Ayşenur Ozderya

Lutfi Kirdar Kartal Education and Research Hospital, İstanbul, Istanbul, Turkey

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Publications (16)29.94 Total impact

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    ABSTRACT: Asymptomatic primary hyperparathyroidism (PHPT) is characterized with autonomous overproduction of parathyroid hormone without signs or symptoms associated with hyperparathyroidism. Before symptoms become obvious, PHPT may affect structures like sacroiliac joints, which consist of bone. So, in the asymptomatic PHPT patients, structural and inflammatory changes in sacroiliac joints may lead to confusion during diagnosis workup of axial spondyloarthropathy. In this study, we evaluated active and chronic sacroiliac magnetic resonance imaging (MRI) changes relevant to sacroiliitis in the patients with asymptomatic PHPT and interpreted bone marrow edema within the scope of Assessment of SpondyloArthritis International Society–Outcome Measures in Rheumatology Clinical Trials (ASAS-OMERACT) criteria. Forty-nine patients with asymptomatic PHPT, 26 patients with newly diagnosed axial spondyloarthropathy (SpA), and 37 healthy controls were enrolled. All subjects were evaluated by sacroiliac MRI for four active (bone marrow edema, enthesitis, capsulitis, and synovitis) and four chronic (subchondral sclerosis, subchondral/periarticular erosions, periarticular fat deposition, and bony bridges/ankylosis) lesions relevant to sacroiliitis. Bone marrow edema compatible with ASAS-OMERACT active sacroiliitis criteria in sacroiliac MRI was fulfilled by 16.3 % (8/49) of the asymptomatic PHPT patients which was similar with controls but statistically lower than axial SpA. Moreover, asymptomatic PHPT patients and controls were similar for other chronic or active MRI findings. Also, we detected lower frequency of all other MRI findings, except enthesis, in asymptomatic PHPT patients according to axial SpA. Acute inflammatory including bone marrow edema fulfilling ASAS-OMERACT active sacroiliitis criteria and chronic structural sacroiliac lesions relevant to sacroiliitis in MRI were detected in asymptomatic PHPT similar frequency with controls but as expected, lower than axial SpA. But, these findings could not be attributed to excessive secretion of parathyroid hormone.
    No preview · Article · Jan 2016 · Clinical Rheumatology
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    ABSTRACT: Objectives/hypothesis: To test the assumption that voice is changed in polycystic ovary syndrome (PCOS) and identify changes that occur. Study design: Cross-sectional pilot study. Methods: Thirty patients with PCOS and a control group of 22 age-matched and body mass index-matched healthy women were included. Demographic data, anthropometric measurement, serum androgens, and Voice Handicap Index-10 were determined. Transnasal fiberoptic laryngoscopy and rigid stroboscopy were performed. Supraglottic hyperfunction was assessed during fiberoptic laryngoscopy. Presence of supraglottic hyperfunction was interpreted as abnormal muscle tension pattern. Glottal closure configuration and vibratory wave characteristics were evaluated via stroboscopy. Acoustic analysis was performed with the Dr. Speech software program version 4 (Tiger DRS Inc., Seattle, WA). Results: Voice complaints and acoustic parameters were similar between groups, whereas serum androgens were significantly higher in patients (P < 0.001). Laryngeal examination detected pathology in 17 (56.7%) patients and two (9.1%) controls (P < 0.001). Fiberoptic examination determined supraglottic hyperfunction in 11 patients but in only two controls (P = 0.023). In stroboscopy, incomplete glottal closure configuration and impaired vocal fold vibration were present in 10 and 11 patients, respectively, whereas only one control had glottal closure abnormality and none of the controls had abnormal vibration (P = 0.028 and P = 0.001, respectively). Conclusion: Abnormal muscle tension patterns and impaired vocal fold vibration are frequent among patients with PCOS; but they are not accompanied by increased vocal symptoms or deteriorated acoustic voice parameters. This may be important for professional voice users or in extensive or extraordinary voice use demands in patients with PCOS. Level of evidence: 3b. Laryngoscope, 2015.
