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Biomedical subjects

R E Ruffin

Publications and source records attributed to R E Ruffin.

At least 55 records · Page 3Linked to original sources
PubMed1992

Accuracy of asthma statistics from death certificates in South Australia.

OBJECTIVE: To assess the accuracy of asthma statistics from death certificates in South Australia. DESIGN: Comparison of death certificate coding with expert panel assessments of causes of death after interviews with certifying doctors, regular medical practitioners and close acquaintances of the deceased. SUBJECTS: 261 subjects for whom the term "asthma", "asthmatic" or "asthmaticus" was recorded in Part I or Part II of death certificates lodged in the 24-month period from May 1988. MAIN OUTCOME MEASURES: Sensitivity, specificity and predictive value of death certificate coding, with expert panel assessments as the reference standard. RESULTS: About 95% of deaths assessed as definitely due to asthma were so coded from death certificates, but only 69% of deaths assessed by the panel as not due to asthma were coded to a "non-asthmatic" cause. Of the 129 deaths coded to asthma, the percentage assessed as definitely or likely to be due to asthma was 56%. For ages under 65 years, this figure was 84% compared with only 38% for older subjects. CONCLUSION: The accuracy of death certificate data on asthma for the age group 65 years and over would be too low at present for most epidemiological purposes.

Abstracting and Indexing↗
PubMed1991

Inhaled respiratory medications and the use of chlorofluorocarbons (CFCs). Thoracic Society of Australia and New Zealand.

OBJECTIVE: To assess the use of chlorofluorocarbons (CFCs) in metered-dose aerosols against the background of community concerns regarding the adverse environmental effects of CFCs. DATA SOURCES: Data on the constituents of currently available metered-dose aerosols were supplied by the manufacturers, and details of chemistry and safety were obtained from monographs and papers published in the medical literature. STUDY SELECTION: Five papers, published in the early 1970s when metered-dose aerosols first became popular, were reviewed for safety data on CFCs. Several chapters in monographs were searched for data on the nature and function of CFCs in metered-dose aerosols, and five papers were the source of information on alternatives to CFCs as vehicles for the delivery of inhaled respiratory drugs. DATA SYNTHESIS: The medical use of CFCs accounts for only 1.5% of the total production in Australia, the majority being used for refrigeration, air-conditioning and other commercial or industrial purposes. The physicochemical properties of CFCs are such that they function as a suitable storage medium for active drugs within the canister and as an ideal vehicle for drug delivery. Approximately 20 s after inhalation of a clinically recommended dose of a bronchodilator metered-dose aerosol, CFCs are detectable in the blood, but the concentrations decline rapidly (half-life less than 40 s). Although CFCs have been shown to sensitise the myocardium to the arrhythmogenic effects of catecholamines in experimental animals, the requisite concentrations can only be achieved by patients if they inhale from a canister on every breath for approximately 20 successive breaths. CONCLUSIONS: CFCs used in metered-dose aerosols are an effective storage medium and a convenient vehicle for drug delivery. They are non-toxic--unless amounts far in excess of the clinically recommended doses are used, when arrhythmogenic effects may occur. The medical use of CFCs has minimal environmental impact compared with their industrial and commercial use. Dry powder delivery systems offer an alternative approach, and future research will yield nonozone-depleting CFCs suitable for replacing those in current metered-dose aerosols.

Administration, Inhalation↗
PubMed1991

Longitudinal study of near fatal asthma.

The effect of careful follow-up and treatment modification for 45 patients with an admission for NFA has been studied. In 24 of 45, inciting events were recognized. BDP was used by 14 patients pre-NFA. In the mean follow-up of 863 days, there have been no deaths and seven patients have been readmitted with asthma. Six of the 45 patients have attained normal FEV1 and PC20H. Blunted perception of breathlessness, change in VAS ratio/change in FEV1, was found when first measured, but normalized to be no different than that of other asthmatic subjects as airway responsiveness became milder. The CO2 ventilatory responses did not differentiate individual NFA patients from non-NFA asthmatic or normal subjects. Comparison of the NFA cohort with the 1985 asthma admission cohort showed that an asthma admission within the last five years was a risk factor for a NFA episode.

Adult↗
PubMed1991

Lack of effect of 4 weeks of oral H1 antagonist on bronchial responsiveness.

