The relationship between Nuclear Factor-Kappa B and Inhibitor-Kappa B parameters with clinical course in COVID-19 patients.

BACKGROUND: We aimed to investigate the serum Nuclear Factor Kappa B (NF-κB) p105, NF-κB p65 and Inhibitor Kappa B Alpha (IκBα) levels in patients with mild/moderate Coronavirus Disease 2019 (COVID-19) and their association with the course of the disease. MATERIALS AND METHODS: Blood was drawn from 35 COVID-19 patients who applied to the Department of Emergency Medicine of Istanbul University-Cerrahpasa at the time of diagnosis and from 35 healthy individuals. The patients were evaluated to have mild/moderate degree of disease according to National Early Warning Score 2 (NEWS2) scoring and computed tomography (CT) findings. The markers were studied in the obtained serum samples, using enzyme-linked immunoassay (ELISA). Receiver Operating Characteristic (ROC) analysis was performed. Statistical significance was evaluated to be p < 0.05. RESULTS: NF-κB p105 levels were significantly higher in the COVID-19 group compared to the control group. C-reactive protein (CRP), D-dimer, ferritin levels of the patients were significantly higher (p < 0.001) compared to the control group, while the lymphocyte count was found lower (p = 0.001). IκBα and NF-κB p65 levels are similar in both groups. Threshold value for NF-κB p105 was above 0.78 ng/mL, sensitivity was 71.4% and specificity was 97.1% (p < 0.05). NF-κB p105 levels at the time of diagnosis of the patients who required supplemental oxygen (O2), were significantly higher (p < 0.01). CONCLUSIONS: The rise in serum NF-κB p105 levels during the early stages of infection holds diagnostic value. Besides its relation with severity might have a prognostic feature to foresee the requirement for supplemental O2 that occurs during hospitalization.

The role of S100A12 and Toll-like receptor 4 in assessment of disease activity in familial Mediterranean fever and juvenile idiopathic arthritis.

OBJECTIVE: Our aim was to investigate the possible relationship between the serum S100A12 and Toll-like receptor 4 (TLR4) levels, and the activity of familial Mediterranean fever (FMF) and juvenile idiopathic arthritis (JIA) in accordance with the routine biochemical parameters. Furthermore, the effectiveness of these 2 biomarkers in distinguishing FMF from JIA has been evaluated. METHOD: Sixty-nine children with FMF, 68 children with JIA, and 35 healthy children were included in this study. S100A12 and TLR4 levels were measured by the sandwich enzyme-linked immunosorbent assay technique. RESULTS: In the FMF patient group, serum S100A12 level was found to be significantly higher than in both the JIA and control groups (P = .000 and P = .000, respectively). Although S100A12 levels were higher in the attack period compared to the attack-free period, this increase was not statistically significant (P > .05). TLR4 levels were statistically significantly higher in the attack period compared to the attack-free period in children with FMF (P < .05). Although there was no relationship between S100A12 levels and disease activity, there is a clear correlation between S100A12 and the Auto-Inflammatory Disease Activity Index in attack-free FMF patients (r = 0.612 P = .000). CONCLUSION: Serum S100A12 levels were not found to be a potentially valuable biomarker for assessing disease activity in either FMF or JIA. However, TLR4 levels were found to be a valuable biomarker for assessing disease activity in children with FMF. Further research which includes serial monitoring of S100A12 and TLR4 levels in a large cohort will provide detailed information about accuracy of these 2 potential biomarkers in both patients group.

Artificial neuronal network analysis in investigating the relationship between oxidative stress and endoplasmic reticulum stress to address blocked vessels in cardiovascular disease.

