Topiramate Reduces Aortic Cross-Clamping-Induced Lung Injury in Male Rats.

BACKGROUND: Topiramate (TPM) decreases cytokine release and generation of reactive oxygen species (ROS). Cytokine and endothelin-1 (ET-1) secretion and ROS formation play an important role in ischemia-reperfusion (I/R) injury. We aimed to evaluate whether TPM prevents damage occurring in lung tissue during I/R. MATERIALS AND METHODS: A total of 27 Wistar albino rats were divided into three groups of nine. To the I/R group, two hours of ischemia via infrarenal abdominal aorta cross-ligation and then two hours of reperfusion process were applied. TPM (100 mg/kg/day) orally for seven days was administered in the TPM treatment group. After the last dose of TPM treatment, respectively, two hours of ischemia and two hours of reperfusion were applied in this group. RESULTS: Tumor necrosis factor-alpha (TNF-α) (p < 0.05), malondialdehyde (MDA) (p < 0.05), myeloperoxidase (MPO) (p < 0.05) and ET-1 (p < 0.05) levels of TPM treatment group's lung tissue were significantly lower than for the I/R group. Caspase-3 and histopathological damage were rather lower than that of the I/R group. CONCLUSIONS: During I/R, lung damage occurs due to excessive TNF-α and ET-1 release and ROS generation. TPM could well reduce development of lung damage by decreasing cytokine and ET-1 release and levels of ROS produced.

Soluble Tumor Necrosis Factor (TNF)-Like Weak Inducer of Apoptosis (Tweak) Independently Predicts Subclinical Atherosclerosis in Behcet's Disease.

BACKGROUND: Vasculopathy is a major cause of mortality and morbidity in Behcet's Disease (BD). Subclinical atherosclerosis can even be detected in the early stage of BD. Soluble tumor necrosis factor-like (TNF) weak inducer of apoptosis (TWEAK) is known as a good marker of the inflammation in vascular tree. The aim of this study is to examine the relationship between carotid artery intima-media thickness (cIMT) and serum TWEAK levels in patients with BD. MATERIALS AND METHODS: In line with International BD Study Group criteria, 48 BD, and 30 controls were included in our study. Disease activity was evaluated according to BD current activity form (BDCAF). C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), lipid parameters, serum TWEAK levels, and cIMT were measured. RESULTS: Disease activity score of BD patients was found as 2 (range 0-7). cIMT, serum TWEAK, CRP and ESR levels of BD patients were significantly higher comparing to cIMT (0.62 ± 0.13 mm vs. 0.43 ± 0.09 mm, p < 0.001), serum TWEAK (667.5 ± 130.6 vs. 603.4 ± 89.6 pg/ml, p = 0.015), CRP (3.9 ± 4.3 vs. 1.4 ± 1.0 mg/dl, p < 0.001) and ESR (10.2 ± 10.0 vs. 5.6 ± 3.7 mm/h, p = 0.005) levels of the control group. There was a positive correlation between serum TWEAK level and disease activity (r = 0.251, p = 0.030) and cIMT (r = 0.463, p < 0.001). Our study also revealed an independent correlation between cIMT and serum TWEAK levels (beta = 0.354, p < 0.001). CONCLUSION: Increased serum TWEAK levels can play a part in the development of atherosclerotic heart disease in BD. Due to their liability to atherosclerosis, patients with BD must followed closely.

Alteration of maternal serum irisin levels in gestational diabetes mellitus.

