A nationwide multicentre study in Turkey for establishing reference intervals of haematological parameters with novel use of a panel of whole blood.

INTRODUCTION: A nationwide multicentre study was conducted to establish well-defined reference intervals (RIs) of haematological parameters for the Turkish population in consideration of sources of variation in reference values (RVs). MATERIALS AND METHODS: K2-EDTA whole blood samples (total of 3363) were collected from 12 laboratories. Sera were also collected for measurements of iron, UIBC, TIBC, and ferritin for use in the latent abnormal values exclusion (LAVE) method. The blood samples were analysed within 2 hours in each laboratory using Cell Dyn and Ruby (Abbott), LH780 (Beckman Coulter), or XT-2000i (Sysmex). A panel of freshly prepared blood from 40 healthy volunteers was measured in common to assess any analyser-dependent bias in the measurements. The SD ratio (SDR) based on ANOVA was used to judge the need for partitioning RVs. RIs were computed by the parametric method with/without applying the LAVE method. RESULTS: Analyser-dependent bias was found for basophils (Bas), MCHC, RDW and MPV from the panel test results and thus those RIs were derived for each manufacturer. RIs were determined from all volunteers' results for WBC, neutrophils, lymphocytes, monocytes, eosinophils, MCV, MCH and platelets. Gender-specific RIs were required for RBC, haemoglobin, haematocrit, iron, UIBC and ferritin. Region-specific RIs were required for RBC, haemoglobin, haematocrit, UIBC, and TIBC. CONCLUSIONS: With the novel use of a freshly prepared blood panel, manufacturer-specific RIs' were derived for Bas, Bas%, MCHC, RDW and MPV. Regional differences in RIs were observed among the 7 regions of Turkey, which may be attributed to nutritional or environmental factors, including altitude.

Assessment of serum chemerin, vaspin and omentin-1 levels in patients with polycystic ovary syndrome.

OBJECTIVE: To determine serum chemerin, vaspin and omentin-1 in overweight and normal weight patients with polycystic ovary syndrome (PCOS) and investigate the possible relationship between these adipokines and metabolic syndrome. METHODS: This cross sectional study enrolled women with PCOS and healthy women. Serum chemerin, vaspin and omentin-1 were assessed by enzyme-linked immunosorbent assay methods. RESULTS: Forty patients with PCOS and 30 healthy controls were included in the study. In the PCOS group, 18 women were overweight (body mass index [BMI] = 25.0-29.9 kg/m(2)) and 22 had normal weight (BMI = 18.5-24.9 kg/m(2)). Chemerin, total cholesterol, dehydroepiandrosterone sulphate and free androgen index (FAI) were significantly higher; and high-density lipoprotein cholesterol and sex hormone binding globulin were significantly lower in overweight PCOS patients compared with normal weight PCOS patients. A positive correlation was found between chemerin and BMI, triglyceride, insulin, homeostatic model assessment of insulin resistance and FAI in the PCOS group. There was no difference in serum chemerin, vaspin and omentin-1 between PCOS patients and healthy controls. CONCLUSION: Circulating chemerin was increased in overweight compared with normal weight PCOS patients. The most predictive variables for circulating chemerin in PCOS patients were BMI, FAI and age.

Maternal Serum S100-B, PAPP-A and IL-6 levels in severe preeclampsia.

AIM: We aimed to investigate the relationship of maternal serum levels of S100-B, PAPP-A and IL-6 with severe preeclampsia. MATERIALS AND METHODS: This prospective case-control study consisted of 27 severe preeclamptic and 36 healthy singleton pregnancies. The groups were matched for parity, maternal age and body mass index. Maternal blood sampling for S100B, PAPP-A and IL-6 was performed at the morning after an overnight fasting. RESULTS: S100-B concentrations were significantly higher in severe preeclampsia group (0.09 ± 0.05 vs. 0.13 ± 0.01 µg/L; p = 0.025). PAPP-A levels were higher (196.54 ± 21.56 vs. 208.80 ± 23.97 mIU/ml; p = 0.707) and IL-6 levels were lower in severe preeclamptic group (68.79 ± 29.89 vs. 37.30 ± 6.46 pg/ml; p = 0.372). AUC value for S100-B was calculated as 0.712. When cutoff level for serum S100-B for predicting severe preeclampsia was regarded as 0.0975 µg/L, sensitivity and specificity were found to be 81.4 % and 58.3 %, respectively. Pregnancies with ≥0.0975 µg/L S100-B levels had 12.75-fold increased risk for having CNS symptoms (OR 12.75; 95 % CI 2.69-60.28) and 3.27-fold increased risk for having HELLP syndrome (OR 3.27; 95 % CI 0.62-17.36). CONCLUSION: Our results suggest that serum S100B levels may be a potential marker in severe preeclampsia for the severity of hypoperfusion both in placenta and brain pointing at subsequent risk of organ failure.

