Evidence-based Clinical Chinese Medicine
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Evidence-based Clinical Chinese Medicine

Volume 1: Chronic Obstructive Pulmonary Disease

Charlie Changli Xue, Chuanjian Lu

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eBook - ePub

Evidence-based Clinical Chinese Medicine

Volume 1: Chronic Obstructive Pulmonary Disease

Charlie Changli Xue, Chuanjian Lu

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About This Book

Evidence-based Clinical Chinese Medicine: Vol. 1 Chronic Obstructive Pulmonary Disease provides a "whole evidence" analysis of the Chinese medicine management of chronic obstructive pulmonary disease (COPD). Evidence from the classical Chinese medicine literature, contemporary clinical literature, and the outcomes of clinical trials and experimental studies are reviewed, analysed and synthesised. The data from all these sources are condensed to provide evidence-based statements which will inform clinical practice and guide future research.

This book has been designed to be an easy reference at the point of care. During a patient consultation, Chinese medicine practitioners can refer to this book for guidance on which Chinese herbal medicine formulas, specific herbs, or acupuncture points, can best treat their patient, and be confident there is evidence which supports its use.

Currently, Chinese medicine practitioners who develop a special interest in a particular health condition such as COPD have to consult a variety of sources to further their knowledge. Typically, they use the contemporary clinical literature to understand the theory, aetiology, pathogenesis and obtain expert opinions on the Chinese medicine management of COPD. They search the electronic literature to identify systematic reviews of clinical trials, if any exists, to obtain assessments of the current state of the clinical evidence for particular interventions. If they have the skills and resources, they may search the classical Chinese medicine literature for an historical perspective on treatments that have stood the test of time.

This book provides all of this information for practitioners in one handy, easy to use reference. This allows practitioners to focus on their job of providing high quality healthcare, with the knowledge it is based on the best available evidence.

Contents:

  • Introduction to Chronic Obstructive Pulmonary Disease
  • COPD in Chinese Medicine
  • Classical Chinese Medicine Literature
  • Methods for Evaluating Clinical Evidence
  • Clinical Evidence for Chinese Herbal Medicine
  • Pharmacological Actions of Common Herbs
  • Clinical Evidence for Acupuncture and Related Therapies
  • Clinical Evidence for Other Chinese Medicine Therapies
  • Clinical Evidence for Combination Therapies
  • Summary of All Evidence


Readership: Graduate students and practitioners in alternative/Chinese medicine, respiratory medicine/pulnomary medicine.
Key Features:

  • The inclusion of classical Chinese medicine literature, comprehensively reviewed using systematic methods, provides the readers with a history of changes in terminology and treatment approaches from pre Tang dynasty (before 618 AD) to modern times. Rigorous processes have been developed to ensure consistency of the search, extraction and synthesis of data from the classical literature into the body of evidence for COPD. Systematic reviews of the clinical trial evidence and clinical practice guidelines tend to limit the evidence to that derived from randomised controlled trials. The books in this series take a broader view by including evaluations of non-randomised controlled trials and non-controlled studies, such as case series studies, in order to include the full scope of clinical studies and provide a clear insight into which Chinese medicine interventions have received clinical research attention
  • This book integrates evidence from the contemporary and classical literatures with the results of clinical studies to make evidence-based statements for easy application at the point of care. In addition, the actions of the Chinese herbs most frequently used in controlled trials are discussed in light of the results of in-vivo and in-vitro studies. This provides the reader with an understanding of how these Chinese herbs exert their effects
  • The authors are internationally recognised, well-respected leaders in the field of Chinese medicine and evidence based medicine with strong track records in research