OBJECTIVES: The aim of our study was to compare serum irisin concentrations in pregnant women with and without ges-tational diabetes mellitus (GDM). MATERIAL AND METHODS: This study was performed at the Tertiary Care Center, Department of Obstetrics and Gynecol-ogy, between January 2014 and April 2014. A total of 45 pregnant women with GDM (diabetes group) and 41 BMI- and age-matched healthy pregnant women (control group) were recruited. Maternal serum irisin levels were measured by enzyme-linked immunosorbent assay kit at 24-28 weeks of gestation. An association between maternal serum irisin lev-els and metabolic parameters was analyzed. Body mass index, serum levels of glucose, insulin and irisin were tested and analyzed in the study group and controls. RESULTS: Pregnant women with GDM had significantly higher fasting plasma glucose (p = 0.001), first-hour OGTT glucose (p = 0.001), second-hour OGTT glucose (p = 0.001), and fasting insulin (p = 0.045) levels as compared to controls. Serum irisin levels were 1.04 ± 0.3 and 1.3 ± 0.2 in pregnant women with GDM and healthy pregnant controls, respectively (p = 0.001). Correlation analysis between irisin levels and anthropometric and biochemical parameters in patients with gestational diabetes revealed that none of the investigated parameters correlated with serum irisin level. CONCLUSIONS: Our results suggest that serum irisin levels might be introduced as a novel marker for GDM, with decreased levels of irisin being indicative of GDM.

Serum fibronectin levels in acute and chronic viral hepatitis patients.

BACKGROUND: The aim of this study was to investigate the serum fibronectin (FN) levels and liver enzyme activities in patients with acute hepatitis (A, B, C) and chronic viral hepatitis (B, C); determine whether the virus types correlated with disease severity; and assess whether FN could be used as a marker of virus type or disease severity in patients. METHODS: A total of 60 subjects were enrolled in the study, including 20 patients with acute hepatitis (A, B, C), 20 with chronic hepatitis (B, C), and 20 healthy controls. Serum fibronectin (FN), aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase (GGT), and albumin were measured in all patients from blood samples. RESULTS: Serum FN levels were significantly lower in acute (122.9 µg/mL (SD 43.1), P < 0.001) and chronic hepatitis patients (135.7 µg/mL (SD 46.0), P < 0 .001) compared to controls 221.4 µg/mL (SD 32.5). A negative correlation was found between serum FN and AST (r(2) = 0.528, P < 0.001), ALT (r(2) = 0.425, P < 0.001), and GGT (r(2) = 0.339, P < 0.001). Additionally, high serum GGT levels (ß = -0.375, P = 0.010), and low serum albumin levels (ß = -0.305, P = 0.008) were associated with low serum FN levels. CONCLUSION: Serum FN levels were lower in both acute and chronic hepatitis patients, and an inverse relationship between serum FN and serum AST, ALT, and GGT levels was found. A decrease in serum FN levels may indicate hepatitis severity as AST and ALT represent hepatocyte damage.

Assessment of peripapillary retinal nerve fiber layer thickness in children with vitamin B12 deficiency.

PURPOSE: Vitamin B(12) deficiency is a worldwide problem. It affects all ages, including children. It is one of the most common nutritional disorders and can cause harmful effects on the nervous system. In this study, we compared the peripapillary retinal nerve fiber layer thickness (RNFLT) in a healthy control group with children with vitamin B(12) deficiency. In our study, we aimed to evaluate the effect of vitamin B(12) deficiency on the RNFLT in children with the optical coherence tomography (OCT) method. METHODS: Sixty-six children with a diagnosis of vitamin B(12) deficiency (patient group) and 66 age- and sex-matched healthy children (control group) were enrolled in this prospectively designed study. Blood counts, vitamin B(12) levels, folate levels, and full biochemical parameters were obtained for all the subjects in each group. Peripapillary RNFLT measurements were performed with Cirrus HD spectral domain OCT. RESULTS: The thickness of the superior retinal nerve fiber layer (RNFL) in the vitamin B(12) deficiency group was significantly lower than that of the control group (p = 0.037). Although the average thickness of the RNFL was lower in the patient group, there was no statistically significant differences (p = 0.216). In the vitamin B(12) deficiency group, the average RNFL thickness and the superior RNFL thickness were significantly correlated with vitamin B(12) levels ((r1) = 0.353, (p1) < 0.004 and (r2) = 0.416, (p2) = 0.001, respectively). CONCLUSION: Our study showed that a deficiency in vitamin B(12), elsewhere it is important for the development of the central nervous system, is associated with a reduction in the thickness of the superior RNFL.