    No preview · Article · Dec 2015 · The Laryngoscope
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    ABSTRACT: Background: In this study, we aimed to investigate whether high parathormone (PTH) levels in obese patients contribute to the metabolic complications of obesity. Methods: A total of 400 obese subjects aged 18-65 years were included. Anthropometric bioelectrical bioimpedance measures, blood tests, and 75 gram oral glucose tolerance test results were evaluated. Results: Of the 400 obese subjects, 335 were female. The mean age was 39 ± 10 years. The median body mass index was 36 (interquartile range 34-41). Subjects were divided into quartiles according to blood PTH levels. Groups included quartile 1 [n = 100, median PTH; 42 (range 36-45)], quartile 2 [n = 100, median PTH; 55 (51-59)], quartile 3 [n = 100, median PTH; 73 (68-78)], and quartile 4 [n = 100, median PTH; 99 (89-125)]. Quartiles were evaluated with a generalized linear model adjusted for age, sex, and season of recruitment. Systolic and diastolic blood pressure, fasting glucose, homeostatic model assessment-estimated insulin resistance, insulin sensitivity index, triglyceride level, and high-density lipoprotein cholesterol (HDL-C) were not different among quartiles. PTH and 25 hydroxyvitamin D (25(OH)D) were not associated with higher odds of prevalent metabolic syndrome in obese subjects (odds ratio, OR, 0.99 [95% confidence interval, CI, 0.981.00], P = 0.38 and 0.99 95% CI 0.96-1.01], P = 0.46, respectively). Decreased 25(OH)D levels were significantly correlated with higher odds of low HDL-C (OR 0.96 [95% CI 0.93-0.99], P = 0.04). Conclusions: PTH does not contribute to the occurrence of metabolic components of obesity, but there is a positive correlation between 25(OH)D and HDL-C.
    No preview · Article · Oct 2015 · Metabolic syndrome and related disorders

  • No preview · Article · Sep 2015 · European Urology Supplements
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    Full-text · Article · May 2015
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    Full-text · Article · May 2015
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    ABSTRACT: Madelung's disease is a rare fat metabolism disorder characterised by benign multiple symmetric, encapsulated lipomatosis. The exact cause of the disease is unknown; it may be associated with chronic alcoholism and mutations in mitochondrial DNA (A8344G), but there have been cases without these factors reported in the literature. A 29-year-old man with a 6-year history of diabetes mellitus was admitted to our hospital for poorly regulated diabetes and decreased libido. He was not an alcohol consumer. His family history was unremarkable. Physical examination revealed that he had a eunuchoid body shape. There was a symmetric excess fat accumulation in his submandibular, deltoid, nuchal, suprapubic and inguinal areas. He was diagnosed with Madelung's disease, and imaging studies supported the diagnosis. Hormonal evaluation revealed a hypergonadotropic hypogonadism. Karyotype analysis revealed a 47,XXY mutation. Genetic research showed no mitochondrial DNA mutation. Metabolic disorders, such as diabetes mellitus, hyperlipidaemia, hyperuricaemia and liver disease, endocrine gland diseases, such as hypothyroidism, and neurological diseases, such as polyneuropathy and cognitive disorders, may accompany Madelung's disease. The present study represents the first reported case of Madelung's disease accompanied by Klinefelter's syndrome. Madelung's disease is a rare fat metabolism disorder characterised by benign multiple symmetric and encapsulated lipid accumulation.The exact cause of the disease is unknown.Metabolic disorders, such as diabetes mellitus, hyperlipidaemia, hyperuricaemia and liver disease, endocrine gland diseases, such as hypothyroidism, and neurological diseases, such as polyneuropathy and cognitive disorders, may accompany Madelung's disease.
    Full-text · Article · Apr 2015
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    ABSTRACT: Aim: To determine whether insulin resistance (IR) accompanies normocalcemic primary hyperparathyroidism (NCPHP).Methods: Twenty-five patients with NCPHP and 25 age, gender, body mass index (BMI) matched controls, were included the study. Patients were diagnosed NCPHP if serum calcium (Ca) concentrations and ionized serum Ca levels were in the normal range but parathyroid hormone (PTH) levels were inappropriately and persistently high. Subjects with 25-hydroxyvitamin D (25[OH]D) levels ≥ 20 ng/dl were included in the study. The upper limit of PTH was calculated using a nomogram (calculated max PTH = 120 - [6 x Ca (mg/dl)] - [1/2 x (25[OH]D) (ng/ml)] - [1/4 x Age (years)]) for each subject. Patients and controls underwent a standard 75-gram oral glucose tolerance test (OGTT). Insulin resistance (IR) was assessed by the homeostasis model assessment (HOMA-IR) and insulin sensitivity index (ISOGTT).Results: There were no differences between the demographic features of patients with NCPHP and the control group. IR frequency was not different between groups (p = 0.14). HOMA-IR was higher and ISOGTT was lower in patients with NCPHP than the control group but the difference was not significant (p = 0.17 and p = 0.22, respectively). We did not find any correlation between PTH and glucose metabolism markers (HOMA-IR, ISOGTT, HBA1C, and BMI) in either of the groups.Conclusion: The results of this study indicate that IR is no more common in patients with NCPHP, and PTH is not related to ISOGTT and HOMA-IR.
