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103. Determination of insulin resistance and its relationship with hyperandrogenemia, anti-Müllerian hormone, inhibin A, inhibin B, and insulin-like peptide-3 levels in adolescent girls with polycystic ovary syndrome.

Author

YETİM ŞAHİN, Aylin, BAŞ, Firdevs, YETİM, Çağcıl, UÇAR, Ahmet, POYRAZOĞLU, Şükran, BUNDAK, Rüveyde, and DARENDELİLER, Feyza

Subjects
*ANTI-Mullerian hormone, *TEENAGE girls, *POLYCYSTIC ovary syndrome, *INSULIN resistance, *GLUCOSE tolerance tests, *INDUCED ovulation
Abstract

Background/aim: This study aims to investigate the association between polycystic ovary syndrome (PCOS) and obesity and insulin resistance (IR) with respect to anti-Müllerian hormone (AMH), inhibin A (INH-A), inhibin B (INH-B), and insulin-like peptide 3 (INSL3) levels, all factors which may have an impact on IR. Materials and methods: In this cross sectional study, 52 adolescent girls diagnosed with PCOS [groups: nonobese (NO), n = 23; overweight/obese (OW/O), n = 29] were included. Blood samples were obtained to measure AMH, INH-B, INH-A, and INSL3 levels, together with hormonal and biochemical assessments. Oral glucose tolerance test (OGTT) was performed and the indexes of IR [homeostasis model assessment: insulin resistance (HOMA-IR) and Matsuda index] were calculated. Results: Insulin resistance was 56.5% with OGTT and 30.4% with HOMA-IR in nonobese-PCOS girls. There was a correlation between INH-A and HOMA-IR even when controlled for body mass index (BMI). INH-B and FAI also had correlations with HOMA-IR which disappeared when controlled for BMI. In regression analyses, AMH (odds ratio = [0.903, P = 0.015) and FAI (odds ratio = 1.353, P = 0.023) are found to be contributors to IR. Their effect was BMI-independent. In ROC analysis, the cutoff value for FAI was 5.93 (sensitivity 71%) to define IR in PCOS girls. Conclusion: AMH and FAI may contribute to IR (defined by OGTT) in PCOS. FAI might be used as a supporting IR marker (defined by OGTT) in adolescent girls with PCOS. [ABSTRACT FROM AUTHOR]

Published
2019
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104. Etiologic Evaluation of Severe Short Stature in Children at a Tertiary Pediatric Endocrinology Centre.

Author

Uçkun, Utkucan, Baş, Firdevs, Poyrazoğlu, Şükran, Şükür, Mine, Darendeliler, Feyza, and Bundak, Rüveyde

Subjects
*SHORT stature, *PEDIATRIC endocrinology, *PITUITARY dwarfism, *GESTATIONAL age, *CHILDREN
Abstract

Objective: The aim of this study was to describe the characteristics and the etiological profile of children with severe short stature evaluated at a tertiary Pediatric Endocrinology centre in Istanbul. Method: Randomly selected 500 patients with the diagnosis of severe short stature height SDS<-3SD) were selected for this study. Among those, 320 patients with at least 12 months of follow-up were included. Results: Among these patients pathological short stature was diagnosed in 94.1%. Endocrine disorders (50.9%) was found to be the leading cause among pathological short stature; followed by specific syndromes and chromosomal abnormalities (13.2%), disproportionate short stature (12.8%), chronic diseases and malnutrition (12.8%), small for gestational age (SGA) with failure of catch-up growth (3.8%) and psychosocial short stature (0.6%). Of those with endocrine disorders; the most common etiology was growth hormone deficiency (GHD) (95.2%). Conclusion: Pathological causes should be ruled out in children with severe short stature. Our results showed that the most common cause was GHD among all subjects. [ABSTRACT FROM AUTHOR]

Published
2019
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105. Endokrin Hastalıklarda Çocukluktan Erişkine Geçiş Deneyimi.

Author

KARAKILIÇ ÖZTURAN, Esin, KARDELEN, Aslı Derya, ÖZTÜRK, Ayşe Pınar, KUBAT ÜZÜM, Ayşe, ÖZÇETİN, Mustafa, BAŞ, Firdevs, POYRAZOĞLU, Şükran, ARAL, Ferihan, DİNÇÇAĞ, Nevin, TANAKOL, Refik, SATMAN, İlhan, and DARENDELİLER, Feyza

Subjects
OBESITY, METABOLIC disorders, PITUITARY dwarfism, PATIENT satisfaction, ADRENOGENITAL syndrome, METABOLIC bone disorders, SEX differentiation disorders
Abstract

Copyright of Journal of the Child / Çocuk Dergisi is the property of Journal of Child and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2018
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106. Transient Neonatal Disorders of Thyroid Function

