Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 3rd Intrenational Conference on Chronic Obstructive Pulmonary Disease Brisbane, Australia.

Day 2 :

  • Track-4: COPD and its Co-Morbidities
    Track-8: Developments in COPD Management
Speaker

Chair

Phil Hansbro

University of Newcastle, Australia

Speaker

Co-Chair

Geertjan Wesseling

Maastricht UMC+, Netherlands

Session Introduction

Joaquim Gea

Dean
Universitat Pompeu Fabra
Barcelona
Spain

Title: COPD and nutritional abnormalities

Time : 10:00 - 10:25

Speaker
Biography:

Joaquim Gea obtained his MD (1979) and PhD (1989) degrees at the Universitat de Barcelona, being specialist in both Internal Medicine (1981) and Respiratory Medicine (1985). He is the Head of the Respiratory Department at Hospital del Mar, Full Professor and Dean of the School of Medicine at Universitat Pompeu Fabra and Deputy Director at the Spanish Network of Excellence for Research in Respiratory Diseases (CIBERES). He has been funded by 65 competitive grants, including 4 projects funded by the European Commission, and published more than 260 Original Articles and Reviews in peer reviewed journals as well as 50 book chapters.

Abstract:

Nutritional abnormalities are often associated with Chronic Obstructive Pulmonary Disease (COPD). Their early detection is important, since they determine the patient's prognosis independently of the degree of lung function impairment. In addition, nutritional abnormalities are involved in muscle dysfunction, which in turn leads to exercise limitation, loss of quality of life and increased mortality. However, the presence/absence of malnutrition is a factor that has not been included in the majority of clinical guidelines. The diagnostic techniques include both anthropometry and measurement of body composition (mainly through bioelectrical impedance). The most commonly used anthropometric variables are body mass index (BMI) and the percentage of ideal body weight, while fat-free mass index (FFMI) is the most commonly used impedance variable. The causes of malnutrition associated with COPD include smoking, systemic inflammation, imbalance between nutrient intakes and energy consumption, impairment in respiratory gas exchange and the effects of anabolic hormones, effects of some drugs, decreased physical activity and comorbidities. All these causes lead mainly to an imbalance between protein synthesis and destruction and a predominance of bone resorption, with loss of muscle, fat and bone mass. The treatment includes an improvement in lifestyle (avoid tobacco smoking, better quality in nutrient intake, increase in physical activity, exercise training) and, if necessary, the use of nutritional support (enteral or even parenteral) and anabolic agents (eg, selective androgen receptor modulators [SARM] or secretagogues of the growth hormone). These drugs seem to be more effective when associated with training.

Ping Yang

Professor
Mayo Clinic College of Medicine
USA

Title: Chronic obstructive pulmonary disease (COPD) complicating early-stage lung cancer (LC)

Time : 10:25 - 10:50

Speaker
Biography:

Prof. Ping Yang has completed her MD from Beijing Medical College in China and PhD at Johns Hopkins University in USA. She has been leading a comprehesive lung cancer research program at Mayo Clinic since 1997, emphasizing patient-centered outcome research with COPD as one of the key interaested areas. She has published more than 200 peer-reviewed papers and has been serving as an editorial board member of Jounal of Clinical Oncology and Associate Editir of Journal of Thoracic Oncology.

Abstract:

COPD is present in 40-60% of LC patients; some existed long before LC diagnosis and others were identified at the time of LC diagnosis. Our clinical research team has been evaluating the impact of different diagnostic time (prior vs. concurrent), severity of COPD, and a subgroup of CT-defined emphysema on long-term survival of patients with early stage non-small cell lung cancer (NSCLC). Two patient cohorts include ~1400 NSCLC with known COPD status and ~1100 with known emphysema status. COPD was defined according to pulmonary function tests (post-bronchodilator FEV1/FVC<0.70) or recorded medical diagnosis; severity was grouped by GOLD criteria (Global Initiative for Chronic Obstructive Lung Disease). Emphysema was based on standard-dose CT scan; percentage quantification was determined through direct inspection and categorized into <5%, 6-24% and 25-60%. Five key findings are summarized as follows: (1) Patients with a prior COPD had a significantly higher proportion of former smokers and moderate airflow obstruction than those with concurrent COPD. (2) Worse survival was significantly associated with prior COPD and moderate to severe airflow obstruction regardless of COPD diagnosis time. (3) In surgically-treated patients, the overall postoperative complications were higher in patients with a greater emphysema score. (4) Increasing emphysema score was significantly associated with worse survival. (5) More specific to resected LC in the predominant emphysematous region, patients with >6% emphysema experienced a mild decrease in FEV1 and an increase in FEV1/FVC. We conclude that COPD in general and emphysema in particular should be taken into careful consideration in LC treatment

