An International Journal for Biomedical Sciences - Biomedicine

Serum α 1 - antitrypsin in smokers with COPD
the Fenton’s and Haber- weiss reactions. Air
pollutants are another exogenous source of
reactive oxygen species in the lungs (2). Smoking
induced chronic obstructive pulmonary disease
(COPD) is the fourth most common cause of
death in adults (3).The increased oxidative
burden occurs in lungs of patients with chronic
obstructive pulmonary disease and this results
in an imbalance between oxidants and anti
oxidants,(4) leads to pathogenesis of COPD(5)
The other reasons are due to excessive smoking,
occupational hazards, emphysema and air
pollution (6). Oxidative stress is also thought to
play an important role in the diseased aspect of
the lungs with systemic consequences ,such as
muscle dysfunction and weight loss(7).
Global Initiative on Obstructive Lung Disease
(GOLD) guidelines defined smoking induced
COPD as “a disease state characterized by air
flow limitation which is to a greater extent
irreversible. Air flow limitation is progressive
and with an abnormal inflammatory response
of the lungs to noxious particles or gases (8).
In alveolar capillary units the unopposed
actions of proteases and oxidants results in
destruction of the alveoli and Emphysema
appears. Smoking induced COPD comprising a
chronic bronchitis, emphysema, smaller air way
disease. Clinical features are similar exertional
dyspnoea , cough and sputum production in
usually a prolonged period. Pathogenesis is
after cigarette smoke, 90% of all patients with
COPD are smokers, almost 20% of these
smokers develop the condition (9). Persistent
reduction in FEV1 (forced expiratory maneuver)
is the common finding in COPD. Diagnosis is
made by measurement of pulmonary function.
(10). Assessment of FEV1/FVC (FEV1, forced
expiratory volume in one second, FVC, forced
vital capacity ) is the indicator for early airway
obstruction. A decline in the pulmonary function
is a good index every year (11). A reduced
FEV1/FVC ratio is characteristic. \
In general the smoking, finally produce
COPD within less than 10 pack /10 years. 1
pack a year is equal to 20 cigarettes/day/1 year.
28
The oxidants are counteracted by enzymatic
antioxidants in airways are superoxide
dismutase, glutathione peroxidase, catalase,
glutathione-S-transferase, xanthin oxidase, etc.
The non-enzymatic antioxidants are Vitamin C,
Vitamin E (Alfa Tocoferol), urate, lipoic acid
and bilirubin(3) RTLF (Respiratory-tract lining
fluid) that covers the respiratory epithelium
contains Vitamin C, reduced glutathione (GSH),
urate, Vitamin E and extracellular superoxide
dismutase (SOD)(9), pulmonary antioxidant
system is excellently adaptive.. Hence the
evaluated parameters in this regard are Alfa 1
Antitrypsin, SOD, Vitamin E and Vitamin C
in the prognostic study of COPD patients.
Methods
A total of 80 COPD male cases with history of
smoking and 20 age and sex matched healthy
controls with no smoking, attending our hospital
were included in the study. Furthermore 80
COPD cases with history of smoking were
classified in to four groups according to GOLD
and number of cigarettes/day. The study was not
done in the acute phase but in the stable chronic
phase. All subjects were studied by spirometry
and classified into controls and four case groups
according to the Global Initiative for Chronic
Obstructive Lung Disease (GOLD)(12) as
follows :
Controls : n = 20, no smoking, normal
spirometry, no risk
Group I : n = 20, 5 – 10 cigarettes/day, FEV1/
FVC ‹ 70%, FEV1 greater than or equal to 80%
predicted, mild COPD.
Group II : n = 20, 11 – 15 cigarettes/day, FEV1/
FVC ‹ 70%, FEV1 greater than or equal to 50%
to ‹ 80% predicted, moderate COPD.
Group III : n = 20, 16 – 20 cigarettes/day, FEV1
greater than or equal to 30% to ‹ 50% predicted,
moderate COPD.
Group IV : n = 20, ≥ 20 cigarettes/day, FEV1/
FVC ‹ 70%, FEV1 ‹ 30% predicted or FEV1 ‹
www.biomedicineonline.org Biomedicine - Vol 31; No.1: 2011