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)

An H1-receptor blocking antihistamine, clemastine, taken before aspirin gave complete or partial protection against flushing, rhinorrhea, cough, and headache in ten asthmatic patients with idiosyncrasy to aspirin. In five of the ten patients aspirin-precipitated bronchoconstriction was also reduced or prevented after pretreatment with clemastine. Thus histamine appears to play a part in the production of most non-respiratory symptoms occurring after aspirin ingestion in intolerant patients with asthma. Bronchial reactions might depend partly on histamine and partly on the action of other spasmogens. It is suggested that inhibition of prostaglandins of the E series by aspirin-like drugs plays a crucial part in the release of histamine from tissue stores in aspirin-sensitive asthmatic patients. Clemastine might be of use in the treatment of acute reactions to aspirin.
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PMID:Inhibition of idiosyncratic reactions to aspirin in asthmatic patients by clemastine. 9 16

Out of 19 patients with extrinsic bronchial asthma challenged with 123 mug histamine acid phosphate by intravenous infusion only 13 responded with a fall in FEV1 of over 10% (mean 16%). Seventeen of these patients were given histamine 2 mg/ml by aerosol, and all responded with a mean decrease in FEV1 of 37.8%. When challenged with allergen extract by aerosol the mean decrease in FEV1 was 37.5%. After 40 mg sodium cromoglycate 15 of the 17 patients showed significant protection against allergen challenge with a mean decrease in FEV1 of only 23.6%. Inhalation of 40 mg sodium cromoglycate, however, failed to protect against histamine given by either the intravenous or aerosol route. Histamine given intravenously to asthmatic patients produces less of a bronchial response than when given by aerosol, even though the intravenous route produces many more systemic symptoms, such as flushing and throbbing headache. The protection of sodium cromoglycate against an allergen inhalation challenge is not due to histamine antagonsim.
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PMID:Bronchial reactivity to histamine before and after sodium cromoglycate in bronchial asthma. 81 11

This study examines the efficacy and side effects of 15-methyl-prostaglandins F2alpha (PGF2a) free acid administered intramuscularly for midtrimester abortion. 50 healthy women aged 14 to 37 years and between 12 to 18 weeks gestation were randomly selected from the abortion clinic at the Los Angeles County/USC Medical Center, Women's Hospital to participate in the study. The prostaglandin preparation was supplied in ampules containing 1.1 mg. in 2.2 ml. of aqueous solution. The injection was given every 2 hours until the fetus was expelled or for a maximum of 12 injections. Vital signs of the patients were closely monitored. 46% (23) of the subjects aborted within 12 hours and 90% within 27 hours. Mean injection-abortion time was 13.5 hours (range, 5 3/4 to 27 hours). The effectiveness and rapidity of abortion was related with gestational age: the lower the gestational age, the shorter the abortion time. Women with more than 17 weeks gestation had a higher failure rate. Mean number of injections was 7.5. 5 patients failed to abort with prostaglandin alone, all of them primigravidas and weighing in excess of 150 lbs; supplemental therapy was provided. Side effects and complications associated with 15-methyl-PGF2a included: emesis (66%); diarrhea (76%); flushing (12%); chills (4%); fever of 100 degrees Fahrenheit (12%); pain requiring medication (16%); and blood loss (6%). The success of this method appears to be related to dosage; parity; gestational age; weight of patient; and frequency of administration. Although there were side effects, these were outweighed by rapid abortion time, mild contractions, and ease of administration. Asthma is the only medical contraindication to prostaglandin therapy.
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PMID:Midtrimester abortion with intramuscular injection of 15-methyl-prostaglandin F2alpha. 113 40

