Herbal medicine: role in the management of chronic obstructive pulmonary disease (COPD).
It is estimated that around 2 million Australians are living with COPD while it remains a largely under recognised condition, under diagnosed and under untreated.
This paper outlines the basic epidemiology, pathophysiology and clinical considerations when it comes to treating someone with COPD. It is very important for the herbal medicine practitioner to be familiar with this chronic condition, its management as well as the management of common co-morbidities in COPD patients.
COPD is most prevalent in middle aged to older patients with average age of diagnosis being in the fifth to sixth decades of life. It affects 12.4% of Australians between 45 and 70 years (Murtagh 2007). There is no gender bias with males and females affected equally (Ferguson 2008).
COPD is a spectrum of conditions predominantly comprising chronic bronchitis, a disease of the small airways, and emphysema. Asthma and bronchiectasis may also be included under this definition (Kumar 2005) however this paper will refer specifically to chronic bronchitis and emphysema in relation to the management of COPD.
In emphysema there is parenchymal destruction with abnormal permanent enlargement of airspaces distal to terminal bronchioles and destruction of bronchiole walls. Depending on the anatomical location of airway destruction, emphysema can be classified into four major subtypes; centriacinar, panacinar, paraseptal and irregular (Kumar 2005).
The major pathophysiologic changes in emphysema include chronic infection, excess mucous and inflammatory edema, entrapment of air in the alveoli and bronchiolar obstruction increasing airway resistance. This pathophysiology results in a grossly abnormal ventilation/perfusion mismatch (V/Q mismatch) resulting in wasted ventilation, and loss of alveolar walls decreases the diffusing capacity of the lungs (Guyton 2006). For a diagnosis of chronic bronchitis there must be persistent cough with sputum for at least 3 months in at least two consecutive years, in the absence of any other identifiable cause. The major pathological changes in the bronchi and bronchioloes include goblet cell metaplasia, clustering of alveolar macrophages, inflammatory infiltration and fibrosis of bronchiolar walls. Chronic bronchitis shows late destruction of alveolar walls compared to emphysema which shows early destruction of alveolar walls (Kumar 2005).
As a result COPD symptoms understandably include dyspnea, cough, decrease in exercise tolerance, fatigue, anemia and weight loss (Murtagh 2007). Much of the fatigue symptoms in COPD patients may be partly due to disturbed sleep due to alveolar hypoventilation and resulting hypoxemia with REM PaO2 levels being reported in some COPD patients at 20 mmHg. This results in increased sleep fragmentation and arousals (Gay 2008).
Exacerbations due to respiratory tract infections are an important cause of hospitalisation in 70-80% of cases especially in chronic bronchitis. Common pathogens include viruses such as respiratory syncytial virus and human metapneumovirus, and bacteria including H. influenzae, Moraxella catarrhalis and Streptococcus pneumoniae. Atypical bacteria such as Chlamydophila pneumoniae in exacerbations of COPD appear to be 3 to 5 percent with Mycoplasma pneumoniae and Legionella spp being even more rare (Bartlett 2008).
Cigarette smoking is a known major modifiable risk factor (level 1 evidence) (Frith 2008) and is involved in 9.7% of disability adjusted life years (DALYs) (Mathers 2000). There is a large variability in individuals' response to smoking, and although smoking is a significant predictor of forced expiratory volume at 1 sec (FEV1), there is no general consensus on variability being exclusively explained by number of pack years smoked.
This leads to the conclusion that there is also a significant genetic/environmental component (Kasper 2005). It is estimated that 85% of COPD patients have a significant smoking history however 15% do not have any direct smoking history (Hanley 2003). Other sources suggest a figure of 80% of COPD patients have a significant smoking history with the other 20% being exposed to causes such as pulmonary infections, air pollution and occupational dusts and chemicals (McPhee 2009).
Other causative factors include familial factors such as genetic predisposition, alpha1-antitrypsin deficiency and bronchial hyper responsiveness (Murtagh 2007) while the etiological role of chronic airway infections in adults and children for development of COPD remains controversial (Kasper 2005).
Observational studies and animal data show that atopic individuals have a more rapid decline in FEV1 and FEV1/ FVC than non atopic individuals and therefore atopy is considered a risk factor for decline in lung function (Weiss 2008).