Background: Cardiovascular disease is the leading cause of death in the world and is associated with significant morbidity. Atherosclerosis is the main cause of cardiovascular disease (CVD), including myocardial infarction (MI), heart failure, and stroke. The mechanism of atherosclerosis has not been well investigated in different aspects, such as the relationship between oxidative stress and endothelial function. This project aims to investigate whether an oxidative enzyme vascular peroxidase 1 (VPO1) and activating transcription factor 4 (ATF4) can be used as biomarkers in highlighting the pathogenesis of the disease and in evaluating the prognosis of the relationship with endoplasmic reticulum and oxidative stress. This paper used artificial neural network analysis to predict cardiovascular disease risk based on new generation biochemical markers that combine vascular inflammation, oxidative and endoplasmic reticulum stress. Methods: For this purpose, 80 patients were evaluated according to the coronary angiography results. hs-CRP, lipid parameters and demographic characteristics, VPO1, ATF4 and Glutathione peroxidase 1(GPx1) levels were measured. Results: We found an increase in VPO1 and hs-CRP levels in single-vessel disease as compared to controls. On the contrary, ATF4 and GPx1 levels were decreased in the same group, which was not significant. Our results showed a significant positive correlation between ATF4 and lipid parameters. A statistically significant positive correlation was also observed for VPO1 and ATF4 (r=0.367, P<0.05), and a negative correlation was found for ATF4 and GPx1 (r=-0.467, P<0.01). A significant negative relationship was noted for GPx1 and hs-CRP in two/three-vessel disease (r=-0.366, P<0.05). Artificial neural network analysis stated that body mass index (BMI) and smoking history information give us an important clue as compared to age, gender and alcohol consumption parameters when predicting the number of blocked vessels. Conclusions: VPO1 and ATF4 might be potential biomarkers associated with coronary artery disease, especially in the follow-up and monitoring of treatment protocols, in addition to traditional risk factors.

Are Interictal Discharges Associated with Neuronal Cell Loss in Electrical Status Epilepticus in Sleep?

OBJECTIVE: Neuron-specific enolase is an established biomarker of neuronal damage. This study aimed to reveal the relationship between serum neuron-specific enolase level and continuous interictal discharges in a group of encephalopathy with electrical status epilepticus in sleep patients for the first time and determine whether there is a neuronal cell loss or damage. MATERIALS AND METHODS: We analyzed serum neuron-specific enolase levels in patients with an electrical status epilepticus in sleep pattern on their electroencephalographs with age- and sex-matched control subjects. Patients with a spike-wave index of at least 50% and acquired neuropsychological regression were included in the study. Magnetic resonance imaging of all electrical status epilepticus in sleep patients and control subjects included in the study was within normal limits. Neuron-specific enolase is measured by the enzyme-linked immunosorbent assay kit based on the sandwich technique. RESULTS: In this study, 14 patients diagnosed with electrical status epilepticus in sleep and 21 healthy controls were included. The median age of electrical status epilepticus in sleep patients was 7.1 years (min-max: 4.5-10.7 years) and 7.7 years (min-max: 3.2-14 years) in the control subjects. According to the results of serum neuron-specific enolase measurements, the mean ± standard deviation level of neuron-specific enolase was 7.61 ± 3.19 ng/dL for the electrical status epilepticus in sleep group and 6.93 ± 2.55 ng/dL for the control group. Serum neuron-specific enolase levels between electrical status epilepticus in sleep patients and the control group were not statistically significant (P = .749). CONCLUSION: No significant difference was observed in serum neuron-specific enolase levels between electrical status epilepticus in sleep patients and control subjects. Our results may indicate that frequent interictal discharges do not result in neuronal cell loss or damage in electrical status epilepticus in sleep patients.

Relationship between LPA SNPs and inflammatory burden in patients with preeclampsia to address future cardiovascular risk.

OBJECTIVE: The study tested whether cardiovascular corresponding LPA risk genotypes improve pre-eclampsia and coronary heart disease (CHD) risk prediction beyond conventional risk factors. BACKGROUND: Studies have shown that women specific risk factors for cardiovascular disease (CVD) have taken an attention recently. It might be possible to identify women who have the highest risk in developing CVD in their further lives. It is well-known that Lp(a) levels have an impact on increased risk of CVD which is affected by LPA gene. Further, LPA risk genotypes are not considered in cardiovascular risk prediction. METHODS: We have included 200 pregnant Turkish women into the study. We stratified the preeclamptic (PE) group: early (EOP) (28.7 ± 3.0 weeks) and late onset (LOP) (36.0 ± 1.4 weeks). 14 LPA SNPs were evaluated in the study. Rs9355296 and rs3798220 were found as independent risk factors for preeclampsia by logistic regression analysis. A positive correlation was found between rs9355296 and the diagnostic criteria of preeclampsia. Further rs9355296 G/* carriers have higher vascular inflammation rather than AA carriers. CONCLUSIONS: The findings reveal that LPA genetic variability with high inflammatory response might be an indication of future cardiovascular events.

