PubMed Health⌕ Search

Biomedical subjects

H Joyce

Publications and source records attributed to H Joyce.

15 recordsLinked to original sources
PubMed2005

Evolution of changes in carbon monoxide transfer factor in men with chronic obstructive pulmonary disease.

Progression of chronic obstructive pulmonary disease (COPD) has been studied predominantly by following change in forced expiratory volume in 1s (FEV1) which reflects both primary airway disease and associated alveolar disease. Carbon monoxide transfer (Tlco) (the product of the transfer coefficient Kco and alveolar volume Va) is the only simple, widely available test of alveolar function, but few studies have followed long-term changes in an individual. Seventeen middle-aged men with moderate chronic airflow obstruction (mean FEV1 56% of predicted values) were observed with yearly measurements of FEV1, Tlco and Kco over a mean of 18.9 yr. At the end of follow-up FEV1 had fallen to 29% of predicted values. Va, measured by single breath dilution, fell in each man. Kco at recruitment ranged from 41% to 110% predicted and remained >75% predicted in eight men at the end of follow-up supporting a phenotype of COPD with predominant airway disease and little emphysema. Fall in FEV1 was faster (2.03% predicted FEV1/yr) in seven men with low initial Kco<75% pred. than in men with initial Kco>75% pred. (1.14% predicted FEV1/yr, P=0.006). Repeated measurements of CO transfer in an individual should increase the present poor knowledge of the contribution of alveolar disease to the progression of chronic airflow obstruction.

Adult↗
PubMed2000

Changes in carbon monoxide transfer over 22 years in middle-aged men.

We measured single breath CO transfer (T(LCO)), single breath alveolar volume (VA), CO transfer coefficient (K(CO)) and forced expiratory volume in 1 sec (FEV1) in 84 men, mean age 40.5 years at recruitment, in 1975 and in 1997. At recruitment, 42 men were cigarette smokers and 42 were not smoking. Mean annual decline in FEV1 was similar in never- (34.2 ml yr(-1)) and ex- (33.1 ml yr(-1)) smokers and faster (51.0 ml yr(-1)) in continuing smokers. In contrast to predictions from cross-sectional reference values, there was no fall in T(LCO) or K(CO) in men who did not smoke over the period of follow-up. In the 16 men who smoked throughout follow-up there was a 10% fall in T(LCO) (P = 0.043) but most of this was due to a significant fall in VA (P = 0.017), presumably reflecting uneven gas mixing. These results indicate the need for population-based longitudinal studies of T(LCO) and K(CO). If single breath estimates of VA are used in subjects with even mild airflow obstruction, K(CO) rather than T(LCO) should be used to assess alveolar function.

Adult↗
PubMed1994

Prenatal diagnosis and post-mortem study of a fetus with mosaic trisomy 14 due to a dic(14)(p11).

Amniocentesis at 17 weeks' gestation revealed a mosaic karyotype--46,XX/46,XX,-14,+dic(14)(p11). No abnormalities were detected on ultrasound. Growth and placentation were normal. The fetus was examined after termination of pregnancy and micrognathia and pulmonary hyperlobation were the only abnormalities detected. Several tissues were set up for cytogenetics, including fetal skin, kidney, ovary, and placenta. The diagnosis was confirmed by these studies. The level of mosaicism varied between tissues, with the trisomy 14 cell line highest in amniotic fluid.

Adult↗
PubMed1993

Influence of smoking habits on change in carbon monoxide transfer factor over 10 years in middle aged men.

