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PUBLISHED DATE: - 10-09-2024
https://doi.org/10.37547/TAJMSPR/Volume06Issue09-04
PAGE NO.: - 16-19
SOME RISK FACTORS FOR PROGRESSION OF
СHRONIC OBSTRUCTIVE PULMONARY
DISEASE
MD.Muminov D.K.
MD, Associate Professor, Tashkent Pediatric Medical Institute, Tashkent, Uzbekistan
Musayev F.T.
Tashkent Pediatric Medical Institute, Tashkent, Uzbekistan
INTRODUCTION
Chronic obstructive pulmonary disease(COPD) is a
disease that has become one of the causes of
morbidity and mortality throughout the world.
This disease is characterized by the fact that it
occurs as an exacerbation and is not always
treatable. This article presents an analysis of
literature data over the past 10 years on risk
factors and pathogenetic aspects of chronic
obstructive pulmonary disease [1].
X-ray comparisons, and in recent years, biopsy
comparisons carried out in the treatment of many
thousands of patients, have shown that in
specialized centers the error rate is 4-5% and tends
to decrease. Correct use of standard examination
methods for patients with COPD, including, first of
all, spirometry, in non-specialized general
practitioners' offices, allows us to increase the
percentage of correct diagnoses to 80
–
85%. The
use of various biopsy options in specialized
pulmonology institutions helps to increase this
percentage to 95-96% [2,3].
As practice shows, general practitioners often
make a diagnosis of COPD based on such shaky
signs as shortness of breath, physical and
radiological data, especially in patients with
frequent exacerbations of lung diseases, without
taking into account risk factors for the onset and
progression of the disease [4].
Diagnosis of COPD using the spirometric method is
gaining new positions every year. Currently, a
classification of COPD has been adopted, in which
the main indicator of the severity of the disease is
FEV1, all values of which relate to post-
bronchodilation. The work of the last decade has
RESEARCH ARTICLE
Open Access
Abstract
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confirmed the correctness of the fundamental
principles about the decisive role of the FEV1
indicator in the diagnosis of COPD. However, in
recent years, justified concerns have emerged that
some overdiagnosis of this disease is possible,
especially when trying to take into account the so-
called microsymptoms and symptoms that cannot
be accurately recorded and measured [5].
I would like to note that reproaches against
modern pulmonology, as well as other medical
disciplines, for departure from clinical thinking are
only fair when the use of a particular technique
becomes an end in itself, and the data obtained are
not scrupulously studied and generalized.
According to experts, the diagnosis of COPD is
possible if the patient’s s
hortness of breath is more
pronounced than that of healthy people of the same
age and gender, and the exacerbation of the
infectious process significantly disrupts the
patient’s lifestyle and if the malaise is long
-lasting
[1,5].
Combating risk factors is the most important
strategic goal in the prevention and treatment of
COPD. There remains a nihilistic attitude towards
COPD among a wide range of physicians due to the
disappointing results regarding primary and
secondary prevention of COPD, in particular
regarding the possibility of eliminating factors
causing the initiation and progression of COPD.
Identification of risk factors is an important step
towards developing strategies for the prevention
and treatment of any disease. Risk factors for COPD
are divided into two groups: exogenous and
endogenous [6].
In addition, the prevailing opinion is that in most
cases, the patient causes the disease to himself.
Thus, smoking continues to be the cause of COPD
and other serious diseases. It has been shown that
smokers have a higher prevalence of symptoms of
respiratory dysfunction, a greater decline in annual
FEV1, and a higher mortality rate compared to non-
smokers. The results of twenty-five-year
observations of smokers in the general population
showed that a large proportion of smokers develop
COPD [7].