Geertjan Wesseling

Professor
Maastricht University, Netherlands

Title: Clustering of comorbidities and implications for secondary care

Time : 11:10 - 11:35

Speaker
Biography:

Geertjan Wesseling has studied Biology and Medicine at the Free University of Amsterdam, Netherland. He has completed his Training in Respiratory Medicine in 1991 and obtained his PhD in 1993. He is a Professor of Respiratory Medicine in Maastricht and coordinates the International Master in Medicine of Maastricht University. He is a former President of the Dutch Pulmonology Society

Abstract:

Comorbidities are very common in COPD. Of patients referred for pulmonary rehabilitation more than 50% report at least one chronic comorbid disorder that is of importance for the rehabilitation and its outcomes. Also, comorbidities have a huge impact on the disease burden, on the risk of hospitalization and on mortality. Recently it was reported that comorbidities come in clusters of which cardiovascular and psychological comorbidities are the most frequently seen. It appears that these comorbidities are in part related to systemic inflammation. Other mechanisms may be relevant as well. Several studies have demonstrated effects of comorbidities on outcomes of pulmonary rehabilitation. These may implicate differentiation of rehabilitation programs according to clusters of comorbidities.

M Rashidul Hassan

Director
National Institute of Diseases of Chest & Hospital
Bangladesh

Title: COPD Basic concept: Understanding the pathophysiology by Simile to convince physicians

Time : 11:35 - 12:40

Speaker
Biography:

Md Rashidul Hassan is the Director cum Professor at National Institute of Diseases of the Chest & Hospital, Dhaka. He has completed his MD Respiratory Medicine from Dhaka University in the year 1995. He is currently a Professor at the Department of Respiratory Medicine, National Institute of Diseases of the Chest and Hospital [NIDCH], Dhaka, Bangladesh. He is also a Founding President of Bangladesh Lung Foundation and Founding Vice President of Evidence Based Clinical Practice Society of Bangladesh. He has published 63 papers in reputed journals and has been serving as Editorial Board Member of Journal of Asia Pacific Society of Respirology (APSR).

Abstract:

Background: Understanding of basic concept of COPD is an important issue for the practicing physicians. Seamless management of COPD needs to understand basic concept of asthma. Use of simile is the best way to understand any basic concepts. A positive role of physicians after proper understanding of basic concept is essential for successful management of COPD. To achieve this goal in Bangladesh, we developed a module COPD presentations and carried out several seminars entitled “COPD: BASIC CONCEPT AND MANANAGEMENT” in different regions of the country. The outcome is encouraging and we assume the module can be used for general physicians as an effective instrument in switching to standard treatment of COPD from conventional treatment. Objectives: Similarity between water movement air movement and pathophysiology of COPD helps in understanding the basic mechanism of COPD and thereby physicians can be easily motivated to switch over to standard treatment of COPD. Methods: An audio-visual module comprising of an interactive lecture were prepared and presented in front of the primary care physicians and respiratory specialists. For this a nation-wide campaign will be out entitled “COPD: BASIC CONCEPT AND MANANAGEMENT” in different regions of Bangladesh including all medical colleges. Atleast two pulmonologists of Bangladesh presented the papers and answered the different questions of the audiences. Discussion: Water movement, like conduction, convection and Diffusion can be easily described and resulting in difficulty in breathing. After water movement simile it is described clearly irritation of smoke and recurrent infection is the main cause of sputum production and exacerbations. After an episode of COPD exacerbation small airway and alveolar destruction leads to different types of emphysema formations and mismatch of Ventilation Perfusion ratio and right to left shunt. This V/Q mismatch and shunted blood leads to progressive exertional dyspnea, Hypoxemia, Hypoventilation, Polycythemia or anemia and ultimately leads to Respiratory Failure. Conclusions: What we don’t see through our necked eyes (pathophysiology of COPD) may be understandable by drawing simile with an event, which we can see with our eyes. The lesson can be remembered like stories by anybody even a layman. This may help to facilitate patient education programs. Recommendations: We may carry this mode pf presentation to popularize COPD management and Update knowledge of physicians. 1.Attract physicians “towards Basic Cocept of COPD” by using such simple simile like water movement 2.Integrate physicians with appropriate knowledge of COPD Management 3.Deal with physicians to take care patients’ value regarding COPD management.

