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Dive into the research topics where Harold Rea is active.

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Featured researches published by Harold Rea.


Thorax | 1986

A case-control study of deaths from asthma.

Harold Rea; R Scragg; R Jackson; R Beaglehole; J Fenwick; D C Sutherland

A population based case control-study was initiated in 1981 to identify risk factors for death from asthma. Over a two year period all deaths in the Auckland population possibly due to asthma, in people less than 60 years of age, were investigated. From the 47 people who died from asthma 44 who had useful reversibility of airways obstruction (records showing greater than 20% variability of peak flow or a history indicating equivalent variability of shortness of breath) before death were selected as cases for the study. Both hospital and community based controls were used. The cases were more likely than were the community controls to have had severe disease, a hospital admission or visits to a hospital emergency department in the previous year (odds ratios 4.4, 16.0, 8.5 respectively). The asthmatic patients who died were more likely than either group of controls to have had a previous life threatening asthma attack. Poor management of the disease and poor compliance on the part of the patient increased the risk of death. In addition, use of three or more types of asthma drug within the past year was associated with an increased risk of dying that was independent of disease severity. Of interest was a similarity between asthmatic patients admitted to hospital and those who died. Nevertheless, a history of a previous life threatening attack and a recent admission to hospital identified a group at high risk.


The Lancet | 2005

Cardiovascular risk factors after antenatal exposure to betamethasone : 30-year follow-up of a randomised controlled trial

Stuart R Dalziel; Natalie Walker; Varsha Parag; Colin D. Mantell; Harold Rea; Anthony Rodgers; Jane E. Harding

BACKGROUND Antenatal betamethasone treatment is widely used for the prevention of neonatal respiratory distress syndrome in preterm infants and substantially reduces neonatal mortality and morbidity. Fetal exposure to excess glucocorticoids has been proposed as one of the core mechanisms of the fetal origins of adult disease hypothesis. We assessed whether antenatal exposure to betamethasone for the prevention of neonatal respiratory distress syndrome affects cardiovascular risk factors at 30 years of age. METHODS We followed up at age 30 years 534 individuals whose mothers participated in a double-blind, placebo-controlled, randomised trial of antenatal betamethasone for the prevention of neonatal respiratory distress syndrome. Mothers received two doses of betamethasone or placebo given by intramuscular injection 24 h apart. Follow-up assessments included anthropometry; measurement of blood pressure, blood lipids (after overnight fasting), and early morning cortisol levels; and a 75 g oral glucose tolerance test. FINDINGS There were no differences between those exposed to betamethasone and to placebo in body size, blood lipids, blood pressure, plasma cortisol, prevalence of diabetes, or history of cardiovascular disease. After a 75 g oral glucose tolerance test, participants exposed to betamethasone had higher plasma insulin concentrations at 30 min (60.5 vs 52.0 mIU/L; ratio of geometric means 1.16 [95% CI 1.03 to 1.31], p=0.02) and lower glucose concentrations at 120 min (4.8 vs 5.1 mmol/L; difference -0.26 mmol/L [-0.53 to 0.00], p=0.05) than did those exposed to placebo. INTERPRETATION Antenatal exposure to betamethasone might result in insulin resistance in adult offspring, but has no clinical effect on cardiovascular risk factors at 30 years of age. Thus, obstetricians should continue to use a single course of antenatal betamethasone for the prevention of neonatal respiratory distress syndrome.


Thorax | 1995

Major reduction in asthma morbidity and continued reduction in asthma mortality in New Zealand: what lessons have been learned?

J Garrett; John Kolbe; G Richards; T Whitlock; Harold Rea

Increasing financial barriers to primary health care against a background of social and economic decline are likely to have contributed to asthma morbidity and mortality in New Zealand. Although there would not have been a sufficient increase in asthma prevalence to have accounted for the threefold increase in mortality rates, whether or not there was an increase in asthma severity in the late 1970s remains open to debate. Misuse or poor use of newly available and potent bronchodilator medications by those with the most severe asthma may simply have contributed to further delays in obtaining appropriate care and therefore to an increase in frequency of severe attacks in the community. Despite substantial increases in the use of bronchodilator therapy in New Zealand, there was no immediate improvement in indices of either asthma morbidity or mortality. The initial reduction in mortality rates in the 1980s happened at a time when first admissions for asthma were still increasing and seems to be best explained by an improvement in utilisation of hospital services (which were free until 1992) rather than a reduction in asthma severity. However, the recent reductions in all measures of asthma morbidity and further reduction in asthma mortality since 1989 does now suggest a reduction in asthma severity and would be best explained by the substantial increase in medium and high dose inhaled corticosteroid use, and to the endorsement of the current management strategies for asthma which are being promoted internationally and which were given considerable publicity in New Zealand in 1989 and 1990. Whilst sales of inhaled beta agonists were higher in 1991 than 1989, this may not reflect their pattern of use by individual patients since the need for an increase in inhaled beta agonist treatment has been accepted as indicating a lack of control and the need for either starting or increasing the dose of inhaled steroid treatment.


Thorax | 1993

Demographic characteristics of patients with severe life threatening asthma: comparison with asthma deaths.