There is limited data that suggests a deficiency in antioxidants such as vitamins E and C may be a risk factor for developing COPD however theoretically the mechanism is plausible especially with regards to antioxidant depletion in smokers (Weiss 2008).
COPD burden of disease
Over recent times there has been a shift in the burden of disease in Western societies towards diseases associated with lifestyle factors and an example of this is COPD. Apart from the many adverse biological/physical effects, COPD has many psychosocial effects such as a decreased work and recreational ability. These psychosocial factors have far reaching adverse consequences on the independence and self esteem of COPD patients. COPD results in increased mortality that is preceded by a long period of disability (Frith 2008). The main causes of death in COPD patients include respiratory acidosis (CO2 retention) and coma, right sided heart failure (cor pulmonale) and massive collapse of the lungs secondary to pneumothorax (Kumar 2005).
The rate of mental illness, especially depression and anxiety, in people with COPD is also much higher than in the general community (40% depression, 36% anxiety, compared with 12.3% and 9% respectively in the general community) (Frith 2008).
In Australia COPD is the sixth highest cause of mortality, accounting for 2.8% of total years lost to mortality (YLL), the eighth highest cause of years lost to disability (YLD) and the third highest with regards to DALYs (Mathers 2000, Frith 2004). Crockett et al (2002) estimate that the cost of COPD to the Australian economy ranges between $818 and $898 million per annum while a recent analysis by Frith et al (2008) has shown that the cost of COPD to the Australian economy now exceeds $1 billion per annum.
The financial burden from COPD management can be divided into direct and indirect costs. United Kingdom data shows the majority of direct costs are related to hospitalisation (54%) (Halpin 2006). In Australia the average length of hospital stay for COPD treatment is 7.1 days compared with 4.2 for all respiratory disease (Australian Institute of Health and Welfare 2008). This is followed by scheduled care and pharmacological treatment (15% each) (Halpin 2006).
Costs associated with hospitalisation of COPD patients has also increased by approximately 50% between 1993 and 2000 (Crockett 2002) and are expected to increase in proportion to an aging population (Crockett 2002). It is suggested that there is a large degree of under diagnosis of COPD within the Australian community (Crockett 2002) and therefore the above costs are presumably an underestimation of true costs.
Despite the high financial cost and personal burden that COPD imposes on the Australian community, it is largely a preventable disease that does not rate National Health Priority status (National Chronic Disease Strategy 2006). This may be partly due to the historical belief that little could be done for COPD prevention and treatment (Thorax 2004) and therefore a sense of nihilism often prevails (McKenzie 2007).
The regional COPD working group (2003) estimated that 80% of patients with COPD in Australia live in urban regions and the remaining 20% in rural regions. Analysis by Ansari et al (2007) of the rates of hospitalisation for patients in Victoria, showed that hospital admission rates were higher for rural regions compared with urban regions and that the rate of admission increases with degree of remoteness (Regional COPD working group 2003). An additional analysis of socioeconomic status showed that admission rates were 55% higher for patients in the most disadvantaged group compared with the least disadvantaged groups (Regional COPD working group 2003). Therefore patients who are least able to be separated from their families due to remote location and/or financial pressures are those who have the highest hospitalisation rates for COPD.
Natural history of COPD
COPD usually shows progressive deterioration over many years with increasing hypoxia and hypercapnia which results in severe, prolonged and devastating air hunger (Guyton 2006). Prognostic factors that predict accelerated lung function decline, diminished physical functioning and/or mortality include:
* Airways responsiveness
* Cigarette smoking
* Low body mass index (BMI [less than or equal to] 21)
* HIV infection
* Increased airway bacterial load
* Decreased exercise capacity
* Decreased peak oxygen consumption (VO2), measured by cardiopulmonary exercise testing
* Elevated C-reactive protein (>3 mg/L) (Weiss 2008)
Patients are generally not cyanosed and lung signs are due to hyperinflation/air trapping. Patients show a barrel shaped chest with an increased anterioposterior diameter. There may be pursed lip breathing with increased end expiratory pressure forcing airways open. There may be use of accessory muscles of inspiration and therefore hypertrophy of the sternocleidomastoid muscles. On palpation there will be reduced chest expansion (<5 cm) and a hyper inflated chest. On percussion there will be a hyper resonant note and decreased liver dullness. Breath sounds will be reduced with early inspiratory crackles while wheeze is often absent. Signs of right heart failure such as peripheral edema and raised jugular venous pressure (JVP) are late and generally indicate a preterminal state.
