Search PubMed⌕ Search

Biomedical subjects

J Burdon

Publications and source records attributed to J Burdon.

36 records · Page 2Linked to original sources
PubMed1998

Comparison of efficacy and ease of handling of salmeterol and terbutaline powder inhalers.

A multicentre, randomised, open, parallel-group study was performed to compare the efficacy, tolerability and ease of handling of salmeterol xinafoate 50 micrograms twice daily via the Diskus inhaler with terbutaline sulphate 500 micrograms four times daily via the Turbuhaler inhaler. Two hundred and sixty-three patients (aged 18-79 years, baseline FEV1 50-90% predicted, mean PEFR 85% of response to salbutamol) were randomised to treatment with salmeterol (n = 136) or terbutaline (n = 127). A statistically significant difference in favour of salmeterol was seen between treatment groups for the primary efficacy variable, mean morning PEFR (difference in adjusted means 25.4 l/min, p < 0.001). Within the groups randomised to each device, ease of handling assessments favoured the Diskus inhaler over the Turbuhaler inhaler. More patients liked the Diskus inhaler than the Turbuhaler inhaler (98% vs 72%, p < 0.001). The Diskus inhaler received better scores than the Turbuhaler inhaler for all features assessed in the device questionnaire.

Adolescent↗
PubMed1996

Effect of inhaled morphine on the development of breathlessness during exercise in patients with chronic lung disease.

BACKGROUND: Inhaled morphine has previously been shown to increase exercise endurance in patients with chronic lung disease. A similar study was performed to determine whether inhaled morphine reduces the sensation of breathlessness in this group of patients. METHODS: A randomised double blind study on the effect of nebulised morphine on both exercise induced breathlessness and maximum achievable power output using isotonic saline as a control was performed in 10 patients with stable chronic lung disease. Each subject performed a progressive exercise test (Jones' stage I) on an electrically braked cycle ergometer. The work load was increased by 10 watts per minute and subjects exercised to exhaustion. At the end of each minute of exercise patients were asked to rate their degree of breathlessness according to a modified Borg scale. All subjects were randomised to receive either inhaled morphine sulphate 1 mg/ml (5 ml) or isotonic saline (5 ml) by wet nebulisation. The effect of morphine and saline on the achieved exercise capacity and the development of breathlessness during exercise was tested on separate days. RESULTS: The mean dose of morphine inhaled was 1.24 mg. There was no difference in maximum power output achieved, minute ventilation at maximum power output, nor the degree of breathlessness at maximum power output between the groups treated with morphine and placebo. The degree of breathlessness was related to the power output achieved during exercise by a power function relationship (mean r: morphine = 0.86, saline = 0.87). However, there was a wide variation in the sensation for any given power output in both groups. There was no difference in the group mean slopes (morphine = 1.15, saline = 1.00) or intercepts (morphine = 0.07, saline = 0.15) in this relationship between the morphine and saline treatment groups. CONCLUSIONS: In patients with severe chronic lung disease inhaled morphine in the doses used in this study does not relieve exercise induced breathlessness nor does it increase maximum power output achieved during progressive exercise.

Administration, Inhalation↗
PubMed1995

Alpha 1-antitrypsin deficiency and anti-proteinase 3 antibodies in anti-neutrophil cytoplasmic antibody (ANCA)-associated systemic vasculitis.

alpha 1-antitrypsin (alpha 1-AT) is a naturally occurring inhibitor of proteinase 3 (PR3) and elastase, two of the target antigens of anti-neutrophil cytoplasmic antibodies (ANCA). An increased incidence of alpha 1-AT phenotypes associated with dysfunctional alpha 1-AT or low serum levels has been reported in patients with anti-PR3 antibodies. We have studied the relationship between ANCA, and phenotypes and serum levels of alpha 1-AT. Phenotypes usually associated with a moderate or severe reduction in alpha 1-AT serum levels or in dysfunctional activity were found more often in individuals with anti-PR3 antibodies than in the general population: four of the 31 patients (13%) with anti-PR3 antibodies had phenotypes MZ (n = 2), S (n = 1) or Z (n = 1) (P < 0.05). However, the corresponding alpha 1-AT serum levels were normal (n = 3) or elevated (n = 1). None of the 31 sera with anti-PR3 antibodies had low levels of alpha 1-AT. No abnormal alpha 1-AT phenotype was demonstrated in seven patients with anti-elastase antibodies, despite a low level of alpha 1-AT in one serum. Anti-myeloperoxidase antibodies are common in patients with ANCA, but no abnormal phenotype or low serum alpha 1-AT level was demonstrated in any of 29 sera containing these antibodies. Finally anti-glomerular basement membrane (GBM) antibodies occur occasionally in patients with ANCA-associated diseases, but again none of 10 sera had an abnormal alpha 1-AT phenotype or low serum level. ANCA were not demonstrated by indirect immunofluorescence in any serum from 73 patients with abnormal alpha 1-AT phenotypes. These results confirm that patients with anti-PR3 antibodies often have alpha 1-AT phenotypes that are usually associated with low serum levels of alpha 1-AT or with dysfunctional protein. Nevertheless, the incidence of anti-PR3 antibodies in patients with abnormal alpha 1-AT phenotypes is very low. This probably reflects the rarity of Wegener's granulomatosis, the major disease associated with anti-PR3 antibodies, and the relative frequency of abnormal alpha 1-AT phenotypes. The mechanism for the development of anti-PR3 antibodies in patients with abnormal alpha 1-AT phenotypes is not clear, but may relate to the increased propensity of unbound and uninhibited PR3 to stimulate autoantibody production.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1995