Ten patients with stable chronic asthma completed a randomized double-blind placebo controlled crossover study examining the effect of 120mg terfenadine twice daily for 4 weeks on bronchial responsiveness. Bronchial responsiveness was measured by methacholine inhalation tests performed by the tidal breathing technique at 0, 2 and 4 weeks of active and placebo treatment periods separated by a one week washout period. There were no significant differences in mean baseline forced expired volume in 1 sec (FEV1) for placebo and terfenadine treatments (p greater than 0.05) and there were no differences between geometric mean provocative concentrations of methacholine to cause a 20% fall in FEV1 (PC20M) at 2 and 4 weeks of terfenadine (0.89 and 0.99 mg.ml.1) from placebo (0.94 and 0.84 mg.ml.1) (p greater than 0.05). Examination of individual PC20M values during terfenadine treatment showed that 5 patients had PC20M's outside their 95% confidence interval; 2 increased both 2 and 4 week values, 1 increased one value and 2 decreased one value each. It is concluded that terfenadine does not produce clinically significant changes in stable asthmatics.

Administration, Oral↗
PubMed1991

New trends in asthma management.

The trend in asthma management is to promote the regular use of preventive medications to reduce airway inflammation and to maintain good control of asthma. Bronchodilators are to be used on an 'as required' basis when symptoms or peak flow rates indicate and in uncontrolled asthma. New delivery devices are becoming available. It is hoped that all asthmatics will have an asthma management plan developed by their doctors, so that patients understand how to control their asthma, how to assess their asthma control, and what to do in the situation of uncontrolled asthma.

Administration, Inhalation↗
PubMed1990

Bronchoconstriction of the asthmatic airway by inhaled and ingested propranolol.

Responsiveness to inhaled histamine and DL propranolol hydrochloride was measured in 31 adult asthmatics and compared with bronchoconstriction provoked by acute oral propranolol dosing (max 160 mg). Twelve asthmatics developed greater than or equal to 15% reduction in the forced expired volume in 1 s (FEV1), 2 h after less than or equal to 100 mg oral propranolol; cardiac beta-adrenoceptor blockade was confirmed by cycle exercise tests in the 19 without airway response. The provocative inhaled dose of each aerosol causing a 20% fall in FEV1 (PC20) was lower, histamine 0.43 mg.ml-1, propranolol 3.12 mg.ml-1, in the 12 with a positive oral test compared with the 19 with a negative test, PC20 histamine 1.65 mg.ml-1, PC20 propranolol 16.2 mg.ml-1 (P less than 0.001 for both aerosols). A correlation was demonstrated between the PC20 values for asthmatics with a negative oral test (r = 0.72, P less than 0.001, n = 19) but not for the remainder (r = 0.14, P greater than 0.05, n = 12). Plasma propranolol concentrations (CL, ng.ml-1) after the final oral dose did not correlate with the % delta FEV1 (26.3) (r = -0.28) when an airway response was provoked or with the reduction in exercise tachycardia (25.9%) (r = 0.31) when no bronchoconstriction occurred. CL exceeded the limit of detection after the final inhaled propranolol dose (7.5 ng.ml-1) and was weakly related to the PC20 propranolol value (r = 0.53, P = 0.01, n = 27). The prevalence of a positive oral challenge was low in this group (39%).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1990

The effect of inhaled fenoterol and ipratropium bromide on propranolol induced bronchoconstriction in the asthmatic airways.

1. The provocative dose of inhaled propranolol, (PC20P, mg/mL) needed to induce a 20% reduction in the forced expired volume in 1 s (FEV1, L) was determined for 15 adult asthmatics following randomized pre-treatment with placebo, ipratropium bromide (40, 160 micrograms) and fenoterol (200, 800 micrograms) aerosols using a double-blind protocol. 2. Fenoterol 200 micrograms, 800 micrograms increased the baseline FEV1 0.28 +/- 0.16, 0.32 +/- 0.16 L (P = 0.04, P = 0.008 respectively). Fenoterol 800 micrograms moved the PC20 P rightwards from placebo geometric mean 10.95, 95% Confidence Intervals (95% CI) 4.43-27.22 mg/mL to mean 20.41, 95% CI 10.13 to 40.64 mg/mL (P = 0.01). Fenoterol 200 micrograms was not protective; mean PC20 16.22, 95% CI 7.83-34.35 mg/mL (P = 0.08). Neither 40 or 160 micrograms ipratropium changed the FEV1 or PC20P values compared with placebo; increase in FEV1 0.15 +/- 0.27 L (P = 0.22), 0.24 +/- 0.12 L (P = 0.14) and geometric mean PC20P 16.59 +/- 0.57 mg/mL, 95% CI 8.01-34.51 mg/mL (P = 0.90), 15.58 +/- 0.66 mg/mL, 95% CI 6.72-36.05 mg/mL (P = 0.34) respectively after ipratropium treatments. 3. Bronchoconstriction induced by inhaled propranolol (P) appears to be only weakly antagonized by inhaled beta-agonist and not reduced by antimuscarinic anticholinergic aerosol. This finding argues against the activation of a cholinergic reflex to explain propranolol induced bronchoconstriction (PIB).

