To evaluate the value of the combination schemes of 10 serological markers in the clinical diagnosis of acute cerebral infarction.The level of total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol, high-sensitivity C-reactive protein, homocysteine (HCY), lipoprotein-related phospholipase A2, ischemia-modified albumin, complement C1q, and lipoprotein a were analyzed in 154 patients with acute ischemic cerebral infarction. The optimized diagnostic combination for acute cerebral infarction was explored by calculating the maximum area under the receiver operating characteristic curves (AUC).The levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol, high-sensitivity C-reactive protein, HCY, lipoprotein-related phospholipase A2, ischemia-modified albumin, complement C1q, and lipoprotein a were significantly higher in the patient vs the control group. Moreover, the positive rate of HCY reached 89.9%. The analysis of the receiver operating characteristic curve of each index and their combinations showed that the minimum AUC of HDL-C alone was 0.543, while the maximum AUC of HCY was 0.853. A multiple logistic regression analysis indicated that HDL-C was a slightly significant variate in the diagnosis of acute cerebral infarction.The value of individual serological markers in the diagnosis of acute cerebral infarction was slightly significant, while the combination of the markers significantly improved the efficiency of its diagnosis.

Background: We aimed to determine the relationship of ischaemia-modified albumin (IMA) with diabetic foot ulcers and its predictive value in the Wagner classification.

Methods: Our cross-sectional study was conducted in 120 diabetic foot patients and 60 healthy individuals with similar body mass index (BMI) and age. Patients with a diabetic foot were classified according to the Wagner classification. Biochemical parameters, C-reactive protein (CRP) and IMA levels ​​were measured in all patients and healthy volunteers. Screening performance characteristics of CRP and IMA were calculated according to Wagner classes and the presence of osteomyelitis.

Results: The levels of BMI, CRP and IMA in diabetic foot patients were significantly higher than the healthy controls. When we grouped the patients according to the Wagner classification, there were no significant differences between the Wagner groups in terms of BMI. The highest IMA levels were detected in Wagner grade 5. CRP had higher sensitivity and specificity than IMA in the discrimination of other grades, except for grade 4-5 separation. For Wagner grade 4-5 distinction, IMA had 84.6% sensitivity and 94.7% specificity.

Conclusion: IMA had a higher predictive value in discrimination of the Wagner grade 4-5. In the management of diabetic foot patients, it may be recommended that IMA is evaluated by clinicians.

Keywords: CRP; Diabetic foot; Ischaemia-modified albumin; Wagner classification.

Background: Ischemia-reperfusion models are used to evaluate treatment options that may minimize cellular damage after ischemia.

Objectives: To investigate the effects of amantadine and topiramate on apoptosis and cellular oxidative damage.

Material and methods: This experiment was performed using 30 male Wistar albino rats. The right internal carotid artery was identified and clamped with an aneurysm clip under general anesthesia, except for animals in the control group. After 10 min of occlusion, the aneurysm clip was removed, allowing reperfusion. After reperfusion and a waiting period of 12 h, the test and control groups were intraperitoneally administered the following solutions: the sham group received 10 mg/kg of isotonic solution, the amantadine group received 20 mg/kg of amantadine, the topiramate group received 40 mg/kg of topiramate, and the amantadine-topiramate group received 20 mg/kg of amantadine and 40 mg/kg of topiramate. After 24 h, the rats were euthanized.

Results: Apoptosis was evaluated using the TUNEL method. Total antioxidant status (TAS), total oxidant status (TOS), total thiol, and ischemia-modified albumin (IMA) levels were measured in both brain tissue and serum samples. The rate of apoptosis in the sham and amantadine groups increased significantly compared to the control group and the non-ischemic counter hemisphere. In the amantadine-topiramate group, both serum TAS and tissue thiol levels decreased. Tissue TOS levels were significantly higher in the topiramate group compared to all other test groups. Tissue TAS levels were significantly higher in the amantadine group compared to all other test groups.

Conclusions: This experimental ischemia-reperfusion model revealed that topiramate reduces apoptosis in the early period after ischemia and that its combination with amantadine does not provide additional benefits against cell death. However, topiramate did not have an inhibitory effect on the oxidative stress biomarkers used in our study (TAS, TOS, IMA, and thiol). Studies that reveal the neuroprotective mechanism of action and long-term effects of topiramate are needed to complement this study.