The protective effect of adrenomedullin on renal injury, in a model of abdominal aorta cross-clamping.

Renal injury induced by aortic ischemia-reperfusion (IR) is an important factor in the development of postoperative acute renal failure following abdominal aortic surgery. The aim of this study was to examine the effect of adrenomedullin (AM) on kidney injury induced by infrarenal abdominal aortic IR in rats. Thirty-two Wistar Albino rats were randomized into four groups (eight per group) as follows: Control group, IR group (120-minute ischemia and 120-minute reperfusion), IR + AM group (a bolus intravenously of 0.05 µg/kg/min AM), and control + AM group. At the end of the experiment, blood and kidney tissue specimens were obtained for biochemical analysis. Immunohistological evaluation of the rat kidney tissues was also done. IR significantly increased (p < 0.05 vs control group) and AM significantly decreased (p < 0.05 vs. IR group) all of the biochemical parameters. Immunohistological evaluation showed that AM attenuated morphological changes as apoptosis associated with kidney injury. The results of this study indicate that AM attenuates both biochemically and immunohistopathologically kidney injury induced by aortic IR in rats.

Prolonged NHE Activation may be both Cause and Outcome of Cytokine Release Syndrome in COVID-19.

The release of cytokines and chemokines such as IL-1ß, IL-2, IL-6, IL-7, IL-10, TNF-α, IFN-γ, CCL2, CCL3, and CXCL10 is increased in critically ill patients with COVID-19. Excessive cytokine release during COVID-19 is related to increased morbidity and mortality. Several mechanisms are put forward for cytokine release syndrome during COVID-19. Here we have mentioned novel pathways. SARS-CoV-2 increases angiotensin II levels by rendering ACE2 nonfunctional. Angiotensin II causes cytokine release via AT1 and AT2 receptors. Moreover, angiotensin II potently stimulates the Na+/H+ exchanger (NHE). It is a pump found in the membranes of many cells that pumps Na+ inward and H+ outward. NHE has nine isoforms. NHE1 is the most common isoform found in endothelial cells and many cells. NHE is involved in keeping the intracellular pH within physiological limits. When the intracellular pH is acidic, NHE is activated, bringing the intracellular pH to physiological levels, ending its activity. Sustained NHE activity is highly pathological and causes many problems. Prolonged NHE activation in COVID-19 may cause a decrease in intracellular pH through H+ ion accumulation in the extracellular area and subsequent redox reactions. The activation reduces the intracellular K+ concentration and leads to Na+ and Ca2+ overload. Increased ROS can cause intense cytokine release by stimulating NF-κB and NLRP3 inflammasomes. Cytokines also cause overstimulation of NHE. As the intracellular pH decreases, SARS-CoV-2 rapidly infects new cells, increasing the viral load. This vicious circle increases morbidity and mortality in patients with COVID-19. On the other hand, SARS-CoV-2 interaction with NHE3 in intestinal tissue is different from other tissues. SARS-CoV-2 can trigger CRS via NHE3 inhibition by disrupting the intestinal microbiota. This review aimed to help develop new treatment models against SARS-CoV-2- induced CRS by revealing the possible effects of SARS-CoV-2 on the NHE.

Effects of venlafaxine and escitalopram treatments on NMDA receptors in the rat depression model.