    Full-text · Article · Aug 2014 · Endocrine Practice
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    ABSTRACT: Endothelin 1 (EDN1) is well established marker of inflammation. The functions of EDN1 are mediated mainly by endothelin receptor type A (EDNRA). The link between EDN1 and EDNRA polymorphisms with several diseases has been previously demonstrated. The etiopathogenesis of Hashimoto's thyroiditis (HT) remains still elusive although the role of chronic inflammation and subsequent endothelial dysfunction has been established. This study examined firstly the possible association of EDN1 (G5665T and T-1370G) and EDNRA (C+70G and G-231A) single nucleotide polymorphisms (SNPs) with the occurrence of HT, and evaluates the relationship between genotypes and clinical/laboratory manifestation of HT. We analyzed genotype and allele distributions of above-mentioned polymorphisms in 163 patients with HT and 181 healthy controls by real-time PCR combined with melting curve analysis. No significant associations between HT and variant alleles of EDN1 5665 and -1370, as well as EDNRA +70 and -231 SNPs were found. Haplotype analysis demonstrated that there was a strong (D'=0.76, r(2)=0.487) and weak (D'=0.403, r(2)=0.086) linkage disequilibrium (LD) between EDN1 -1370 and 5665, and between EDNRA -231 and +70 SNPs, respectively. However, haplotype frequencies in patients were similar to those in controls. In addition, it was observed that the EDNRA +70 G allele had protective effect against early (at age before 40years) disease onset of HT (OR: 0.51, 95% CI=0.32-0.79, p=0.003). Although no significant associations between susceptibility to HT with EDN1 5665 and -1370, as well as with EDNRA +70 and -231 SNPs were found, EDNRA +70 polymorphism was related with decreased risk for early onset HT.
    Full-text · Article · May 2014 · International immunopharmacology
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    ABSTRACT: Graves' disease (GD) arises due to complex interactions between genetic and environmental factors. Transforming growth factor β1 (TGFβ1) is required to maintain immune homeostasis, and is implicated in lymphocyte infiltration, thyroid follicular cell hyperplasia, and production of autoantibody in the thyroid gland of patients with GD. The aim of the present study was to investigate the possible association of Leu10Pro (c.869T>C) and Arg25Pro (c.915G>C) single nucleotide polymorphisms (SNPs) of TGFβ1 gene with the occurrence of GD. We analyzed the genotype and allele frequencies of these SNPs in 171 patients with GD and 197 healthy controls using PCR-restriction fragment length polymorphism (RFLP). The distribution of Leu10Pro (c.869T>C) genotype and allele frequencies in the control and GD groups were not significantly different. However, there was a significant increase of Arg25Pro (c.915G>C) C allele frequency in patients with GD compared with healthy controls (p<0.0001, OR=4.77, 95% CI=3.32-7.03). In addition, C allele carrying subjects (CG+CC) had 5.31-fold increased risk for developing GD according to GG homozygotes (p<0.0001, 95% CI=3.43-8.44). No association between polymorphisms and GD phenotypes was observed. This study indicates that the Arg25Pro (c.915G>C) polymorphism of TGFβ1 gene may be related to occurrence of GD.
