Profile of patients with severe chronic obstructive pulmonary disease in a tertiary care hospital in central India

Sharma P 1, Thakur PK 2

1Dr. Parag Sharma, Assistant professor, Department of Pulmonary medicine, Chirayu Medical college, Bhopal, MP, India, 2Dr. Praveen Kr. Thakur, Assistant professor, Department of ENT,  Chirayu Medical college, Bhopal, MP, India

Address for correspondence: Dr Parag Sharma, Email: roshanchanchlani@gmail.com



Abstract

Chronic obstructive pulmonary disease (COPD) is a public health problem. Tobacco smoking is the major cause, but not the only one. Air pollution, exposure to chemicals, environmental smoke exposure, and passive smoking are among other contributing causes; viral and bacterial infections also being risk factors. Gender and weight are associated with the severity of the disease. Co-morbidity is frequent. Objective: To characterize a population of COPD patients. Methods: Questionnaires were applied to patients with COPD. The data included gender, age, weight, body mass index (BMI), oxygen delivery users, and FEV1, exposure to tobacco smoke, exposure to wood smoke, history of tuberculosis and co-morbid diseases. Results: Of the 110 patients enrolled in the study, 70% (77) were men with an average age of 64 ± 10 years, average weight of 63 ± 16 kg and average BMI of 22 ± 5 kg/m 2. Mean FEV 1 was 35 ± 14% and 45.7% were oxygen dependent. Sixteen (17.6%) patients never smoked, while 16.3% had quit tobacco smoking). Eighteen (19.8%) were exposed to wood smoke. Eight (8.8%) patients had tuberculosis, Five (4.5%) complained of asthma symptoms, 2 (1.8%) had bronchiectasis, Thirteen (11.8%) diabetes mellitus, Sixty two (56.3%) hypertension, and Fourteen (12.7%) Corpulmonale. Conclusion: Other possible COPD etiologies must be investigated. Determinants of the pulmonary injury could be environmental smoke exposure associated to former infections. Men with low BMI are typically representative of this severe patient population. Hypertension and Cor Pulmonale are frequent co-morbidity factors.

Keywords: Chronic obstructive pulmonary disease, Tuberculosis, Asthma, Diabetes mellitus, Smoking



Manuscript received 12th February 2016, Reviewed: 24th February 2016
Author Corrected: 4th March 2016, Accepted for Publication: 15th March 2016

Introduction

Chronic obstructive pulmonary disease (COPD) is a public health problem [1]. All over the world, millions of people suffer from this illness and die prematurely due to its complications. Currently, COPD is the 12 th most prevalent disease in the world and the World Health Organization reckons it will be the fifth by the year 2020. From the sixth cause of death, it will be the third in the same time period [2]. COPD is a clinical entity characterized by the presence of obstruction or chronic limitation of the airflow, presenting a slow and usually irreversible evolvement [1,3]. Tobacco smoking is the main cause of COPD [4]. However, not all smokers develop COPD: only 15% of smokers present the phenotype of the disease, suggesting that, together with the individual susceptibility, additional factors are involved in the establishment of the disease [5]. The need to improve strategies for the reduction of tobacco smoking is vital; however, smoking is not the only cause of COPD. Environmental pollution, chemical exposure, inhaled smoke, passive smoking [6], viral [7] and bacterial [8] infections, alpha-1-antitripsine deficiency [5] and other associated illnesses are considered important risk factors for the development of COPD. COPD diagnosis seems to be more prevalent in men than in women, suggesting higher severity of the disease for males [9]. Weight and muscle mass loss, as well as depletion of organic tissues, are frequent findings in chronic inflammatory diseases such as COPD. These alterations may indicate a worse prognosis as a consequence of impairment of the peripheral muscle function and reduction of exercise capacity [10]. The purpose of this study is to characterize a population of COPD patients assisted in the ambulatory of an outsourced health service.

Methodology

110 patients suffering from COPD attending the Department of Pulmonary medicine, CMCH, Bhopal were enrolled. A written informed consent was taken from the patients and standard questionnaires were applied to them. Data collected included: gender, age, weight, body mass index (BMI), smoking (starting and quitting age, years of smoking, number of years/pack, use of corn husk cigarette), contact with wood burning smoke, previous history of lung tuberculosis, associated diseases, such as asthma, bronchiectasis, diabetes mellitus, systemic hypertension and corpulmonale, use of home oxygen and pulmonary function (forced expiratory volume in the first second – FEV1 ).