Speaker
Biography:

Hiroaki Kume obtained his MD from Toyama Medical and Pharmaceutical University in 1982. He has completed his PhD in Department of Medicine (II), Nagoya University School of Medicine in 1990, and postdoctoral studies from School of Veterinary Medicine, University of Pennsylvania (Dr. Michael I. Kotlikoff’s Lab). Currently, he works at Department of Respiratory Medicine and Allergology, Kindai University Faculty of Medicine and Department of Respiratory Medicine, Rinku General Medical Center, Izumisano City, Osaka 598-8577, Japan, and focuses on investigating the characteristics of COPD with the goal of rational therapy for COPD

Abstract:

Rationale: Eosinophil inflammation in the airways is observed in some patients with chronic obstructive pulmonary disease (COPD) independent of asthma. However, little is known about not only mechanisms but also therapy in this clinical phenotype of COPD. This clinical study was designed to determine whether inhaled glucocorticosteroids (ICS) are useful for airway eosinophilia in COPD. Methods: Once-daily inhalation of indacaterol (LABA) was firstly administrated to the patient with COPD. After symptoms were stable, sputum examination was done. When a percentage of eosinophil in the induction sputum is >3%, once-daily inhalation of ciclesonide (ICS) was administered. Results: 20 patients with COPD (GOLD 2-3) with airway eosinophilia were enrolled. After administration of indacaterol, COPD Assessment Test (CAT) score was decreased from 15.1 to 7.9 (P<0.05), and frequency of SABA on demand for symptom relief was also decreased from 1.6 to 0.8 puffs/week (P<0.05). In lung function test, forced expiratory volume in 1 sec (FEV1) and inspiratory capacity (IC) were increased by 210.0 (P<0.05) and 311.5 mL (P<0.01), respectively. After addition to ciclesonide, values of CAT score and frequency of SABA were markedly decreased to 4.9 points and 0.3 puffs/week, respectively (each P<0.05 vs LABA). Moreover, FEV1 and IC were further increased by 147.0 and 227.6 mL, respectively (each P<0.05 vs LABA). Conclusions: Not only LABA but also ICS is needed to improve lung function and to achieve better maintenance in COPD with airway eosinophilia. Ciclesonide is effective for these cases. Eosinophil infiltration to airways may be indication of ICS therapy for COPD.

Speaker
Biography:

Gunilla Lindqvist is a Registered Nurse (RN), Master´s degree in Public Health, Senior Lecturer, Doctor of Philosophy (PhD) and Post doctor within the subject of Health and Caring Science. Gunilla is working as a Senior Lecturer at School of Health and Caring Sciences, Linnaeus University Campus Kalmar and Växjö and has now a postdoctoral position at Linnaeus University. Gunilla Lindquist’s research focuses on Chronic Obstructive Pulmonary Disease, the sufferer themselves and their spouses. Gunilla works in a research project focusing on innovative solutions to meet future healthcare needs and preferences of older people and their carers.

Abstract:

Chronic obstructive pulmonary disease (COPD) is an increasing health problem that affects about 600 million people globally, and it is expected to be the third most common cause of death worldwide by 2020. COPD is a chronic long-term condition that is irrevocable. Cigarette smoking is the most commonly encountered risk factor for COPD, and it has also been shown that passive smoking impairs lung function. When the disease progresses, not only is the lung fiction impaired, but there are also other consequences as physical, psychological and social. Aim The aim of the study was to generate a theory, grounded in empirical data, to reveal the main concerns of people who suffer from COPD and how they handle everyday life. Method The constant comparative method of grounded theory, developed by Glaser and Strauss (1967), was used. Data was collected by interviewing 23 people with COPD all having different grades of the disease, from mild to severe. Findings A substantive theory was generated showing that the main concern for people suffering from COPD was feelings of guilt due to self-inflicted disease associated with smoking habits. This includes feelings of living in the shadow of death. This core category was linked to five categories termed making sense of existence, adjusting to bodily restrictions, surrendering to faith, making excuses for the smoking related cause, and creating compliance with daily medication. These categories form a pattern of behavior that explains how feelings of guilt were handled by people living with COPD.

Qian Zeng

General Practitioner
Medi7 Clinic Bentleigh
Australia

Title: A New Anti-inflammatory Therapy for COPD

Time : 14:15 - 14:40

Speaker
Biography:

Dr. Qian Zeng made Self-research on anti-inflammatory therapy for chronic inflammatory diseases from 2001 to 2011, and Working as a general practitioner at Medi7 Clinic Bentleigh, Melbourne and continuing research on anti- inflammatory therapy from 2012 until now. His main Interest is to combine Modern Western Medicine with Traditional Chinese Medicine to develop a new anti-inflammatory therapy for treating chronic inflammatory diseases.

