DİSCUSSİON
It is estimated that about a third of the world’s population lives with
latent TB. Continuing to be one of the most important causes of death
until recent years, TB is an important public health problem worldwide
[21]. Therefore, biomarkers are very important in the diagnosis of
tuberculosis disease, in the follow-up of treatment and in determining
the outcome effectively and accurately. We need new biomarkers in the
prognosis and treatment process of the disease.
Degenerative lung diseases such as tuberculosis are associated with lung
oxidant-antioxidant imbalance [22]. Mycobacterium tuberculosis is an
intracellular pathogen, which grows and replicates in the host
macrophages. It is well known that macrophages undergo respiratory burst
after contact with this microorganism. Increased amounts of ROS are
produced as a result of respiratory burst [23].
Under physiological conditions, antioxidant production also increases to
neutralize the harmful effects of increased ROS in tissues. However, the
delicate balance between antioxidants and oxidants is key to tissue
homeostasis, and when disrupted, it causes irreversible cell damage with
pathological consequences [24]. There are many studies showing that
oxidant parameters increase and antioxidant parameters decrease in
tuberculosis disease. One study showed that thiol/disulfide homeostasis
is impaired in TB diseases [25]. In other studies, serum SOD
activities were significantly reduced and serum MDA levels increased in
tuberculosis patients compared to healthy controls [26-28]. This
result shows that oxidative stress is increased in patients with
pulmonary tuberculosis. Most of the thiols in plasma are associated with
albumin, and SH groups are oxidized in the presence of oxidative stress,
thus causing structural changes in albumin [29].
The production mechanism of ischemia modified albumin is unclear.
However with OS, some changes occur in the N-terminal part of albumin,
resulting in reduced binding to heavy metals such as copper and cobalt
[16]. OS may promote an increase in IMA levels as it affects
albumin’s ability to associate with metals such as cobalt [30]. It
has been shown that increased IMA concentrations are associated with
inflammation, oxidative stress and endothelial dysfunction [18].
Elevated IMA levels were detected in patients with COPD [31] and
inflammatory bowel disease [32]. In another study, significantly
higher IMA values were found in pulmonary embolism patients compared to
the control group [33]. In a study, it was shown that there is an
inverse relationship between IMA and albumin levels [34]. In another
study, serum IMA levels were significantly increased in
community-acquired pneumonia patients [35]. Albumin, which has an
antioxidant effect, constitutes 70% of the total antioxidant capacity
of the serum [14]. Therefore, albumin modification can be
informative about the body’s response to OS.
Limited data is available on the relationship between IMA and lung
diseases. Determination of IMA levels in diseases where oxidative stress
plays a major role in pathogenesis would be important. In our study, IMA
levels in the patient group were significantly higher than in the
control group. Albumin levels were significantly lower in the patient
group than in the control group. In this study, we can say that the
increase in ROS released from macrophages in patients with pulmonary
tuberculosis disrupts the structure of albumin, which makes up most of
the serum proteins, causing an increase in serum IMA levels and a
decrease in serum albumin levels.