three times daily given in random, double-blind manner for 8 weeks. A double-blind, cross-over study comparing nicardipine with placebo was then undertaken. After 5 months of open treatment with nicardipine 90 or 120 mg day-1, patients received either placebo or nicardipine for 3 weeks, each followed by the alternative treatment for an additional 3 weeks and further open-label treatment with nicardipine for another 3-5 months. There were no significant changes in the PR, QRS or QT intervals, or in the QRS pattern during the short-term and long-term studies. There were no significant differences in mean heart rate after nicardipine compared with baseline. During treatment with nicardipine 120 mg day-1, patients reported significantly fewer anginal attacks compared with placebo, and nitroglycerin consumption also decreased. Nicardipine increased treadmill time, time to onset of angina, and time to one mm ST segment depression. These effects were maintained after 6 months of continued nicardipine therapy. Adverse effects were minor and well tolerated and included headache, dizziness, gastrointestinal upset, flushing paraesthesia and pedal oedema. Abrupt withdrawal of nicardipine at the end of the study resulted in a rapid return of the original symptoms but without further deterioration from the baseline measurements. Nicardipine was effective in the treatment of stable effort angina pectoris; this benefit was maintained for the entire year of treatment.
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PMID:Short- and long-term treatment of stable effort angina with nicardipine, a new calcium channel blocker: a double-blind, placebo-controlled, randomised, repeated cross-over study. 392 59


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