Abstract:

COPD is a chronic progressive inflammatory lung disease. It is caused by various stimuli, like smoking, air pollution, exposing to noxious chemicals and recurrent infections. All these stimuli can cause small airway and lung tissue injury, which induces an inflammatory reaction. Prolonged inflammation further damages small airway and lung tissue, subsequently the inflammation becomes self-perpetuating, i.e. the inflammation will last for ever even when the initial stimuli are eliminated. The activated neutrophil and alveolar macrophage produce neutrophil elastase and macrophage elastase, these two proteolytic enzymes cause disruption of the wall of alveoli and fusion of alveoli, resulting in decreased gas-exchanging surface. Activated inflammatory cells also produce various inflammatory factors, which stimulate secretion of mucus and cause fibrosis and thickening of the wall of small airway, all these increase the obstruction of small airway, reduce the air flow. The ongoing inflammation in small airway and lung tissue will continue to cause tissue damage, as a result, the lung function in COPD patients will progressively deteriorate. The key in treating COPD is to treat the inflammation. Current treatment of COPD are LAMA, LABA and ICS. LAMA and LABA only treat the symptoms of COPD by dilating the small airway, they do not target the underlying mechanism of COPD (the inflammation). ICS can only temporarily supress the inflammation in COPD, cannot really terminate the inflammatory reaction and therefore it cannot stop the progression of COPD, though it is the mainstay of treatment of COPD. The inflammation in COPD is partially resistant to steroid. The underlying mechanism sustaining the chronic inflammation in COPD is due to a bidirectional intercellular reactions between T cell and alveolar macrophage and/or neutrophil. The activated T cell produces cytokines, which activate alveolar macrophage and/or neutrophil, in turn, activated alveolar macrophage and neutrophil produce interleukins XII and other cytokines to activate T cell. Once this vicious intercellular reaction established, it cannot be disrupted and will last for ever. This is the common mechanism of all self-perpetuating chronic inflammation, no matter what the initial stimuli are or in what tissue or organ the inflammatory reaction occurs. Steroid resistant is a big issue in treating COPD and other chronic inflammatory lung diseases, like asthma, pulmonary fibrosis. In order to effectively treat COPD, we must find new anti-inflammatory therapies or developing new anti-inflammatory drugs.

Geertjan Wesseling

Professor
Maastricht UMC
Netherlands

Title: What we shouldn’t do in COPD

Time : 14:40 - 15:10

Speaker
Biography:

Geertjan Wesseling (1956) studied biology and medicine at the Free University of Amsterdam. He completed his training in Respiratory Medicine in 1991 and obtained his PhD in 1993. He is a professor of Respiratory Medicine in Maastricht and coordinates the international master in medicine of Maastricht University. He is a former president of the Dutch Pulmonology Society

Abstract:

Chronic Obstructive Pulmonary Disease causes significant morbidity and mortality worldwide. Most patients can be treated in primary care. However, even in patients with relatively mild airflow obstruction referral to a specialist may lead to important findings, both related to the COPD and to comorbidities. Several classifications and gradings have been proposed throughout the years that help in categorizing patients, yet not all have direct consequences for the management, that typically includes lifestyle changes, of which smoking cessation and increased physical activity or even rehabilitation are paramount, and pharmacotherapy. Inhaled medication is aimed at improving expiratory flow, reducing hyperinflation and inflammation, to slow-down disease progression and improve quality of life and prognosis. Longacting bronchodilators have clinically significant effects and are widely used, also in mild-to-moderate disease. In recent years the Astma COPD Overlap Syndrome has been proposed, which is a misnomer and often an excuse to skip an adequate diagnostic process and prescribe triple-therapy in patients who would do well with only one or two different drugs. Unfortunately, the majority of COPD patients are on inhaled steroids, but effects are small, often not clinically relevant and side-effects such as an increased risk of pneumonia should warrant clinicians to be more prudent in prescribing those. Selfmanagement is considered an important component of management strategies, even if effects on various outcomes are limited. Repeated lung function measurements are often performed both in primary care and in the hospital.with limited if any effects on management. Taken together, appropriate COPD management is not only about what we should do but certainly also about what we shouldn’t.

Annemarie Lee

Postdoctoral research fellow
West Park Healthcare Centre
Canada

Title: Forgotten Co-morbidities in COPD

Time : 15:10 - 15:35

Speaker
Biography:

Roger Goldstein is the Director of the Respiratory program at West Park Healthcare Centre and a Professor of Medicine at the University of Toronto. His research
interests include chronic respiratory disease, exercise training and pulmonary rehabilitation. Dr Annemarie Lee is a postdoctoral research fellow at West Park
Healthcare Centre and a physiotherapist in pulmonary rehabilitation, with an interest in comorbidities in COPD, including pain and gastro-oesophageal reflux. She
has published more than 50 papers in peer reviewed journals.