Evaluation of the thyroid disorders in children with familial Mediterranean fever.

Although it is well-known that autoimmune thyroid diseases are more common in most of the autoimmune connective tissue diseases, the relationship between autoinflammatory diseases and autoimmune thyroid diseases has not well-evaluated yet and still remains unclear. The aim of this study was to investigate the frequency of autoimmune diseases of the thyroid gland and to evaluate thyroid function tests in children with familial Mediterranean fever. Thyroxine, thyroid-stimulating hormone, and thyroid autoimmune markers such as thyroid peroxidase and thyroglobulin antibodies, and thyroid ultrasound findings of 133 patients with familial Mediterranean fever and 70 healthy controls were evaluated. Serum levels of thyroid-stimulating hormone, free thyroxine, and thyroid autoimmunity markers were similar in patients with familial Mediterranean fever compared with healthy controls. There was no relationship between the duration of the disease and thyroid-stimulating hormone, free thyroxine, anti-thyroid peroxidase, and anti-thyroglobulin levels. This study revealed that incidence of thyroid dysfunction and autoimmunity is not increased in patients with familial Mediterranean fever. In conclusion, routine screening of serum thyroid function tests and thyroid antibody levels is not required in patients with familial Mediterranean fever in the absence of clinical symptoms or family history. Key Points • It is well-known that autoimmune thyroid diseases are common in autoimmune diseases. • The relationship between autoimmune thyroid diseases and autoinflammatory diseases like familial Mediterranean fever is still unclear. • In this study, we report the similar frequency of the autoinflammatory thyroid diseases in patients with familial Mediterranean fever and healthy controls. • A routine screening of serum thyroid function tests and thyroid antibody levels may not be required in patients with familial Mediterranean fever in the absence of clinical symptoms or family history.

Non-invasive diagnosis of endometriosis and moderate-severe endometriosis with serum CA125, endocan, YKL-40, and copeptin quadruple panel.

Considering the complex pathogenesis of endometriosis, which is associated with many cellular or molecular processes, such as proliferation, angiogenesis, inflammation, we evaluated the diagnostic value of a quadruple panel of serum markers CA125, endocan, YKL-40 and copeptin, for the prediction of endometriosis and moderate - severe endometriosis. Seventy women with endometriosis and 70 women without endometriosis were evaluated. Serum CA125, endocan, copeptin and YKL-40 levels were significantly increased in women with endometriosis compared to the women without endometriosis and in the minimal - mild endometriosis group compared to the no-endometriosis group. YKL-40, endocan and copeptin levels were significantly increased in the moderate - severe endometriosis group compared to the mild -moderate endometriosis group but the difference in CA125 levels remained non-significant. The quadruple panel score had an AUC of 0.954, a sensitivity of 96.5% and specificity of 84.6% for prediction of moderate - severe endometriosis. Zero or one positive marker had a sensitivity of 91.4% and specificity of 88.57% to rule out endometriosis. In conclusion, a quadruple panel of serum markers-CA125, endocan, YKL-40, and copeptin may be beneficial for the diagnosis of endometriosis and especially moderate - severe endometriosis. Further studies are needed to prove the efficacy of this panel.Impact statementWhat is already known on this subject? Many serum markers including CA125 have been investigated so far and suggested to be associated with endometriosis. However, none of these markers is sensitive and specific enough to diagnose endometriosis.What do the results of this study add? A quadruple panel score (CA125, endocan, YKL-4 and copeptin) had an AUC of 0.954, a sensitivity of 96.5% and specificity of 84.6% for prediction of moderate - severe endometriosis.What are the implications of these findings for clinical practice and/or further research? A high score may be beneficial to warn the surgeon about the risk of moderate to severe endometriosis if the patient will be operated anyway. A negative test of the quadruple panel may show high odds that there is no endometriosis which may prevent unnecessary surgery.

The relationship between epileptic seizure and melatonin in children.

