CLINICAL PRACTICE ARTICLE

Post-Tuberculous Chronic Obstructive Pulmonary Disease

Inam Muhammad Baig1, Waseem Saeed2 and Kanwal Fatima Khalil2

ABSTRACT
Objective: To determine the frequency of chronic obstructive pulmonary disease (COPD) as a sequel of treated
pulmonary tuberculosis.
Study Design: A case series.
Place and Duration of Study: Department of Pulmonology, Military Hospital, Rawalpindi, from April to November 2007.
Methodology: Forty seven adults, previously treated for pulmonary tuberculosis and presenting subsequently with chronic
exertional dyspnoea for which no other alternate cause was found were included. Those having a probability of re-activated
TB, having history of current or previous smoking or occupational exposure, asthmatics and cases of interstitial lung
disease and ischemic heart disease were excluded. Pre- and post-dilator FVC, FEV1 and FEV1/FVC were recorded in
each case through simple spirometry on Spirolab-II MIR S/N 507213. Stage and pattern of COPD was recorded.
Results: There were 76.5% (n=36) males. Mean age was 56.4 and 44.2 years in males and females respectively. Twenty
six (55.3%) were found to have an obstructive ventilatory defect of different degrees: severe/stage III in 69.2% (n=18),
moderate/stage II in 23.0 % (n=6) and mild/stage I in 5.9% (n=2). Fourteen (29.7%) were found to have a restrictive pattern
and 7 (14.8%) revealed a mixed obstructive and restrictive pattern.
Conclusion: Chronic obstructive pulmonary disease can occur as one of the chronic complications of pulmonary
tuberculosis and the obstructive ventilatory defect appears more common among various pulmonary function
derangements.
Key words:

Tuberculosis. COPD. Pulmonary function tests. Restrictive ventilatory defect. Obstructive pulmonary ventilatory defect.

INTRODUCTION
Chronic obstructive pulmonary disease (COPD) and
tuberculosis are among the worlds first ten most
prevalent diseases, the main burden of the later being in
the developing countries, in the form of pulmonary
tuberculosis. In the global burden of disease, COPD and
tuberculosis have been ranked as sixth and eighth
respectively, in terms of disability and death in low and
middle income communities world wide.1 However, the
impact of pulmonary tuberculosis on the prevalence of
COPD has often remained neglected.2 Pulmonary
functional impairment as a complication of tuberculosis
manifests in various patterns but mainly as airflow
limitation.3
Chronic obstructive airways disease as a complication
of pulmonary tuberculosis has been re-studied recently
in many regions of the globe.2-4 In the executive
summary of the 2006 update of the Global initiative for
chronic obstructive lung disease (GOLD) guidelines,5
the role of tuberculosis in the development of chronic
1

Department of Medicine, Combined Military Hospital, Multan

Cantt.
Department of Pulmonology and Critical Care, Military
Hospital, Rawalpindi.
Correspondence: Dr. Inam Muhammad Baig, Classified
Medical Specialist and Pulmonologist, Combined Military
Hospital, Multan Cantt.
E-mail: inammbaig@yahoo.com
Received April 10, 2009; accepted April 10, 2010.

542

airways obstruction has been recognized. According to

the GOLD Workshop summary, chronic bronchitis or
bronchiolitis and emphysema can occur as complications
of pulmonary tuberculosis.6 A study performed to
assess the impact of pulmonary tuberculosis on the
prevalence of COPD, found that the prevalence of
COPD increased from 3.7-5% by including participants
with past history of TB treatment.7
Pakistan is one of the 22 countries in the world that
accounts for 80% of TB cases according to World Health
Organization.8 In Pakistan, post-tuberculosis respiratory
morbidity is common and constitutes a significant subgroup of chronic lung disease patients presenting to
medical out patients. Recognizing this respiratory
disorder and assessing its severity would rationalize its
management and could minimize the frequency of unnecessary treatment given to patients on the presumption
of active or reactivated tuberculosis.9
The objective of this study was to determine the occurrence
of post-tuberculous COPD in the local setting.