Abstract:

Chronic obstructive pulmonary disease (COPD) is a complex multi-component condition whose clinical presentation is often complicated by co-morbidities and extrapulmonary clinical features. This presentation will highlight three of them. Affecting between 17% and 78% of people is gastro-oesophageal reflux disease (GORD). Due to the possibility of pulmonary microaspiration GORD may influence lung disease severity and is a predictor of acute exacerbations. Pain is common in people with COPD, affecting 66% of individuals with moderate to very severe disease. Higher pain intensity is associated with increased dyspnea, fatigue, poorer quality of life, lower levels of physical activity and a greater number of comorbidities. Pain imposes limitations on exercise behaviour and participation in pulmonary rehabilitation. The common locations of pain are the upper and lower back and lower limbs. In COPD, postural alterations may be influenced by musculoskeletal comorbidities including osteoarthritis and osteoporosis. Common postural abnormalities include alterations in the degree of cervical lordosis and thoracic kyphosis, and altered scapula position. Postural alterations are associated with reduced pulmonary function and may contribute to exercise limitations and increased functional impairment.

Sulaiman Ladhani

Professor
Prince Aly Khan Hospital
Mumbai University
India

Title: COPD- The Indian Scenario
Speaker
Biography:

Sulaiman Obtained his MBBS degree from Mumbai University in 1996 and Post graduation in Respiratory medicine and Tuberculosis in 2002 from B Y L Nair Hospital Mumbai. he has more than 13 years experience in private practice and research . Areas of expertise include Asthma,COPD, Interstial lung disease,Sleep apnea syndrome and Tuberculosis esp multi drug resistant and XDR tuberculosis Awarded Mahatma Gandhi gold medal in 2014 for outstanding contribution in field of Respiratory medicine, community health and research. Have many publications in Internarional journals and participated in many international conferences . Am Principal Investigator in many research projects at present and part of Advisory committee of ICMR and CCDC Delhi for Non communicable diseases Have been Director with Aga Khan Health Service India for 7 years and at present am a Governing board of Prince Aly khan. Hospital since 2012. Am also the Chairman of Hospital based Authorisation commitee and Brainstem Death committee at Prince Aly Khan hospital

Abstract:

A global healthcare survey of WHO highlighted some health concerns for India viz. vulnerability of young children, poor sanitation and limited insurance with only 3%-5% of Indians covered under health insurance. There is a high percentage of ageing population as well. Chronic diseases like COPD add to this pre-existing burden on healthcare systems. The current COPD burden is limited but is expected to increase as the population ages.There is a lot of variation in COPD prevalence in India in rural and urban population.In India, cigarette smoking is just one of the major risk factors for COPD. Exposure to tobacco smoke from hookahs, chillums and bidis, burning of biomass fuel like animal dung and wood, burning of mosquito coils, also poses a great risk. This is coupled with under-diagnosis of COPD withSpirometry still being underutilized. Comorbid conditions like ischemic heart disease, hypertension, skeletal muscle dysfunction, osteoporosis, depression, diabetes and renal conditions add to the morbidity. The Indian guidelines for COPD classify severity simply as mild, moderate and severe whereas GOLD guidelines have a combined assessment of COPD in the form of a grid which is classified as mild, moderate, severe and very severe. Management options include SABAs/SAMAs, LAMAs and LABAs, inhaled corticosteroids, antibiotics and the preferred device being MDI with spacer or nebulization. Due to diversity of COPD stages at which patients present themselves along with urban and rural prevalence, it will be interesting to ponder over different treatment algorithms based on some case studies.

Mark Olfert

Professor
West Virginia University School of Medicine
Morgantown
USA

Title: Exercise and muscle function in COPD
Speaker
Biography:

Dr. Olfert completed his PhD in Physiology from Loma Linda University (Loma Linda, CA) and postdoctoral studies in pulmonary physiology in School of Medicine at University of California San Diego (La Jolla, CA). He is currently an Associate Professor (with Tenure) at West Virginia University School of Medicine, and Member in the Center for Cardiovascular and Respiratory Sciences, the Mary Babb Randolph Cancer Center, and the West Virginia Clinical and Translational Science Institute. He has published more than 45 papers in ruptable peer reviewed journals and is currently serving as an editorial board member on 3 respected journals. He is a standing member on 2 national grant reveiw panels within the USA, as well as ad hoc reveiwer for several international grant agencies.

Abstract:

Exercise limitation is a hallmark of chronic lung diseases, such as COPD. There is evidence of systemic contributions that contribute to exercise limitation above and beyond central pulmonary dysfunction, but the cellular mechanisms remain poorly understood. This talk will review currentl and new data obtain from muscle biopsys in patients with COPD in the regards to exercise function and expression of angiogenic regulators and inflammatory molecules in skeletla muscle. Importantly, this discussion will highlight evidence obtained in a diversity of COPD patients, which include cigarette smoked induced COPD, as well as the genetic variant of COPD resulting from alpha-1-antitrypsin deficient (AATD) individuals. Further insight will be glean from data obtain in AATD individuals that have developed COPD and AATD who have not develop COPD. The focus of the presentation will address whether abnormalities in the muscle angiogenic response to exercise are a consequence of systemic inflammation stemming from lung damage, or if these are based on O2 transport limitation, and what effect exercise training and/or physical fitness exhibits in this context. The central premise of the talk is based on observation that deregulation of several key angiogenic regulators is responsible for many of the structural and functional alterations found in skeletal muscle of patients with COPD, especially those with a cachectic phenotype, and that these abnormalities produce a phenotype that is unable to protect skeletal muscle from chronic inflammation. Exercise training can help to restore and/or minimize the abnormal angio-metabo signal axis in muscle, thereby increasing muscle capillarity and improving muscle function.

