Disease relevance of Peak Expiratory Flow Rate

• The variations in histamine, S.R.S.-A and IgE gave a highly significant negative correlation with the peak expiratory flow-rate, suggesting that chemical mediators of hypersensitivity may play some role in the pathogenesis of airways obstruction in this disease [1].
• Sputum eosinophilia correlated with the arylsulphatase IIB concentration but not with the peak expiratory flow-rate, IgE, histamine, or S.R.S.-A, a finding consistent with the view that eosinophils accumulate at the site of type I reactions after the peak of mediator release [1].
• In 11 patients with bronchial asthma and regular overnight falls in PEFR of greater than 15%, we demonstrated significant bronchodilation restricted only to large airways after the administration of a single dose of 10 mg of nifedipine [2].
• Spirometry, twice daily measurements of peak expiratory flow rate, and self assessment of asthma symptom scores showed significant improvement during triamcinolone treatment; less extra prednisolone was required and there was significant weight loss [3].
• In one treatment study involving 525 patients with asthma or chronic obstructive pulmonary disease, zanamivir recipients had a small but significantly increased mean morning peak expiratory flow rate (PEFR) and evening PEFR compared with placebo during the treatment period (days 1 to 5) [4].

High impact information on Peak Expiratory Flow Rate

• MAIN OUTCOME MEASURES--Decline in lung function (FEV1), change in bronchial hyperresponsiveness, indicated by a provocative concentration of histamine causing a 20% fall in FEV1 (PC20), morning peak expiratory flow rate (PEFR), diurnal PEFR, week-to-week variation of PEFR, bronchial symptoms, and exacerbations [5].
• Ten of 17 patients had better control during cloprednol therapy than during previous prednisone regimens, and significant improvement was noted in peak expiratory flow rate during the study period (P less than .001) [6].
• Histamine challenge in atopic asthmatics at concentrations giving a comparable change in PEFR/FEV1 to that evoked by exercise or inhaled antigen was not associated with the appearance of circulating NCF [7].
• Patients treated with salmeterol had reduced bronchodilator responses to salbutamol in terms of FEV1 and peak expiratory flow rate (PEFR) than those treated with placebo [8].
• Cyclosporin therapy resulted in a mean increase above placebo of 12.0% in morning peak expiratory flow rate (PEFR; p less than 0.004) and 17.6% in FEV1 (p less than 0.001) [9].

Chemical compound and disease context of Peak Expiratory Flow Rate

• A significant difference in the degree of bronchospasm after exercise (as shown by the maximal % fall in the peak expiratory flow rate), was seen when patients with increased urinary LTE4 excretion were compared with those with decreased excretion (60.4 +/- 17.3 versus 24.1 +/- 14.3%, p less than 0.01) [10].
• Prior to hospital admission, a bolus of 3 g IV magnesium sulfate was infused with complete abatement of her bronchospasm, significantly increasing peak expiratory flow rate without any significant side effects [11].
• We studied 20 patients with severe COAD (mean age 66, mean FEV1 0.81 l) and little reversibility (less than 20% increase in FEV1 post-inhaled salbutamol 200 micrograms and less than 25% increase in peak expiratory flow rate, PEFR, on oral steroids) [12].
• BACKGROUND: This prospective study was undertaken to evaluate the efficiency of intercostal nerve block (ICNB) with 0.5% bupivacaine (Marcaine) for pain relief in patients with rib fractures and to correlate the degree of pain relief with changes in the peak expiratory flow rate (PEFR) and oxygen saturation (Sao2) [13].
• Bornaprolol significantly reduced resting heart rate, dose-dependently lowered exercise-induced tachycardia and decreased peak expiratory flow rate and plasma renin activity [14].

Biological context of Peak Expiratory Flow Rate

• Corticosteroid resistance was defined by failure of forced expiratory volume in 1 s (FEV1) and peak expiratory flow rate to improve by at least 15% after a 2-week trial of corticosteroids (prednisolone 20 mg daily for 1 week, then 40 mg daily for 1 week) despite more than 15% improvement with inhaled beta agonists [15].
• All three cetirizine doses produced significantly greater increases than placebo in FEV1 and forced expiratory flow rate between 25% and 75% of vital capacity for 8 hours and in peak expiratory flow rate for 7 hours (p < 0.02) [16].
• In the former, theophylline induced an early and potent bronchodilatation (60% rise in PEFR), the kinetics of which correlated with plasma concentration [17].
• Peak expiratory flow rate, wheezing scores, difficulty breathing scores, nocturnal awakenings requiring salbutamol, and puffs of salbutamol per day also indicated a greater improvement in respiratory function and symptoms of asthma with MF DPI 50 or 100 microg twice daily than with placebo [18].
• The expected diurnal variation in peak expiratory flow rate (PEFR) was found (significant in the whole group--p less than 0.05); but PEFR did not change significantly when measured before and immediately after coughing caused by citric acid inhalations [19].