It is important to note that emphysema patients do not show hemoptysis or finger clubbing. These signs would be more consistent with lung cancer (Tally 2006). Advanced disease patients may show significant weight loss and this is an independent poor prognostic factor (Kasper 2005).
* Assessing severity
* Sputum production
* Chest tightness
* Fatigue, anorexia and weight loss are especially important with advanced disease (Murtagh 2008)
Assessment using these main symptoms as a guideline is useful with regards to developing a herbal management program that can be individualised for each patient.
Spirometry is the gold standard for diagnosis of COPD. COPD is defined via spirometry as post bronchodilator FEV1/FVC <0.70 and FEV1 <80% predicted for age (Murtagh 2008). The important factor is that the airways obstruction is not reversible with bronchodilators such as salbutamol.
Other useful adjunct investigations to spirometry include:
* Chest X ray may show late changes but important to help exclude lung cancer >1 cm. Lung cancer is two to four times more common in COPD patients than in the general community with men being affected more than women (Mannino 2008).
* Blood gases may show a raised PaCO2 and decreased PaO2 in advanced disease
* ECG may be useful in determining the extent of right heart disease (cor pulmonale) due to airway obstruction
* Sputum culture may be indicated if a resistant organism is suspected
* Full blood evaluation is important to identify anemia and polycythemia (Murtagh 2008)
* CT has a higher sensitivity and specificity for detecting COPD than a plain chest film and can determine centriacinar from panacinar (Rennard 2008).
Current medical recommendations for treatment/management
All models of care, be it primarily self managed, GP or multidisciplinary team including tertiary respiratory specialists, should aim to manage COPD following the COPDX guidelines. Naturopathic management of COPD may also follow these guidelines. These guidelines were developed by the Australian Lung Foundation and the Thoracic Society of Australia and New Zealand to provide a frame work for the optimal diagnosis and management of COPD patients.
The COPDX guidelines are as follows:
* C = Confirm diagnosis
* O = Optimise function
* P = Prevent deterioration
* D = Develop a self management plan and manage
* X = Xacerbations
These naturally lead onto the following goals of:
* Primary prevention of smoking
* Improving rates of smoking cessation
* Early detection of airflow limitation in smokers before disablement
* Improved management of stable disease and prevention of exacerbations (McKenzie 2007).
Current orthodox medicine management
Short acting [beta]2 agonists (salbutamol terbutaline) relieve wheeze and shortness of breath. The anticholinergic drugs may also be used and the main drug in this case is ipratropium bromide (Atrovent). If airway disease is severe (<40% FEV1 predicted), a longer acting [beta]2 agonists such as salmeterol or eformoterol may be initiated. Other options include longer acting anticholinergics such as tiotropium and inhaled corticosteroids.
Oral corticosteroids are not recommended for long term treatment however may be needed following an acute exacerbation in patients with severe COPD. Commonly used corticosteroids include prednisolone and prednisone orally, or if this cannot be tolerated IV hydrocortisone may be used (Murtagh 2008).
Physiotherapy with regular chest 'tune ups' and breathing exercises is also recommended. Long term oxygen therapy may be needed especially for those patients who are hypoxic and with PaO2 of constantly less than 55 mmHg (Murtagh 2008). Surgical pathways include lung transplantation for severe disease and lung volume reduction surgery which shows symptom and mortality benefit (Kasper 2005).
* Coleus forskohliimay potentiate the effects of salbutamol. Increased serum levels of salbutamol may result in increased heart rate, cardiac arrhythmias and tremor (Brunton 2006).
* Licorice (Glycyrrhiza glabra) may potentiate the effects of corticosteroids (Braun 2006). Supra-physiological levels of corticosteroids may result in general suppression of the HPA axis, electrolyte abnormalities especially hypokalemia, hypertension, hyperglycemia and glycosuria, increased susceptibility to infection, osteoporosis, myopathy and the characteristic habitus of steroid overdose as seen in Cushing's syndrome (Brunton 2006).
