Background:The aim of this study is to evaluate dysfunctional high-density lipoprotein cholesterol (HDL) by measuring myeloperoxidase (MPO)/paraoxonase 1 (PON1) ratio in patients with rheumatoid arthritis (RA) and to investigate the relationship between dysfunctional HDL and cardiovascular disease (CVD) in RA patients.Methods: Sixty-seven healthy individuals and 130 RA patients were included in the study. Routine lipid panels (triglyceride (TG), low-density lipoprotein cholesterol (LDL), HDL, total cholesterol (TC), PON1 and MPO levels were measured. Disease activity scores-28 (DAS28) of RA patients were calculated. Cardiological examination records of the patients were assessed to detect patients who also have CVD.Results: There were no significant differences between RA and control groups in routine lipid profiles (P > .05 for all). MPO/PON1 ratios were significantly elevated in the RA group compared with the control group (P < .001). MPO/PON1 ratios were higher in RA patients with CVD history compared with those without CVD (P < .05).MPO/PON1 ratios were correlated with DAS28 scores (rho: 0.357, P < .001). Conclusion:HDL dysfunction determined by the MPO/PON1 ratio may be associated with the pathophysiology of increased CVD in RA. Thus, evaluating dysfunctional HDL levels by measuring the MPO/PON1 ratio in RA patients may allow more detailed patient follow-up, as well as the reduction of CVD events in RA patients with therapeutic agents aiming to increase the functional properties of HDL by decreasing this ratio.

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BackgroundOsteoporosis is a common bone metabolism disease, characterized by low bone mass and pathological fractures. This disease is caused by loss of balance in bone resorption and formation. It is thought that this imbalance is associated with increasing in reactive oxygen species (ROS) and/or insufficiency of antioxidant defense (1). ROS adversely affect the formation and life cycle of osteoclasts, osteoblasts and osteocytes (2).Albumin has many functions such as the transport of molecules, the oncotic pressure of plasma and antioxidation. The damage of the ROS to the N-terminal of the albumin reduces the carrying capacity of the albumin and thus the antioxidant capacity. This damage is evaluated by decreasing the cobalt binding capacity of albumin called ischemia modified albumin (IMA), and IMA shows oxidative damage (3).ObjectivesThe aim of this study was to determine IMA levels of patient with osteoporosis.MethodsOP was diagnosed by t score of bone mineral density (BMD). IMA, albumin levels and IMA/Albumin ratio (IMAR) were studied from the sera of patients with osteoporosis (OP) and healthy volunteers (control) (4). Patients who had any chronic disease such as diabetes mellitus, hypertension, and etc. and any acute disease such as infection were excluded from study. Results were shown as mean ± standard deviation or median (IQR) according to the distribution of variables. p<0.05 was considered significant.ResultsThe study included 28 female patients in OP group and 26 female volunteer in control groups. The mean age was 65.5 ± 5.4 and 66.4 ± 7.4 for OP and control groups, respectively (p:0.616). Median (IQR) lumbar t scores of BMD of OP group were -3.1 (-3.32; -2.85). The albumin values of OP and control groups were 4.38 ± 0.13 and 4.40 ± 0.11, respectively; and no significant difference was found between the groups (p = 0.441). The IMA and IMAR results of the OP group were 0.65 (0.61; 0.74) and 0.15 (0.14; 0.17), respectively; and 0.46 (0.40, 0.55), and 11 (0.09; 0.13) in the control group, respectively. (Figure 1). Both IMA and IMAR results were significantly lower in the OP group than in the control group (high ABSU) (p <0.001; for all).ConclusionCobalt binding capacity of albumin was decreased in patients with osteoporosis. To the best of our knowledge, this study is the first determining IMA levels in osteoporosis. It is known that the cobalt binding capacity of albumin decreased after oxidative damage. It is shown that IMA is increased in some diseases associated with oxidative stress. Similarly, it was showed that thiol-disulphide balance was shifted to disulphide side in postmenopausal osteoporosis and it was an indicator of oxidative stress (1, 2). In the light of these results, oxidative stress is thought to play role in the pathophysiology of osteoporosis. As a result, antioxidant replacement such as N-acetyl cysteine, lipoic acid, vitamin C, etc. may be recommended to the patients with osteoporosis.References[1] Altindag O, Erel O, Soran N, Celik H, Selek S. Total oxidative/anti-oxidative stat...

Myofascial pain syndrome (MPS) is a regional pain syndrome characterised by the presence of trigger points in the muscle or fascia.One of the most important causes of neck and shoulder pain are the trigger points in the trapezius muscle. Myofascial trigger points (MTPs), characterised by hypersensitive nodules, can be palpated in stretched bands in the affected muscles. 1 Compared to other muscles, the trapezius is the muscle with the highest incidence of MPS and its symptoms can affect the entire neck and shoulder region. The prevalence of MPS caused by trigger points varies between 30% and 85%. 2The etiopathogenesis has not been fully elucidated, but it is considered that neuromuscular junction or motor endplate activity is altered, and the sensitisation process develops in central and peripheral nerves. 3 MPS causes muscle spasm, stiffness, referring pain and

Background & Objective: To evaluate the relationship between the clinical outcome of subacute stroke patients and extracellular thiol-disulphide (SH-SS) and intracellular oxidized-reduced glutathione (GSSG-GSH) homeostasis and the effect of the rehabilitation program on these homeostasis. Methods: In this prospective observational study, outcome assessments (National Institutes of Health Stroke Scale Scores (NIHSS), modified Rankin Scale (mRS), and Barthel Daily Living Activities Index (BI)) and SH-SS and GSSG-GSH homeostasis parameters were investigated from 42 patients with subacute stroke before and after 4-week rehabilitation treatment protocol. Also, SH-SS and GSSG-GSH homeostasis parameters were measured from 35 healthy volunteers. Results: SS/SH and GSSG/GSH ratios were significantly higher in the patient group at baseline and post-rehabilitation than the control group (p<0.05). SS/SH ratio, GSSG/GSH ratio, NIHSS and mRS values significantly decreased with the rehabilitation (p<0.05). The baseline SS/SH and GSSG/GSH ratios were correlated with baseline and post-rehabilitation NIHSS, mRS and BI scores (p<0.05). Conclusions: The better outcomes of patients with higher baseline antioxidant thiol groups suggest that active thiol groups may play a role in achieving better outcomes in subacute stroke. In addition, rehabilitation treatment increased clinical scores and additionally shifted intracellular and extracellular thiol groups to the antioxidant side.