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.