Person: CESUR, YAŞAR
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Publication Metadata only Psychotic disorder, hypertension and seizures associated with vitamin B-12 deficiency: a case report(2012-04-01T00:00:00Z) Dogan, M.; Ariyuca, S.; Peker, E.; Akbayram, S.; Dogan, S. Z.; Özdemir, Ömer Faruk; Cesur, YAŞAR; CESUR, YAŞARThis report highlights a rare presentation of vitamin B-12 deficiency (concurrent psychotic disorder, seizures and hypertension). A 16-year-old girl presented with nervousness that had been persisting for 2 weeks. She had stopped eating and there was decreased self-care and she could not walk and sleep. Two days prior to admission, generalized tonic clonic convulsions were noted. On physical examination, vital signs were normal, except for hypertension (150/100 mm Hg). She did not respond to conversation; she could not answer the questions. Mood was depressive and hallucinations were noted. Laboratory analyses were normal, except for a low vitamin B-12 level (<150 pg mL(-1)). The patient was not given any treatment of hypertension, psychosis or seizures, except vitamin B-12 injections. After that, she showed improvement within 1 week. In the 7 days of hospitalization, the arterial blood pressure returned to normal, psychotic symptoms were resolved, the visual hallucinations and the depressive mood subsided, and she could eat and speak clearly. No hypertension or convulsions have been detected on the control examinations, and she has now been followed-up without any symptoms or findings. In conclusion, with this report we emphasized that psychosis, seizures and hypertension can be a rare manifestation of vitamin B-12 deficiency, which is reversible with therapy and serum vitamin B-12 level should be checked in patients who do not have an obvious cause for psychosis, seizures or hypertension.Publication Metadata only Congenital hypothyroidism with isolated fibula agenesis Fi̇bula agenezi̇si̇ i̇le bi̇rli̇kte konjeni̇tal hi̇poti̇roi̇di̇(2010-05-01T00:00:00Z) Doǧan, Murat; Yilmaz, Cahide; Çaksen, Hüseyin; Cesur, YAŞAR; AKPINAR, Fuat; GÜVEN, Ahmet Sami; CESUR, YAŞARPublication Metadata only Novel TSHR mutations in consanguineous families with congenital nongoitrous hypothyroidism(2010-11-01T00:00:00Z) Cangul, Hakan; Morgan, Neil V.; FORMAN, Julia R.; Saglam, Halil; AYCAN, Zehra; Yakut, Tahsin; Gulten, Tuna; TARIM, Omer; Bober, Ece; Cesur, YAŞAR; Kirby, Gail A.; Pasha, Shanaz; Karkucak, Mutlu; EREN, Erdal; CETINKAYA, Semra; BAS, Veysel; Demir, Korcan; Yuca, Sevil A.; Meyer, Esther; Kendall, Michaela; Hogler, Wolfgang; Barrett, Timothy G.; Maher, Eamonn R.; CESUR, YAŞARObjective Nonsyndromic autosomal recessively inherited non-goitrous congenital hypothyroidism (CHNG) can be caused by mutations in TSHR, PAX8, TSHB and NKX2-5. We aimed to investigate mutational frequencies of these genes and genotype/phenotype correlations in consanguineous families with CHNG.Publication Metadata only Evaluation of therapeutics management patterns and glycemic control of pediatric type 1 diabetes mellitus patients in Turkey: A nationwide cross-sectional study(2016-09-01) Hatun, Sukru; DEMIRBILEK, Huseyin; DARCAN, ŞÜKRAN; Yuksel, Aysegul; Binay, Cigdem; Simsek, Damla Goksen; Kara, Cengiz; CETINKAYA, Ergun; UNUVAR, Tolga; UCAKTURK, Ahmet; Tutunculer, Filiz; Cesur, YAŞAR; Bundak, Ruveyde; Saglam, Halil; Simsek, Enver; Bereket, Abdullah; CESUR, YAŞARAims: To evaluate the management strategies, glycemic control and complications of pediatric type 1 diabetes mellitus (T1DM) patients in Turkey.Publication Open Access Correlation of Brain Neuropeptide (Nesfatin-1 and Orexin-A) Concentrations with Anthropometric and Biochemical Parameters in Malnourished Children(2015-09-01) Kahraman, Feyza Ustabas; Vehapoglu, Aysel; Ozgen, Ilker Tolga; Terzioglu, Sule; Cesur, YAŞAR; Dundaroz, Rusen; VEHAPOĞLU TÜRKMEN, AYSEL; USTABAŞ KAHRAMAN, FEYZA; ÖZGEN, İLKER TOLGA; TERZİOĞLU, ŞULE; CESUR, YAŞAR; İŞCAN, AKINObjective: Malnutrition continues to be a leading cause of stunted growth in many countries. This study aimed to investigate serum nesfatin-1 and orexin-A levels in underweight children and the potential correlations of these levels with anthropometric and nutritional parameters. Methods: The study enrolled 44 prepubertal children (between 2 and 12 years of age) with thinness grades of 1-3 and 41 healthy age- and gender-matched children. The demographic, clinical and laboratory parameters including nesfatin-1 and orexin-A concentrations were compared between the two groups. The correlations of nesfatin-1 and orexin-A with biochemical and anthropometric parameters were investigated. The receiver operating characteristic (ROC) analysis were also performed for evaluating nesfatin-1 and orexin-A in distinguishing children with malnutrition from healthy controls. Results: Thyroid-stimulating hormone, vitamin B12 and insulin levels were significantly lower in the study group than controls (p=0.001, p=0.049 and p=0.033, respectively). Mean nesfatin-1 levels in the malnourished group was also significantly lower compared to the healthy controls (3871.2 ± 1608.8 vs. 5515.0 ± 3816.4 