Keywords: amantadine; apoptosis; cerebral ischemia-reperfusion; oxidative stress; topiramate.

Objective: The pathophysiological mechanisms of idiopathic pulmonary fibrosis (IPF) are not well elucidated. It is assumed that oxidative stress and inflammation are the key underlying culprits for its onset and progression. To gain deeper insight into these processes, we have evaluated several oxidative stress parameters, inflammation markers [i.e., high sensitivity C-reactive protein (hsCRP), serum amyloid A1 (SAA1)], soluble programmed cell death-ligand 1 (sPD-L1), and 25-hydroxyvitamin D [25(OH)D] in IPF patients.

Patients and methods: Biochemistry analyses were done in 30 consecutive IPF patients and 30 age and gender-matched healthy control group (CG).

Results: IPF patients had significantly higher advanced oxidation protein products (p<0.001), pro-oxidant-antioxidant balance (p=0.010), total oxidative status (p<0.001), and ischemia modified albumin (p<0.001) compared to CG. Lower total antioxidant status and total sulfhydryl groups (tSGH) and significantly higher sPD-L1, hsCRP (p<0.001 for all), SAA1 proteins (p=0.014) and [25(OH)D] severe deficiency [11.0 (9.6-15.1) nmol/L] in IPF patients compared to CG were observed. Paraoxonase 1 activity and hsCRP level were lower, while tSHG and sPD-L1 were higher in IPF patients with more severe disease (i.e., II+III stage compared to I stage, p<0.05 for all).

Conclusions: IPF patients are in a state of profound oxidative stress compared to healthy people. The inflammatory component of the disease was confirmed by higher hsCRP and SAA1, but lower [25(OH)D] in IPF than in healthy people. Also, higher levels of sPD-L1 in patients with IPF compared to healthy individuals suggest that sPD-L1 may have a significant role in immune response in IPF.

Despite significant progress in trisomy 21 (T21) diagnostic tools, amniocentesis is still used for the confirmation of an abnormal fetal karyotype. Invasive tests carry the potential risk of miscarriage; thus, screening biomarkers are commonly used before undergoing invasive procedures. In our study, we investigated the possible application of oxidative stress markers in the prenatal screening of trisomy 21. The DNA/RNA oxidative stress damage products (OSDPs), advanced glycation end (AGE) products, ischemia-modified albumin (IMA), alfa-1-antitrypsin (A1AT), asprosin, and vitamin D concentrations were measured in both maternal plasma and amniotic fluid in trisomy 21 (T21) and euploid pregnancies. The obtained results indicated increased levels of DNA/RNA OSDPs and asprosin with simultaneous decreased levels of vitamin D and A1AT in the study group. The diagnostic utility of the plasma measurement based on the area under the received operative characteristic (ROC) curve (AUC) calculation of asprosin (AUC = 0.965), IMA (AUC = 0.880), AGE (AUC = 0.846) and DNA/RNA OSDPs (AUC = 0.506) in T21 screening was demonstrated. The obtained results indicate a potential role for the application of oxidative stress markers in the prenatal screening of T21 with the highest screening utility of plasma asprosin.

Keywords: Down syndrome; antioxidant protein; oxidative stress; prenatal screening; trisomy 21.

Introduction: Oxidative stress as observed in fetal growth restriction (FGR) and preeclampsia (PE) can be identified by decreased levels of systemic free thiols (FT) and increased levels of plasma ischemia-modified albumin (IMA), which may serve as biomarkers in maternal blood for pregnancy complications. We evaluate the performance of oxidative stress-associated potential biomarkers for FGR and PE, and their relationship with clinical characteristics.

Methods: A prospective clinical pilot study was performed in healthy controls and women with pregnancies complicated by severe FGR with or without PE. Blood samples were taken directly after inclusion and analyzed for FT; IMA; soluble FMS-like tyrosine kinase-1 (sFlt-1); placenta growth factor (PlGF); and biomarkers like leptin and soluble receptors for advanced glycation end products (sRAGE). Placentas were examined microscopically. Descriptive statistics and receiver operating characteristics statistics were performed.

Results: Mothers with both severe FGR and PE had significantly reduced FT levels (p < 0.001) and PlGF levels (p < 0.001), and increased levels of plasma IMA (p < 0.05), sFlt (p < 0.001), leptin (p < 0.05) and sRAGE (p < 0.01) compared to women with FGR only. Systemic FT levels were significantly inversely associated with blood pressure (p < 0.01) and plasma IMA (p < 0.001), leptin (p = 0.01) and sRAGE (p < 0.001). Systemic FT and leptin showed significant discriminative ability to differentiate mothers with both FGR and PE from mothers with uncomplicated pregnancies or pregnancies complicated by FGR only.