* There should be no interaction concerns with the inhaled anticholinergic drugs such as ipratropium bromide.
Role of the herbal medicine practitioner in treatment and management of COPD
It is vitally important that herbalists are considered part of a multidisciplinary team when it comes to chronic disease management within the community. It is however, not the aim of this paper to discuss the details about how herbalists will be able to become officially recognised as part of allied health care in Australia as this is a complex and often emotive debate. This paper does explore the management goals that herbal medicine practitioners may take in treatment and support of their COPD patients.
Management goal 1--assisting patients to stop smoking
As already mentioned smoking is the greatest recognised risk factor for development of COPD and contributes to the exacerbations experienced by COPD patients. Smoking accelerates decline in lung function in people diagnosed with COPD who continue to smoke (Weiss 2008). It is vitally important to assist COPD patients to quit smoking, or better still to not start.
This outcome can be achieved in numerous ways. Important aims in helping patients quit smoking include:
* Stress reduction--meditation, exercise, herbal medicines, improve sleeping patterns, regular massage
* Psychological support--cognitive behavioral therapies (CBT) or other psychological support Pharmacological--nicotine replacement (patches, gum), varenicline tartrate (Champix), buproprion hydrochloride (Zyban)--for PBS subsidy there must be a 6 month gap between taking Zyban and beginning on Champix (MIMS 2008).
* Herbal medicines--non specific measures such as herbal treatment for stress reduction or detoxification. The herbal product Remotiv (Flordis) has been trialed at the Brain Sciences Institute, Swinburne University Melbourne, as an alternative to pharmacotherapy for smoking cessation. Remotiv is a patented extract (Ze 117) of Hypericum perforatum.
* Community support services--there are numerous local and Federal initiatives for assistance in stopping smoking.
Management goal 2--optimising lung function The following mechanisms of action may be addressed when using natural medicines for the optimising of lung function in COPD patients:
Bronchodilator action and mucous clearance
Chronic tracheobronchial mucous secretion is a significant contributor to the symptoms of COPD and hypersecretion of mucous is associated with increased mortality, accelerated decline in FEV1 and increased risk of hospitalisation (Aboussouan 2008). The mechanisms of action of herbal medicines that would be most indicated include the mucolytics/expectorants and bronchodilators.
The bronchodilator action of Coleus forskohlii makes it a reasonable first choice, not only due to its bronchodilator activity but also to its positive inotropic effect on the myocardium (Bone 1996). In vitro studies have also shown that forskolin has a synergistic effect with salbutamol and therefore may reduce the required dose of the short acting bronchodilators (Gaby 2006).
Useful warming mucolytics/expectorants include Angelica archangelica, Cinnamomum zeylandicum and Zingiber officinalis which have the added benefit of being general aromatic digestives, a beneficial action in emphysema patients. For expectorant/mucolytic action, small doses of chilli (Capsicum annum) may be added to a liquid herb mix or incorporated into food. The sulphur containing compounds in garlic (Allium sativum) are useful mucolytic agents (Mills 2000).
Thymus vulgaris has valuable mucolytic and expectorant actions. It loosens obstructive secretions in the respiratory tract and is strongly antibacterial to the respiratory mucosa--an important indication for COPD patients (Mills 1991).
Inula helenium may be used not only for its stimulating expectorant effects but also to support digestion and a debilitated constitution (Mills 1989).
Adhatoda vasica is an important bronchodilator and expectorant (Bone 1996). Its antiasthmatic actions are useful should there be a component of reversible airway obstruction in the COPD patient.
The expectorant and anti inflammatory actions of Asclepias tuberosa may assist COPD patients however this herb is contraindicated in patients taking digoxin (Hoffman 2003).
Inadequate hydration status seems a logical mechanism in obstructive bronchial mucous however there is currently little evidence to support hydration as a means of reducing reduce mucous obstruction (Aboussouan 2008). Within a naturopathic framework it may be recommended for these patients to consume 2 to 3 litres of water daily as a general good health guideline. This may be contraindicated if the patient is on any daily fluid restrictions due to cor pulmonale or congestive heart failure or other co-morbidities such as end stage renal failure.