Risk factors for COPD include genetic
predisposition; the most studied genetic disorder
that may cause the disease is alpha-1-antitrypsin
deficiency, which is the main cause of emphysema
in non-smokers, organic and inorganic industrial
hazards, household chemicals, and poorly
ventilated areas. In addition, insufficient growth
and development of the lungs in the perinatal
period, oxidative stress, gender, age, respiratory
tract infections, a history of tuberculosis,
socioeconomic status, poor nutrition, and
comorbid conditions are considered risk factors for
COPD [7,8].
It is known that COPD is a polygenic inherited
disease. In particular, deficiency in the production
of α1
-antitrypsin, the most important circulating
inhibitor of serine proteases, is a documented risk
factor for the development of COPD. Although α1
-
antitrypsin deficiency is a recessively inherited and
relatively rare disease, this disease is a clear
example illustrating the interaction between
genotype and environmental factors leading to the
development of COPD [9].
Scientists have conducted a number of studies to
draw parallels between hereditary biological
defects and the risk of developing COPD. In
particular, the role of transforming growth factor
β1 (TGF
-
β1), microsomal apoxide hydrolase 1
(mEPHX1), and tumor necrosis factor α (TNFα) in
the pathogenesis of COPD was studied. However,
the unconditional role of these factors in the
pathogenesis of COPD has not been proven [7,9].
Infectious agents (viral and bacterial agents) may
play a role in both the initiation of COPD and the
progression of the disease through exacerbations.
Researchers have proven the connection between
severe infectious lung diseases suffered in
childhood and an increased risk of clinically
significant COPD in adulthood. A high susceptibility
to viral infections of the respiratory tract may be
associated with birth weight, which is also a risk
factor for the development of COPD [10,11]. One of
the risk factors for the development of COPD may
be individual underdevelopment of the lungs in the
perinatal period.
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The course of COPD varies among patients and
depends on the severity of symptoms (especially
breathing and decreased physical activity),
systemic manifestations, and comorbidities that
contribute to airflow limitation. At the same time,
COPD itself has a number of systemic
(extrapulmonary) manifestations that lead to the
development of comorbid conditions. [12]
The statement that bronchial asthma may be a risk
factor for the development of COPD is not
conclusive. COPD can coexist with bronchial
asthma. It has been established that in bronchial
asthma,
a
sensitizing
antigen
promotes
inflammation through CD4+ T lymphocytes and
eosinophils. In this case, the obstruction is
reversible. Whereas in COPD, the damaging agent
promotes inflammation through CD8+ T
lymphocytes, macrophages and neutrophils, and
the obstruction is only partially reversible [13].
In recent years, malnutrition, or malnutrition or
trophological deficiency observed in patients with
COPD, has been the subject of close study, due to
the fact that it is considered by scientists as an
independent unfavorable factor that aggravates
the prognosis and course of the disease [14]. The
cause of malnutrition is probably the progressive
loss of muscle mass in COPD, as well as muscle
weakness due to increased apoptosis or muscle
inactivity.
It is believed that post-transplant osteoporosis is
one of the unfavorable consequences of
immunosuppressive therapy (taking cytostatics
and glucocorticosteroids). However, in patients
with so-called terminal pulmonary pathology,
including COPD, there are a number of risk factors
for the development of osteopenic syndrome:
hypogonadism, physical inactivity, poor nutritional
status leading to vitamin D deficiency and calcium
absorption,
long-term
therapy
with
glucocorticosteroids,
hypoxemia,
systemic
inflammation [15].
Systemic manifestations of COPD, in addition to
musculoskeletal disorders associated with
apoptosis and hypodynamic atrophy, include
depression, anemia (usually normochromic,
normocytic), depression, diabetes, and sleep
disturbances. These combinations obviously
worsen the prognosis of patients with COPD [16].
Thus, COPD is a disease that (according to the
definition of GOLD experts) can be prevented and
treated by carefully studying the comorbid
background, conducting a differential diagnosis of
the severity of comorbid conditions in each patient
with obstructive syndrome. The strategy to combat
COPD should include early identification of
patients with COPD, timely diagnosis, identification
and monitoring of factors contributing to the
progression of the disease.
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