Discussion: There is a significant discriminative capacity of FT, IMA, leptin and sRAGE that harbor potential as biomarkers of pregnancies complicated by combined FGR and PE.

Keywords: Biomarker; Free thiols; Hypoxia; Ischemia-modified albumin; Leptin; sRAGE.

Background: Acute cholecystitis (AC) is caused by chemical and bacterial inflammation of the gallbladder. The use of Tokyo guidelines is recommended in determining the diagnosis of AC and its clinical severity. In the early stages of AC, many cytokines are secreted due to the local inflammatory cell activation, leading to exacerbation of inflammation and organ failure. Ischemia modified albumin (IMA) is a type of albumin that occurs in ischemia and oxidation and is used as a marker of hypoperfusion and oxidative stress. This study aims to investigate the effectiveness of ischemia modified albumin, C-reactive protein (CRP), and some other inflammation parameters in predicting the severity of the AC on admittance.

Methods: Forty-two patients diagnosed with AC and 30 healthy individuals in the control group were included in the study. The severity assessment of the patients was performed based on the revised Tokyo guidelines (TG 13). The patients were divided into 3 groups according to severity of the disease. Blood samples were taken from the subjects on admittance. Serum IMA levels were studied using an ELISA kit. SPSS 22.00 package program was used for statistical analysis.

Results: Thirty (71.4%) of the participants were in the mild group, while 12 (28.6%) were in the moderate group. There were no patients in the severe group. Leukocyte, CRP, and IMA values in the patient group were higher than those of the control group (p > 0.05). According to the Tokyo classification, a significant difference was found between the groups with mild and moderate grades in terms of CRP and IMA values (p < 0.001 and p < 0.05, respectively). When the cutoff value of IMA was 84 ng/mL, the sensitivity was found to be 76% and specificity was determined to be 40% (AUC: 0.665, p = 0.017, 95% Confidence Interval).

Conclusions: It is considered that IMA could be useful in predicting the clinical severity of TG13-based acute cholecystitis and, therefore, could be used in the management of treatment by the clinician such as medical treatment, early surgery, and interval surgery.

Background: Dialysis patients have an increased risk of mortality. Recently treatment with haemodiafiltration (HDF) has been reported to reduce mortality, particularly cardiovascular mortality, compared to standard high-flux haemodialysis (HD). However, why HDF may offer a survival advantage remains to be determined. So, we conducted a pilot study to explore differences in middle-molecules, inflammation and markers of vascular disease in patients treated by HD and HDF.

Methods: Observational cross-sectional study measuring serum β2-microglobulin (β2M), Advanced Glycosylation End Products (AGEs) by skin autofluorescence (SAF), oxidative stress with ischaemia modified albumin ratio (IMAR) and peripheral vascular disease assessment using Ankle-Brachial Index (ABI), and arterial stiffness using Cardio-Ankle Vascular Index (CAVI).

Results: We studied 196 patients, mean age 69.1 ± 12.4 years, 172 (87.8%) treated by HD and 24 (12.2%) by HDF. Age, body mass index, co-morbidity and dialysis vintage were not different between HD and HDF groups. Middle molecules; β2M (31±9.9 vs 31.2±10 ug/mL) and SAF (2.99±0.72 vs 3.0±0.84 AU), ABI (1.06±0.05 vs 1.07±0.10) and CAVI (9.34±1.55 vs 9.35±1.23) were not different, but IMAR was higher in the HD patients (38.4±14.8 vs 31.3 ± 17.4, P = 0.035).

Conclusions: In this pilot observational study, we found patients treated by HDF had lower oxidative stress as measured by IMAR, with no differences in middle molecules. Lower oxidative stress would be expected to have diverse protective effects on the cardiovascular system Although we found no differences in ABI and CAVI, future studies are required to determine whether reduced oxidative stress translates into clinically relevant differences over time.