BACKGROUND: Emphysema is associated with a reduction in carbon monoxide transfer coefficient (TLCO/VA), but little is known about the evolution of changes in TLCO/VA in middle aged smokers at risk of developing chronic airflow obstruction. METHODS: TLCO/VA (single breath method) was measured on two occasions 10 years apart in 122 middle aged men. RESULTS: Initially TLCO/VA averaged 97% predicted in never smokers (n = 42, mean age 37.2 years), 99% predicted in ex-smokers (n = 21, mean age 41.9 years), and 85% predicted in those who smoked over 15 cigarettes a day (n = 42, mean age 42.0 years). Mean rates of decrease in TLCO/VA over 10 years, however, were similar in the three groups, so that differences between smokers and non-smokers did not increase during the 10 years. Seventeen men (mean age 40.9 years) who initially were smokers became sustained ex-smokers within two years of the first measurement; in these men mean absolute values of TLCO/VA rose, averaging 89% predicted at the first assessment but 102% predicted 10 years later. CONCLUSION: By the age of about 40 years TLCO/VA was lower in smokers than in never smokers but this difference did not increase over the following 10 years. Sustained ex-smokers had values similar to those of never smokers even when TLCO/VA was known to have been reduced while they were smoking. Changes in TLCO/VA associated with stopping smoking were considerably larger than could be explained by carbon monoxide back pressure, indicating that mechanisms other than irreversible increase in the size of terminal air spaces underlie the lower values in smokers. To detect emphysema in smokers it is necessary to use reference equations that take account of current smoking.

Adult↗
PubMed1992

Failure of inhaled corticosteroids to modify bronchoconstrictor or bronchodilator responsiveness in middle-aged smokers with mild airflow obstruction.

We have compared the effects of three-month periods of treatment with an inhaled corticosteroid, budesonide 600 micrograms twice daily and with placebo on bronchial responses to inhaled histamine and to bronchodilators in a double-blind crossover trial in 14 middle-aged male smokers (mean age, 59.6 years) with mild airways obstruction (mean FEV1 2.42 L, 80 percent predicted [range, 48 to 110 percent]). Responsiveness to inhaled histamine was assessed monthly by the provocative concentration (mg/ml) reducing FEV1 by 20 percent (PC20). Bronchodilator response to a combination of inhaled salbutamol (5 mg) and ipratropium (0.5 mg) was assessed before and after three months' treatment. Compliance with treatment was checked by weighing aerosol canisters, and by measuring plasma budesonide and metabolites. There was no significant change in FEV1 (budesonide mean 2.38 L [SEM 0.17] vs placebo 2.40 L [0.17]), vital capacity (budesonide mean 3.69 L [0.17] vs placebo 3.81 L [0.17]) or in bronchodilator responsiveness (mean increase over baseline FEV1, budesonide 11.6 [2.7] percent vs placebo 10.5 [3.2] percent). There was a small overall reduction in bronchoconstrictor responsiveness over the period of the trial, but there was no effect of 12 weeks of budesonide treatment compared with 12 weeks of placebo treatment (mean log PC20 during budesonide 0.595 [SEM 0.063], placebo 0.591 [SEM 0.055]). Following the three-month crossover trial, six men continued for nine more months to receive budesonide in a single-blind trial and the results were compared with those in six men who took no active treatment for the subsequent nine months. No improvements in baseline spirometry, home peak flow measurements, bronchoconstrictor or bronchodilator responsiveness were observed after 12 months of budesonide treatment. Thus, a regimen of budesonide treatment that consistently attenuates bronchial responsiveness in asthmatic subjects had no effect in these men; larger and longer trials will be required to establish whether a subgroup of smokers shows a favorable response.

Administration, Inhalation↗
PubMed1991

Plasma leucocyte elastase concentrations in smokers.