Result

One hundred and ten COPD patients were included in the study. Average forced expiratory volume in the first second (FEV1) was 0.8 ± 0.42 litters or 35.5 ± 13.63% of the expected. Forty nine patients (44.5%) depended on oxygen at the time of the clinical evaluation. Seventy seven (70%) patients were male and 33 (30%), female. Age ranged from 40 to 83 years, with a mean of 64 ± 9.71 years. The patients´ weight varied from 38 to 110 kg, with a mean of 63 ± 15.95 kg and the body mass index, from 15.67 and 38.06 with an average of 22.46 ± 5.03 kg/m 2 (Figure 2). Of the 110 patients studied, sixteen (17.6%) had never smoked; 76 were still smoking (69%) and 18 (16.3%) had quit smoking (78.8%). The mean smoking onset age was 16 ± 7.15 years and the mean smoking period was 38 ± 11.10 years/pack, 1.3 ±0.81packs/day in average. Eighteen patients (19.8%) reported having had contact with wood burning smoke; two of them smoked a little and one had never smoked. Eight patients (8.8%) had diagnosed pulmonary tuberculosis, treated in the past. Among the associated diseases, five patients (4.5%) presented sibilant-related dyspnea and positive response to bronchodilator (12% increase of FEV1 and 200 ml), two (1.8%) had bronchiectasis observed at high-resolution computer assisted tomography; thirteen (11.8%) had diabetes mellitus, 62 (56.3%) were treated for systemic hypertension and 14 (12.7%) were diagnosed with corpulmonale.

Discussion

Chronic obstructive pulmonary disease is characterized by limitation of the airflow, which is not completely reversible. This limitation is caused by an impairment of the small airway (obstructive bronchiolitis) and pulmonary destruction (emphysema). The population of patients evaluated in this study has moderate COPD, according to international patterns – Stage II B of GOLD [1] , since mean FEV1 is between 30 and 50% of expected. COPD incidence is higher in men than in women and increases considerably with age. The gender differences may result from the higher prevalence of tobacco smoking and occupational exposure among men. With the increase of smoking among women, the findings may change in the future [3]. Recent evidence indicates that women may be more susceptible to the side effects of cigarette smoke than men; the active search of early COPD cases by spirometry reduces the difference of COPD prevalence between men and women [9].

In this population of severe patients the BMI was lower than 25 kg/m 2, even though the upper and lower weight limits showed a large variation. Weight loss, reduction of muscle mass and tissue depletion are common findings in COPD patients. The loss of free fat mass is directly related to the impairment of respiratory and peripheral muscles and to the reduction of the exercise capacity that occurs in COPD patients. These systemic alterations in COPD may be associated to a worse prognosis, indicating that patients with lower BMI survive less [10].

Three mechanisms participate in the evolvement of limited airflow in COPD: bronchial alterations with inflammation and metaplasia of cells, hypertrophy of smooth muscle and fibrosis can narrow lumen of the respiratory tract. Chronic inflammation occurs as a response of the individual to smoke exposure. The reduction of tobacco use is related to health benefits and consequently, to a drop of the prevalence, morbidity and mortality of COPD patients [11]. One cigarette has more than 4,000 substances producing pulmonary lesions. However, for some years, the wood burning smoke has been recognized as a COPD pathogenic agent [12-15]. In this population of COPD, 25.7% of the individuals reported having been exposed to wood burning smoke, and in three of them, cigarette could not be the main COPD causal factor.

Recent studies show that infections of the respiratory tract in children make these patients become more susceptible to develop COPD from exposure to potentially noxious agents [16]. In smokers, decrease of mucociliary clearing and of autoimmune local defenses allow infectious agents (virus, bacteria) to colonize the lower respiratory tract. These pathogenic agents and their degradation products can elicit even more mucociliary damage, due to an increased production of mucous secretion, interruption of normal ciliary activity and damage to the airway epithelium [16-18] .

In this COPD population, five (4.5%) patients had clinical characteristics of asthma. This number is in agreement with the international literature data, which puts the intersection between asthma and COPD in 10% [19]. The inflammatory cellular mechanisms of typical COPD differ from those of asthma [20,21] . There is, however, a group of patients characterized as COPD carriers who present characteristics common to asthma, including increased eosinophils in the exacerbated sputum. The use of steroids (oral or inhalatory) would be beneficial in this group of patients, differing of typical COPD patients, in which corticosteroids do not prevent the progressive loss of pulmonary function. The name “sibilant bronchitis” has been proposed for the pulmonary disease in this subgroup of patients [19].

The most frequently diseases associated to COPD found in this sample of patients, systemic hypertension and diabetes mellitus, could be directly related to the chronic use of systemic corticoids [22].