Depression may relate to neurocognitive impairment that results from alteration of N-methyl-D: -aspartate receptor (NMDAR) levels. Venlafaxine and escitalopram are two drugs commonly used to treat depression. The drugs may affect expression of NMDARs, which mediate learning and memory formation. The aim of the study was to examine whether the effects of venlafaxine and escitalopram treatments are associated with NMDARs in a rat model of depression. Forty male Wistar albino rats were randomly divided into four groups (n = 10) as follows: control group, chronic mild stress group (CMS), venlafaxine (20 mg/kg body weight per day) + CMS, and escitalopram (10 mg/kg body weight per day) + CMS. After induction of depression, a decrease in the concentration of NR2B was observed; venlafaxine treatment prevented the reduction of NR2B expression. Escitalopram treatment did not effect the reduced levels of NR2B resulting from depression. There was no significant difference in NR2A concentration among groups. The present data support the notion that venlafaxine plays a role in maintaining NR2B receptor in experimental depression. It may be possible that treatment with escitalopram has no effect on NMDARs in experimental depression.

Can emapalumab be life saving for refractory, recurrent, and progressive cytokine storm caused by COVID-19, which is resistant to anakinra, tocilizumab, and Janus kinase inhibitors.

Although many potent drugs have been used for cytokine storm, mortality is high for patients with coronavirus disease-2019 (COVID-19), which is followed up in the intensive care unit. Interferons (IFNs) are the major cytokines of the antiviral defense system released from many cell types. However, IFN-γ plays a key role in both primary and secondary cytokine storms. If the cytokine storm is not treated urgently, it will be fatal; therefore, it should be treated immediately. Anakinra, an interleukin-1 (IL-1) antagonist, tocilizumab, an IL-6 antagonist, and Janus kinase (JAK) inhibitors are successfully used in cytokine storm caused by COVID-19. However, sometimes, despite these treatments, the patient's clinical course does not improve. Emapalumab (Eb) is the human immunoglobulin G1 monoclonal antibody and is a potent and noncompetitive antagonist of IFN-γ. Eb can be life saving for cytokine storm caused by COVID-19, which is resistant to anakinra, tocilizumab, and JAK inhibitors.

Could ferritin, vitamin B12, and vitamin D play a role in the etiopathogenesis of fibromyalgia syndrome?

Introduction. Fibromyalgia syndrome (FS) comprises general body pain, sleep disturbances, and fatigue. Vitamin B12 (VB), vitamin D (VD), and iron deficiencies lead to similar complaints. First, this study aimed to evaluate the VB, VD, and ferritin levels of patients with FS. Second, it aimed to investigate whether there was a relationship between these parameters and FS severity. Material and methods. The study included 58 female patients with FS and 58 healthy females as a control group. The patients completed the Fibromyalgia Impact Questionnaire (FIQ), Visual Analog Scale (VAS), fatigue questionnaire, Pittsburgh sleep quality scale, and the Short Form-36 (SF-36). This study examined the VD, VB, and ferritin levels of the patient and control groups. Results. The VB (240.0 [110.0-394.0] vs 291.0 [210.0-609.0] pg/ml, p<0.001), VD (12.5 [3.0-45.0] vs 20.0 [5.0-54.0] ng/ml, p=0.013), and ferritin levels (21.2 [4.0-86.0] vs 32.0 [7.1-120.0], ng/ml, p=0.009) of the FS patients were determined to be significantly lower than those of the control group. A negative correlation was determined between the number of tender points and VB, VD, and ferritin levels. In the regression analysis, we found low ferritin levels (odds ratio [OR] 1.036, 95% confidence interval [CI] 1.015-1.058, p<0.001) and VB (OR 1.010, CI 1.002-1.018, p=0.010) to be an independent risk factor for FS. Conclusions. There may be a relationship between VB, VD, and ferritin levels and the number of tender points in patients with FS. Levels of iron and VB may play a vital role in FS etiopathogenesis. However, VD levels may not be a risk factor for FS etiopathogenesis.

Monocyte to Lymphocyte Ratio, Neutrophil to Lymphocyte Ratio, and Red Cell Distribution Width are the Associates with Gouty Arthritis.

