Background Osteoporosis 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). Objectives The aim of this study was to determine IMA levels of patient with osteoporosis. Methods OP 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. Results The 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). Conclusion Cobalt 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 status and relation to bone mineral density in osteoporosis. Rheumatology international. 2008;28(4):317-21. [2] Korkmaz V, Kurdoglu Z, Alisik M, Turgut E, Sezgin OO, Korkmaz H, et al. Thiol/disulfide homeostasis in postmenopausal osteoporosis. Journal of endocrinological investigation. 2017;40(4):431-5. [3] Ellidag HY, Eren E, Yilmaz N, Cekin Y. Oxidative stress and ischemia-modified albumin in chronic ischemic heart failure. Redox report : communications in free radical research. 2014;19(3):118-23. [4] Bar-Or D, Lau E, Winkler JV. A novel assay for cobalt-albumin binding and its potential as a marker for myocardial ischemia-a preliminary report. The Journal of emergency medicine. 2000;19(4):311-5. Disclosure of Interests None declared

Fibromyalgia syndrome (FMS) is a multifactorial condition characterized by chronic widespread pain, fatigue, and sleep disturbances, often accompanied by biochemical and psychosocial alterations. Sleep quality plays a critical role in disease severity and patient functionality. Recent evidence suggests that magnesium may influence both pain and sleep regulation. This observational cross-sectional study aimed to investigate the relationship between sleep quality and serum magnesium levels in patients with FMS and to explore their associations with clinical characteristics such as pain severity and functional status. Eighty-two patients diagnosed with FMS were grouped based on their Pittsburgh Sleep Quality Index (PSQI) scores: PSQI ≤ 5 (n = 27) and PSQI > 5 (n = 55). Demographic and clinical parameters, including age, body mass index, tender points, Fibromyalgia Impact Questionnaire (FIQ), and serum magnesium levels, were compared between the groups. Correlation analyses were performed to assess associations between magnesium levels and clinical variables. No significant differences were found between the groups in terms of age and body mass index (P > .05 for all). The PSQI > 5 group demonstrated significantly higher tender points (P = .035), visual analog scale scores (P = .002), FIQ scores (P < .001), and lower serum magnesium levels (P = .038) compared to the PSQI ≤ 5 group. Significant negative correlations were observed between magnesium levels and tender points (ρ = −0.293, P = .008), visual analog scale score (ρ = −0.252, P = .023), FIQ scores (ρ = −0.242, P = .028), PSQI scores (ρ = −0.324, P = .003). The findings indicate that lower serum magnesium levels are associated with poorer sleep quality, higher pain severity, and greater functional impairment in patients with FMS. These findings suggest a potential link between magnesium levels and the pathophysiology of sleep disturbances in FMS. However, due to the cross-sectional nature of the study and possible confounding influences, further longitudinal and interventional research is required to determine whether magnesium supplementation could offer clinical benefits in this population.