OBJECTIVE: Studies about the relationship between epileptic seizures (ESs) and melatonin are limited in children and have been performed in heterogeneous patient groups and with different methods. In this study, it was planned to investigate this relationship according to seizure and epilepsy characteristics. MATERIAL AND METHODS: In 91 children with ES, serum melatonin levels were measured within half an hour following the seizure and on a seizure-free day. Seizures were categorized according to the diagnosis, semiology, etiology, duration, electroencephalography (EEG) findings, and response to treatment. Melatonin levels were compared between each group and control group. In addition, basal melatonin levels of 21 patients with electrical status epilepticus in sleep (ESES) were compared with a control group. RESULTS: Basal melatonin levels were found to be lower in children with ESs and ESES group compared with the control group (p < 0.001, p < 0.001). Likewise, similar results were obtained in subgroups except for remote symptomatic etiology, severe EEG findings, and refractory epilepsy. No significant difference was observed between basal and postseizure levels of melatonin. CONCLUSION: This is the first study to reveal the relationship between ESs and basal melatonin levels according to all the characteristics of seizure and epilepsy in the largest patient group. It also demonstrates the need for more detailed studies on the role of melatonin in the pathogenesis of both ESs and ESES, which may provide a basis for a future treatment.

Serum KL-6 level as a biomarker of interstitial lung disease in childhood connective tissue diseases: a pilot study.

Krebs von den Lungen-6 (KL-6) has been described as a promising biomarker in the diagnosis and determining the severity of interstitial lung disease in adults with connective tissue disease. This study was performed to determine whether the serum KL-6 level is useful as a biomarker for detecting the interstitial lung disease (ILD) in pediatric cases of connective tissue disease (CTD). In total, 88 patients [36 patients with systemic juvenile idiopathic arthritis (sJIA), 27 patients with juvenile systemic lupus erythematosus (JSLE), 14 patients with juvenile dermatomyositis (JDM), and 11 patients with juvenile systemic sclerosis (JSSc)] and 68 healthy controls were included in this study. Age, sex, and duration of CTD and ILD (if any) were recorded. Blood samples from all the patients and controls were examined by ELISA. Eleven of the 88 patients with CTD (12.5%) had ILD and all of them were symptomatic. Subgroup analysis indicated that eight patients had JSSc, two had JSLE, and one had systemic JIA. The median serum KL-6 level was 1450.5 U/mL (interquartile range (IQR) 742.9-2603.2) in the CTD with ILD group, 415.9 U/mL (IQR 233.4-748.4) in the CTD without ILD group, and 465.9 U/mL (IQR 273.6-1036) in the control group. KL-6 levels were significantly higher in the CTD with ILD group than the CTD without ILD group and the control group (p = 0.003). At a cut-off of 712.5 U/ml identified by ROC curve, serum KL-6 yielded a sensitivity of 81% and specificity of 72% for CTD with ILD group. There was no significant difference in serum KL-6 level among the disease subgroups (sJIA, JSLE, JSSc, JDM), in either the CTD with ILD group or the CTD without ILD group (p > 0.05). In conclusion, KL-6 is a useful biomarker of CTD with ILD in pediatric patients.

Prevalence and Clinical Features of Celiac Disease in Healthy School-Aged Children.

BACKGROUND/AIMS: The aim of this study was to determine the prevalence of celiac disease (CD) in healthy school-aged children in the northern region of Cyprus and to investigate the existence of potential markers that may accompany CD. This is the first study to measure the prevalence of CD in the northern region of Cyprus. METHODS: This study included 3792 school-aged children who were between the ages of 6 and 10 years between January 2015 and October 2016. CD was screened using total serum IgA, IgA anti-tissue transglutaminase (tTG), and IgA antiendomysial (EMA) antibodies. Subjects with selective IgA deficiency were further tested for IgG-tTG. Small intestinal biopsies were performed on all subjects with tTG antibody positivity. Risk factors and symptoms related to CD were evaluated using questionnaires in both the CD and control groups. RESULTS: Of the 3792 subjects, 39 were antibody positive (IgA-tTG was positive only in 14 subjects, IgA-tTG plus IgA-EMA in 21 subjects, and IgG-tTG in 4 subjects). IgA deficiency was detected in 11 subjects (0.29%). IgG-tTG was positive in 4 subjects with IgA deficiency (36.3%). Intestinal biopsies were performed on 28 of the 39 seropositive subjects. The biopsy findings of 15 children were consistent with CD (IgA-tTG positive in 3, IgA-tTG and IgA-EMA positive in 10, and IgG-tTG positive in 2). Thus, biopsies confirmed CD in 1:256 children (0.39%). CONCLUSIONS: Our study, which is the first study of school-aged children from the northern region of Cyprus, revealed that CD is a prevalent disease in this region.