Conclusion

The high morbidity-mortality of COPD, demands a better care in the way the suspected patients are investigated. The early diagnosis is essential with the determination of possible aggravating or triggering factors. COPD must be considered not as a simple disease caused by individual abuses, but rather as an addiction disease.

Funding: Nil, Conflict of interest: None initiated.
Permission from IRB: Yes

References


1. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease NHLB/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop Summary. Am J RespirCrit Care Med 2001;163:1256-76.

2. Barnes PJ. Chronic obstructive pulmonary disease. N Engl J Med. 2000 Jul 27;343(4):269-80.


3. I ConsensoBrasileiro de Doença Pulmonar Obstrutiva Crônica (DPOC). J Pneumol 2000;26:S1-S52.

 
4. Snider GL. Chronic obstructive pulmonary disease: a definition and implications of structural determinants of airflow obstruction for epidemiology. Am Rev Respir Dis. 1989 Sep;140(3 Pt 2):S3-8.
[PubMed]

5. Turato G, Zuin R, Saetta M. Pathogenesis and pathology of COPD. Respiration. 2001;68(2):117-28.
[PubMed]

6. Singh N, Davis GS. Review: occupational and environmental lung disease. Curr Opin Pulm Med. 2002 Mar;8(2):117-25.
[PubMed]

7. Hogg JC. Role of latent viral infections in chronic obstructive pulmonary disease and asthma. Am J Respir Crit Care Med. 2001 Nov 15;164(10 Pt 2):S71-5.
[PubMed]

8. Murphy TF, Sethi S. Bacterial infection in chronic obstructive pulmonary disease. Am Rev Respir Dis. 1992 Oct;146(4):1067-83.
[PubMed]

9. Chapman KR, Tashkin DP, Pye DJ. Gender bias in the diagnosis of COPD. Gender bias in the diagnosis of COPD. Chest. 2001 Jun;119(6):1691-5.
[PubMed]

10. Wouters EF, Creutzberg EC, Schols AM. Systemic effects in COPD. Chest. 2002 May;121(5 Suppl):127S-130S.
[PubMed]

11. Petty TL. COPD in perspective. Chest. 2002 May;121(5 Suppl):116S-120S.
[PubMed]

12. Dennis RJ, Maldonado D, Norman S, Baena E, Martinez G. Woodsmoke exposure and risk for obstructive airways disease among women. Chest. 1996 Jan;109(1):115-9.


13. Pérez-Padilla R, Regalado J, Vedal S, Paré P, Chapela R, Sansores R, Selman M. Exposure to biomass smoke and chronic airway disease in Mexican women. A case-control study. Am J Respir Crit Care Med. 1996 Sep;154(3 Pt 1):701-6.
[PubMed]

14. Albalak R, Frisancho AR, Keeler GJ. Domestic biomass fuel combustion and chronic bronchitis in two rural Bolivian villages. Thorax. 1999 Nov;54(11):1004-8.
[PubMed]

15. Tzanakis N, Kallergis K, Bouros DE, Samiou MF, Siafakas NM. Short-term effects of wood smoke exposure on the respiratory system among charcoal production workers. Chest. 2001 Apr;119(4):1260-5.
[PubMed]

16. Ward SA, Casaburi R. 21st century perspective on chronic obstructive pulmonary disease. Respiration. 2001;68(6):557-61.
[PubMed]

17. Saetta M, Turato G, Maestrelli P, Mapp CE, Fabbri LM. Cellular and structural bases of chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2001 May;163(6):1304-9.
[PubMed]

18. Barnes PJ. Future Advances in COPD Therapy. Respiration. 2001;68(5):441-8.
[PubMed]

19. Barnes PJ. Mechanisms in COPD: differences from asthma. Chest. 2000 Feb;117(2 Suppl):10S-4S.
[PubMed]

20. Cotrim D, et al. Pneumologia: atualização e reciclagem. Vol. IV. Vivaldi Editora, 2001. 


21. Croxton TL, Weinmann GG, Senior RM, Hoidal JR. Future research directions in chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2002 Mar 15;165(6):838-44.


22. Rice KL, Rubins JB, Lebahn F, Parenti CM, Duane PG, Kuskowski M, Joseph AM, Niewoehner DE. Withdrawal of chronic systemic corticosteroids in patients with COPD: a randomized trial. Am J Respir Crit Care Med. 2000 Jul;162(1):174-8.




How to cite this article?

Sharma P, Thakur PK, Profile of patients with severe chronic obstructive pulmonary disease in a tertiary care hospital in central India: Int J Med Res Rev 2016;4(4):664-667.doi: 10.17511/ijmrr.2016.i04.32.