Antioxidant therapy may be beneficial in COPD patients particularly those who continue to smoke. N-acetylcysteine supplementation may have the benefit of reducing the frequency of exacerbations and improving subjective symptoms (Weiss 2008) however has no effect as a mucoactive agent at 600 mg twice daily (Stoller 2008). This was confirmed in the multicentre European BRONCHUS trial where 523 COPD patients were randomly assigned to acetylcysteine or placebo groups (Aboussouan 2008).
Circulatory and cardiac support
Clinically patients with emphysema often have poor peripheral perfusion and therefore circulatory support with herbs such as Zingiber officinalis and Ginkgo biloba may be indicated.
For this clinical action Crataegus species cannot be overlooked. Due to the increased incidence of cor pulmonale as a secondary complication in long term emphysema patients the actions of Crataegus species with its positive inotropic effects and decreased oxygen demand of the myocardium make it highly indicated (Mills 2000). The antioxidant effects are also of some benefit in these patients.
Coleus forskohlii works synergistically with Cragaegus to increase left ventricular function and therefore help to maintain sufficient cardiac output (Bone 1996).
Anti inflammatory action
Glycyrrhiza glabra has duel activity being not only anti inflammatory but also a stimulating expectorant (Mills 2000). Often emphysema patients have an ineffective cough and a combination of Glycyrrhiza with other mucolytic herbs will help remove congestion from the lungs. Stimulating expectorants are indicated in emphysema but the regular use of antitussives in stable COPD is contraindicated (Murtagh 2008).
Management goal 3--reducing exacerbations
As respiratory tract infections are the most common cause of exacerbation in COPD patients and responsible for hospitalization, it is vitally important for the naturopathic practitioner to help to minimise these disturbing and costly events. The following mechanisms of action may be addressed when using natural medicines for the reduction of exacerbations in COPD patients:
* Immune herbs for emphysema include Echinacea spp, Andrographis paniculata and Astragalus.
* If RSV infection is suspected, antiviral herbs such as Thuja occidentalis are indicated. Thuja has the added benefit of promoting expectoration (Hoffman 2003).
Anti bacterial action
Common infective micro-organisms in emphysema patients include H. influenzae, S. pneumoniae and Moraxella catarrhalis. Specific antimicrobial treatment is indicated whenever there is an increase in cough/ dyspnea together with increased sputum volume and/or purulence (Murtagh 2008).
Herbal medicines particularly indicated here are Thymus vulgaris, Hydrastis canadensis and Inula helenium however it may be necessary to avoid Hydrastis if there is evidence of hypertension (Mills 2000).
Inhalations of tea tree or eucalyptus oil are beneficial during acute infective exacerbations.
Other management goals Increase in exercise
A retrospective cohort study showed that in those with a COPD diagnose and who continue to smoke, regular physical activity may mitigate lung function decline (Weiss 2008). It would be logical to suggest that physical activity would also be advantageous in COPD patients who have quit smoking.
Bitters such as Angelica archangelica are indicated.
Prevention of osteoporosis
As many COPD patients may have been exposed to prolonged periods of corticosteroid use the risk of osteoporosis is markedly increased. Glucocorticoids are the most common cause of medication induced osteoporosis (Kasper 2005).
Ensure adequate intake of calcium, vitamin D and magnesium. Encourage small amounts of daily sun exposure and gentle weight bearing exercise to a tolerated level. Often this may prove difficult with patients who are profoundly hypoxic or otherwise immobile.
It is not within the scope of this paper to discuss the micronutrient treatment options for COPD patients. However the use of co enzyme Q10 is warranted for its wide therapeutic action, specifically for COPD patients with their symptoms of fatigue and congestive heart failure. This has been confirmed in numerous randomised controlled clinical trials (Osiecki 2002). Co enzyme Q10 may be important for those patients taking a statin for lowering of cholesterol. Supplementation of co enzyme Q10 has been shown to significantly improve maximum oxygen consumption and increase maximum expired volume in COPD patients (Braun 2006).
Management of psychiatric co-morbidities
COPD patients have a higher incidence of depression than in the general community.
Hypericum perforatum (St John's wort) is indicated not only due to its antidepressant/anxiolytic actions but also for improving sleep patterns via its influence on nocturnal melatonin levels (Mills 2000). Along side the well known interaction between St John's wort and SSRIs, it should be avoided in patients taking digoxin (Gaby 2006).