Possible effects of lipoprotein-associated phospholipase A2 single-nucleotide polymorphisms on cardiovascular risk in patients with preeclampsia.

PURPOSE: Lipoprotein lipase-associated phospholipase A2 (Lp-PLA2) is a vascular inflammatory marker associated with cardiovascular diseases (CVD). Women with preeclampsia (PE) have elevated vascular inflammation and at higher CVD risk in the later life. We hypothesize that vascular inflammation related genetic variations increase the risk for developing future cardiovascular disease in women with PE. To test this hypothesis, we studied PLA2G7 gene polymorphisms, Lp-PLA2 mass, activity, index, and other cardiovascular risk factors in women with preeclampsia. METHODS: A total of 200 pregnant women were included into the study. We stratified the PE group: early (28.7 ± 3.0 weeks) and late onset (36.0 ± 1.4 weeks). Serum Lp-PLA2 mass in the early PE and the late PE group were significantly higher than the control group (p = .000). Lp-PLA2 index, Hs-C-reactive protein (CRP), serum amyloid A (SAA), calprotectin, and PTX3 levels were higher in early and late PE (p = .000). Single-nucleotide mutations of PLA2G7 rs1805017 (r = -0.228, p < .05) and rs9381475 (r = 0.216, p < .05) were correlated with LpPLA2 mass for the early PE group. Logistic regression analysis showed that LP-PA2 mass an independent risk factor for early PE with rs1805017 and rs9381475 carriers. CONCLUSIONS: Lp-PLA2 genetic variability with vascular inflammatory markers might contribute the incidence of future cardiovascular events.

Is there any relationship between adipocytokines and angiogenesis factors to address endothelial dysfunction and platelet aggregation in untreated patients with preeclampsia?

PURPOSE: Preeclampsia is a multisystem disorder and its etiology remains still unclear. Recent hypotheses rely on imbalance between angiogenic and antiangiogenic factors and disruption of endothelial function of spiral arteries. In addition; increased VTE (venous thromboembolism) risk is still unclear in preeclampsia. Our aim was to investigate the relationship between endothelial dysfunction, adipocytokines, platelet function, and vasculogenesis in preeclampsia. METHODS: Plasma angiogenic (PlGF, VEGF), antiangiogenic factors (sflt-1, endoglin) with adipocytokines (leptin, adiponectin, ghrelin), endothelial dysfunction markers (vWF, NO), and platelet function markers (ADP and collagen induced platelet aggregation, P-selectin) were examined in 30 early-onset, 22 late-onset preeclampsia, and 27 healthy pregnants. Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum biomarker levels except NO. NO levels were determined using colorimetric method. RESULTS: Endoglin, leptin, and vWF levels were increased in preeclampsia (P < 0.001), whereas PlGF, P-selectin (P < 0.001), and col-induced platelet aggregation slope (P < 0.05) were decreased in the same counterpart as compared to healthy pregnants. Endoglin also correlated with sflt-1 in preeclamptic patients. CONCLUSION: Increase in the levels of antiangiogenic factors and leptin herewith decline in the level of other angiogenic factor PlGF, did not affect nitric oxide and platelet aggregation markers significantly. Increased levels of vWF and endoglin might be result of endothelial dysfunction, so our findings suggest that an impaired angiogenesis may address endothelial dysfunction, but not platelet aggregation for preeclampsia.

The Relationship of Disordered Eating Attitudes with Stress Level, Bone Turnover Markers, and Bone Mineral Density in Obese Adolescents.