Background: Acute aortic dissection is a potentially fatal cardiovascular disorder associated with high mortality. However, current predictive models show a limited ability to efficiently and flexibly detect this mortality risk, and have been unable to discover a relationship between the mortality rate and certain variables. Thus, this study takes an artificial intelligence approach, whereby clinical data-driven machine learning was utilized to predict the in-hospital mortality of acute aortic dissection. Methods: Patients diagnosed with acute aortic dissection between January 2015 to December 2018 were voluntarily enrolled from the Second Xiangya Hospital of Central South University in the study. The diagnosis was defined by magnetic resonance angiography or computed tomography angiography, with an onset time of the symptoms being within 14 days. The analytical variables included demographic characteristics, physical examination, symptoms, clinical condition, laboratory results, and treatment strategies. The machine learning algorithms included logistic regression, decision tree, K nearest neighbor, Gaussian naive bayes, and extreme gradient boost (XGBoost). Evaluation of the predictive performance of the models was mainly achieved using the area under the receiver operating characteristic curve. SHapley Additive exPlanation was also implemented to interpret the final prediction model. Results: A total of 1,344 acute aortic dissection patients were recruited, including 1,071 (79.7%) patients in the survivor group and 273 (20.3%) patients in non-survivor group. The extreme gradient boost model was found to be the most effective model with the greatest area under the receiver operating characteristic curve (0.927, 95% CI: 0.860-0.968). The three most significant aspects of the extreme gradient boost importance matrix plot were treatment, type of acute aortic dissection, and ischemia-modified albumin levels. In the SHapley Additive exPlanation summary plot, medical treatment, type A acute aortic dissection, and higher ischemia-modified albumin level were shown to increase the risk of hospital-based mortality.

Keywords: acute aortic dissection; extreme gradient boost; in-hospital mortality; machine learning; prediction.

Objectives: Serum ischemia-modified albumin (IMA) is higher in patients with cerebral infarction (CI). In this study, we aimed at studying the association between IMA and CI.

Methods: Patients with CI were divided to severe stenosis group and mild stenosis group according to the stenosis of vertebrobasilar artery. Digital subtraction angiography (DSA) and magnetic resonance imaging (MRI) were used for diagnosis. Cobalt-combined with Albumin test was used to determine the serum IMA levels. Serum IMA levels in patients with CI and healthy volunteers were compared by t test. Receiver operating characteristic (ROC) curve was performed for evaluating the diagnostic efficiency of serum IMA for CI. The correlation between IMA level and the National Institute of Health Stroke Scale(NIHSS) score after treatment was analyzed.

Results: Serum IMA levels in patients with CI was increased compared to healthy volunteers(P < .05). Patients in severe stenosis group had a higher serum IMA level than mild stenosis group(P < .05). Serum IMA level at admission was associated with NIHSS score on the 7th day after treatment(P < .05).

Conclusions: Serum IMA level was correlated with vertebrobasilar artery stenosis and short-term prognosis in patients with acute CI.

Keywords: Ischemia modified albumin; cerebral infarction; receiver operating characteristic curves; vertebrobasilar artery stenosis.

Objective: To investigate the effects of low-flow and high-flow anesthesia techniques, administered with sevoflurane during laparoscopic cholecystectomy, on thiol/disulphide homeostasis and serum ischemia-modified albumin (IMA) levels.

Study design: Double-blind, randomised study.

Place and duration of study: Department of Anesthesiology and Reanimation, Health Science University, Bursa Yuksek Ihtisas Training and Education hospital, Bursa, Turkey from January to October 2020.

Methodology: Patients over the age of 18 years, scheduled for elective laparoscopic cholecystectomy, were included in the study. The patients were divided into two groups: Group 1 (low-flow, 1 L/min) and Group 2 (high-flow, 2 L/min). The blood samples for thiol/disulphide homeostasis and serum IMA levels were collected as follows: 5 minutes before induction of anesthesia (T0), 5 minutes after induction of anesthesia (T1) and postoperative 24th hour (T2).

Results: The final analysis included 104 patients. The two groups did not differ significantly in terms of any of the demographic characteristics (p >0.05). There were also no inter-group differences in terms of thiol/disulphide homeostasis parameters or serum IMA levels at T0, T1, or T2. However, in both groups, there were statistically significant changes in serum disulphide and IMA levels from T0 to T1 and T0 to T2 (p=0.000, and p=0.005, respectively).

Conclusion: There was no difference between low-flow and high-flow anesthesia during laparoscopic cholecystectomy in terms of hemodynamics or thiol/disulphide homeostasis. Key Words: Low-flow anesthesia, High-flow anesthesia, Thiol/disulphide homeostasis, İschemia-modified albumin (IMA), Laparoscopic cholecystectomy.