Behera

Senior Professor
Dept. of Pulmonary Medicine
Postgraduate Institute of Medical Education & Research
Chandigarh
India

Title: Indoor Air Pollution and COPD
Speaker
Biography:

Dr. D. Behera is the Senior Professor & Head,Dept. of Pulmonary Medicine,(WHO Collaborating Centre for Research & Capacity Building in Chronic Respiratory Diseases)Postgraduate Institute of Medical Education & Research, Chandigarh - 160012 (INDIA). He has the experience as a teacher, researcher and clinician over 35 years. He has 425 scientific publications and is the author of two text books on Pulmonary Medicine and Respiratory Diseases. Has also has authored books on bronchial asthma and lung cancer, and tuberculosis. He has many National and International Scientific awards to his credit. He has been A Fellow and Member of many International and National scientific bodies. He has been the President and office bearer of a couple of scientific bodies and is associated with a number of scientific journals.

Abstract:

More than 400 million people worldwide suffer from COPD. The estimated burden in India is about 15 million cases (~9 million males and ~6 million females)[INSEARCH study IJTLD 2012]. Besides smoking air pollution, particularly indoor air pollution is one important risk factor for COPD in iNdia and other developing countries. Women who cook with solid fuels have increased respiratory symptoms including chronic cough and phlegm. Decrease in lung function and COPD is present in 7 % of biomass using women who never smoked in their life. In contrast, only 1.8% of never-smoking LPG users had COPD. A number of studies have showed that in India, the incidence of chronic cor pulmonale is similar in men and women despite the fact that 75% of the men and only 10% women are smokers. In women, chronic cor pulmonale was found to be more common in younger age. This has been attributed to domestic air pollution as a result of the burning of solid biomass fuels leading to chronic bronchitis and emphysema which result in chronic cor pulmonale. A number of studies by us (Behera et al) have shown that exposure to biomass fuel produces various respiratory symptoms including COPD, impaired lung functions (Lung function, particularly FVC, is affected by indoor air pollution due to domestic cooking more so with biomass fuel), high levels of blood carboxyhemoglobin levels, and respiratory symptoms in children (Mixed fuel and kerosene fuel had worst effects on respiratory system in children whose households used these fuels).

Mohammad Hossein Boskabady

Professor
Applied Physiology Research Centre and Dept. of Physiology
Mashhad University of Medical Sciences
Mashhad IR
Iran

Title: Airway responsiveness to various agoists and antagonists, experimental and human evidences
Speaker
Biography:

MH Boskabady Finished MD in Mashhad University of Medical in 1981 and PhD in London University, Charring Cross and Westminister Medical School in 1991. He Published more than 170 papers in English language and more than 10 in Farsi and Presented more than 240 abstract in National and International Congresses He Received several national research awards His main intersts are; Asthma, COPD, Airway Pharmacology, Chemical warfare and Respiratory Diseases, Inhaled toxicology, Smoking

Abstract:

Increased airway responsiveness to different stimuli is the main characteristic feature of asthma. However, airway hyper responsiveness is reported in COPD patients and smokers. In a series of studies airway responsiveness to various pharmacological agonists and antagonists were examined. In animal studies, increased tracheal responsiveness to histamine as histamine concentration caused 50% of maximum response (EC50) and hisataminie (H1) receptor blockade by chlorpheniramine as shift in concentration response to histamine (CR-1) in guinea pig model of COPD by their exposing to cigarette smoke as well as in sensitized animals were shown. Tracheal responsiveness to both isoprenaline and beta-adrenoreceptor blockade by propranolol in cigarette smoke exposed and sensitized guinea pigs and a close correlation in responsiveness to isoprenaline and propranolol between COPD and asthmatic animals were demonstrated. Increased tracheal responsiveness to methacoline and muscarinic receptor blockade by atropine in an animal model of COPD was also reported. Tracheal hyper responsiveness to methacholine in sulfur mustard exposed guinea pigs was also shown. In human studies, increased airway responsiveness to methacholine and salbutamol and the relationship between the two was demonstrated in smokers. Airway hyper responsiveness to salbutamol in COPD patients was also shown. Airway hyper responsiveness to methacholine as well as to salbutamol in chemical war victims were also shown in two studies. Increased airway responsiveness to different pharmacological agonists and antagonists in exposed animal to cigarette smoke and sulfur mustard, smokers, COPD patients and chemical war victims were documented.