OBJECTIVE: To investigate the effect of stress caused by disordered eating attitudes on bone health in obese adolescents. METHODS: A cross-sectional study comprising 80 obese adolescents was performed from November 2013 to September 2014. Twenty-four-hour urinary free cortisol levels were measured as a biological marker of stress. Bone turnover was evaluated using bone-specific alkaline phosphatase, serum osteocalcin, and urinary N-telopeptide concentrations. Bone mineral density was measured using dual-energy X-ray absorptiometry. The Eating Disorder Examination Questionnaire, Dutch Eating Behavior Questionnaire, Children's Depression Inventory, and the State-Trait Anxiety Inventory for Children were used to assess eating disorders, depression, and anxiety. Psychiatric examinations were performed for binge eating disorders. RESULTS: In the Pearson's correlation test, a positive correlation was found between the 24-hour urinary cortisol level and Dutch Eating Behavior Questionnaire total and restrained eating subscale scores (p<0.05 for both). In linear regression analyses, the Dutch Eating Behavior Questionnaire total and restrained eating subscale scores were found to be significant contributors for urinary cortisol level (ß=1.008, p=0.035; ß=2.296, p=0.014, respectively). The femoral neck areal bone mineral density was found to be significantly higher in subjects who had binge eating disorder compared with those without binge eating disorder (p=0.049). CONCLUSION: Despite the lack of apparent effects on bone turnover and bone mineral density in our obese adolescents at the time of the study, our results suggest that disordered eating attitudes, and especially restrained eating attitudes, might be a source of stress. Therefore, studies in this area should continue.

Maternal serum atrial natriuretic peptide (ANP) and brain-type natriuretic peptide (BNP) levels in gestational diabetes mellitus.

OBJECTIVE: The aim of the study is to evaluate maternal serum atrial natriuretic peptide (ANP) and brain-type natriuretic peptide (BNP) levels in patients with getational diabetes mellitus compared with a control group. METHODS: We have measured maternal serum ANP and BNP levels in 35 otherwise healthy and 45 gestational diabetic women between gestational week 24 and 28 referred to our unit in a cross-sectional study. Independent samples t-test or the Mann-Whitney U-test was used for comparison of two groups where appropriate. RESULTS: Mean maternal serum homeostasis model assessment of insulin resistance (HOMA-IR), HbA1c, fasting glucose and insulin levels in gestational diabetes mellitus (GDM) group were significantly higher than the control group (p < 0.01). Mean maternal serum ANP and BNP levels of women with GDM were significantly lower than the control group (12.9 ± 9.9 versus 34.8 ± 16.9 pg/ml, p < 0.001; 416.6 ± 209.7 versus 629.7 ± 162.2 mg/dl, p < 0.001, respectively). Maternal serum ANP and BNP levels were negatively correlated with insulin levels, HbA1c and HOMA-IR values (p < 0.05). CONCLUSIONS: Maternal serum ANP and BNP levels are significantly lower in patients with GDM. These biomarkers might be valuable in clinical setting for identifying high-risk women for developing diabetes during pregnancy.

Maternal serum copeptin concentrations in early- and late-onset pre-eclampsia.

OBJECTIVE: Early-onset pre-eclampsia is primarily associated with placental dysfunction, whereas late-onset pre-eclampsia is defined as a maternal constitutional disorder. As a protein cosynthesized with vasopressin, copeptin is a potential marker of metabolic syndrome and insulin resistance, which shares similar risk factors with pre-eclampsia. The aim of this study was to investigate the copeptin levels in patients with early-onset and late-onset pre-eclampsia. MATERIALS AND METHODS: A total of 80 pregnant women receiving antenatal and obstetric care were recruited. The patients were subdivided into four groups: Early-onset pre-eclampsia (n = 20), late-onset pre-eclampsia (n = 20), and two control groups of similar gestational ages for both pre-eclamptic groups (n = 20 in each group). The maternal serum copeptin levels were measured using an enzyme-linked immunosorbent assay. RESULTS: The mean copeptin levels were 0.92 ± 0.57 ng/mL and 1.65 ± 0.95 ng/mL in the early-onset and late-onset pre-eclampsia groups, respectively. These values were higher compared with the control groups (0.54 ± 0.25 ng/mL and 1.15 ± 0.94 ng/mL, respectively). However, the difference was only statistically significant in the early-onset pre-eclampsia group (p = 0.011). Copeptin levels were associated only with gestational age and systolic-diastolic blood pressure. CONCLUSION: Our results suggest that copeptin levels might be useful in the evaluation of the severity of pre-eclampsia. However, copeptin might be involved in early- rather than late-onset pre-eclampsia.