Background: The present study investigates cardiovascular risk and kidney damage in patients with solitary kidneys.

Methods: Included in the study were 40 children with a unilateral functioning kidney and 60 healthy controls, all of whom were evaluated for carotid intima-media thickness, ischemia-modified albumin and oxidative stress parameters, and 24-h ambulatory blood pressure monitoring.

Results: Serum creatinine and urine microalbumin levels were higher and creatinine clearance was lower in the patient group than in the control group, and serum ischemia-modified albumin, carotid intima-media thickness, aldosterone, plasma renin activity and blood pressure were all higher in the patient group than in the control group. In addition, the patient group was showed a non-dipper pattern.

Conclusion: Children with a normal functioning solitary kidney are likely at higher risk of developing cardiovascular disease and such patients should be followed closely before marked kidney impairment occurs.

Keywords: 24-h ambulatory blood pressure monitoring; Cardiovascular risk; Carotid intima-media thickness; Children; Ischemia-modified albumin; Solitary kidney.

Background: Urticaria is an unknown, sudden, and itchy skin disease that is recognized with redness, swelling, and is sometimes seen with angioedema. It is classified as acute or chronic, depending on the duration of symptoms. Thiols in plasma are powerful antioxidants that physiologically eliminate free radicals. The mostly and rapidly affected proteins are thiols that contain the sulfhydryl group. In the present study, the thiol/disulfide homeostasis was investigated as a brand new indicator of oxidative stress in patients who had acute urticaria and presented to the emergency department.

Objective: In the present study, the thiol/disulfide homeostasis, ischemia-modified albumin (IMA), and and neutrophil lymphocyte ratio (N/L ratio) were investigated in the etiopathogenesis of acute urticaria.

Material and method: A total of 37 patients and 40 healthy volunteers were included in the study. Thiol/disulfide homeostasis (TDH) [total thiol-native thiol/disulfide changes] was measured in both groups (patient group and control group) using a brand novel method developed by Erel and Neselioglu. Half of the difference between total thiol and native thiol concentrations gives the amount of disulfide bond.

Results: Total thiol and native thiol levels in blood were found to be low. The levels of total thiol (P = 0.218) and native thiol (P = 0,001) were significantly lower in patients with acute urticaria than in the control group. At the same time, the level of disulfide was significantly higher in the patient group than in the control group (P = <0.001). The level of IMA was higher in the patient group than in the control group (P < 0.001).

Conclusion: While total thiol and native thiol are low in acute urticaria, the levels of disulfide and IMA are high.

Keywords: Acute urticaria; ischemia-modified albumin; neutrophil lymphocyte ratio; oxidative stress; thiol-disulphide homeostasis.

Background: Among one of the common hereditary causes of chronic kidney disease is autosomal-dominant polycystic kidney disease (ADPKD), and its incidence rate is reported as one between 500 and 1.000 individuals. The most common complications of ADPKD are hypertension (HT) and end-stage renal disease (ESRD). HT occurring in the early stage of ADPKD leads to deteriorations in renal function.

Aims: It was aimed to investigate the ischemia-modified albumin (IMA) levels and the effect of renin-angiotensin-aldosterone system (RAAS) blockers on serum IMA levels in patients with ADPKD.

Methods: One hundred and fifteen patients were included as ADPKD (n = 50), HT (n = 35), and healthy control (HC) groups (n = 30). Patients with ADPKD and HT were divided into two subgroups as RAAS blocker-users and non-users.

Results: Serum IMA levels were detected as 0.42 (0.17-0.80) in ADPKD and 0.28 (0.04-0.51) in HT and 0.36 (0.22-0.56) in HC groups as absorbance units (ABSU), and the highest serum IMA level was seen in Group ADPKD. Serum IMA levels were 0.33 ± 0.14 in RAAS blocker-users and 0.41 ± 0.11 ABSU in non-users with ADPKD. Serum IMA levels were witnessed to be significantly lower in RAAS blocker-users in Groups ADPKD (p = 0.038) and HT (p = 0.004), compared to non-users. Given basal and 6-month values of those with ADPKD, the levels of serum IMA within 6 months were significantly lower (p = 0.002).

Conclusions: We consider that serum IM levels should be assessed in oxidative stress (OS)-related conditions, such as ADPKD, and RAAS blockers may be effective in reducing serum IMA levels in ADPKD and HT patients.