1. The aim of the study was to compare the efficacy and the tolerability of treatment with atenolol (50-100 mg once daily), nitrendipine (20-40 mg once daily) and their combination (atenolol 50 mg + nitrendipine 20 mg) once daily in patients with mild to moderate essential hypertension. 2. The study was a randomised, double-blind, placebo controlled parallel groups design: blood pressures were measured at 'trough' effect (i.e. 24 h after dosing) to assess the adequacy of once-daily treatment. 3. Mean blood pressures (mm Hg) recorded on four occasions over 12 weeks of treatment were significantly lower both with atenolol (155/97 sitting: 155/104 standing) and with the combination of atenolol plus nitrendipine (153/96 sitting: 152/104 standing) than with placebo (169/108 sitting: 169/114 standing). Nitrendipine alone had no significant effect on blood pressure 24 h after dosing (165/104 sitting: 165/110 standing). 4. Withdrawals due to adverse effects were more common during treatment with nitrendipine: 7/32 of the patients experienced adverse effects attributable to intense systemic vasodilatation (e.g., flushing, erythema, headache). 2/37 patients taking atenolol were withdrawn: one because he developed a psoriatic rash and the other because of impaired peripheral circulation. Of the 35 patients taking combination treatment, two were withdrawn: one developed headaches and dyspnoea, and the other asthma. 5. The results suggest that once daily dosing with nitrendipine does not control blood pressure throughout the 24 h period in the majority of patients, and is associated with a considerable burden of adverse effects. Combination treatment was better tolerated but appeared to offer no advantages over atenolol alone in terms either of blood pressure control or adverse effects.
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PMID:Comparison of once daily atenolol, nitrendipine and their combination in mild to moderate essential hypertension. 218 68

Allergic reactions from handling psyllium have been reported since 1970. Health professionals and workers in laxative-manufacturing plants are at greatest risk. Sensitized people are at risk of life-threatening anaphylactic reactions. Two illustrative cases are presented. The first is A 39-year-old female dialysis nurse with a 3-year history of nasal and eye symptoms from exposure to psyllium. She obtained an over-the-counter psyllium bulk laxative, took it for constipation and developed flushing, tachycardia, urticaria, angioedema, laryngeal edema, and lightheadedness. An epicutaneous skin test and radioallergosorbent test for psyllium were both strongly positive. The second is a 42-year-old female nurse with a history of asthma who had allergic nasal and eye symptoms while dispensing psyllium. She received a prescription for crystallized psyllium, took it by mouth, and developed immediate flushing, tachycardia, urticaria, and angioedema. With subsequent ingestion of psyllium she had, in addition, severe wheezing, lightheadedness, and loss of consciousness. A psyllium epicutaneous skin test was strongly positive. These patient reports illustrate the risk of severe allergic reactions in sensitized people. Ingestion by sensitized people, such as from a routine postoperative and postpartum order, is potentially dangerous.
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PMID:Psyllium anaphylaxis. 225 44

Platelet activating factor, a potent mediator of inflammation, causes a sustained increase in airway responsiveness to methacholine in man and has been implicated in asthma. The effect of the beta 2 agonist salbutamol (200 micrograms by inhalation) on platelet activating factor induced bronchoconstriction and airway hyperresponsiveness was studied in seven normal subjects in a double blind, crossover study. Salbutamol only partially inhibited the platelet activating factor induced fall in partial flow at 30% of vital capacity (Vp30) (mean percentage fall 47.6 (SEM 7.9); p less than 0.001), whereas it completely blocked a similar degree of bronchoconstriction induced by methacholine. Salbutamol did not prevent the accompanying transient flushing and chest irritation and did not affect the transient neutropenia (mean % fall 69.5 (13.6); p less than 0.01) or the rebound neutrophilia (mean % increase 84.7 (24.7); p less than 0.05) that followed platelet activating factor. There was an increase in the airway responsiveness to methacholine following inhalation of platelet activating factor, the maximum mean change being a three fold increase in PC40 (the provocative concentration of methacholine causing a 40% fall in Vp30) on day 3 (p less than 0.01). Salbutamol caused a significant attenuation of this response on day 3 (p less than 0.02) but had no significant effect on days 1 and 7. Thus a therapeutic dose of salbutamol caused partial inhibition of platelet activating factor induced bronchoconstriction and had a minimal effect on the increased bronchial responsiveness following platelet activating factor.
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PMID:Effects of salbutamol on bronchoconstriction, bronchial hyperresponsiveness, and leucocyte responses induced by platelet activating factor in man. 264 45