METHODOLOGY
It was a descriptive study carried out at the Department
of Pulmonology, Military Hospital, Rawalpindi, from April
to November 2007.
The inclusion criteria were adults aged 18-65 years, who
had a definite past history of pulmonary tuberculosis,
had received complete anti-tuberculosis therapy course
and then presented with chronic exertional dyspnoea
with or without cough. Only those were included who

Journal of the College of Physicians and Surgeons Pakistan 2010, Vol. 20 (8): 542-544

Post-tuberculous chronic obstructive pulmonary disease

had radiological evidence of very typical post-TB lesions

in the form of scarring, fibrosis, cavitations, emphysema
and other destructive lung changes in their latest chest
radiographs. It was otherwise difficult to ascertain their
past diagnosis by any laboratory records. Presence of
any clinical feature leading to a probability of active
disease meant exclusion. Other conditions considered
for exclusion in this study were history of current or
previous smoking, history of occupational exposure,
diagnosed cases of asthma and COPD, ischaemic heart
disease, interstitial lung disease, bilateral extensive
bronchiectasis, severe anemia and renal failure. Those
showing more than 12% reversibility in the post-dilator
FEV1 were also excluded.
Patients meeting the criteria were interviewed after their
consent and data were recorded on pre-designed forms
as case number, age, gender and timing of the anti-TB
treatment. Patients were then called for spirometry on
Spirolab-II-MIR S/N 507213 according to convenience
without any pre-medication. The technique was
explained and actual measurements were done after
subjects became familiar with a correct technique. Three
attempts were recorded and only considered if the
variation between two best reading was less than 5%.
Spirometric values were recoded as FVC, FEV1 and
FEV1/FVC. Those not meeting the American Thoracic
Society Criteria for quality for spirometry and those
showing significant post dilator reversibility (more than
12%) were excluded. The subjects showing an
obstructive ventilatory defect were then classified as
mild, moderate and severe according to the GOLD
guidelines.10
Data was analyzed using SPSS version 10. Descriptive
statistics were used to describe the data i.e. mean and
standard deviation for numeric variables and frequency
along with percentages for categoric variables.

RESULTS
During the study period a total of 92 individuals having a
past history of being treated for pulmonary tuberculosis
and presenting with chronic dyspnoea were interviewed.
Fifty-four subjects fulfilling all the inclusion/exclusion
criteria underwent spirometry. Three were excluded as
their post-dilator reversibility was significant (more than
12%) although they had no previous history of asthma
and four were excluded due to sub-optimal spirometric
technique.
Forty-seven individuals were finally considered in the
study. 76.5% (n=36) were males. The age in males
ranged between 24 and 65 years with a mean of 56.4
years. In females, it ranged between 33 and 59 years
with a mean of 44.2 years. Among those 55.3% (n=26)
were found to have an obstructive ventilatory defect of
different degrees: severe/stage-III in 69.2% (n=18),
moderate/stage-II in 23.0% (n=6) and mild/stage-I in

5.9% (n=2). Fourteen (29.9%) were found to have a

restrictive pattern in their spirometry and 7 (14.8%)
revealed a mixed obstructive and restrictive pattern. In
those showing irreversible airflow obstruction, 15
(57.6%) had been treated between 10 and 15 years ago,
30.7% (n=8) had been treated in less than 10 years and
11.3% (n=3) had a history of receiving treatment more
than 15 years before.

Figure 1: Patterns of pulmonary function impairment.

DISCUSSION
This study found that 55.3% of treated pulmonary
tuberculosis patients presenting with dyspnoea, had an
obstructive ventilatory defect. Previous studies had also
revealed that an obstructive pattern of pulmonary
functional impairment following treated pulmonary
tuberculosis was more common.11,12,13 PLATINO study,
a recent large study, found that FEV1 is reduced
compared to FVC in most cases.14 However, another
previous study had found after 15 years follow-up of 40
patients that there was a higher yearly decline in FVC
compared to FEV1.15 An inverse relation ship between
FEV1 and the extent of the disease on the original chest
radiograph in treated pulmonary TB has been
documented.16
This study also found that 65% of those patients showing
an obstructive ventilatory defect had been treated more
than 10 years earlier. An earlier study revealed that the
obstructive changes become pro-nounced after 10
years of follow-up in treated cases and co-related with
the residual scarring on chest radiograph regardless of
the findings on original chest radiographs.16
PLATINO study, a latest large population based multicentre study, carried out in 5 Latin American countries
(n=5,571 participants) included subjects on the criteria
of a past diagnosis of pulmonary tuberculosis by a
physician and performed spirometry in the field. This
study had a small sample size and was hospital based.
It included only those presenting to the hospital
with dyspnoea. Along with exclusion of other possible