BACKGROUND: Neutrophils, monocytes, and macrophages activations are associated with a gout attack. Monocyte to lymphocyte ratio (MLR), neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), red cell distribution width (RDW), and mean platelet volume (MPV) are well-known inflammation markers. In this study, we aimed to investigate whether they could be a predictive marker to the gout attack. MATERIAL AND METHODS: A hundred and ten gout patients (male/female, 86/24) and 90 (male/female, 64/26) age-, gender-, and body mass index-matched volunteer controls were included in the study. Blood samples were obtained in the intercritical and attack period of the patients. Hemogram, serum uric acid (SUA), C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) values were studied. RESULTS: In the attack period NLR (p < 0.001), PLR (p < 0.05), MLR (p < 0.001), RDW (p < 0.05), MPV (p < 0.05), ESR (p < 0.001), CRP (p < 0.001) and SUA (p < 0.001) values were significantly higher than intercritical period values. According to the results of regression analysis; There was an independent strong relationship between the gout attack and SUA, (Beta [ß] = 0.352, p < 0.001), ESR (ß = 0.329, p < 0.001), CRP (ß = 0.286, p < 0.001), MLR (ß = 0.126, p < 0.001), RDW (ß = 0.100, p = 0.003) and NLR (ß = 0.082, p = 0.014). CONCLUSIONS: MLR, RDW, and NLR may be a strong predictive marker for a gout attack. MPV and PLR values in the gout attack may be associated with systemic inflammation.

Evaluation of serum thiol/disulfide homeostasis in patients with ankylosing spondylitis by a novel method.

OBJECTIVE: Increased reactive oxygen species may play an important role in Ankylosing spondylitis (AS) etiopathogenesis. The thiol group is a very potent antioxidant. In this study, we aimed to investigate the presence of oxidative stress in patients with AS by evaluating thiol/disulfide homeostasis. METHODS: In this study, a total of 66 AS patients (27 male, 39 female) and 66 healthy controls (21 male, 45 female) were enrolled. Recently, a novel method for the thiol measurement was found. Thiol and disulfide values were measured by the novel methods. RESULTS: Native thiol (NT) (p<0.001) and native thiol/total thiol (NTT) (p<0.001) levels of AS patients were significantly lower compared to the values of the healthy group. However, disulfide (p<0.001), disulfide/native thiol (DNT) (p<0.001) and disulfide/total thiol (DTT) levels of AS patients were a strongly higher control group. A negative correlation was found between BASFI and NTT. Also, a negative correlation was found between BASDAI and NT, NTT levels. A positive correlation was found between BASFI and disulfide, DNT and DTT levels. A positive correlation was found between BASDAI and disulfide, DNT and DTT levels. CONCLUSION: The findings revealed that thiol-disulfide homeostasis deteriorated in patients with AS in favor of disulfide amounts. Thiol-disulfide homeostasis can play roles in the etiology and severity of AS.

Thiol/Disulfide homeostasis in patients with rheumatoid arthritis.

BACKGROUND: Oxidative stress may play an important role in rheumatoid arthritis (RA) etiopathogenesis. The thiol group is a very strong antioxidant. In this study, we aimed to investigate the presence of oxidative stress in patients with RA by evaluating thiol/disulfide homeostasis. MATERIAL AND METHODS: A total of 50 female RA patients and 50 healthy female controls were included in this study. Thiol and disulfide values were calculated utilizing novel methods. RESULTS: Native thiol (p < 0.001) and total thiol (p < 0.001) levels of RA patients were significantly lower compared to values in the control group. However, the disulfide (p < 0.001) levels of RA patients were strongly higher than in healthy individuals. A negative correlation was found between thiol and disease activity score-28 among the patients, whereas a positive correlation was found between disulfide and disease activity score-28 among the patients. CONCLUSION: We found that the thiol-disulfide rate deteriorated in RA patients, with the proportion of disulfide increasing. There is a strong correlation between the decrease in thiol levels, increase in disulfide levels and the disease activity scores.

Alteration of Thiol-Disulfide Homeostasis in Fibromyalgia Syndrome.