The associations between cigarette smoking, plasma leucocyte elastase concentration, peripheral leucocyte count and FEV1 were examined in 148 men, 72 of whom were current cigarette smokers, 40 of whom were ex-smokers, and 36 who had never smoked. All men were part of a long-term survey. Smokers had significantly higher plasma leucocyte elastase concentrations than ex-smokers or those who had never smoked. Mean current FEV1 was lower, and the annual decline in FEV1 in the preceding 10 years was faster in smokers than the other two groups. A few smokers had slight increases in serum C-reactive protein concentrations. Although peripheral blood leucocyte counts were higher in smokers than in non-smokers or ex-smokers, no association was found in any of the three groups of men between plasma elastase concentration and peripheral leucocyte count, nor between either of these two variables and annual decline in FEV1 or current level of FEV1. There was also no relation between plasma elastase concentration and reported daily cigarette consumption or mixed expired carbon monoxide in smokers. The results indicate that some male smokers have increased in vivo release of elastase from peripheral blood neutrophils at a time when there is no evidence of acute infection. Because leucocyte elastase is a strong candidate for pulmonary tissue damage, further studies of the mechanisms that increase plasma concentrations are indicated.

Adult↗
PubMed1990

Abnormal regional distribution of ventilation in middle-aged smokers: comparison of changes in 81Krm ventilation scans and computed tomography of the lung.

In 1980 we found that abnormalities in regional distribution of ventilation, as assessed by 81Krm lung scans, were common in middle-aged smokers with normal chest radiographs and mild impairment of overall lung function. In 1984 we repeated 81Krm scans in 16 continuing smokers then aged 50-64 years and with mean forced expiratory volume in one second 93% (20 SD) of predicted values who had previous 81Krm scans performed in 1980. To assess the role of disease of the peripheral airspaces in causing abnormal regional ventilation, we also obtained computed tomograms (CT) of the lungs and measured carbon monoxide transfer of the lungs in these men. Krypton scans in seven men who had normal or minor focal defects of ventilation in 1980 were unchanged in 1984. Scans in seven of the nine men who had abnormal scans in 1980 remained abnormal in 1984 but there was no overall deterioration in the abnormality of ventilation in these men; in men with similar grading in 1980 and 1984 some of the peripheral defects present in 1980 had resolved and some new abnormal areas had appeared. Minor localised abnormalities of CT scans, as assessed visually, were present in eight of the 16 men and were associated with lower values of carbon monoxide transfer coefficient (mean 78% vs 98% predicted in men with normal scans, P less than 0.01) and lung density (mean -894 vs -869 HU in men with normal scans, P less than 0.054) suggesting the CT changes were due to alveolar destruction. Abnormality of the krypton scan was not significantly associated with abnormality of the CT scan or with a reduction in carbon monoxide transfer. The results of the krypton lung scans confirm that non-uniformity of regional ventilation is often present in asymptomatic middle-aged smokers and suggest that this non-uniformity is in part due to temporary occlusion of airways. Abnormality in regional ventilation was not associated with the anatomical changes shown by the CT scan, suggesting that airway narrowing was more important than alveolar destruction in causing regional abnormalities of ventilation in these men.

Forced Expiratory Volume↗
PubMed1990

Effects of nonsteroidal anti-inflammatory drugs on the bronchial hyperresponsiveness of middle-aged male smokers.

Bronchial hyperresponsiveness (BHR) in smokers is believed to be a consequence of airway wall inflammation. We have examined the effects of treatment with nonsteroidal anti-inflammatory drugs (NSAID) on BHR to inhaled histamine, measured as the provocative concentration reducing forced expiratory volume in one second (FEV1) by 20% (PC20), in middle-aged male cigarette smokers in two separate double-blind, placebo-controlled, cross-over trials. Baseline FEV1 in these smokers ranged from 41-117% predicted values. In the first study 15 men (mean age 58 yrs, FEV1 2.20 l) were examined before and one hour after a single dose of 1.2 g aspirin. There was no significant change in PC20 (geometric mean 1.88 mg.ml-1 pre-aspirin, 1.89 mg.ml-1 post-aspirin) or baseline FEV1 and we observed no tachyphylaxis to the effects of inhaled histamine at one hour after placebo. In the second study 10 men (mean age 60 yrs, FEV1 2.53 l) were examined before and after three days' treatment with the NSAID flurbiprofen 50 mg t.d.s. Baseline PC20 was higher in this group than in the first study. There was no relationship between the excretion of urinary thromboxane metabolites and the intensity of BHR under baseline conditions; flurbiprofen greatly reduced the urinary excretion of thromboxane metabolites, but baseline FEV1 was not altered. Analysis of change in PC20 was complicated by a difference in baseline PC20 before the two treatments, but treatment with flurbiprofen did not significantly attenuate BHR. The results suggest that thromboxane or other cyclo-oxygenase products of arachidonic acid metabolism do not play an important role in the short-term maintenance of BHR to histamine in middle-aged male cigarette smokers.