Administration, Inhalation↗
PubMed1989

A comparative bronchodilator study of salbutamol and salbutamol sulphate that were administered by metered-dose inhalers.

Twenty-one patients with mild-to-moderately-severe asthma participated in a placebo-controlled, double-blind, cross-over, randomized bronchodilator study of 200 micrograms of salbutamol (Glaxo) and 200 micrograms of salbutamol in the form of salbutamol sulphate (Riker; 50-microL and 25-microL valves) that were administered by metered-dose inhalers. The mean baseline forced expired volumes in one second (FEV1) were similar for the four separate study days. The three active treatments caused a significantly-greater FEV1 response than did placebo for four hours (P less than 0.05) and no difference was found between the treatments (P greater than 0.05). The power of the study was 75% with a clinically-significant difference in the FEV1 response of 25%. The administration of 200 micrograms of salbutamol (Glaxo) caused the same FEV1 response as did that of 400 micrograms of salbutamol at the end of that study day (P greater than 0.05), but both 200-micrograms doses of salbutamol sulphate (Riker) caused a smaller FEV1 response than did the 400 micrograms of salbutamol sulphate (P less than 0.05). These observations indicate that no clinically-significant difference occurs between the bronchodilator effects of salbutamol and those of salbutamol sulphate which is administered as 200 micrograms of salbutamol equivalent, with different propellant mixtures, dispersal agents and valvular systems.

Adult↗
PubMed1989

Appearance of allergen-induced increases in airway responsiveness only after repeated allergen inhalations in two subjects.

Observations in two subjects undergoing three allergen challenges for a drug study suggested 'priming' of the late sequelae, namely allergen-induced increase in airway responsiveness. Both subjects had rhinitis and asthma limited to the ragweed season, near normal out-of-season histamine PC20, and extreme IgE sensitivity to ragweed. Both had an isolated early response with no change in histamine PC20 after the first allergen challenge. Significant (3.5- to 5.8-fold) reductions in histamine PC20 occurred after the second and third allergen challenge in Subject 1, and after the third challenge in Subject 2; this was associated with equivocal 5-8% late responses. Such a 'priming' effect, the prevalence of which is not known, may be important in the pathogenesis of naturally occurring allergic asthma, and in the design of clinical trials involving repeated allergen inhalations.

Adolescent↗
PubMed1989

Psychological defenses and coping styles in patients following a life-threatening attack of asthma.

Twenty-five patients who have suffered a near miss asthma death (NMAD) have undergone a comprehensive psychiatric evaluation on average 13 months following this event. Forty percent of the patients were judged to have psychiatric disorders at the time of assessment. All patients had very high levels of denial and following the NMAD, patients appeared to either decompensate psychiatrically, usually exhibiting symptoms of anxiety disorders, or further increase their levels of denial. Those patients who had psychiatric illnesses at the time of the study were more constitutionally vulnerable towards developing these disorders and had a reduced perception of their quality of life compared with the patients who increased their levels of denial following the NMAD. The effects of the NMAD on patients and their families ranged from mutual anger and anxiety, although the anger was often repressed, to mutual overinvolvement and overdependence. The presence of high levels of denial of asthma and a history of psychiatric illness in the patient appear to be factors that may increase the likelihood of death from asthma.

Adaptation, Psychological↗
PubMed1988

Psychiatric morbidity in patients with life-threatening asthma: initial report of a controlled study.

Thirteen patients who have suffered a "near-miss" death of asthma have been compared to 36 patients with asthma who had not experienced such an episode. Contrary to expectations, there were no differences between the groups in their levels of psychiatric morbidity, their degree of life-style and social restrictions or in their levels of compliance with prescribed medication. However, both groups did show higher than expected levels of psychiatric morbidity, severe life-style and social restrictions and an unexpectedly-high compliance with prescribed medication. The main psychiatric diagnoses that were noted were anxiety disorders. It is concluded that more comprehensive asthma education and close medical follow-up are likely to improve the physical and psychological health of asthmatic patients. The high-risk patients in this study who received such follow-up have shown hospital-admission rates that have been reduced by a half while maintaining good asthma control. This South Australian longitudinal study is continuing.

Acute Disease↗
PubMed1988

Biochemical studies of N-methyltransferase in human and guinea-pig lung: no apparent role in the pathogenesis of asthma.