    Full-text · Article · Apr 2014 · International immunopharmacology
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    ABSTRACT: Graves' disease (GD) is a consequence of genetic and environmental factors. Endothelin 1 (EDN1) is a strong angiogenic and mitogenic factor, playing a key role in hypervascularization, thyroid follicule cell hyperplasia, and lymphocyte infiltration in the thyroid gland of patients with GD. EDN1 induces angiogenesis and mitogenesis via endothelin receptor type A (EDNRA). Relationships between their polymorphisms with several diseases have been found. This study examined the possible association of EDN1 (G5665T and T-1370G) and EDNRA (C+70G and G-231A) single nucleotide polymorphisms (SNPs) with the occurrence of GD, and evaluates the relationship between genotypes and clinical/laboratory manifestations of GD. We analyzed genotype and allele distributions of EDN1 and EDNRA polymorphisms in 165 patients with GD and 181 healthy controls by real-time PCR combined with melting curve analysis. No significant associations between GD and variant alleles of the studied polymorphisms were observed. However, the anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-TG) levels in EDN1 G5665T GG genotype were higher than those in T allele carriers (GT+TT) (p=0.001 and p=0.026, respectively). In addition, anti-TPO levels in EDN1 T-1370G wild-type homozygous patients were found to be higher than in mutant gene carrying patients (GT+GG) (p=0.006). The presence of EDNRA+70G allele was associated with 3.37-fold increased risk for development of ophthalmopathy in GD patients (p=0.009). Although there were no associations between EDN1 (G5665T and T-1370G) and EDNRA (C+70G and G-231A) SNPs and susceptibility to GD, EDN1 G5665T and T-1370G polymorphisms were related to alterations of autoantibody production and EDNRA C+70G polymorphism is related with increased risk for ophthalmopathy in GD patients.
    Full-text · Article · Nov 2013 · International immunopharmacology
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    ABSTRACT: The etiopathogenesis of Graves' disease (GD) has not been clearly elucidated although the role of chronical inflammation and endothelial dysfunction has been established. Adhesion molecules such as intercellular adhesion molecule 1 (ICAM1), vascular cell adhesion molecule 1 (VCAM1), and E-selectin are secreted from vascular endothelium and promote accummulation of leukocytes in damaged endothelial areas. This study examined the possible association of ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) single nucleotide polymorphisms (SNPs) with the occurence of GD. ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) SNPs in DNA from peripheral blood leukocytes of 171 patients with GD and 259 healthy controls were investigated by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes. We did not find significant differences in the distributions of studied polymorphisms, nor in the haplotype frequencies between patients with GD and healthy control. However, the anti-TPO levels in E-selectin 128R allele carrying subjects (SR + RR) were higher than S128S genotype (p < 0.05). In addition, the decline of TSH levels was more prominent in ICAM1 469 E carrying subjects (KE + EE) in comparison with wild homozygotes (p < 0.05). Although there is not assosiation between ICAM1 (G241R and K469E), VCAM1 (T-1591C and T-833C), and E-selectin (S128R) SNPs and susceptibility to GD, higher anti-TPO in E-selectin 128 SR + RR, and lower TSH in ICAM1 469 KE + EE subjects suspect that these genotypes are prone to increased antithyroid autoantibody production with more accentuated TSH suppression in GD. Further studies with a larger cohort, analyzing other polymorphisms in ICAM, VCAM1 and E-selectin genes are necessary to support our observations.
    Full-text · Article · Dec 2012 · Molecular Biology Reports
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    ABSTRACT: This study examined firstly the possible association of G241R and K469E single nucleotide polymorphisms (SNPs) of ICAM-1 gene with the occurrence of Hashimoto thyroiditis (HT). G241R and K469E SNPs in DNA from peripheral blood leukocytes of 190 HT and 247 healthy controls were investigated by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes. There was a significant increase of ICAM-1 241R allele frequency in patients with HT compared with healthy controls (P = 0.04, OR = 1.84, 95 % CI = 1.00-3.37). Regarding ICAM-1 K469E polymorphism, patients homozygous for E allele had 1.73-fold increased risk for developing HT according to KK homozygotes (P = 0.04, 95 % CI = 1.00-3.01). The 469E allele frequency was higher in HT patients according to controls, however the difference was at borderline significance (P = 0.05, OR = 1.30, 95 % CI = 1.00-1.70). No associations between polymorphisms and HT phenotypes were observed. We suggest that the G241R and K469E SNPs of ICAM-1 gene may be related to occurrence of HT. However, more studies with larger sample size including other loci of the ICAM-1 gene are necessary to support our findings before any definite statement can be made about the relationship between HT and ICAM-1 polymorphism.