Monika Szturmowicz

Professor in National Tuberculosis and Lung Diseases Research Institute, Warsaw, Poland

Title: Pulmonary hypertension in COPD – is it always the consequence of end-stage disease?
Speaker
Biography:

Monika Szturmowicz is a Professor of Medicine afficiated at I Department of Lung Diseases, National Tuberculosis and Lung Diseases Research Institute, Warsaw Poland. In 2010—2014 she was the Editor-in-Chief of Polish Pneumonology and Allergology, the peer-reviewed official Journal of the Polish Respiratory Society. Dr. Szturmowicz is an active member of ACCP (FCCP since 2003), ERS and IASLC, directly involved in the clinical research concerning pulmonary hypertension in lung diseases. She is the author of 99 papers published in peer-reviewed international journals, Hirsh Index -13.

Abstract:

Pulmonary hypertension (PH) defined as mean resting pulmonary artery pressure (mPAP) equal or higher than 25 mmHg ( measured directly), is found in 50% of the patients with end-stage COPD. In most cases mild PH is observed. Nevertheless in 2-7% of patients, severe PH (defined as mPAP>35 mmHg or CI<2.5 l/min) develops. What’s most interesting, severe PH in COPD is not always combined with end-stage disease. The differential diagnosis on such occassion should exclude the influence of other comorbidities on PH ( left heart disease, venous thromboembolism and sleep disordered breathing). Latest publications indicate that clinical phenotype of severe PH in COPD is characterised by: profound hypoxemia, hypocapnia and very low diffusion capacity of the lung for carbon dioxide (DLCO), despite mild or moderate aiway obstruction. It is still not known, if such phenotype is combined with certain genetic rearangements. According to latest PH guidelines, optimal COPD treatment combined with long therm oxygen therapy in the patients with PaO2 below 60 mmHg, is indicated in PH-COPD. Nevertheless in the patients with servere PH, the referral to an expert center is advised. Latest results of clinical trials with PH-specific drugs are disappointing. Despite the improvement in pulmonary haemodynamics, no significant changes in exercise capacity or quality of life of the patients are reported. Future research should be directed towards the identification of those PH-COPD patients, in whom maximal exercise capacity is limited by low cardiac output, and not by the exhaused ventilatory reserve.

Speaker
Biography:

Department of Respiratory Medicine, King George’s Medical University, Lucknow-226003, Uttar Pradesh, India

Abstract:

Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease (COPD). Oxidative stress has been known for having a key role in pathogenesis of many diseases. The aim of this study was to investigate the serum cytokines levels in [Interleukin-1β (IL-1β), Interleukin-6 (IL-6), Tumor necrosis factor-α (TNF-α)] and their correlation with smoking categories, oxidative stress and also the relationship between antioxidant system statuses and lung function in patients with COPD and smokers and non-smokers subjects. Diagnosis was made by spirometry. METHODS: Total 100 newly diagnosed patients from 30-80 years were included in the study. Participants diagnosed as COPD were selected for the systemic serum cytokines levels. 5 ml of venous blood were collected from each patient in a plain vial and centrifuged for 10 minutes at 2655 g at 40 C, serum collected; it was stored at -80° C for further analysis. For oxidative stress 30 subjects with COPD, 30 smokers, and 30 healthy non-smokers participated in this study. The investigation included determination of the lung function and the measurements of total antioxidant capacity, and also erythrocyte glutathione peroxidase, glutathione reductase, superoxide dismutase, and catalase. RESULTS: The results shows that among the smoking categories there was significant difference in the level of TNF-α (p=0.03), IL-6 (p=0.01) and IL-1β (p=0.02) among the different categories of smoking habit. The pos-hoc analysis revealed TNF- α (pg/ml) was significantly (p<0.05) higher among ex-smoker than non-smokers. Erythrocyte glutathione peroxidase and glutathione reductase were not significantly different between the studied groups. Subjects with COPD and smokers had lower catalase and superoxide dismutase activity (P < .001) than the non-smoker group. Levels of antioxidant capacity were significantly lower in subjects with COPD and smokers than in the non-smoker group (P < .001). Regression analysis revealed no correlations between antioxidant status and spirometric data. CONCLUSION: Decreased total antioxidant capacity in plasma of subjects with COPD and smokers suggests an increased oxidative stress in this group. However, no relationship was found between lung function and antioxidant systems status in COPD subjects. Smoking may influence TNF-α mediated systemic inflammation, which, in turn, may account for some of the benefits observed in patients with COPD who stop smoking.

