Biomedical subjects

A Laverty

Publications and source records attributed to A Laverty.

6 recordsLinked to original sources

PubMed2007

Standardizing lung function laboratories for multicenter trials.

Multi-center studies provide advantages in clinical research but differences between centers can introduce bias. Three specialist pediatric respiratory laboratories standardized their methodology and examined differences between centers. The specific aims were to (i) assess the variability of measurements on adults within and between centers and (ii) to exchange and cross-analyze data from children to assess the extent of agreement between centers. Each laboratory used identical equipment and software. Inter-laboratory visits were used to (i) standardize protocols for data collection and analysis and (ii) make spirometric and plethysmographic measurements on participating staff at each location. Staff also had repeat measurements in their home laboratories. Measurements from children in each laboratory were exchanged on disk, cross-analyzed, and data compared by ANOVA. There were no significant within-subject, between-center differences in FVC, FEV1, FEF50, FRCpleth, or VC. There was a slight trend for TLC and RV (P=0.07) to be higher at one center. The 95% limits of agreement within and between centers were similar for all parameters. There were no differences between centers in cross-analyzed data from 10 children. By standardizing hardware, software, and protocol, potential inter-laboratory differences can be minimized. We recommend that this approach be adopted prior to multi-center studies.

Adult↗

PubMed2002

The use of nasal continuous positive airway pressure to treat obstructive sleep apnoea.

AIM: To review 66 children with obstructive sleep apnoea (OSA) for whom a trial of nasal continuous positive airway pressure (nCPAP) was proposed. METHODS: Baseline sleep studies were performed to assess OSA severity; a trial of nCPAP was performed where moderate to severe OSA, not relieved by adenotonsillectomy, was found. The nCPAP trial was considered either technically successful (ST), if the child accepted the mask for sufficient time to determine nCPAP efficacy, or a technical failure (FT) if otherwise. Patients with an initial FT were offered a period of home acclimatisation to familiarise them with wearing the mask during sleep. ST patients in whom nCPAP was effective were established on long term therapy. RESULTS: Nasal CPAP trials were successful (ST) in 49/66 (74%) patients. Nasal CPAP efficacy could not be determined in the remaining 17 FT patients (26%), generally because of their poor nCPAP tolerance. These patients were subsequently considered for other treatment. A total of 42/49 (86%) ST patients were established on long term nCPAP therapy, 2/49 (4%) derived no benefit from nCPAP, while 5/49 (10%) refused long term nCPAP therapy. Of patients on long term nCPAP, the most frequently reported side effects were skin irritation and nasal dryness; however, these were not serious enough to require any patients to discontinue therapy. A period of home acclimatisation was found to be effective in increasing nCPAP acceptance, with 26% of FT children being subsequently successfully reassessed for nCPAP. CONCLUSION: The use of nCPAP was feasible in a significant proportion of a paediatric OSA population. Failure was usually because of the child's intolerance of the nCPAP equipment. Nasal CPAP was an effective treatment in the majority of patients where it could be assessed, and was adopted as a long term therapy in most cases. We have successfully used nCPAP to treat OSA across a wide range of ages. Motivated parents and skilled support staff have proved essential for the success of nCPAP in a paediatric setting.

Adolescent↗

PubMed1998

A step in the right direction: assessing exercise tolerance in cystic fibrosis.

Exercise tolerance may be reduced in patients with cystic fibrosis, but it is not always possible to predict this from standard lung function measurements. Formal exercise testing may, therefore, be necessary, and the test should be simple and readily available. We have developed a "3-minute step test" and compared it with the standard 6-minute walking test. Subjects stepped up and down a 15-cm-high single step at a rate of 30 steps per minute for 3 minutes. The effect of the step test on spirometry was tested first in 31 children with CF (mean age, 12.0 years), who had a mean (range) baseline forced expired volume in 1 second (FEV1) of 64% (18-94%) of predicted values. The step test was then compared with the standard 6-minute walk in a further 54 patients with cystic fibrosis (mean age, 12.5 years), with mean (range) baseline FEV1 of 61% (14-103%) of predicted values. Outcome measures were minimum arterial oxygen saturation (SaO2), maximum pulse rate, and the modified Borg dyspnea score. Post-step test spirometry showed mean (95% CI) changes of -1.1% (-6.0 + 3.9%) for forced vital capacity, of -1.6% (-4.2 + 1.1%) for FEV1, and +0.25% (-2.8 + 3.3%) for peak expiratory flow, although 5/31 children showed >15% drop in one or more parameters. The step and walk tests both produced significant changes (P < 0.0001) in all outcomes, with a mean (range) minimum SaO2 of 92% (75-98%) versus 92% (75-97%), a maximum pulse rate of 145 b.p.m. (116-189) versus 132 (100-161), and a Borg score of 2.5 (0-9) versus 1.0 (0-5), respectively. Comparison of the two tests showed that the step test increased breathlessness (mean change Borg score, 2.3 vs. 0.8; P < 0.0001) and pulse rate (mean change, 38% vs. 24%, P < 0.0001) significantly more than the walk, whereas the decrease in SaO2 was similar (mean change, -2.9% vs. -2.6%; P = 0.12). Some patients with a significant drop in SaO2 (>4%) would not have the decrease predicted from their baseline lung function. Reproducibility for the two tests was similar. The step test is quick, simple and portable, and is not dependent on patient motivation. Although the step test is more tiring, its effect on SaO2 is similar to the 6-minute walking test. It is a safe test that may prove to be a valuable measure of exercise tolerance in children with pulmonary disease, although longitudinal studies are now needed.