Vitamin D Deficiency and Hashimoto's Thyroiditis in Children and Adolescents: a Critical Vitamin D Level for This Association?

OBJECTIVE: Vitamin D has been suggested to be active as an immunomodulator in autoimmune diseases such as Hashimoto's thyroiditis (HT). The goal of the present study was to investigate the vitamin D status in HT patients. METHODS: This prevalence case-control study was conducted on 90 patients with HT (of ages 12.32 ± 2.87 years) and 79 age-matched healthy controls (11.85 ± 2.28 years). Serum 25-hydroxyvitamin D3 [25(OH)D3] levels were measured in all 169 subjects. RESULTS: The prevalence of vitamin D deficiency in HT patients (64 of 90; 71.1%) was significantly higher than that in the control group (41 of 79; 51.9%) (p=0.025). Mean serum 25(OH)D3 level in the HT group was significantly lower compared to the control group (16.67 ± 11.65 vs. 20.99 ± 9.86 ng/mL, p=0.001). HT was observed 2.28 times more frequently in individuals with 25(OH)D3 levels <20 ng/mL (OR: 2.28, CI: 1.21-4.3). CONCLUSION: Vitamin D deficiency is associated with HT in children and adolescents. Levels lower than 20 ng/mL seem to be critical. The mechanism for this association is not clear.

Barnidipine ameliorates the vascular and renal injury in L-NAME-induced hypertensive rats.

The present study was aimed to investigate the influence of Barnidipine treatment on early stage hypertension by determining the function and morphology of the mesenteric and renal arteries as well as the kidney in N(ω)-Nitro-L-Arginine Methyl Ester (L-NAME)-induced hypertensive rats. Barnidipine (3 mg/kg/day p.o) was applied to rats after 2 weeks of L-NAME (60 mg/kg/day) administration, and continued for the next 3 weeks concomitantly with L-NAME. The systolic blood pressure (SBP) of rats was determined to decrease significantly in Barnidipine treated hypertensive group when compared to that of rats received L-NAME alone. Myograph studies demonstrated that the contractile reactivity to noradrenaline were significantly reduced in both of the resistance arteries while endothelium-dependent relaxations to acethylcholine were significantly diminished particularly in the mesenteric arteries of L-NAME-induced hypertensive rats. The impaired contractile and endothelial responses were completely restored by concomitant treatment of Barnidipine with L-NAME. Histopathological examinations verified structural alterations in the arteries as well as the kidney. Moreover, a decrease in endothelial nitric oxide synthase (eNOS) expression was presented both in the arteries and kidney of hypertensive rats which were increased following Barnidipine treatment. Elevated plasma levels of malondialdehyde (MDA) and myeloperoxidase (MPO) were also reduced in Barnidipine treated hypertensive rats. In conclusion, besides to its efficacy in reducing the elevated SBP, amelioration of vascular function, modulation of arterial and renal eNOS expressions as well as reduction of the plasma levels of oxidative and inflammatory biomarkers are possible supportive mechanisms mediating the favorable implications of Barnidipine in L-NAME-induced hypertension model.

Evaluation of Lp-PLA2 mass, vitronectin and PAI-1 activity levels in patients with preeclampsia.