Aged↗
PubMed1989

Effects of smoking on changes in respiratory resistance with increasing age.

1. The oscillation method for measuring total respiratory resistance (Rrs) is a simple method of assessing airway dimensions which can be applied in epidemiological surveys and potentially might be useful for detecting mild airway disease in smokers. However, it is not known whether abnormalities in Rrs are only present when there are also abnormalities in simple spirometric tests. 2. We have compared values of Rrs and its frequency-dependence (fR) using the oscillation technique applied over the frequency range 6-26 Hz in 42 healthy, non-asthmatic men who were never-smokers (aged 26-61 years) and in 41 male cigarette smokers (aged 32-64 years). The results were compared with those for spirometry and the single-breath N2 test which are the most commonly used techniques in epidemiological surveys for detecting the effects of smoking on the lungs. 3. There was a strong trend for Rrs (especially at lower oscillation frequency) and fR to increase with increasing age in smokers. Increases in Rrs and fR were usually present when forced expiratory volume in 1 s was less than 80% of predicted and the forced expiratory volume in 1 s/vital capacity ratio was less than 65%, but abnormal fR was present in some smokers whose spirometry was within conventional normal limits. 4. Abnormalities in Rrs and fR were weakly associated with abnormality of the single-breath N2 manoeuvre.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Changes in bronchial responsiveness to inhaled histamine over four years in middle aged male smokers and ex-smokers.

Bronchial hyperresponsiveness to inhaled histamine in smokers is associated with an accelerated annual decline in FEV1 and low baseline FEV1 values. The evolution of bronchial hyperresponsiveness and whether it precedes or follows the accelerated decline in FEV1 and reduction in FEV1 is unknown. Measurements of the provocative concentration of inhaled histamine required to reduce FEV1 by 20% (PC20) were repeated after a four year interval in 27 male smokers (mean age 59 years, smoking on average 27 cigarettes a day in 1986) and 16 men who were ex-smokers in 1982 and who remained non-smokers until 1986 (mean age 53 years in 1986). These men were originally recruited to a prospective study in 1974 and had their first PC20 measurement in 1982. PC20 was positively related to baseline FEV1 in both smokers and ex-smokers in both 1982 and 1986 (r ranging from 0.56 to 0.76, p less than 0.01). In smokers mean FEV1 fell from 83% to 77% predicted (p less than 0.001) and geometric mean PC20 from 7.11 to 3.27 mg/ml (p less than 0.001) between 1982 and 1986. The change in PC20 in individual smokers over the four years was related to change in FEV1 (p = 0.012). In ex-smokers mean FEV1 was 93% predicted both in 1982 and in 1986 and there was no significant difference in geometric mean PC20 between 1982 (6.68 mg/ml) and 1986 (5.98 mg/ml). Thus in smokers there was an accelerated annual decline in FEV1 and an increase in bronchial hyperresponsiveness as FEV1 fell. The ex-smokers had comparable levels of bronchial hyperresponsiveness in 1982. Mean PC20 values were unchanged in 1986 in these men, who showed a normal age related decline in FEV1. These longitudinal results emphasise the importance of baseline airway geometry in influencing bronchial hyperresponsiveness to histamine in middle aged smokers and ex-smokers.

Airway Resistance↗
PubMed1985

Smoking, allergy, and the differential white blood cell count.