Journal of the College of Physicians and Surgeons Pakistan 2010, Vol. 20 (8): 542-544

543

Inam Muhammad Baig, Waseem Saeed and Kanwal Fatima Khalil

confounding factors, smokers and subjects with more

than 65 years were also excluded as an earlier study
had revealed that the severity of obstructive airway
disease changes in subjects treated for tuberculosis with
advancing age and number of cigarettes smoked.17

5.

Rabe KF, Hurd S, Anzueto A, Barnes PJ, Buist SA, Carverley P,

et al. Global initiative for chronic obstructive lung disease. Global
strategy for the diagnosis, management, and prevention of
chronic obstructive pulmonary disease: GOLD executive
summary. Am J Respir Crit Care Med 2007; 176:532-55. Epub 2007
May 16.

Only those subjects who previously received a full course

of anti-tuberculosis treatment, had a chest radiograph
evidence of scarring or destructive changes and who
had no features of active disease were included to
clearly differentiate it from active endobronchial tuberculosis which may also present with dyspnoea and
wheezing as a main feature.18

6.

Pauwels RA, Buist AS, Carverley PM, Jenkins CR, Hurd SS.
GOLD Scientific Committee. Global strategy diagnosis,
management and prevention of chronic obstructive pulmonary
disease: NHLBI/WHO Global initiative for chronic obstructive
lung disease (GOLD) Workshop Summary. Am J Respir Crit Care Med
2001; 163:1256-76. Comment in: p.1047-8.

7.

The limitations of this study, need to be mentioned. Due

to the high prevalence and incidence of pulmonary
tuberculosis in this region, a large sample was expected
however, due to many exclusion criteria, the sample size
finally remained small. Being a hospital based study
only those subjects presenting with dyspnoea were
interviewed, it would not represent the over all
prevalence of post-TB COPD, which is possible by
population based studies. Since it was carried out in a
military set-up, with a male majority, the ratio of male to
female may actually be different in community setting.

World Health Organization. Stop TB partnership. Tuberculosis in

countries [Internet]. [updated 2009 Mar 20]. Available from:
http://www.stoptb.org/countries/

9.

Khan MB, Tahir M, Qureshi SM, Ashraf HM. Errors in the

diagnosis and treatment of pulmonary tubercuosis. Pak Armed
Forces Med J 2007; 57:135-42.

11. Snider GL, Doctor L, Demas TA, Shaw AR. Obstructive airway
disease in patients with treated pulmonary tuberculosis. Am Rev
Respir Dis 1971; 103:625-40.

Chronic functional effects of extensive post-tuberculous

lung scarring manifested mainly as a COPD like
syndrome, which showed same patterns of pulmonary
function abnormalities on spirometry. In view of the fact
that smokers and other possible causes had been
excluded, this study finds pulmonary tuberculosis as an
independent etiological factor for chronic obstructive
pulmonary disease.

12. Lee JH, Chang JH. Lung functions in patients with chronic airflow
obstruction due to tuberculous destroyed lung. Respir Med 2003;
97:1237-42.
13. Patricio Jimnez P, Vivianne Torres G, Paula Lehmann F, Elisa
Hernndez C, Mauricio Alvarez M, Mnica Meneses M, et al.
Chronic airways obstruction in patients with tuberculosis sequel:
a comparison with COPD. Rev Chil Enf Respir 2006; 22:98-104.
14. Menezes AMB, Hallal PC, Perez-Padilla R, Jardim JRM, Muin
OA, Lopez MV, et al. Latin American Project for the investigation
of obstructive lung disease (PLATINO) team. Tuberculosis and
airflow obstruction: evidence from the PLATINO study in Latin
America. Eur Respir J 2007; 30:1180-5. Epub 2007 Sep 5.

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