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)

A 33-year-old female presented with a 2-month history of right cervical and submandibular lymphadenopathy. She had recent onset of a nonproductive cough but was otherwise asymptomatic. The usual symptoms of carcinoid syndrome such as cutaneous flushing, abdominal pain, and asthma were absent.
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PMID:Atypical carcinoid of the lung with cervical and submandibular lymphadenopathy: a case report. 842 88

Salbutamol inhibits neutropenia, increased airway resistance, and gas exchange abnormalities provoked by platelet-activating factor (PAF) challenge in normal persons. To further explore the intriguing dissociation between spirometric abnormalities and gas exchange defects shown in patients with asthma, we investigated whether the salbutamol-induced improvement in gas exchange disturbances after PAF is the result of bronchodilation by comparing this effect with that of ipratropium bromide. We hypothesized that ipratropium bromide, an anticholinergic agent without vascular effects, should block PAF-induced bronchoconstriction but not interfere with its systemic, neutropenic, and gas exchange effects. We studied eight nonsmokers with mild asthma (26 +/- 2.0 SE yr of age) who, prior to PAF challenge (18 micrograms), inhaled either ipratropium bromide (80 micrograms) or salbutamol (300 micrograms) in a randomized, double-blind, crossover fashion 1 wk apart. Peripheral blood neutrophils, respiratory system resistance (Rrs), arterial blood gases and ventilation-perfusion (VA/Q) inequalities were measured 5, 15, and 45 min after PAF. Compared with pretreatment with salbutamol, ipratropium bromide also blocked the increase of respiratory system resistance (Rrs) but did not prevent facial flushing and neutropenia (p < 0.03) at 5 min nor the decrease of PaO2 (p = 0.08 and 0.05), the increase of AaPO2 (p < 0.02 each), and the deterioration of VA/Q relationships (p < 0.05 each) at 5 and 15 min, respectively. This functional pattern was similar to that observed previously in normal subjects and in nonpremedicated asthmatic patients after PAF, with return to baseline values at 45 min. By contrast, salbutamol blocked PAF-induced increased Rrs, in addition to all the other PAF-induced abnormalities. These findings indicate that, in patients with mild asthma, salbutamol inhibits PAF-induced neutropenia and gas exchange abnormalities by mechanisms involving other than airway smooth muscle narrowing, possibly by acting on both the bronchial and pulmonary circulations.
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PMID:Inhibition of PAF-induced gas exchange defects by beta-adrenergic agonists in mild asthma is not due to bronchodilation. 923 Jul 20

Alcohol and histamine metabolic pathways in the body have the common enzymes aldehyde dehydrogenase and aldehyde oxidase. The metabolite of ethanol, acetaldehyde, can effectively compete with the metabolites of histamine, methylimidazole acetaldehyde, and imidazole acetaldehyde. At the periphery, alcohol and acetaldehyde liberate histamine from its store in mast cells and depress histamine elimination by inhibiting diamine oxidase, resulting in elevated histamine levels in tissues. Histamine mediates alcohol-induced gastric and intestinal damage and bronchial asthma as well as flushing in Orientals. On the other hand, alcohol provokes food-induced histaminosis and histamine intolerance, which is an epidemiological problem. There are many controversial reports concerning the effect of H2 receptor antagonists on ethanol metabolism and the activity of alcohol dehydrogenase in the stomach. In addition, alcohol affects histamine levels in the brain by modulating histamine synthesis, release, and turnover. Histamine receptor antagonists can affect ethanol metabolism and change the sensitivity of animals to the hypnotic effects of alcohol. In contrast to other neurotransmitters, the involvement of the brain histamine system in the mechanisms of the central actions of alcohol and in the pathogenesis of alcoholism is poorly studied and understood.
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PMID:Alcohol-histamine interactions. 1034 73

In unusual cases of flushing and anaphylaxis, and after the elimination of the more obvious causes of anaphylaxis or those that may be evaluated by readily available techniques, it is possible to confront a limited and difficult differential diagnosis, which includes idiopathic flushing, anaphylaxis, and neoplastic syndromes associated with mastocytosis and carcinoid tumor. Interestingly, there are rather few features that distinguish one of these possibilities from another. However, the presence of allergic signs and symptoms tend to favor the diagnosis of recurrent idiopathic anaphylaxis; and right-sided valvular heart disease, the presence of excessive 5-HIAA in the urine, and a response to somatostatin favor the diagnosis of carcinoid syndrome. The distinguishing features of mastocytosis include the presence of characteristic skin lesions and diagnostic histopathologic findings on bone marrow biopsy. Counts of absolute mast cell numbers in the skin are less helpful. Following such guidelines, it is often possible to focus on the most likely diagnosis, be it idiopathic anaphylaxis, benign cutaneous flushing, mastocytosis, or carcinoid tumor.
Allergy Asthma Proc
PMID:Differential diagnosis of the patient with unexplained flushing/anaphylaxis. 1074 48