Dutch workers have proposed that people with asthma and those smokers who develop chronic airflow obstruction share a common allergic constitution. To study whether smoking itself is associated with indicators of allergy, we have examined 237 men aged 51-61 years (120 smokers, 73 ex-smokers, and 44 non-smokers) who were recruited to a long term study of lung function in 1974, at which time men with a clinical diagnosis of asthma were excluded. Smokers, ex-smokers, and non-smokers did not differ in personal or family history of allergic disease, but the prevalence of positive responses to skinprick tests was greater in ex-smokers (59%) than in the other two groups (33% and 34%). In men with negative responses to skinprick tests total serum IgE was greater in smokers (log10 mean 1.41 IU/ml) and in ex-smokers (log10 mean 1.53 IU/ml) than in non-smokers (log10 mean 1.12 IU/ml). In men with positive skin test responses serum IgE was similar in the three groups (log10 mean ranging from 1.68 to 1.78 IU/ml). Geometric mean total white cell counts in the peripheral blood were higher in smokers (7.34 X 10(9)/l) than in non-smokers (5.82 X 10(9)/l); the value in ex-smokers (6.16 X 10(9)/l) was intermediate. Absolute blood eosinophil counts were increased in smokers disproportionately to the increase in total white cell count. Thus smoking is associated with small increases in some markers of allergy. These changes are probably acquired after the onset of smoking but sequential studies are required to amplify these cross sectional observations. Smokers whose skin test responses are positive appear more likely to give up smoking.

Adult↗
PubMed1985

Bronchial reactivity to inhaled histamine and annual rate of decline in FEV1 in male smokers and ex-smokers.

We examined the relations between bronchial reactivity, baseline FEV1, and annual decline of height corrected FEV1 (delta FEV1/ht3) over 7.5 years in 227 men (117 smokers, 71 ex-smokers, and 39 non-smokers). Men with a clinical diagnosis of asthma or receiving bronchodilator treatment were excluded. Bronchial reactivity was determined as the provocation concentration (PC20) of inhaled histamine sufficient to reduce FEV1 by 20%; subjects were divided into reactors (PC20 less than or equal to 16 mg/ml) and non-reactors (PC20 greater than 16 mg/ml). Thirty per cent of smokers, 24% of ex-smokers, and 5% of non-smokers were reactors. When smokers who were reactors were compared with non-reactors, the reactors showed a lower baseline FEV1 as percentage predicted in 1981-2 (85% v 108%), and a faster delta FEV1/ht3 (14.1 v 9.2 ml/y/m3). Baseline FEV1 correlated with PC20 in both smokers (rs = 0.51) and ex-smokers (rs = 0.61), and all 15 subjects with an FEV1 under 80% of the predicted value were reactors. In ex-smokers delta FEV1/ht3 was similar in reactors and non-reactors (m 9.0 v 7.4 ml/y/m3), despite significant differences in baseline FEV1. When analysis was confined to men with a baseline FEV1 over 80% predicted, the prevalence of reactors was significantly increased among smokers and slightly increased among ex-smokers compared with non-smokers, though the mean FEV1 was higher in the non-smokers. Bronchial reactivity was not increased in smokers aged 35 years or less. In smokers delta FEV1/ht3 was faster in those with a personal history of allergy (usually allergic rhinitis), but was not related to a family history of allergic disease, total serum immunoglobulin E level, absolute blood eosinophil count, or skinprick test score. delta FEV1/ht3 was also faster in all subjects taking beta blocker drugs. Thus increased bronchial reactivity was associated with accelerated decline of FEV1 in smokers. Although the association could be a consequence of a lower lower baseline FEV1, a trend towards increased reactivity was found in smokers with normal baseline FEV1 and delta FEV1/ht3 was dissociated from increased reactivity in ex-smokers. These findings are compatible with the "Dutch hypothesis," but the association between allergic features and accelerated delta FEV1/ht3 was relatively weak, and increased reactivity may follow rather than precede the onset of smoking.

Bronchi↗