Other herbs that may be of benefit include the adaptogenic herbs such as Eleutherococcus senticosus (contraindicated if the patient is on digoxin and higher doses are cautioned if the patient is suffering from any tachyarrythmias or hypertension) and Withania somnifera (Mills 2000). The nutrient S-adenosyl-L-methionine (SAMe) may be a useful addition due to its efficacy in depression and its anti-inflammatory and anti-oxidant actions (Braun 2007).
COPD is a chronic illness with far reaching consequences across a biopsychosocial spectrum. It poses a significant burden of disease within the Australian community and is often under recognised and treated.
Complementary medicine practitioners such as herbalists are in a prime position to help in the primary community level management of these chronic health conditions.
The use of herbal medicines, nutritional advice and supplements together with general advice on lifestyle modifications has a vitally important role in COPD treatment and management. Naturopathic philosophy and herbal medicine treatment protocols for COPD can stand along side other forms of treatment for the optimal management of COPD patients. Improving management and reducing exacerbations will relieve some of the burden of an already struggling hospital system.
It is important that complementary health practitioners such as herbalists are seen to be an integral part of primary care management for COPD patients and integrated into allied health care teams.
Clinicians need to be realistic about treatment goals, however it is reasonable to expect a significant improvement in subjective symptoms such as general wellbeing, dyspnea and shortness of breath, cough, fatigue and sleep quality within a short treatment period.
Managing respiratory tract infections is essential due to the fact that infections are the main cause of hospitalisation in these patients. This management will greatly improve the quality of life of COPD patients.
No conflict of interest
Aboussouan L. 2008. Role of mucoactive agents in the treatment of COPD. Qld Health current database.
Anasari Z, Dunt D, Dhamage S. 2007. Variations in hospitalisations for chronic obstructive pulmonary disease in rural and urban Victoria, Australia. Respirol 12:874-80.
Australian Institute of Health and Welfare (AIWH). Prevalence of risk factors for chronic diseases http://www.aihw.gov.au/cdarf/data_pages/prevalence_risk_factors/ index.cfm#tobacco, accessed 31 Aug 2008
Bartlett JG, Sethi S. 2008. Role of infection in acute exacerbation of chronic obstructive pulomonary disease. Qld Health current database.
Bone K. 1996. Clinical application of Ayurvedic and Chinese herbs. Sydney: Phytotherapy Press.
Bourbeau J, Collet JP, Schwartzman K, Ducruet T, Nault D, Bradley C. 2006. Economic benefits of self-management education in COPD. Chest 130:1704-11.
Braun L, Cohen M. 2006. Herbs and Natural Supplements, An Evidence Based Guide 2nd ed. London: Churchill Livingston.
Brunton L, Lazo J, Parker K. 2006. Goodman's and Gilman's The Pharmacological Basis of Therapeutics 11th ed. Sydney: McGraw Hill.
Cecins N, Geelhoed E, Jenkins SC. 2008. Reduction in hospitalisation following pulmonary rehabilitation in patients with COPD. Aust Health Rev 32:415-22.
Cramond T. 1996. Home Oxygen. Aust Prescriber 19:69-71.
Cranston JM, Crockett AJ, Moss JR, Pegram RW, Stocks NP. 2008. Models of chronic disease management in primary care for patients with mild-to-moderate asthma or COPD: a narrative review. Med J Aust 188:S50-2.
Crockett A, Cranston J, Moss J. 2002. Economic Case Statement Chronic Obstructive Pulmonary Disease. Aust Lung Foundation.
Ferguson G, Make B. 2008. Management of stable chronic obstructive pulmonary disease. Qld Health current database.
Frith P. 2004. Chronic Obstructive Pulmonary Disease (COPD) in Australia: An under-recognised and under-treated burden. Aust Lung Foundation http://www.copdx.org.au/resources/ documents/lung_health_sur_2004Nov.pdf
Frith P, Cafarella P, Duffy J. 2008. Chronic obstructive pulmonary disease (COPD) is a major personal and public health burden in Australia. Aust NZ J Public Health 32:139-41.