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Information

Publisher
WSPC
Year
2016
ISBN
9789814723114

1

Introduction to Chronic Obstructive Pulmonary Disease

Overview
Chronic obstructive pulmonary disease (COPD) is a major contributor to the burden of disease globally. COPD was ranked as the fifth leading cause of disease in 2002, and is projected to be third by 2030. Symptoms of COPD include dyspnoea, cough and excess sputum production, and the progressive worsening of lung function. The progression of COPD cannot be fully reversed. The majority of COPD cases are associated with tobacco smoking, with other causes including workplace dust, chemical exposure, and indoor and outdoor air pollution. People with COPD should be encouraged to stop smoking. Pharmacotherapy may be prescribed to alleviate symptoms and reduce the frequency of acute exacerbations. While treatments are effective at managing symptoms, they cannot completely cure the disease, and side effects have been reported with some drugs. This chapter describes the risk factors for COPD, pathological process, diagnosis and severity assessment, as well as pharmacological and non-pharmacological management.
Chronic obstructive pulmonary disease (COPD) is a disorder that includes chronic bronchitis and emphysema. It is characterised by chronic inflammation of the airways and lungs that worsens over time.1 COPD is commonly caused by smoking; therefore, it is largely preventable.1 Airflow is limited by the inflammatory process, excessive mucus, thickening of the airway wall and increased tone of the bronchial smooth muscle.2 The diagnosis, management and treatment of COPD is largely guided by recommendations from The Global Initiative for Chronic Obstructive Lung Disease.1 It defines COPD as a common preventable and treatable disease [that] is characterised by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients’.
Despite the common COPD symptoms (i.e. dyspnoea, cough and excess sputum production), the extent of COPD’s underlying pathologies, chronic bronchitis and emphysema, are difficult to determine in an individual patient. Chronic bronchitis is defined as the presence of chronic or recurrent cough and sputum production that persists on most days for a minimum of three months per year, for at least two consecutive years, which is not attributed to other pulmonary or cardiac causes.3 Emphysema, on the other hand, is defined anatomically, usually by X-ray, as a permanent, destructive enlargement of airspaces distal to the terminal bronchioles in the absence of obvious fibrosis.4 Patients with COPD will primarily be in the stable stage; however, they may have episodes of exacerbation, which are characterised by worsening symptoms, leading to a change in medication.1
COPD is a growing health and economic concern. Worldwide, it was the fifth leading cause of death in 2002 and is projected to be third by 2030.5 Based on estimates by the World Health Organisation, 80 million people suffer from moderate to severe COPD, which causes 5% of global deaths. COPD mostly affects middle-aged or older people, and with a globally ageing population, COPD is increasing. Historically, it was more common in men than in women. However, due to increased tobacco use in high-income countries and increased exposure to indoor air pollution in low-income countries, women are now equally affected by COPD as men.5
From a patient’s perspective, COPD has a profound effect on quality of life. People living with COPD are limited in their basic daily activities due to shortness of breath, they often cannot work, and require the assistance of health services and emergency care.

Risk Factors

Smoking is associated with the majority of COPD cases, but COPD may also be attributed to workplace dust, chemical exposure and occupational fumes.6,7 Indoor and outdoor air pollution are also associated with the development of COPD. For example, cooking or heating using biomass fuels, performing domestic work in poorly ventilated buildings and living in urban cities are all significant risk factors for COPD.810 Although smoking or exposure to noxious gases is closely related to COPD, approximately 10% of sufferers have never smoked. Hence, COPD susceptibility results from existing genetic factors interacting with environmental factors.11 The interaction is complex and is not fully understood. alpha1-antitrypsin deficiency is one genetic cause, which increases the susceptibility of an individual to develop COPD; however, this deficiency is rare.12 As people age, they are more likely to develop COPD; this may be due to a natural decline in lung function and/or exposure to noxious exposures over a lifetime.1

Pathological Processes

Chronic exposure to irritants such as tobacco smoke causes a complex inflammatory process in the lungs. There is an abnormal and increased immune response leading to lung tissue repair and remodelling. Oxidative stress and the migration of inflammatory cells also contribute to this process.1 Inflammatory cells, including macrophages, T-lymphocytes, B-lymphocytes and neutrophils migrate into the lung and release a variety of pro-inflammatory cytokines and inflammatory mediators, most notably leukotriene-4, interleukin-8 and tumour necrosis factor-α. The cytokines and inflammatory mediators attract inflammatory cells from the circulation, resulting in cyclical amplification of the inflammatory process.13
In addition to inflammation, evidence suggests there is an imbalance between proteases and antiproteases. Proteases break down connective tissue and antiproteases protect connective tissue. The major proteases involved in the pathogenesis of COPD are produced by neutrophils (elastase, cathepsin G and proteinase-3), macrophages (cathepsins B, L and S) and various matrix metalloproteases. The major antiproteases involved in the pathogenesis of COPD include, α1-antitrypsin, secretory leukoprotease inhibitor and tissue inhibitors of matrix metalloproteases.13
Oxidants present in cigarette smoke can stimulate alveolar macrophages to produce reactive oxygen species. Oxidative stress is therefore a major feature in the pathogenesis of COPD leading to increased neutrophils, increased pro-inflammatory mediators, inactivation of antiproteases, injury to airspace epithelial cells and mucus hyper-secretion.14

Diagnosis

Diagnosis of COPD should be considered in patients with dyspnoea, cough, and excess sputum production and a history of exposure to risk factors, such as smoking.1,15 Because COPD develops gradually over many years, patients learn to adjust their lifestyles to avoid the uncomfortable feeling of dyspnoea. Therefore, they have lower activity levels than other people of their age.16

Symptoms

Dyspnoea is persistent and becomes worse over time. It often occurs during exercise, especially when walking up hills or stairs. Patients will avoid activities that cause breathlessness; however, as airways obstruction worsens, dyspnoea will be unavoidable.15 Cough may be intermittent or persistent. In mild and moderate COPD, cough may only be present in the early morning, but as COPD progresses, cough will be persistent during the day. The cough is often productive and some patients may consider it associated with their smoking; however, even when smoking is stopped, the cough persists. Sputum follows the pattern of cough and in mild and moderate cases, it is present in the morning, but in more severe cases, it persists throughout the day. The sputum is usually thick and clear, but if the colour or volume changes, it indicates an infection.15

Testing

A clinical diagnosis of COPD using lung function ‘spirometry’ is required because history and physical examination is not sensitive enough.1 Whe...

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