INTRODUCTION
Pulmonary thromboembolism (PTE) occurs when a blood clot originating from any systemic vein blocks one or more branches of the pulmonary arteries [1]. PTE can develop as a result of an acute or chronic process. PTE; It is divided into three types: massive with high mortality, submassive with moderate mortality, and non-massive with low mortality [2]. PTE; It is the third most common cardiovascular disease after acute myocardial infarction and stroke [3]. Some patients die before being diagnosed. Therefore, its net prevalence is not known [4]. Clinical symptoms and signs; It may vary depending on the size, number, location of the embolus, the development of an infarction, the resolution rate, the recurrence or not, the age of the patient and the reserve of cardiopulmonary functions. The most common symptoms; dyspnea, pleuritic chest pain, cough, syncope, and hemoptysis [5]. Suspecting pulmonary thromboembolism is the most important step in diagnosis. Suspicion of disease should be based on risk factors, symptoms, examination findings, electrocardiogram, biochemical data, and chest radiography findings. clinical evaluation alone is not reliable to diagnose or rule out PTE. However, both clinical follow-up and clinical predictive rules are useful in determining the probability of PTE before examination [6].
Thiol; It is an organic compound containing sulfhydryl (-SH) group, which has a critical role in preventing the formation of oxidative stress in cells. Plasma thiols show pro-oxidant or mostly antioxidant effects in physiological and biological events. Thiol groups of sulfur-containing amino acids (such as cysteine, methionine) in protein are the primary target of reactive oxygen species (ROS). ROS transfer their electrons to other species. Thiols have standard reducing potential and therefore act as fast electron acceptors. In this way, the oxidant is reduced by thiols and neutralized to a less harmful product. The thiol molecule is oxidized and transformed into disulphide (C-S-S-C). This reaction is reversible and normally exists in the body in equilibrium. [7].
In previous studies, native thiol and total thiol values were found to be lower in the patient group compared to the control group in cases such as pneumonia and stomach cancer [8, 9], and these values were found to be higher in psoriasis and lichen planus patients [10, 11]. Disulphide values were found to be lower in colon cancer, multiple myeloma and fibromyalgia compared to the control group [9, 12], whereas these values were found to be higher in diabetes and pneumonia [13, 7].
It is known that oxidative stress plays an important role in the pathogenesis of cell and tissue damage. Antioxidants are thought to be an effective treatment method for preventing oxidative tissue damage [7]. There are various biochemical markers used with the aim of identifying oxidative stress (OS) and inflammation. One of these markers is dynamic thiol/disulphide balance. Thiol / disulphide homeostasis (TDH) plays a critical role in many cellular activitie, such as antioxidant protection, detoxification, cell growth, apoptosis, signal transduction, and enzyme activities [7, 14]. Thiols, forming a significant proportion of total antioxidants in the body. They are compositions containing sulfur and play a substantial role in aiding the body’s defense versus reactive oxygen species. Plasma thiols scavenge free radicals through a variety of mechanisms. They are commonly accepted as playing a physiologic role by acting as antioxidants [15]. The aim of this study is to determine how thiol disulphide balance changes in PTE cases and to examine its usability as a new biomarker.