BACKGROUND: Fibromyalgia syndrome (FMS) is an extra-articular rheumatological disease, characterized by widespread pain and somatic symptoms. The etiology has not yet been clarified. Oxidative stress may play an important role in FMS etiology. Thiol group is a very strong antioxidant. We aimed to investigate whether thiol/disulfide homeostasis in FMS is altered or not. MATERIAL AND METHODS: A total of 80 female FMS patients and 64 healthy female control individuals were included in this study. Thiol and disulfide values were measured by Erel's novel methods. RESULTS: Native thiol (330.6 ± 46.1 vs. 356.8 ± 55.5 µmol/L, p = 0.005) and native thiol/total thiol (89.4 ± 3.2 vs. 93.3 ± 4.0, p < 0.001) levels of FMS patients were significantly lower when compared to the values of control group. However, disulfide (19.4 ± 6.3 vs. 12.2 ± 6.3 µmol/L, p < 0.001) levels of FMS patients were significantly higher than healthy individuals. A negative correlation was found between the native thiol/total thiol and fibromyalgia impact questionnaire (FIQ) score among the FMS patients. A positive correlation was found between disulfide values and FIQ score among the patients. CONCLUSIONS: In FMS patients, there was a significant correlation between the decrease in the thiol levels and an increase in the disulfide levels with the FIQ scores. We determined that thiol-disulfide rate was deteriorated in FMS patients and it increases in favor of disulfide amounts.

Atherogenic index of plasma: a useful marker for subclinical atherosclerosis in ankylosing spondylitis : AIP associate with cIMT in AS.

Ankylosing spondylitis (AS) is associated with an increased risk of atherosclerotic cardiovascular disease (ACD). The atherogenic index of plasma (AIP), which is the logarithmic transformation of the plasma triglyceride (TG) level to the high-density lipoprotein level (HDL) ratio, has been suggested to be a novel marker in the identification of atherosclerosis risk. Therefore, this study aims to determine if the AIP can act as an accurate marker for the detection of subclinical atherosclerosis. Fifty-two male patients with AS and 52 age-, gender-, and body mass index (BMI)-matched healthy control subjects were included in the study. For each patient, AIP and total cholesterol (TC)/HDL values were calculated and carotid artery intima-media thickness (cIMT) was measured. The mean (SD) cIMT and median (range) AIP values for AS patients were higher than that of the healthy control subjects (0.60 ± 0.18 vs. 0.51 ± 0.10, p = 0.003 and 0.23 [- 0.32 to 0.85] vs. 0.09 [- 0.53 to 0.49], p = 0.007, respectively). A positive correlation was found between the patients' cIMT and AIP values (r = 0.307, p = 0.002) and TC/HDL values (r = 0.241, p = 0.014). Regression analysis revealed an independent association between the subclinical atherosclerosis and AIP (beta [ß] = 0.309, p = 0.002). There were no independent correlations between subclinical atherosclerosis and TC (ß = 0.245, p = 0.065), TG (ß = 0.185, p = 0.515), HDL (ß = 0.198, p = 0.231), TC/HDL (ß = 0.032, p = 0.862), and low-density lipoprotein (LDL) (ß = 0.151, p = 0.246). A strong and independent correlation exists between AIP and cIMT values. Therefore, the AIP could serve as a better marker than the TC/HDL ratio for the detection of subclinical atherosclerosis in AS patients.

The Relationship Between Atherogenic Index and Carotid Artery Atherosclerosis in Familial Mediterranean Fever.

Familial Mediterranean fever (FMF) is a disease characterized by chronic inflammation. Atherogenic index of plasma (AIP) is a logarithmic value of the triglyceride to high-density lipoprotein cholesterol ratio and it is a good marker for atherosclerotic heart disease and cardiac risk. In this study, we investigated subclinical atherosclerosis and cardiac risks in patients with FMF. Patients with FMF (78 men and 84 women) and healthy controls (74 men and 82 women) were included in this study. The AIP values of the patients were calculated and carotid intima-media thicknesses (cIMTs) were measured. The cIMT ( P < .001) and AIP ( P < .001) values of patients with FMF were higher than the values of the control group. There was a positive correlation between cIMT and AIP values ( r = .304, P < .001). In regression analysis, we detected an independent relationship between cIMT and AIP (ß = .248, P = .001). Atherogenic index of plasma may be highly correlated with the subclinical atherosclerosis. Particularly, male patients with FMF may have a high cardiac risk.