The efficacy of intranasal triamcinolone acetonide in seasonal and allergic rhinitis has been evaluated in clinical trials and has been compared with antihistamines and other intranasal corticosteroids. Intranasal corticosteroids are either as equally effective as or more effective than comparative drugs. Intranasal corticosteroids are particularly useful as they decrease membrane permeability and inhibit both early and late phase reactions to allergens. They minimise the nasal secretory response and reduce the sensitivity of local nasal irritant receptors. A potential benefit of topical application is the flushing action of the nasal mucosa, which may reduce allergens and secretions. In addition to seasonal and perennial rhinitis, intranasal corticosteroids have additional benefits when used to reduce inflammation in the treatment of sinusitis and may help in decreasing secondary rhinovirus infections. Furthermore, suboptimal control of asthma can be avoided by treatment of allergic rhinitis with intranasal corticosteroids. In clinical trials, common adverse effects for triamcinolone acetonide include sneezing, dry, mucosa, nasal irritation, sinus discomfort, throat discomfort, epistaxis and headache. Posterior subcapsular cataract formation has not been seen with triamcinolone acetonide. Recent literature evaluating systemic absorption of intranasal corticosteroids have shown surprising results where significant absorption has occurred with intranasal budesonide and fluticasone propionate. Growth and hypothalamic pituitary axis (HPA) function studies have been reviewed, with some intranasal corticosteroids showing changes with continual use. A retrospective study in children receiving daily triamcinolone acetonide for 12 months showed no effect on height and bodyweight. Triamcinolone acetonide at standard dosages (110 or 220microg once or twice a day) does not appear to suppress adrenal gland function and is effective in relieving most symptoms of allergic rhinitis. The International Consensus Conference Proceedings on Rhinitis now currently recommends the use of intranasal corticosteroids as first line therapy, since they have been found to be well tolerated and effective with minimal adverse effects and, specifically, no cognitive impairment. The recommended maximum dose of aqueous triamcinolone acetonide in adults and children is 220microg once a day. The aerosol form may be recommended in children between 7 and 12 years old, up to 440microg once a day or in divided doses. Duration of allergy treatment is generally for the length of each allergy season. If symptoms are perennial, then a reduction of dosage is made to the lowest effective dose with monitoring every 3 months for risk and benefit assessment. Complications to watch for include bleeding, and possible septal perforation and nasal candidiasis, although these are rare.
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PMID:A risk-benefit assessment of intranasal triamcinolone acetonide in allergic rhinitis. 1105 Dec 18

The objective of this study was to evaluate the effects of adding ketamine to standard emergency department (ED) therapy for patients with status asthmaticus. This was a prospective observational study. Ten patients with an acute exacerbation of asthma who were unresponsive to standard therapy were enrolled in the ED. Upon enrollment, children received ketamine at a loading dose of 1 mg/kg intravenously (i.v.), followed by a continuous infusion of 0.75 mg/kg/hr (12.5 microg/kg/min) for 1 hr. Clinical asthma score (CAS), vital signs, and peak expiratory flow (PEF) measurements were obtained prior to ketamine administration, within 10 min after ketamine administration was completed, and 1 hr after infusion. Median CAS on ED arrival was 15 (range 7-23) and did not significantly change immediately prior to infusion of ketamine (median 14, range 8-21). Median CAS decreased to 10.5 immediately after infusion and to 9.51 hr post ketamine infusion (37% reduction, p < 0.05 by ANOVA vs. preketamine CAS). Median respiratory rate (RR) also decreased from 39 prior to ketamine to 30 immediately following ketamine administration (25% decrease vs. preketamine; p < 0.05). Oxygen saturation significantly improved after ketamine infusion, although 5 patients remained on oxygen. Median PEF improved after infusion, but was not statistically significant. Four patients experienced mild side effects including mild hallucinations, diffuse flushing, and moderate hypertension. Side effects resolved with benzodiazepines or with discontinuation of the infusion. Addition of ketamine to standard therapy was associated with improved indices of acute asthma severity. Side effects were transitory and comparable to previous studies. However, a double-blinded randomized controlled trial needs to be conducted to determine if improvement is attributable to the addition of ketamine to standard asthma therapy.
J Asthma 2001 Dec
PMID:Emergency department use of ketamine in pediatric status asthmaticus. 1175 94