Keywords: Autosomal dominant polycystic kidney disease; Ischemia modified albumin; Oxidative stress; Renin–angiotensin–aldosterone blockade.

Purpose: Thiols are sulfhydryl-containing organic compounds that have an important role in preventing cellular oxidative stress. This study compares the blood oxidative stress marker levels in bronchiectasis cases during their stable periods with healthy controls.

Materials and methods: Seventy-seven patients (49 patients with stable bronchiectasis/28 healthy controls), followed up by the chest disease clinic, were included in the study. Peripheral blood thiol-disulfide parameters (NT: native thiol (-SH); TT: total thiol (-SH + SS); SS: disulfide (-SS); SS-SH: disulfide/native thiol index; SS-TT: disulphide/total thiol index; SH-TT: native thiol/total thiol index), and ischemia-modified albumin (IMA) levels were examined in the stable bronchiectasis group and the control group. Thiol-disulfide homeostasis was evaluated using a novel and automated assay. Findings and Result. Blood native thiol levels in patients with stable bronchiectasis were found to be significantly higher compared with healthy controls. A positive correlation between the total airway disease score and IMA levels was present. Our findings revealed that native thiol levels, which constitute a part of the antioxidant defense system, are increased in patients with stable bronchiectasis.

Objectives: In this study, our aim was to determine the differences between intrauterine growth restriction (IUGR) and normal birth weight fetuses in terms of ischemia modified albumin (IMA) levels. For this purpose, we measured ischemia modified albumin levels in the cord blood of fetuses and the mothers.

Material and methods: This study is a prospective study conducted at University of Health Sciences Tepecik Training and Research Hospital between January 2018 and December 2019. According to the inclusion/exclusion criteria, 227 patients were included in the study. Participants were divided into two groups according to the presence (patient group) or absence (control group) of intrauterine growth restriction (IUGR). In addition to routine parameters recorded during pregnancy, the IMA levels and Doppler USG findings of all participants were recorded.

Results: The mean cord blood serum IMA levels of the patient group were significantly elevated compared to controls (p = 0.038). Whereas mean maternal blood serum IMA levels were similar among groups (p = 0.453). The cord blood and mother blood serum IMA levels were not significantly different with regard to the presence or absence of perinatal asphyxia.

Conclusions: In the literature, studies evaluating IMA levels in the cord and maternal blood of IUGR fetuses are limited. In IUGR patients, IMA level is expected to increase and in our study, IMA levels were significantly increased but the presence of oxidative stress has not been found to affect IMA levels.

Keywords: asphyxia; cord blood; intrauterine growth restriction (IUGR); ischemia modified albumin (IMA); oxidative stress.

Introduction Primary myelofibrosis (PM) has a lower overall survival rate than other myeloproliferative neoplasms, and leukemic transformation is the most common cause of death. Increased oxidative stress has an important role in leukemic transformation in these patients. In this study, we aimed to find an answer to the question, "Could Ruxolitinib, which has been widely used in patients with myelofibrosis in recent years, have a role in reducing oxidative stress in these patients?". Methods A total of 106 patients with PM and 111 healthy volunteers were included in this study. We collected the serum samples of healthy volunteers and patients with myelofibrosis at the time of diagnosis and one month after the initiation of Ruxolitinib treatment. Ischemia modified albumin (IMA), native thiol, total thiol, and disulfide levels were studied. The disulfide/native thiol, disulfide/total thiol, and native thiol/total thiol ratios were calculated. Results IMA, native thiol, total thiol, disulfide levels, disulfide/native thiol, and disulfide/total thiol ratios at the time of diagnosis were significantly different in patients with myelofibrosis compared to the control group (p=0.001). Ruxolitinib significantly reduced oxidative stress when the measurements in the first month after Ruxolitinib were compared with those at the time of diagnosis (p=0.001). In patients with ASXL1 mutation, intermediate-2 risk, and high-risk according to the Dipps-plus score, the decrease in oxidative stress in the first month of treatment was more significant than at the time of diagnosis. Conclusion Ruxolitinib may be an effective treatment for reducing oxidative stress in patients with PM. The reduction in oxidative stress parameters with treatment in patients with ASXL1 mutation, intermediate-2, and high-risk patients was observed to be higher.

Keywords: disulfide; oxidative stress; primary myelofibrosis; ruxolitinib; thiol compounds.