Relationship of serum osteoprotegerin with arterial stiffness, preclinical atherosclerosis, and disease activity in patients with ankylosing spondylitis.

Patients with ankylosing spondylitis (AS) reportedly have a higher mortality and morbidity risk. Osteoprotegerin (OPG) was recently defined as an important cardiovascular (CV) marker in the general population. We aimed to assess the relationship of serum OPG levels with arterial stiffness, carotid intima media thickness (CIMT), and clinical and laboratory data in AS patients. We examined 60 AS patients without CV disease or risk factors and 50 healthy controls. Disease activity was evaluated using the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and the Ankylosing Spondylitis Disease Activity Score (ASDAS), whereas functional capacity was evaluated using the Bath Ankylosing Spondylitis Functional Index (BASFI). Serum OPG levels were measured with the enzyme-linked immunosorbent assay. Carotid-femoral pulse wave velocity (PWV) was used as an indicator of arterial stiffness, whereas CIMT (examined via carotid ultrasonography) was used to evaluate preclinical atherosclerosis. The mean serum OPG level, PWV, and CIMT were significantly higher in AS patients than in controls (106.7 ± 50.9 vs. 58.1 ± 12.7 pg/mL; 7.4 ± 1.8 vs. 6.2 ± 1.2 m/s; 0.72 ± 0.13 vs. 0.57 ± 0.07 mm, respectively; P < 0.001 for all). In AS patients, the serum OPG levels were not significantly correlated with PWV and CIMT but were significantly correlated with erthrocyte sedimentation rate, BASFI, and ASDAS. AS patients without CV disease or risk exhibited high OPG levels and increased PWV and CIMT values. Although OPG levels were not significantly correlated with PWV or CIMT, future long-term follow-up studies will help define the predictive value of OPG in these patients.

Relationship between site of myocardial infarction, left ventricular function and cytokine levels in patients undergoing coronary artery surgery.

BACKGROUND: The purpose of this study was to examine the relationship between left ventricular (LV) function, cytokine levels and site of myocardial infarction (MI) in patients undergoing coronary artery bypass grafting (CABG). METHODS: Sixty patients undergoing CABG were divided into three groups (n = 20) according to their history of site of myocardial infarction (MI): no previous MI, anterior MI and posterior/inferior MI. In the pre-operative period, detailed analysis of LV function was done by transthoracic echocardiography. The levels of adrenomedullin, interleukin-1-beta, interleukin-6, tumour necrosis factor-alpha (TNF-α) and angiotensin-II in both peripheral blood samples and pericardial fluid were also measured. RESULTS: Echocardiographic analyses showed that the anterior MI group had significantly worse LV function than both the group with no previous MI and the posterior/inferior MI group (p < 0.05 for LV end-systolic diameter, fractional shortening, LV end-systolic volume, LV end-systolic volume index and ejection fraction). In the anterior MI group, both plasma and pericardial fluid levels of adrenomedullin and and pericardial fluid levels of interleukin-6 and interleukin- 1-beta were significantly higher than those in the group with no previous MI (p < 0.05), and pericardial fluid levels of adrenomedullin, interleukin-6 and interleukin-1-beta were significantly higher than those in the posterior/inferior MI group (p < 0.05). CONCLUSIONS: The results of this study indicate that (1) patients with an anterior MI had worse LV function than patients with no previous MI and those with a posterior/inferior MI, and (2) cytokine levels in the plasma and pericardial fluid in patients with anterior MI were increased compared to patients with no previous MI.