    Full-text · Article · Oct 2012 · Molecular Biology Reports
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    ABSTRACT: Background: Although prooxidant and antioxidant status were reported to be changed in clinical and experimental hypothyroidism, obtained results are conflicting. In addition, in subclinical hypothyroidism, scarced and controversial data are available about oxidative stress. Therefore, we aimed to investigate prooxidant-antioxidant status only in Hashimoto's thyroiditis (HT) patients with subclinical (sHT) and overt hypothyroidism (oHT). Subjects and methods: Thirty sHT and 18 oHT patients and 30 healthy control subjects were included in the study. Endogenous and prooxidant 2,2'-azobis-(2-amidinopropane) hydrochloride (AAPH)-induced malondialdehyde (MDA), diene conjugate (DC), protein carbonyl (PC) and nitrotyrosine (NT) levels as well as ferric reducing antioxidant power (FRAP) were determined in serum. In addition, endogenous DC and copper-induced MDA levels were measured in low density lipoprotein (LDL) fraction. Results: Although there were no significant difference in serum endogenous MDA and DC levels, AAPH-induced MDA levels were significantly increased in sHT patients. All these parameters increased in oHT patients. Serum PC levels were detected to be increased in both sHT and oHT patients. Serum FRAP values did not alter in sHT patients, but they lowered in oHT patients. Endogenous DC and copper-induced MDA levels in LDL fraction did not change in sHT patients. However, these parameters were detected to be increased significantly in oHT patients as compared to controls and sHT patients. Conclusion: In conclusion, there were significant increases in oxidative stress parameters in serum and LDL-fraction in oHT patients. However, oxidative stress was detected to stimulate partly in serum, but not LDL fraction in sHT patients.
    Full-text · Article · Aug 2012 · International immunopharmacology
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    ABSTRACT: Oxidative DNA damage, caused by either endogenous or exogenous sources of reactive oxygen species (ROS), has been linked several diseases including Graves' disease (GD). 7,8-Dihydro-8-oxoguanine (8-oxoG) is a major lesion produced by ROS and is considered a key biomarker of oxidative DNA damage. In humans, 8-oxoG is mainly repaired by 8-oxoguanine DNA N-glycosylase-1 (hOGG1), which is an essential component of the base excision repair (BER) pathway. The functional studies showed that hOGG1 Ser326Cys polymorphism is associated with the reduced DNA repair activity and increased risk for some oxidative stress-related diseases. In this study, we firstly investigated hOGG1 Ser326Cys polymorphism in GD. According to our results, Cys/Cys genotype frequency in the GD patients (23.4%) was significantly higher than the controls (9.2%). Cys/Cys genotype had an 3.5-fold [95% CI (confidence interval): 2.10-6.01, p < 0.001] the Cys allele had 1.83-fold (95% CI: 1.43-2.34, p < 0.001) increase in the risk for developing GD. Our results suggest that Ser326Cys polymorphism of the hOGG1 gene is associated with GD risk.
    No preview · Article · Apr 2011 · Cell Biochemistry and Function
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    ABSTRACT: Oxidative stress has been implicated in etiopathogenesis of Graves' disease (GD). Increased lipid peroxidation and oxidative DNA damage have been found in GD patients. Oxidative DNA damage is mainly repaired by the base-excision repair (BER) pathway. Polymorphisms in DNA-repair genes have been associated with the increased risk of various diseases and could also be related to the etiology of GD. Therefore, we conducted a study including 197 patients with GD and age- and sex-matched 303 healthy subjects to examine the role of single-nucleotide polymorphisms of BER genes, APE/Ref-1 (codon 148) and XRCC1 (codons 194 and 399) as a risk factor for GD. These polymorphisms were determined by quantitative real-time PCR and melting curve analysis using LightCycler. No significant association was observed between the variant alleles of APE/Ref-1 codon 148 [odds ratio (OR) = 0.89, 95% confidence interval (CI) = 0.69-1.17], XRCC1 codon 194 (OR = 1.24, 95% CI = 0.79-1.94), and XRCC1 codon 399 (OR = 1.12, 95% CI = 0.86-1.46) and GD. These preliminary results suggest that APE/Ref-1 (codon 148) and XRCC1 (codons 194 and 399) polymorphisms are not significant risk factors for developing GD.
    No preview · Article · Sep 2009 · Cell Biochemistry and Function