Relationship of neutrophil gelatinase-associated lipocalin (NGAL) and procalcitonin levels with the presence and severity of the preeclampsia.

OBJECTIVE: The aim of the present study was to evaluate changes in maternal serum neutrophil gelatinase-associated lipocalin (NGAL) and procalcitonin (PCT) concentrations in preeclampsia. MATERIAL AND METHOD: This case-control study consisted of 40 preeclamptic and 40 healthy singleton pregnancies matched for age and body mass index. Serum NGAL and PCT levels were compared between the groups. Diagnostic performance and clinical association of these markers were evaluated. RESULTS: NGAL and PCT concentrations were significantly higher in preeclamptic group (p < 0.0001 and p = 0.001, respectively) and their levels were correlated with the severity of the preeclampsia. There were significant positive correlation between these markers and mean arterial pressure (MAP) and spot urine protein excretion. There was negative correlation between NGAL and apgar scores and fetal birth weight. Pregnancies with higher NGAL (OR: 4.89; 95% CI: 1.81-13.21) and higher PCT (OR: 6.67; 95% CI: 2.44-18.21) concentrations had higher risk for preeclampsia. CONCLUSION: NGAL and PCT may be potential biomarkers for preeclampsia. Their levels increase significantly in preeclampsia and they are related to the severity of the disease. These results are in agreement with the generalized endothelial damage and persistant inflammatory status in preeclampsia. NGAL may also be an indicator for adverse neonatal outcomes with decreased placental hypoperfusion.

Effect of erythropoietin on acoustically traumatized rat cochlea: an immunohistochemical study.

OBJECTIVE: To investigate the audiological and histopathological effects of erythropoietin on acoustic overstimulation in rats. STUDY DESIGN: Twenty-two male Wistar albino rats were divided into 3 groups: sham group (n = 7), erythropoietin injection group (n = 8), and saline injection group (n = 7). Both erythropoietin and saline injection groups were exposed to white noise (100 decibel [dB] sound pressure level [SPL]) for 3 hours. Auditory brainstem responses were measured before, immediately after, and on the 7th day of noise exposure. All animals were sacrificed on the 7th day and temporal bones were collected. The serial sections of the cochleae were stained by caspase-3 and caspase-9 immunostaining and by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method in order to detect apoptotic cells. RESULTS: In the saline group statistically significant differences were detected between the baseline and immediate postacoustic overstimulation thresholds of click and 6 kHz stimuli. However, when the baseline and immediate postacoustic overstimulation thresholds of click and 6 kHz stimuli were compared in the erythropoietin injection group, no statistically significant difference was determined. Histopathologic evaluations demonstrated that erythropoietin decreased the amount of apoptotic cells in the cochlea. CONCLUSION: Erythropoietin is likely to prevent the acute threshold changes and decrease the amount of apoptosis in cochlea after acoustic overstimulation in rats.

Oxidative stress impairs endothelial nitric oxide levels in Behçets' disease.

BACKGROUND: Behçet's disease (BD) is an inflammatory vasculitis. Endogenous nitric oxide (NO), produced by endothelial cells, has pleiotropic effects such as vasodilatator, antiplatelet, antiproliferative. Reactive oxygen species (ROS) are produced at sites of endothelial inflammation. ROS target polyunsaturated lipids, which results in malondialdehyde (MDA) production. OBJECTIVE: The aim was to investigate the oxidative stress in BD patients by measuring MDA and total antioxidant status (TAS) levels and to establish a possible relationship with respect to NO levels regarding disease activity. MATERIALS AND METHODS: 55 BD patients (30 active/25 inactive) and 20 healthy volunteers were included in the study. Blood samples were drawn following an overnight fasting. TAS and MDA levels were determined spectrophotometrically. Serum nitrite (NO(2-)) and nitrate (NO(3-)) levels were measured to estimate NO production. Data were expressed as mean ± SD. RESULTS: TAS levels were significantly lower in BD patients than the controls (1.19 ± 0.34 vs. 3.29 ± 0.89 mmol/L). In the active BD group, MDA levels (0.36 ± 0.19 nmol/mL) were significantly higher than both the inactive BD group (0.25 ± 0.18 nmol/mL) and controls (0.18 ± 0.41 nmol/mL). NO levels were significantly lower in the active group compared to the inactive group (18.0 ± 2.80 vs. 19.40 ± 2.70 µmol/L). MDA levels correlated negatively with NO levels in the active group. CONCLUSION: Decreased NO levels mediated by increased oxidative stress significantly contribute to endothelial dysfunction observed in BD.