pg/mL, p=0.012). No significant difference was observed in the orexin-A levels between the two groups (malnourished vs. control groups: 1135.7 ± 306.0 vs. 1025.7 ± 361.6 pg/mL, p=0.141). Correlation analyses revealed a positive correlation of nesfatin-1 and a negative correlation of orexin-A with body mass index (BMI) z-score. ROC analysis demonstrated that nesfatin-1 and orexin-A cannot be used to distinguish children with malnutrition from healthy controls (AUC: 0.620, p=0.061 for nesfatin-1 and AUC: 0.584, p=0.190 for orexin-A). Conclusion: The positive correlation of nesfatin-1 and the negative correlation of orexin-A with BMI suggest that these neuropeptides may be a part of a protective mechanism in the maintenance of nutritional status and that they may have a role in regulating food intake in undernourished children.Publication Open Access Thyroid Hormone Levels in Obese Children and Adolescents with Non-Alcoholic Fatty Liver Disease(2014-01-01) Torun, EMEL; Ozgen, Ilker Tolga; Gokce, Selim; Aydin, SİNEM; Cesur, YAŞAR; TORUN, EMEL; ÖZGEN, İLKER TOLGA; VEHAPOĞLU TÜRKMEN, AYSEL; AYDIN, SİNEM; CESUR, YAŞARObjective: We aimed to determine the association of thyroid functions with the components of metabolic syndrome (MS) and non-alcoholic fatty liver disease (NAFLD) in pediatric obese patients. Methods: The study included 109 obese children (aged 9-15 years) and a control group of 44 healthy age and gender-matched children of normal weight. NAFLD was diagnosed by conventional ultrasound examination. We assessed the anthropometric data and serum biochemical parameters including lipid profile, alanine aminotransferase (ALT), fasting glucose and insulin levels and thyroid stimulating hormone (TSH), free thyroxine (fT4) and free triiodothyronine (fT3) levels. The homeostasis model assessment of insulin resistance (HOMA-IR) was calculated as a measure of IR. Results: The mean age and gender distributions in the groups were similar (p=0.23). The mean body mass index (BMI) z-scores of obese children with grade 2-3 NAFLD were significantly higher than those of the obese children without hepatic steatosis (p<0.001). Mean ALT, triglyceride (TG) and LDL cholesterol increased and HDL-cholesterol significantly decreased as the hepatic steatosis increased (p<0.05). HOMA-IR levels in obese subjects with grade 2-3 NAFLD were significantly higher than those in both obese children without NAFLD and grade 1 NADFL (p=0.05 and 0.001, respectively). In the obese subjects, TSH levels were increased significantly as the degree of steatosis increased (p=0.04) but fT3 and fT4 levels were not different. In correlation analysis, TSH was significantly correlated with ALT, BMI SDS and the degree of steatosis. Conclusions: Obese children demonstrate an increase in TSH levels as the degree of steatosis increased.Publication Metadata only Evaluation of children with nutritional rickets(2011-03-01T00:00:00Z) Cesur, YAŞAR; Dogan, Murat; ARIYUCA, Sevil; BAŞARANOGLU, Murat; BEKTAS, Mehmet Selcuk; PEKER, Erdal; AKBAYRAM, Sinan; CAKSEN, Huseyin; CESUR, YAŞARAim: To evaluate the clinical findings, risk factors, therapy and outcome in 946 children with nutritional rickets.Publication Metadata only Late onset arginine succinate lyase deficiency with normal plasma ammonia level Normal plazma amonyak düzeyi ile seyreden geç başlangiçli argininosüksinat liyaz eksikliǧi(2011-01-01T00:00:00Z) Yilmaz, Cahide; Doǧan, Murat; Cesur, YAŞAR; Çaksen, Hüseyin; Yuca, Sevil Ari; ATAŞ, Bülent; TUNCER, Oǧuz; CESUR, YAŞARPublication Metadata only Congenital primary hypothyroidism diagnosed at advanced ages(2010-01-01T00:00:00Z) Yuca, Sevil Ari; Cesur, YAŞAR; Yilmaz, Cahide; CESUR, YAŞARPublication Metadata only Vitamin D-Dependent Rickets: Eight Cases(2016-01-01T00:00:00Z) Cesur, YAŞAR; Yuca, Sevil Ari; Bektas, Selcuk; Yilmaz, Cahide; Dulger, Haluk; Temel, Hayrettin; CESUR, YAŞARObjective: Vitamin D is essential for bone development and health, and deficiency resulting in rickets and skeletal deformities is seen mainly during rapid growth. Hereditary vitamin D dependent rickets type I and type II rickets is a very rare form of rickets, characterized by 1-alpha-hydroxylase deficiency or end-organ resistance to vitamin D. We aimed to investigate, clinical and laboratory characteristics of eight cases with Vitamin D-dependent rickets (VDRR). Method: The mean age of patients during diagnosis was 2.6 years. Excluding one patient, others were males (87.5%). Results: Mean laboratory values during referral was calcium 7.5 +/- 1,5 mg/dl, phosphorus 4 +/- 1.2 mg/dl, alkaline phosphatase (ALP) 1679 +/- 641 U/L and parathyroid hormone (PTH) 524 +/- 498 pg/ml. Patients received 1.2 mu g/kg/day calcitriol. During follow-ups serum ALP and PTH values of patients turned to normal levels. Conclusion: In rickets, cases with persistent increased serum ALP and PTH levels it will be appropriate to investigate serum 25 (OH) D levels in cases diagnosed with vitamin D-dependent rickets even though hypocalcaemia is absent. Administration of adequate doses of calcitriol in some cases is able to clinical and laboratory values return to normal.