Platelet activating factor (PAF), a phospholipid inflammatory mediator, was given as an aerosol to eight normal subjects. PAF caused a dose-dependent bronchoconstriction in all subjects. This did not correlate well with responsiveness to methacholine. Some subjects showed tachyphylaxis to PAF-induced bronchoconstriction. No subject had a late bronchoconstriction response. Transient facial flushing and an increase in heart rate (mean 7 beats/min) occurred but there was no consistent change in blood pressure. Lyso-PAF, the inactive precursor and major metabolite of PAF, had no effect on pulmonary or cardiovascular responses. Six of the subjects took part in a double-blind, randomised, placebo-controlled, crossover study in which bronchial responsiveness to methacholine was measured over the 3 days after administration of PAF or lyso-PAF. PAF had a greater effect in raising responsiveness (p less than 0.01). Its maximum effect occurred at 3 days and returned to baseline in 1 to 4 weeks. PAF may contribute to the pathogenesis of bronchial hyperresponsiveness, which is the most characteristic abnormality in asthma.
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PMID:Effects of inhaled platelet activating factor on pulmonary function and bronchial responsiveness in man. 287 40

The inhalation of platelet activating factor (PAF) produces bronchoconstriction in normal and asthmatic subjects. To identify the mechanism by which PAF-induced bronchoconstriction occurs in humans, bronchoprovocation testing was performed in 7 subjects (3 normal, 4 with mild asthma) after pretreatment with phosphate-buffered saline (PBS), atropine, chlorpheniramine, or indomethacin. We determined the nebulizer concentration of PAF which reduced specific airway conductance (SGaw) 35% (PC35 SGaw) and the slope of the PAF dose-response curve. Atropine produced baseline bronchodilatation (SGaw increased 50%), while chlorpheniramine and indomethacin had no effect on baseline pulmonary function. Atropine increased airway responsiveness to PAF: the PC35 SGaw decreased 40% (p less than 0.05) and the slope of the PAF dose-response curve increased 86% (p less than 0.05). In contrast, chlorpheniramine inhibited the airway response to PAF: the PC35 SGaw increased 87% (p less than 0.05), while the slope of the PAF dose-response curve decreased an insignificant 37%. Indomethacin did not affect either measurement. Chlorpheniramine also prevented the PAF-induced facial flushing and feeling of warmth; atropine and indomethacin did not. These results suggest that PAF-induced bronchoconstriction in humans is mediated at least in part by histamine release, not by cholinergic or cyclooxygenase-dependent mechanisms. Other indirect effects, such as the release of sulfidopeptide leukotrienes, or a direct effect on airway smooth muscle may also contribute to PAF-induced bronchoconstriction. Why atropine heightened the airway response to PAF is unclear.
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PMID:Mechanism of platelet activating factor-induced bronchoconstriction in humans. 319

Nifedipine, 30 mg/day for 4 weeks, was compared to placebo in a double-blind, randomized, crossover study, as an additional drug added to the usual treatment of 14 patients with bronchial asthma. Nifedipine did not significantly change peak expiratory flow rates or subjective symptoms like cough, sputum, wheezing, shortness of breath, or disturbed sleep. Nifedipine did not decrease the number of salbutamol rotacaps inhaled per day. Arterial blood pressure significantly decreased (p less than 0.01) after nifedipine treatment, and side effects (headache and flushing) were not uncommon. In this study, long-term treatment with nifedipine had essentially no effect on subjective symptoms at peak expiratory flow rates.
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PMID:Nifedipine treatment of patients with bronchial asthma. 329 78

Acetylsalicylic acid (ASA) and other nonsteroidal anti-inflammatory drugs (NSAID) cause a variety of symptoms in patients sensitive to these drugs. These include wheezing, rhinorrhea, flushing, pruritus, urticaria, hypotension and loss of consciousness. Conversely, improvement of asthma with the use of these drugs in patients who do not have idiosyncratic reactions to ASA (ASA-nonsensitive) has also been observed both with respect to clinical symptoms and pulmonary function tests.
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PMID:Asthma improved by acetylsalicylic acid and other nonsteroidal anti-inflammatory agents. 347 42


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