The beneficial effects of physical exercise on antioxidant status in asthmatic children.

BACKGROUND: The pathogenesis of asthma involves both airway inflammation and an oxidant/antioxidant imbalance. It is demonstrated in asthmatic adults that exercise programmes improve lung function, a mechanism yet to be elucidated. The purpose of this study was to investigate the possible beneficial effects of physical exercise on antioxidant status in asthmatic children which may lead to ameliorated lung function. METHODS: The study enrolled thirteen control and thirty asthmatic children. The asthmatic group was subdivided into two: the first group receiving only pharmacological treatment (n=15) and the second receiving pharmacological treatment with exercise programme (n=15) for 8 weeks. Blood samples were drawn from the subjects before and after treatment periods. As oxidant stress markers blood levels of malondialdehyde (MDA) and total nitric oxide (NO), and as antioxidant status, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) enzyme activities were assessed. RESULTS: Before any treatment was initiated, MDA and NO levels in the asthmatic group were significantly higher than the controls (3.40±0.96 nmol/ml vs 2.46±0.58 nmol/ml, and 12.53±2.10 vs 9.40±1.39 micromol/L, respectively). Both SOD (p=0.0001) and GSH-Px (p=0.023) activities were significantly lower in the asthmatic group. Pharmacological treatment and exercise programme together significantly improved lung performance and decreased the levels of oxidant stress markers, in concordance with a significantly increase in antioxidant enzyme activity measures when compared to the pharmacological treatment. CONCLUSION: Structured exercise programme in asthmatic children resulted in better lung function, which may be attributed to its effect on antioxidant status.

Vitamin D status among adults in the Aegean region of Turkey.

BACKGROUND: Vitamin D is a lipid-soluble hormone found in certain foods and synthesized from precursors in the skin when exposed to ultraviolet light. Vitamin D plays a critical role in bone metabolism and many cellular and immunological processes and low levels have been associated with several chronic and infectious diseases. Vitamin D status is assessed by measuring the concentration of serum 25-hydroxyvitamin D [25(OH)D]. Vitamin D deficiency is reported to be common worldwide, but little has been reported about the vitamin D status of adults in Turkey. In this cross-sectional study, we determined the prevalence of 25(OH)D deficiency in adults residing in a city in the Aegean region of Turkey. METHODS: A survey was conducted on a representative sample of adults over 20 years old in a non-coastal city at the end of the winter season. Of the 209 households selected by random sampling, 8.6% (n = 18) were unoccupied and 21.5% (n = 45) refused to participate. Blood samples were taken and questions about medical history, vitamin supplementation, sunlight exposure, and dietary calcium and vitamin D intake were asked in face-to-face interviews of 391 adults living in the remaining households. RESULTS: The mean serum 25(OH)D concentration was 16.9 ± 13.09 ng/mL, with 74.9% of the subjects having 25(OH)D deficiency (<20 ng/mL), 13.8% having insufficiency (20-29.99 ng/mL), and 11.3% of the subjects having sufficient 25(OH)D (≥ 30 ng/mL) levels. 25(OH)D deficiency was more common among females (78.7%) than males (66.4%, p < 0.05). CONCLUSION: Adults living in an urban, non-coastal setting in Turkey have a high prevalence of vitamin D deficiency.

Endothelial dysfunction in preeclampsia. Increased homocysteine and decreased nitric oxide levels.

Endothelial dysfunction underlies the pathogenesis of preeclampsia, but its mechanism has not yet been completely understood. Elevated oxygen free radicals may partially explain the endothelial cell damage. In this study, we have aimed to measure homocysteine (Hcy) and nitric oxide (NO) levels as endothelial dysfunction markers in preeclamptic women. Nineteen preeclamptic (33.9 +/- 1.4 weeks) and 15 gestational-age-matched normal pregnant women (35.5 +/- 0.7 weeks) were included in the study. Mean NO level was significantly lower (p < 0.001) and mean Hcy level was significantly higher (p < 0.001) in the preeclamptic group. Elevated Hcy and oxygen free radical levels could decrease NO levels due to the reaction with each other and reduced NO may increase blood pressure and ischemia in preeclamptic patients. We have concluded that increased Hcy and oxygen free radical levels, and decreased NO levels are closely associated with preeclampsia-related endothelial dysfunction.