Mohammad Hossein Boskabady

Professor
Applied Physiology Research Centre and Dept. of Physiology
Mashhad University of Medical Sciences
Mashhad IR
Iran

Title: Therapeutic potential for COPD treatment, evidence for stem cell and natural product therapy
Speaker
Biography:

MH Boskabady Finished MD in Mashhad University of Medical in 1981 and PhD in London University, Charring Cross and Westminister Medical School in 1991. He Published more than 170 papers in English language and more than 10 in Farsi and Presented more than 240 abstract in National and International Congresses He Received several national research awards His main intersts are; Asthma, COPD, Airway Pharmacology, Chemical warfare and Respiratory Diseases, Inhaled toxicology, Smoking

Abstract:

In a series of studies various possible therapeutic potential of natural product and stem cell for treatment of COPD were examined. The effect of adipose derived stromal cells (ASCs) on tracheal responsiveness, interleukin-8 (IL-8), total and differential white blood cells (WBC) counts in animal model of COPD was shown. The effect of ASCs on lung histopathologic changes and serum level of malondialdehyde (MDA) in COPD animals was also demonstrated in another study. The effect of Zataria multiflora and its constituent, carvacrol on systemic inflammation including serum levels of IL-8 and MDA as well as total and differential white blood cell (WBC) in the blood of guinea pig COPD model was documented in two studies. The preventive effect of Zataria multiflora and carvacrol on thiol groups, IL-8, total and differential WBC broncho-alveolar lavage fluid (BALF), lung pathology and tracheal responsiveness, were also demonstrated. Tracheal responsiveness to both methacholine and ovalbumin reduced in COPD animal model due to Nigella sativa extract and vitamin C treatment. The preventive effect of vitamine E, dexamethazone and the extract of Nigella sativa on tracheal responsiveness and lung inflammation of sulfur mustard exposed animals was studied. Significant improvement in pulmonary function tests and respiratory symptoms in chemical war victims treated with the extract of Nigella sativa for two month was also observed. The results of these studies indicated a promising therapeutic potential for stem cell and natural product in the treatment of COPD which should be clinically evaluated in further

Kanala Kodanda RamiReddy

Professor
Divison of Human Genetics
Sri Venkateswara University
Tirupati
India

Title: Genetic Determinants of Chronic Obstructive Pulmonary Disease in South Indian Male Smokers
Speaker
Biography:

Dr. Reddy, currently faculty member in the Division of Human Genetics, Department of Anthropology. His expertise is clinical nutrition, clinical trials and genetic epidemiology. He has published 67 research papers in various journals of repute and completed three ad-hoc projects funded by Government of India and one clinical trial is under progress.

Abstract:

The development of chronic obstructive pulmonary disease, upon exposure to tobacco smoke, is the cumulative effect of defects in several genes. With the aim of understanding the genetic structure that is characteristic of our patient population, we selected forty two single nucleotide polymorphisms of twenty genes based on previous studies and genotyped a total of 382 samples, which included 236 patients and 146 controls using Sequenom Mass ARRAY system. Allele frequencies of rs2276109 (MMP12) and rs1800925 (IL13) differed significantly between patients and controls (p = 0.013 and 0.044 respectively). Genotype analysis showed association of rs2276109 (MMP12) under additive and dominant models (p = 0.017, p = 0.012 respectively), rs1800925 (IL13) under additive model (p = 0.047) and under recessive model, rs1695 (GSTP1; p = 0.034), rs729631, rs975278, rs7583463 (SERPINE2; p = 0.024, 0.024 and 0.012 respectively), rs2568494, rs10851906 (IREB2; p = 0.026 and 0.041 respectively) and rs7671167 (FAM13A; p = 0.029). The minor alleles of rs1695 (G), rs7671167 (T), rs729631 (G), rs975278 (A) and rs7583463 (A) showed significant negative association whereas those of rs2276109 (G), rs2568494 (A), rs10851906 (G) and rs1800469 (T; TGF-b) showed significant positive association with lung function under different genetic models. Haplotypes carrying A allele of rs2276109, G allele of rs1695 showed negative correlation with lung function. Haplotypes carrying major alleles of rs7671167 (C) of FAM13A and rs729631 (C), rs975278 (G), rs7583463 (C) of SERPINE2 had protective effect on lung function. Haplotypes of IREB2 carrying major alleles of rs2568494 (G), rs2656069 (A), rs10851906 (A), rs965604 (C) and minor alleles of rs1964678 (T), rs12593229 (T) showed negative correlation with lung function. In conclusion, our study replicated the results of most of the previous studies. However, the positive correlation between the minor alleles of rs2568494 (A) and rs10851906 (G) of IREB2 and lung function needs further investigation.