Alpha-1-antitrypsin PLowell: a normally functioning variant present in low concentration.

BACKGROUND: Alpha-1-antitrypsin deficiency is associated with a high risk for the development of emphysema, particularly for phenotype Pi ZZ, which is both deficient and an abnormal inhibitor of the powerful proteolytic enzyme, human neutrophil elastase. The rare variant PLowell is also expressed at abnormally low levels, but its anti-elastase activity has not been described. AIM: To study the anti-elastase activity of alpha-1-antitrypsin PLowell and compare it to the common M, S and Z proteins. METHOD: Alpha-1-antitrypsin from a female patient aged 75 years with the rare genotype PLowell NullBellingham was studied for its ability to inhibit human neutrophil elastase in a time dependent manner. RESULTS: PLowell has near normal function as an inhibitor of human neutrophil elastase with an association rate constant of 7.4 x 10(6) M-1 S-1 at 25 degrees C, similar to that of M and S. CONCLUSION: Alpha-1-antitrypsin PLowell is associated with a severe deficiency of alpha-1-antitrypsin similar to Z, but unlike that protein it has near normal function as an anti-elastase.

Aged↗
PubMed1994

Absence of alpha-1-antitrypsin (Pi Null Bellingham) and the early onset of emphysema.

BACKGROUND: Alpha-1-antitrypsin is the body's major inhibitor of human neutrophil elastase, a powerful proteolytic enzyme capable of degrading the common tissue components. There are over 70 genetic variants of alpha-1-antitrypsin, with the Z allele being of greatest clinical relevance. Individuals homozygous for this allele (approximately one in 2500 in Caucasians) have low serum alpha-1-antitrypsin levels (10-20% of normal) and are predisposed to emphysema, especially if they smoke. Much rarer are mutations which result in the complete or almost complete absence of alpha-1-antitrypsin in the serum. AIM: To determine the cause of complete absence of alpha-1-antitrypsin in a patient who at age 27 years had both emphysema and idiopathic cardiomyopathy. METHODS: Molecular biology techniques were used to sequence the alpha-1-antitrypsin gene. Allele specific amplification was used to show the presence of the mutations in other family members. RESULTS: Investigation showed that the proband was homozygous for the Pi Null Bellingham variant of alpha-1-antitrypsin due to the mutation Lys 217 (AAG) to Stop (TAG). His grandmother was heterozygous for Pi Null Bellingham and the additional rare variant P Lowell, Asp 256 (GAT) to Val (GTT), a variant that also results in alpha-1-antitrypsin deficiency. CONCLUSION: Patients with complete absence of alpha-1-antitrypsin develop premature emphysema not having smoked or after only minimal exposure, and much earlier than the more common Pi Z individuals who have the usual form of alpha-1-antitrypsin deficiency.

Adult↗
PubMed1993

Culture-positive tuberculosis at St Vincent's Hospital, Melbourne, 1962-1989.

The disease type and demography of patients with culture confirmed tuberculosis (TB) diagnosed at St Vincent's Hospital, Melbourne between the years 1962 to 1989 were reviewed. Four hundred and eighty-two patients with culture-positive TB were identified whose origins were as follows: Australia 194; Northern Europe 38; The Mediterranean 98; Asia 60 and other or unknown 92. Patients whose country of birth was in Asia or the Mediterranean area accounted for 57% of patients in the 1980s; they presented at a younger age, with a higher proportion of extrapulmonary disease and a more equal sex distribution than did Australian born patients. The main types of extrapulmonary disease also differed for the various ethnic groups. The overall proportion of patients with an isolate resistant to at least one of the anti-TB drugs was 10.0% but in the Asian born was 21.7%. This survey, the longest series of bacteriologically confirmed cases of TB reported from a single institution in Australasia, has identified several changes in how TB is presenting for diagnosis.