Adolescent↗

PubMed1998

Distinct patterns of respiratory difficulty in young children with achondroplasia: a clinical, sleep, and lung function study.

AIM: Achondroplasia can result in respiratory difficulty in early infancy. The aim of this study was to document lung growth during infancy, together with the cause of any cardiorespiratory and sleep dysfunction. PATIENTS AND METHODS: Seventeen prospectively ascertained infants (14 boys and three girls) with respiratory symptoms starting before 1 year of age underwent clinical, sleep, and lung function studies. RESULTS: Three distinct groups were identified. Group 1 (n = 6) were the least symptomatic and only had obstructive sleep apnoea. Group 2 (n = 6) had obstructive sleep apnoea of muscular aetiology and, neurologically, hydrocephalus and a small foramen magnum were common. Group 3 (n = 5), the most severely affected group, all developed cor pulmonale, with three deaths occurring as a result of terminal cardiorespiratory failure. All five had obstructive sleep apnoea with a muscular aetiology (a small foramen magnum predominated) with severe or moderately severe gastro-oesophageal reflux. Initially, lung function studies found no evidence of restriction or reduced lung volumes standardised according to weight. However, with growth these infants had worsening function, with raised airway resistance and severe reductions in respiratory compliance. CONCLUSIONS: These groups appear to be distinct phenotypes with distinct anatomical aetiologies: "relative" adenotonsillar hypertrophy, resulting from a degree of midfacial hypoplasia (group 1); muscular upper airway obstruction along with progressive hydrocephalus, resulting from jugular foramen stenosis (group 2); and muscular upper airway obstruction, but without hydrocephalus, resulting from hypoglossal canal stenosis with or without foramen magnum compression and no jugular foramen stenosis (group 3). The aetiology of these abnormalities is consistent with localised alteration of chondrocranial development: rostral, intermediary and caudal in groups 1, 2, and 3, respectively.

Achondroplasia↗

PubMed1996

Reduced upper airway nitric oxide in cystic fibrosis.

Nitric oxide (NO) produced within the respiratory tract is detectable in exhaled and nasal air. Its synthesis may be induced by inflammatory cytokines and reduced by glucocorticoids. Increased concentrations have been found in asthma and bronchiectasis. In this study, NO concentrations were determined in 63 children with cystic fibrosis, of whom 13 were on inhaled steroids (mean age 13.3 years) and 50 were not (mean age 12.3 years); 57 normal children (mean age 12.2 years) were also studied. NO was measured by chemiluminescence analyser, exhaled NO following a relaxed vital capacity manoeuvre, and nasal NO with the breath held following a full inspiration. Mean concentration of exhaled NO in cystic fibrosis patients (no steroids) was 4.7 parts per billion (ppb) (95% confidence interval (CI) 4.0 to 5.3); this did not differ from values in normal children (mean 4.8 ppb, 95% CI 3.8 to 5.8) or in cystic fibrosis patients on inhaled steroids (mean 3.6 ppb, 95% CI 2.5 to 4.8). Nasal concentrations were significantly lower in cystic fibrosis patients, with or without inhaled steroids, than in normal children (cystic fibrosis, no inhaled steroids: 460 ppb, 95% CI 399 to 520; cystic fibrosis, inhaled steroids: 522 ppb, 95% CI 313 to 730, v normal children: 1024 ppb, 95% CI 896 to 1152, p < 0.0001). Considering the inflammatory nature of cystic fibrosis, it is surprising exhaled NO levels were not increased, but this may have been due to alteration in NO diffusion through thick mucus. The low nasal NO concentrations, which are probably the result of impaired flow from the paranasal sinuses, may contribute to the recurrent respiratory infections typical of cystic fibrosis.

Administration, Inhalation↗

PubMed1993

Bronchial hyperresponsiveness in children with atopic dermatitis.

Using histamine provocation tests, bronchial responsiveness was measured in 43 children with atopic dermatitis, aged 7 to 15 years, who had attended pediatric dermatology clinics within the past 5 years. The children were divided into two groups, one group of 21 children in whom asthma had been previously diagnosed and in whom symptoms of asthma had occurred in the preceding year, and the other comprising 22 children who denied any such symptoms. Bronchial hyperresponsiveness (as defined by a 20% fall in forced expiratory volume in 1 second at a provoking dose of histamine of 7.8 mumol or less [PD20]) was demonstrated in all but 1 of the children with atopic dermatitis and asthma, in 18 of the 22 children with atopic dermatitis alone, but in only 3 of a control group of 18 children without atopic dermatitis or asthma. The asthmatic subjects (median PD20 = 0.22 mumol) had more severe bronchial hyperresponsiveness than the nonasthmatic subjects (median PD20 = 2.10 mumol). This study confirms the strong association between atopic dermatitis and bronchial hyperresponsiveness, even in the absence of overt asthmatic symptoms.

Adolescent↗