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Background/Aim: Anti-epileptic drugs are long-term medications; thus, side-effects are frequently seen. An important but insufficiently known side-effect is the emergence of metabolic bone diseases. The mechanism of this entity is not clearly known, but it is usually seen with the use of cytochrome P450 enzyme-inducing anti-epileptics. However, recent studies demonstrated that non-enzyme-inducing molecules also cause bone mineral impairment. The aim of this study was to shed light on the pathogenesis of anti-epileptic metabolic bone disease using bone turnover markers. Methods: This comparative, prospective case-control study included 37 patients followed-up in our outpatient clinic and 39 healthy control subjects. All the patients were female, aged over 18 years and in the premenopausal period, and had received the same anti-epileptic treatment for at least 3 months. Male patients, females who were <18 years old, pregnant, in the postmenopausal period, those with osteoporosis, gastrointestinal malabsorption, physical impairment that may prevent normal ambulation, endocrine and metabolic disease, musculoskeletal and joint disease or a history of medication use were excluded from the study. A healthy control group was formed of age-matched premenopausal women, with no disorders causing gastrointestinal malabsorption, no physical impairment preventing normal ambulation, no endocrine or metabolic disorder, or history of medication use that may affect bone turnover. The levels of serum calcium, alkaline phosphatase, 25-hydroxyvitamin D, osteoprotegerin and bone-specific alkaline phosphatase were assessed, and the results were recorded. Results: Evaluation was made of 37 female epilepsy patients with a mean age of 30.8 (8.1) years and a healthy control group of 39 age- and body mass index-matched females (P=0.69, P=0.85, respectively). The mean duration of AED use was 6.1 (5.5) years. The calcium (P=0.09), phosphate (P=0.906) and alkaline phosphatase (P=0.22) levels were similar in both groups. The levels of 25-hydroxyvitamin D (P=0.049), osteoprotegerin (P=0.025), and bone- specific alkaline phosphatase (P=0.037) were significantly lower in the epilepsy group. Conclusion: Our study showed that serum levels of osteoprotegerin and bone-specific alkaline phosphatase, which are markers of increased bone formation, were lower in epilepsy patients. Probably many factors cause the bone mineral disorder seen in epilepsy patients. Antiepileptic use is one of them. These results suggest that antiepileptics may not only affect enzyme induction but also bone turnover. Neurologists should be aware of this issue and monitor patients regularly with respect to bone mineralization to enable early treatment when necessary. [ABSTRACT FROM AUTHOR]

Purpose: Preeclampsia is a form of hypertensive disorders of pregnancy and defined as the presence of new-onset hypertension and proteinuria or other end organ damage occurring after 20-week gestation. Preeclampsia can be a destructive process that can cause maternal and infant mortality. The exact etiopathogenesis of preeclampsia is still undefined. We aimed to compare serum amphiregulin and cerebellin-1 levels of severe preeclampsia patients with healthy pregnant women and healthy control subjects.Materials and Methods: A total of 88 women were enrolled in this study. Patients diagnosed with severe preeclampsia were group 1 (n = 28), healthy non-pregnant normotensive women group 2 (n = 30), and healthy pregnant women group 3 (n = 30). The participants in each group were matched for age. Pregnant women in groups 1 and 3 were also matched for gestational age. Serum amphiregulin and cerebellin-1 levels were measured using ELISA.Results: Serum amphiregulin levels were 3413 ± 1.38 ng/ml (1748-7739), 8510 ± 7213 ng/ml (2019-24,000), and 6580 ± 5360 ng/ml (2484-24,000) in preeclampsia patients, controls and healthy pregnant women, respectively. Amphiregulin levels were significantly lower in preeclampsia patients than healthy pregnant women (p=.008) and controls (p = .015). Amphiregulin levels were similar between healthy controls and healthy pregnant women (p  =  1.00). Cerebellin-1 levels were 222.039 ± 92.681 pg/ml (138,580-557,757) in preeclamptic patients, 537.043 ± 525.117 pg/ml (150,432-1,600,000) in controls and 415.091 ± 436.580 pg/ml (137,284-1,600,000) in healthy pregnant women. Cerebellin-1 levels were similar among groups (p = .272). Serum amphiregulin and cerebellin-1 levels were significantly and positively correlated with each other in preeclampsia patients (r  =  0.693, p < .001), controls (r  =  0.882, p < .001), and healthy pregnant women (r  =  0.591, p = .001). Serum level of amphiregulin ≤3590 pg/ml had a sensitivity of 67.9% and specificity of 63.3% in the diagnosis of preeclampsia (AUC: 0.751; p = .001).Conclusions: Serum amphiregulin decreases in severe preeclampsia patients. [ABSTRACT FROM AUTHOR]