Anatomical context of Peak Expiratory Flow Rate

• T-lymphocytes from the asthmatic patients showed a range of sensitivity to the antiproliferative effects of cyclosporin, but this could not be correlated with improvements in peak expiratory flow rate (PEFR) or forced expiratory volume in one second (FEV1) during cyclosporin therapy as compared with placebo [20].
• A moderate inverse correlation was revealed between sputum ECP and %PEFR in the foggy season (r= -0.55, P<0.005) [21].
• AIMS: To investigate the effect of the potent gastric acid inhibitor omeprazole 40 mg orally daily on peak expiratory flow rate (PEFR), asthma symptoms and histamine bronchial responsiveness in adult patients with both asthma and GOR [22].

Associations of Peak Expiratory Flow Rate with chemical compounds

• The reduction in response equated with a 2.5-fold and a fourfold greater dose of salbutamol being required to produce a given FEV1 and PEFR, respectively [8].
• Salmeterol remained effective in terms of disease control, with a significant improvement in morning PEFR compared with placebo that was maintained over the 4 week treatment period.(ABSTRACT TRUNCATED AT 250 WORDS)[8]
• 14 asthmatic patients with nocturnal symptoms and morning dips in peak expiratory flow rate (PEFR) were treated with regular inhaled salbutamol for 1 or 2 weeks, followed by regular inhaled beclomethasone dipropionate, in addition to salbutamol, for a further 2 weeks [23].
• Beclomethasone treatment was associated with improvement in peak expiratory flow rate, alleviation of symptoms, and a decrease in the number of exacerbations in both patient groups [24].
• Initially, the theophylline group improved significantly more in symptom scores, beta-agonist usage, and peak expiratory flow rate, but at maximal effect there was no significant difference [25].

Gene context of Peak Expiratory Flow Rate

• Among the patients with emergency asthma flares, those who responded to asthma treatment with an increase in peak expiratory flow rate by an amount equal to at least 20% of their predicted normal value had lower eotaxin levels than those who did not (410 pg/mL [210, 800 pg/mL] and 660 pg/mL [300, 1480 pg/mL], respectively; P =.04) [26].
• In Group I this was associated with improvements in PEFR, FEV1 and night time wheeze and reduced percentages of CD4/CD25 and CD4/HLA-DR peripheral blood T cells [27].
• RESULTS: Patients with increased IFN-gamma changes from baseline showed significantly increased changes in morning (P = 0.02) and evening (P < 0.05) PEFR compared with those with decreased IFN-gamma changes [28].
• Plasma TARC concentration showed inverse correlation with peak expiratory flow rate at presentation [29].
• We measured daily peak expiratory flow rate (PEFR) and daily respiratory symptoms for 1 yr in 70 COPD patients (52 male, 18 female, mean age [+/- SD] 67.5 +/- 8.3 yr, FEV1 1.06 +/- 0.45 L, FVC 2.48 +/- 0.82 L, FEV1/FVC 44 +/- 15%, FEV1 reversibility 6.7 +/- 9.1%, PaO2 8.8 +/- 1.1 kPa) [30].

Analytical, diagnostic and therapeutic context of Peak Expiratory Flow Rate

• METHODS: This study employed a prospective sequential design in which the influence of 0.5 and 1.0 mg of ipratropium bromide on peak expiratory flow rates (PEFR), hospital admissions, and length of stay (LOS) in the emergency department (ED) was evaluated [31].
• The immediate asthmatic response in peak expiratory flow rate and the elevation in NCA were inhibited by the prior oral administration of either disodium cromoglycate (DSCG) or oral beclomethasone dipropionate (BDP) [32].
• Systolic blood pressure, serum cholesterol, glucose levels, smoking, alcohol intake, body mass index, homocysteine and peak expiratory flow rate were entered as independent variables into a multiple regression model, after adjustment for age and education [33].
• METHODS--Serum concentrations of IL-5 were measured in 29 patients with stable oral glucocorticoid-dependent chronic severe asthma (mean PEFR 59.7% predicted) and seven normal controls using a specific enzyme-linked immunoassay calibrated with recombinant human IL-5 standards (lower limit of sensitivity 40 pg/ml) [34].
• MEASUREMENTS AND RESULTS: Vital signs, O2 saturation by pulse oximetry, PEFR, forced vital capacity, forced expiratory volume at 1 second, and physical examination were serially recorded for 110 minutes, with serum magnesium concentrations measured before and after the 20-minute infusion [35].

References