PURPOSE: The aim of the current study is to determine, correlate and compare the plasma lipoprotein-associated phospholipase A2 (Lp-PLA2), vitronectin (Vn), Plasminogen activator inhibitor-1 (PAI-1) activity and tissue plasminogen activator (t-PA) levels in early-onset preeclampsia, late-onset preeclampsia and in control pregnant women. METHODS: A total of 79 individuals, 30 early-onsets, and 22 late-onset preeclamptic and 27 control pregnant women were included into the scope of this study. Enzyme-linked immunosorbent assay procedure was used to determine the serum Lp-PLA2 and plasma Vn, t-PA antigen and PAI-1 activity levels. Serum C-reactive protein (CRP) levels were measured immunoturbidimetrically in routine clinical chemistry analyser. RESULTS: In patients with preeclampsia, Lp-PLA2, PAI-1, t-PA, CRP and blood pressures levels were increased (p = 0.000) and correlated with each other. Vn levels were decreased (p = 0.016) but not correlated with other parameters in preeclamptic patients. CONCLUSION: We are of the opinion that increased Lp-PLA2 levels may partially contribute to endothelial dysfunction by the progression of inflammation. In addition, increased complex formation with Vn is likely to bring about the increase of PAI-1 activity in patients with preeclampsia. Moreover, increased t-PA and decreased Vn levels may also be the consequences of compensatory mechanisms against disease progression.

Histopathologic changes in the middle ear mucosa after exposure to pepsin and unconjugated bile acid.

OBJECTIVE: An increasing number of studies indicate that pepsin and bile acid cause damage to the ear, nose, and throat structures as a result of extraesophageal reflux. The aim of this study was to evaluate and compare the damaging effect of bile acids and pepsin on the middle ear mucosa. MATERIAL AND METHODS: Twenty-nine healthy rats were included in this study. The animals were divided into 5 groups. A single daily dose of 40 µmol/L chenodeoxycholic acid, 40 µg/mL pepsin, and saline were injected separately into the right middle ear of the rats. On day 30, all rats were decapitated, and formalin-fixed, paraffin-embedded samples of the middle ear both from the control and experimental rats were prepared. A semiquantitative analysis was performed. RESULTS: Inflammatory response was seen in all middle ear mucosa of rats except control group 1. The degree of inflammatory response was higher in the bile acid group when compared with the other groups. Epithelial metaplastic changes with varying number of goblet cells were observed in both the bile acid- and pepsin-injected groups. These metaplastic changes were also higher in the bile acid-induced group than in the pepsin-injected group. CONCLUSIONS: This is the first study on the middle ear mucosal damage of both pepsin and bile acid. Our results demonstrate that bile acids were associated with more extensive mucosal injury at pH 7 in comparison to pepsin in a rat animal model. Inflammatory response and metaplastic changes may play an important role in the etiology of middle ear pathologies.

Maternal serum apelin and YKL-40 levels in early and late-onset pre-eclampsia.

OBJECTIVE: The aim of the present study is to investigate whether alterations in the serum levels of apelin and YKL-40 differ between early and late onset pre-eclampsia and whether there is a correlation between apelin and YKL-40 in women who subsequently develop early and late pre-eclampsia. MATERIALS AND METHODS: A total number of 80 pregnant women, 40 with normal pregnancy and 40 with pre-eclampsia, were included in the present study. Both the normal pregnant and pre-eclamptic subjects were subdivided into two groups. Serum YKL-40 and apelin concentrations were measured. RESULTS: Mean maternal serum YKL-40 levels were both lower in women who subsequently developed early (87.45 ± 3.07 versus 103.40 ± 4.29) or late (96.43 ± 4.06 versus 99.87 ± 3.63) pre-eclampsia than those who remained normotensive. The difference was significant in early-onset preeclamptic women (p < 0.05) rather than late-onset pre-eclamptic ones (p > 0.05). Mean maternal serum apelin levels were both higher in women who subsequently developed early (8.6 ± 3.6 versus 5.7 ± 1.2) or late (9.6 ± 2.5 versus 8.1 ± 1.8) pre-eclampsia than those who remained normotensive. The difference was significant in early-onset preeclamptic women (p < 0.05) rather than late-onset pre-eclamptic ones (p > 0.05). There was a significant negative correlation between serum apelin and YKL-40 levels (r = -0.48, p = 0.001). CONCLUSION: Circulating levels of apelin are significantly increased in early-onset pre-eclampsia, indicating the role of apelin in the discrimination of the early-onset of pre-eclampsia. On the other hand, maternal serum YKL-40 levels are not elavated significantly, indicating that adipose-derived apelin is primarily involved in the vascular pathogenesis of early-onset pre-eclampsia than macrophage-derived YKL-40.