G Richards; John Kolbe; J Fenwick; Harold Rea

BACKGROUND--Studies of mortality from asthma have suggested that a very severe asthma attack identifies a group at greatly increased risk of subsequent death from the disease. This study compares the demographic characteristics of asthmatic patients who required management in an intensive care unit for a severe life threatening attack between 1981 and 1987 with a group who died of asthma between 1980 and 1986. The outcome of the group admitted to an intensive care unit is described. METHODS--The groups comprised all cases aged between 15 and 49 years arising from the Auckland Area Health Board (AAHB) population who required admission to an intensive care unit for asthma between 1981 and 1987 (n = 413) and all deaths from asthma in those aged 15 to 49 years arising from the New Zealand population between 1980 and 1986 (n = 466). Details of age, sex, and information on the day and month of the attack were collected. For the group requiring admission to an intensive care unit, outcome in terms of mortality and readmission to intensive care was determined. RESULTS--The age distributions of the two groups were dissimilar, with the severe life threatening attack group having an excess of asthmatic patients under 30 years old. The distribution of events by calendar month was uniform in both groups, but there was an unexpected increase in frequency of attacks on Sundays in both groups. Over the study period, mortality fell from 5.3 per 100,000 to 3.5 per 100,000 but the admission rate to intensive care increased from 10.8 per 100,000 to 17.9 per 100,000. At least 24% of asthma deaths occurring in the AAHB region during the study period had previously experienced a severe life threatening attack. CONCLUSIONS--The similarities between the groups suggest that asthmatic patients who experience severe life threatening attacks are likely to come from the same subgroup of the asthma population as those who die. The group who experience severe life threatening attacks are at high risk of subsequent morbidity and mortality and further studies may produce information relevant to reducing mortality from asthma.


Respiratory Medicine | 2010

The clinical utility of long-term humidification therapy in chronic airway disease

Harold Rea; Sue McAuley; Lata Jayaram; Jeffrey Garrett; Hans Hockey; Louanne Storey; Glenis O'Donnell; Lynne Haru; Matthew Jon Payton; Kevin Peter O'Donnell

AIM Persistent airway inflammation with mucus retention in patients with chronic airway disorders such as COPD and bronchiectasis may lead to frequent exacerbations, reduced lung function and poor quality of life. This study investigates if long-term humidification therapy with high flow fully humidified air at 37 degrees C through nasal cannulae can improve these clinical outcomes in this group of patients. METHOD 108 patients diagnosed with COPD or bronchiectasis were randomised to daily humidification therapy or usual care for 12 months over which exacerbations were recorded. Lung function, quality of life, exercise capacity, and measures of airway inflammation were also recorded at baseline, 3 and 12 months. RESULTS Patients on long-term humidification therapy had significantly fewer exacerbation days (18.2 versus 33.5 days; p = 0.045), increased time to first exacerbation (median 52 versus 27 days; p = 0.0495) and reduced exacerbation frequency (2.97/patient/year versus 3.63/patient/year; p = 0.067) compared with usual care. Quality of life scores and lung function improved significantly with humidification therapy compared with usual care at 3 and 12 months. CONCLUSION Long-term humidification therapy significantly reduced exacerbation days, increased time to first exacerbation, improved lung function and quality of life in patients with COPD and bronchiectasis. Clinical trial registered with www.actr.org.au; Number ACTRN2605000623695.


Health Expectations | 2015

Patients' engagement in primary care: powerlessness and compounding jeopardy. A qualitative study

Nicolette Sheridan; Timothy Kenealy; Jacquie Kidd; Jacqueline Schmidt-Busby; Jennifer Hand; Deborah Raphael; Ann McKillop; Harold Rea

Primary health care does not adequately respond to populations known to have high needs such as those with compounding jeopardy from chronic conditions, poverty, minority status and age; as such populations report powerlessness.


Thorax | 2006

Long-term effects of antenatal betamethasone on lung function: 30 year follow-up of a randomised controlled trial

Stuart R Dalziel; Harold Rea; Natalie Walker; Varsha Parag; Colin D. Mantell; Anthony Rodgers; Jane E. Harding

Background: Antenatal betamethasone is routinely used for the prevention of neonatal respiratory distress syndrome in preterm infants. However, little is known of the long term effects of exposure to antenatal betamethasone on lung function in adulthood. Methods: Five hundred and thirty four 30 year olds whose mothers had participated in the first and largest randomised controlled trial of antenatal betamethasone were followed. Lung function was assessed by portable spirometric testing. The prevalence of asthma symptoms was assessed using the European Community Respiratory Health Survey questionnaire. Results: Fifty (20%) betamethasone exposed and 53 (19%) placebo exposed participants met the criteria for current asthma (relative risk 0.98 (95% CI 0.74 to 1.30), p = 0.89). 181 betamethasone exposed and 202 placebo exposed participants had acceptable spirometric data. There were no differences in lung function between betamethasone and placebo exposed groups (mean (SD) forced vital capacity in the betamethasone and placebo groups 105.9 (12.0) v 106.6 (12.6)% predicted, difference = −0.7 (95% CI −3.2 to 1.8), p = 0.59; mean (SD) forced expiratory volume in 1 second in the betamethasone and placebo groups 98.9 (13.4) v 98.5 (13.6)% predicted, difference = 0.3 (95% CI −2.4 to 3.1, p = 0.80)). Conclusions: Antenatal exposure to a single course of betamethasone does not alter lung function or the prevalence of wheeze and asthma at age 30.


Chest | 1988

International Trends in Asthma Mortality: 1970 to 1985

Rodney Jackson; Malcolm R. Sears; Robert Beaglehole; Harold Rea


The New Zealand Medical Journal | 1987

Lessons from the national asthma mortality study: circumstances surrounding death.

Harold Rea; Malcolm R. Sears; Robert Beaglehole; Fenwick J; Rodney Jackson; Gillies Aj; O'Donnell Tv; Holst Pe; Rothwell Rp


Thorax | 1996

Risk of severe life threatening asthma and beta agonist type: an example of confounding by severity.

J Garrett; S F Lanes; John Kolbe; Harold Rea

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John Kolbe

University of Auckland

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