1. N-Methyltransferase activity was measured in surgical specimens of human lung using phenylethanolamine as substrate. Thirty-three male and seven female patients, age range 19-78 (median 62.5) years were studied. The activity in lung homogenates was 0.59 x 10(-6) units/mg of protein (SEM 0.03, n = 40), with a range of 0.16-1.16 x 10(-6) units/mg of protein. There was no difference (P = 0.97) in activity between males and females. 2. Non-specific N-methyltransferase activity was estimated in 17 of the surgical specimens using beta-phenylethylamine as substrate. This activity was 38.9% (SEM 5.3) of that with phenylethanolamine. Comparative studies with rabbit lung, which has a well-characterized non-specific N-methyltransferase, showed significant differences in substrate specificity between the two species. 3. The apparent Km and Vmax for phenylethanolamine in seven human lung homogenates was 22.0 (SEM 4.6).mmol/l and 1.82 x 10(-6) units/mg of protein (SEM 0.36). The noradrenaline N-methyltransferase (NMT; EC 2.1.1.28) inhibitors SKF 64139-A and LY 134046 did not inhibit this activity up to a concentration of 100 mumol/l. This activity was inhibited 51.4% (SEM 8.6, n = 6) by 100 mumol/l S-adenosyl-L-homocysteine. Immunohistochemistry did not reveal immunoreactive NMT in human lung sections. 4. Comparative studies with guinea-pig lung homogenates demonstrated non-specific N-methyltransferase activity in this species which is similar to the human lung.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Hydroxyphenethylamine↗
PubMed1988

The effect of trifluoperazine on bronchial responsiveness in asthma.

1. The protective effects of oral trifluoperazine (TFP) (7 mg) against standardized methacholine and histamine inhalation tests (MIT and HIT) were examined 2 and 22 h post-treatment in eight stable asthmatics using a randomized double-blind protocol. 2. A preliminary study tested whether a preceding MIT influenced the result of a subsequent HIT. 3. The mean baseline forced expiratory volumes in 1 s (FEV1) were similar prior to placebo and TFP. The mean FEV1 values 2 h after ingestion of placebo or TFP were not different from the baseline values. 4. TFP did not alter bronchial responsiveness to inhaled methacholine or histamine 2 h post-ingestion, but at 22 h the PC20 methacholine was greater than placebo, while PC20 histamine did not change. This change in methacholine responsiveness was not clinically significant. 5. There was a correlation between geometric mean provocative concentration of histamine to cause 20% fall in FEV (PC20H) for HIT performed in isolation ('separate day') and for HIT performed after MIT ('same day'). 6. The effect of inhaled TFP (10 mg/ml, nebulized for 5 min) was examined single-blind and placebo-controlled in a separate group of six stable asthmatics. 7. Inhaled TFP had a bronchoconstrictor effect in all six asthmatics. The mean fall in FEV1 was 36.4% after inhaled TFP and 2.1% after saline. 8. In the asthmatics studied, ingested TFP exhibited a weak anticholinergic effect 22 h post-treatment, but a brisk spontaneously self reverting bronchoconstrictor response was invariably seen when TFP was inhaled.

Adolescent↗
PubMed1987

Psychiatric morbidity in patients with chronic airflow obstruction.

Fifty consecutive patients with chronic airflow obstruction who were admitted to a respiratory unit were assessed medically and psychiatrically. A high rate of psychiatric morbidity (58%) was detected with panic and other anxiety disorders (34%) being particularly prevalent. Various physiological and psychological reasons for the high rate of anxiety disorders are discussed.

Adult↗
PubMed1987

Combined bronchodilator protection against histamine-induced bronchoconstriction in man.

Sixteen stable asthmatics had the protective effects of inhaled fenoterol (200 micrograms) and inhaled ipratropium bromide (60 micrograms) against standardized histamine inhalation tests at 1 h examined in a randomized double blind fashion. There was no significant difference in the baseline forced expired volume in 1 s (FEV1) for the two study days (P greater than 0.05). There was an increase in FEV1 at 1 h on the fenoterol and ipratropium day compared with the fenoterol day (0.26 versus 0.17 l; P less than 0.05). The geometric mean provocative concentration of histamine to cause a 20% fall in FEV1 (PC20) was 6.31 mg/ml after fenoterol and 8.51 mg/ml after fenoterol and ipratropium (P = 0.038). There was no significant relationship between bronchodilator effect of the bronchodilators and the increase in PC20 from pre-study values, r = 0.307 (P = 0.25) for fenoterol alone and r = 0.195 (P = 0.47) for fenoterol and ipratropium. The relationship between pre-study histamine responsiveness and the increase in PC20 caused by the bronchodilators just failed to reach statistical significance, r = -0.441 (P = 0.09) for fenoterol alone and r = -0.47 (P = 0.06) for fenoterol and ipratropium. The study has shown a greater right shift of histamine responsiveness for combined inhaled fenoterol and ipratropium compared with inhaled fenoterol alone in this group of asthmatics.

Adult↗