Paclitaxel (Taxol) a taxane antineoplastic agent causing irreversible microtubule aggregation with activity against breast, ovarian, lung, head and neck, bladder, testicular, esophageal, endometrial and other less common tumors was derived from the bark of the Pacific yew (Taxus brevifolia). Phase I trials conducted in the late 1980s were almost halted because of the high frequency of hypersensitivity-like reactions. Respiratory distress (dyspnea and/or bronchospasm), hypotension, and angioedema were the major manifestations, but flushing, urticaria, chest, abdomen, and extremity pains were described also. Reactions occurred on first exposure in the majority of cases raising etiologic questions. The vehicle for paclitaxel Cremophor EL (polyoxyethylated castor oil in 50% ethanol) was strongly suspect as a direct (non-immunoglobulin E dependent) histamine releaser. Premedication regimens and longer infusion times lowered the incidence of reactivity allowing phase II and III trials to progress through the early 1990s. The mechanism(s) underlying paclitaxel hypersensitivity-like reactions is still unknown, and clinical data on probable complement and mast cell activation are lacking. The original clinical trial protocols for paclitaxel required discontinuation of therapy for patients who experienced hypersensitivity-like reactions. Here, we review the current etiologic knowledge of these reactions and describe our clinical approach to allow completion of chemotherapy with this powerful plant-derived agent.
Allergy Asthma Proc
PMID:Taxol reactions. 1212 9

(1) Dry mouth (xerostomia) is a frequent complication of radiation therapy for cancers of the ear nose and throat. Local measures such as saliva substitutes and anetholtrithione are either moderately effective, inadequately evaluated or little better than placebo. (2) Marketing authorization has been granted in France for an oral formulation of pilocarpine, an old parasympathomimetic agent, in the treatment of radiotherapy-induced xerostomia. (3) According to the results of two double-blind trials, pilocarpine (15-30 mg/day) improves symptoms in about 50 % of patients, compared to improvement in 25% of patients taking placebo. The drug is slow to take effect and has little impact on daily life. It is not known whether pilocarpine helps prevent the complications of xerostomia. (4) Most adverse effects of pilocarpine are due to its parasympathomimetic effects, such as sweating, urinary frequency, flushing, rhinitis and nausea. Pilocarpine must therefore be used with caution in patients with asthma, cardiac arrhythmia, iridocyclitis, and closed-angle glaucoma. (5) In France, this pilocarpine formulation costs 18 times more than a preparation of pilocarpine 2% eye drops used orally (off licence). (6) In practice, patients needing symptomatic treatment of xerostomia after radiotherapy may benefit from oral pilocarpine but, given its limited efficacy and its adverse effects, other local treatments should be tried first.
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PMID:Oral pilocarpine: new preparation. Xerostomia after radiation therapy: moderately effective but costly. 1219 76

Mechanical ventilation (MV) during exacerbation of asthma or chronic obstructive pulmonary disease (COPD) is unequivocally needed when apnoea, cardiorespiratory arrest, coma, hypoxia or treatment failure is present. The need is less clear when the patient can respond, has intact airway reflexes and spontaneous respiration. In this situation, acidosis is an important factor in the decision to institute MV. This study aimed to provide a clinical means of identifying patients with acute respiratory acidosis (ARA) in a setting where blood gas analysis is unavailable. We undertook a prospective, observational study of consecutive patients who presented to two emergency departments with severe and life-threatening exacerbation of asthma or COPD. Each underwent clinical assessment, treatment and blood gas analysis. The outcome measure was ARA or mixed ARA and metabolic acidosis. A total of 127 episodes in patients aged 15-90 years (65.3% males and 34.7% females) were included in the study. Of these, 62.2% had asthma and 37.8% had COPD; 71.7% had life-threatening and 28.3% had severe attacks. Overall, the adjusted odds ratio (and 95% confidence intervals) for predictors of ARA were 7.09 (1.79-28.06) for drowsiness, 4.11 (1.31-12.88) for flushing, 3.34 (1.01-11.02) for having COPD and 2.86 (1.01-8.07) for intercostal retractions. In conclusion, with drowsiness, the likelihood of ARA is about seven times higher. The presence of flushing, COPD and intercostal retractions also increase the risk of ARA.
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PMID:Clinical predictors of acute respiratory acidosis during exacerbation of asthma and chronic obstructive pulmonary disease. 1239 18

Australian tea tree oil has been used as a veterinary antiseptic for many years and, more recently, has been extended into human use. There have been many reports of allergic contact dermatitis and toxicity reactions, but it has never been implicated in immediate systemic hypersensitivity reactions. A 38-year-old man experienced immediate flushing, pruritus, throat constriction, and lightheadedness after topical application of tea tree oil. Our purpose was to determine whether this represented an immunoglobulin E (IgE)--mediated reaction. Skin-prick and intradermal testing was performed, as well as enzyme-linked immunosorbent assays for specific IgG and IgE against tea tree oil. The patient had a positive wheal and flare reaction on intradermal testing with tea tree oil. All five patient controls were negative on skin testing. No specific IgG or IgE was detected. We present the first reported case of an immediate systemic hypersensitivity reaction occurring after topical application of Australian tea tree oil, confirmed by positive wheal and flare reaction on skin testing.
Allergy Asthma Proc
PMID:Immediate systemic hypersensitivity reaction associated with topical application of Australian tea tree oil. 1263 81


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