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.