Adolescent↗
PubMed1991

Carbamylated haemoglobin, urea kinetic modelling and adequacy of dialysis in haemodialysis patients.

Urea kinetic modelling (UKM) has increasingly been used for assessing adequacy of dialysis and protein nutritional status of dialysis patients. Using a precise HPLC method we developed, we measured carbamylated haemoglobin (CarHb) values in 20 stable twice-weekly dialysed patients and attempted to correlate their CarHb values with their UKM-derived indices. Based on these indices, 11 patients were found to have been adequately dialysed with sufficient protein intake, three patients were adequately dialysed but malnourished and six patients were under-dialysed. Estimated dietary protein intake correlated poorly with calculated daily protein catabolic rate in our patients. CarHb values were found to correlate strongly with the time-averaged urea concentrations, suggesting that CarHb might be a time-integrated urea-derived index. Those adequately dialysed patients have a mean (SD) CarHb value of 142 (29) micrograms CV/gHb against the underdialysed patients, 197 (30) micrograms CV/gHb (t-test, P = 0.002). We suggest that a CarHb value less than 175 micrograms CV/gHb may represent satisfactory uraemic exposure, whereas CarHb value greater than 175 micrograms CV/gHb is undesirable.

Adult↗
PubMed1988

Synthesis and nuclear magnetic resonance spectroscopic, mass spectroscopic, and plasma amine oxidase inhibitory properties of analogues of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine.

Seventeen analogues of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine were synthesized using three reaction pathways: condensation of phenols with 1-methyl-4-piperidone, reaction of Grignard reagents with 1-methyl-4-piperidone followed by dehydration of the product, and aminomethylation of olefins. The identity of the products of synthesis was established by nuclear magnetic resonance spectroscopy, mass spectroscopy, and elemental analysis. Thirteen analogues were shown to inhibit the oxidation of benzylamine by bovine plasma amine oxidase. Increasing the length of the aliphatic chain of N-substituted analogues resulted in increased inhibition. In 4-phenyl-substituted analogues, both the position and electronic character of the substituent group affected the degree of inhibition.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1988

Comparison of the effects of nebulized terbutaline with intravenous enprofylline in patients with acute asthma.

We compared the bronchodilating effects of intravenously administered enprofylline (2 mg/kg) with nebulized terbutaline (10 mg) in patients presenting to hospital with acute asthma in a multicenter double-blind parallel study. One hundred twenty three patients were randomized into the study, and 69 of these fulfilled the inclusion criteria and a retrospective time to study entry criterion; 34 received enprofylline and 35 received terbutaline. There was no significant difference in maximum increase in forced expired volume in 1 second (FEV1) between the enprofylline group (0.24 +/- 0.33 L) and the terbutaline group (0.25 +/- 0.28 L) (p greater than 0.05), nor for the increase in FEV1 over the 1-hour study period. Tremor was reported more in the group receiving terbutaline, and nausea was reported more in the group receiving enprofylline. Two patients experienced hypotension and one patient had a vasovagal episode with enprofylline treatment. Both agents acted as bronchodilators with similar efficacy in patients with acute asthma in this study.

Acute Disease↗
PubMed1985

Mitochondrial myoneuropathy with respiratory failure and myoclonic epilepsy. A case report with biochemical studies.

A 55-year-old man is presented who developed severe multifocal myoclonus and tonic clonic seizures in his early thirties, and progressive limb weakness in his mid forties, when a ragged red fibre myopathy was diagnosed. He went on to develop a distal motor neuropathy and respiratory failure. Respiratory function tests indicated respiratory failure secondary to respiratory muscle weakness and a central hypoventilation syndrome. CT scan revealed brain stem atrophy and brain stem evoked responses were abnormal. A sural nerve biopsy showed severe axonal degeneration. Cytochrome difference spectra and polarographic studies on isolated intact muscle mitochondria were normal. This study reports the association of respiratory failure and sleep apnoea with Fukuhara's syndrome and presents biochemical data suggesting that the mitochondrial respiratory chain may be intact in some patients with this syndrome.

Adenosine Diphosphate↗