Gaby A. 2006. A-Z guide to Drug-Herb-Vitamin Interactions. New York: Three Rivers Press.
Gay P. 2008. Sleep disorded breathing in COPD. Qld Health current database.
Guyton AC, Hall JE. 2006. Textbook of Medical Physiology. Sydney: Elselvier.
Halpin D. 2006. Health Economics of Chronic Obstructive Pulmonary Disease. Proc American Thoracic Soc 3:227-33.
Hanley M, Welsh C. 2003. Lange, Current Diagnosis and Treatment in Pulmonary Medicine. Sydney: McGraw Hill.
Hoffman D. 2003. Medical Herbalism. London: Healing Arts Press.
Kasper DL, Fauci AS, Braunwald E, Hauser SL, Jamison JL, Longo DL. 2005. Harrison's Principles of Internal Medicine 16th ed. London: McGraw-Hill.
Kumar V, Abbas AK, Fausto N. 2005. Robbins and Cotran Pathological Basis of Disease 7th ed. Sydney: Elsevier.
Mannino D. 2008. Cigarette smoking and other risk factors for lung cancer. Qld Health current database.
McKenzie D, Abramson M, Crockett A, Glasgow N, Jenkins S, McDonald C et al. 2007. The COPD-X Plan: Australian and New Zealand Guidelines for the management of Chronic Obstructive Pulmonary Disease.
McPhee J, Papadakis E, Gonzales R, Zeiger R. 2004. Current Medical Diagnosis and Treatment. Sydney: McGraw-Hill.
Mills S, Bone K. 2000. Principles and Practice of Phytotherapy. London: Churchill Livingston.
Mills S. 1989. The Complete Guide to Modern Herbalism. London: Thorsons.
Mills S. 1991. The Essential Book of Herbal Medicine. Arkana. MIMS. 2008. Issue 3 June/July.
Monninkhof E, van der Valk P, van der Palen J, van Herwaarden C, Zielhuis G. 2003. Effects of a comprehensive self-management programme in patients with chronic obstructive pulmonary disease. Eur Respir J 22:815-20.
Monninkhof E, van der Valk P, Schermer T, van der Palen J, van Herwaarden C, Zielhuis G. 2004. Economic evaluation of a comprehensive self-management programme in patients with moderate to severe chronic obstructive pulmonary disease. Chron Respir Dis 4;1:7-16.
Mathers C, Vos E, Stevenson C, Begg S. 2000. The Australian Burden of Disease Study: measuring the loss of health from diseases, injuries and risk factors. MJA 172:592-6.
Murtagh J. 2007. Murtagh's General Practice 4th ed. Sydney: McGraw Hill.
National Health Priority Action Council (NHPAC). 2006. National Chronic Disease Strategy. Canberra: Australian Government Department of Health and Aging.
Osiecki H. 2002. The Nutrient Bible. Australia: BioConcepts Publishing.
Regional COPD working group. 2003. COPD prevalence in 12 Asia-Pacific countries and regions: Projections based on the COPD prevalence estimation model. Respirol 192-8.
Rennard S. 2008. Chronic obstructive pulmonary disease: definition, clinical manifestations, diagnosis and staging. Qld Health current database.
Simpson AC, Rocker GM. 2008. Advanced chronic obstructive pulmonary disease: rethinking models of care. QJM Jul 31.
Stoller J. 2008. Management of acute exacerbations of chronic obstructive pulmonary disease. Qld Health current database.
Tally N, O'Connor S. 2006. Clinical examination, A systematic guide to physical examination. 5th ed. Sydney: Churchill Livingston.
Weiss ST. 2008. Chronic obstructive pulmonary disease: risk factors and risk reduction. Qld Health current database.
Wilkinson M, Marmot M. 2006. Social Determinants of Health. The Solid Facts, 2nd edition. London: Oxford Press.
Stuart Glastonbury BSc(Med) DipWHM MNHAA MAIMA
|Printer friendly Cite/link Email Feedback|
|Publication:||Australian Journal of Medical Herbalism|
|Date:||Mar 22, 2009|
|Previous Article:||Nature's Sunshine Products of Australia Pty Ltd 'still hot after 28 years'.|
|Next Article:||Clinical evaluation of a herbal formulation in liver disorders.|