Objective: To compare the serum level of the chemokine, CXCL 16, in preeclamptic and healthy pregnant patients.Methods: This prospective case control study was conducted between January and December 2018 in a tertiary level hospital. The study group was formed of 70 pregnant women diagnosed with preeclampsia, and the control group was formed of 70 healthy pregnant women matched to the study group in respect of age, gestational week and body mass index (BMI). The study group was separated into two subgroups of mild preeclampsia (n = 35) and severe preeclampsia (n = 35). The groups were compared in terms of demographic and clinical parameters and the levels of serum CXCL 16.Results: No statistically significant difference was determined between the study and control groups in respect of maternal age, gravida, parity, BMI, and gestational age at sampling. Neonatal birth weight was significantly lower in the study group than in the control group. Mean serum alanine aminotransferase (ALT), aspartate amino transferase (AST) and creatinine levels of the study group were significantly higher than those of the control group (p < .05 for all). There was a statistically significant difference between the study and control groups regarding the mean platelet count. Compared to the control group, the severe and mild preeclampsia groups had a significantly higher serum level of CXCL 16. The serum level of CXCL 16 was significantly higher in patients with severe preeclampsia than in patients with mild preeclampsia (2.94 ± 3.89 pg mL-1 vs. 1.08 ± 1.87 pg mL-1, p = .14). Correlation analysis revealed a significant positive correlation of serum CXCL 16 level with serum ALT level (r = 0.320, p ≤ .001) and serum AST level (r = 0.373, p ≤ .001) and serum creatinine level (r = 0.279, p = .01) in both groups. High values indicated presence of preeclampsia, with a diagnostic cut-off point of 0.225, sensitivity of 75.7% and specificity of 72.9% for CXCL 16 (area under curve: 0.820, p < .001 CI: 0.753-0.888).Conclusions: This is the first study in literature to show a significantly higher level of CXCL 16 in patients with severe preeclampsia compared to those with mild preeclampsia. The study can also be considered of value in respect of showing that CXCL 16 could play a role in the etiopathogenesis of preeclampsia and the emergence of renal-hepatic damage. Blocking the CXCL 16/CXCR six axis in preeclampsia treatment could lay the ground for the development of new drugs which could be used in the treatment of preeclampsia. [ABSTRACT FROM AUTHOR]

Objectives: This study aims to analyze the G-protein coupled estrogen receptor (GPER/GPR30) activity in patients with fibromyalgia syndrome (FMS). Patients and methods: We enrolled 40 female patients with FMS (mean age 42.9±11.2 years; range, 18 to 64 years) diagnosed according to the 2010 American College of Rheumatology classification criteria and 30 age- and body mass index-matched female healthy controls (mean age 43.7±13.6 years; range, 19 to 64 years). Sex hormones of patients (morning) including estradiol, follicle stimulating hormone, luteinizing hormone, and prolactin (PRL) were recorded. FMS severity was assessed by Fibromyalgia Impact Questionnaire (FIQ). Serum GPER levels were measured by using a quantitative sandwich enzyme-linked immunosorbent assay method with a commercial kit. Results: G-protein coupled estrogen receptor levels were 0.11 (0.02-0.9) ng/mL in the FMS patients and 0.059 (0.01-0.13) ng/mL in controls, with a statistically significant difference (p=0.037). GPER levels were positively correlated with age and negatively correlated with PRL, while they were not correlated with FIQ. Differential diagnosis for FMS with receiver operating characteristic (ROC) analysis for the serum GPER levels was statistically significant (area under the ROC curve: 0.653, confidence interval: 0.522-0.785, p=0.029). High values indicated FMS, with a threshold of >0.075, sensitivity of 60%, and specificity of 60%. Conclusion: The GPER levels of FMS patients were higher than those of the controls. Thus, GPER levels may be considered as a biomarker in the diagnosis of FMS independent of disease severity. [ABSTRACT FROM AUTHOR]