Author

Saka, Nurçin, Baş, Firdevs, and Berik, Pınar

Subjects
endocrine system, endocrine system diseases
Abstract

Congenital hypothyroidism represent one of the most common preventable causes of mental retardation The incidence of congenital hypothyroidism detected by screening varies from 1 in 3500 to 1 in 4500 Transient disorders of thyroid function detected at screening but disappear subsequently in a few days or weeks may be seen as transient primary hypothyroidism transient hyperthyrotropinaemia or transient hypothyroxinaemia Transient primary hypothyroidism: This disorders is characterized by low serum T4 and high TSH concentrations The prevalance varies geographically being higher in iodine deficient areas which is approximately 1 2000 1 8000 in Europe 1 50000 in USA Administration of iodine containing drugs to the mother in utero or in postnatal period amniotic injection of radiographic contrast agents for amniofetography or use of iodinated skin disinfectants in the neonate may induce hypothyroidism Premature and low birth weight infants are more susceptible to the externally applied iodine induced hypothyroidism Antithyroid drugs used in the pregnant woman with Graves disease may cause transient hypothyroidism by crossing the placenta TSH receptor blocking antibodies may also cause thyroid deficiency on the nervous system justify the treatment with thyroid hormones Therapy is subsequently discontinued according to the underlying cause If the diagnosis is not certain therapy may be continued up to 3 years of age and thyroid hormone status re evaluated after 6 weeks of therapy Transient hyperthyrotropinaemia: This is characterized by high TSH and normal T4 levels Intrauterine iodine excess or deficiency and intrauterine antithyroid drug exposure may result in transient hyperthyrotropinemia Affected infants do not require treatment but prolonged follow up is necessary to exclude the possibility of a permenant disorder such as an ectopic thyroid or an inborn detect in thyroid hormonogenesis Transient hypothyroxinaemia: Serum T4 is low TSH is normal Immaturity of hypothalamo pituitary thyroid axis is the main cause of this disorder which is seen in 3 9 of neonates with higher prevalence in the premature infants Serum T4 concentrations increase with progressive maturation The effect of transient hypothyroxinemia on mental developmental in early infancy is not known thus the treatment of affected infants is controversial In addition to these disorders low T3 syndrome in preterm infants is a normal condition which may last up to 6 7 weeks Key words: Transient Primary Hypothyroidism Congenital Hypothyroidism Neonatal Thyroid Disorders Hyperthyrotropinemia Hypothyroxinaemia Cretinism Goiter Topical Povidone Iodine, SummaryCongenital hypothyroidism represent one of the most common preventable causes of mental retardation The incidence of congenital hypothyroidism detected by screening varies from 1 in 3500 to 1 in 4500 Transient disorders of thyroid function detected at screening but disappear subsequently in a few days or weeks may be seen as transient primary hypothyroidism transient hyperthyrotropinaemia or transient hypothyroxinaemia Transient primary hypothyroidism: This disorders is characterized by low serum T4 and high TSH concentrations The prevalance varies geographically being higher in iodine deficient areas which is approximately 1 2000 1 8000 in Europe 1 50000 in USA Administration of iodine containing drugs to the mother in utero or in postnatal period amniotic injection of radiographic contrast agents for amniofetography or use of iodinated skin disinfectants in the neonate may induce hypothyroidism Premature and low birth weight infants are more susceptible to the externally applied iodine induced hypothyroidism Antithyroid drugs used in the pregnant woman with Graves disease may cause transient hypothyroidism by crossing the placenta TSH receptor blocking antibodies may also cause thyroid deficiency on the nervous system justify the treatment with thyroid hormones Therapy is subsequently discontinued according to the underlying cause If the diagnosis is not certain therapy may be continued up to 3 years of age and thyroid hormone status re evaluated after 6 weeks of therapy Transient hyperthyrotropinaemia: This is characterized by high TSH and normal T4 levels Intrauterine iodine excess or deficiency and intrauterine antithyroid drug exposure may result in transient hyperthyrotropinemia Affected infants do not require treatment but prolonged follow up is necessary to exclude the possibility of a permenant disorder such as an ectopic thyroid or an inborn detect in thyroid hormonogenesis Transient hypothyroxinaemia: Serum T4 is low TSH is normal Immaturity of hypothalamo pituitary thyroid axis is the main cause of this disorder which is seen in 3 9 of neonates with higher prevalence in the premature infants Serum T4 concentrations increase with progressive maturation The effect of transient hypothyroxinemia on mental developmental in early infancy is not known thus the treatment of affected infants is controversial In addition to these disorders low T3 syndrome in preterm infants is a normal condition which may last up to 6 7 weeks Key words: Transient Primary Hypothyroidism Congenital Hypothyroidism Neonatal Thyroid Disorders Hyperthyrotropinemia Hypothyroxinaemia Cretinism Goiter Topical Povidone Iodine

Published
2014

107. Atnalı Böbrek Anomalisi ile Birlikte Rastlanan Diğer Bulgular

Author

Baş, Firdevs, Alpay, Harika, Nayır, Ahmet, Emre, Sevinç, Şirin, Aydan, Kadıoğlu, Alev, and Tanman, Faik

Abstract

Horseshoe kidney is the most common fusion anomaly of the kidney and can be associated with certain syndromes While 2 3 of the cases may be asymptomatic throughout life 1 3 of may be merged with hydronephrosis calculus formation recurrent urinary tract infection or hypertension at different stages of life Out of 11 horseshoe kidney cases followed by the Istanbul University Faculty of Medicine Pediatric Nephrology Department 27 were Turner syndrome 27 had lumbar meningomyelocele 18 showed severe growth retardation and 9 had congenital heart disease VSD aorta insufficiency Forty five percent also had recurrent urinary tract infection 18 had hydronephrosis 18 had vesicoureteral reflux and 9 nephrolithiasis These results show the importance of genetics nephrourologic evaluation and follow up of children with horseshoe kidney Key words: Urinary Tract Abnormalities Hydronephrosis Nephrolithiasis Hypertension, Atnalı böbrek böbrek füzyon anomalilerinin en sık görülenidir Bu anomali bazı sendromlara eşlik edebilir Tüm atnalı olgularının 2 3 ü asemptomatiktir 1 3 oranında ise hayatın çeşitli dönemlerinde hidronefroz taş oluşumu tekrarlayan infeksiyonlar ve hipertansiyon ortaya çıkabilir nbsp; İstanbul Tıp Fakültesi Çocuk Nefrolojisi polikliniğinde atnalı böbrek anomalisi tanısı ile izlenen 11 olgunun 27 si Turner sendromu 27 si lomber meningomiyelosel 18 i ağır büyüme gelişme geriliği 9 u konjenital kalp hastalığı VSD ve aort yetersizliği ile birlikteydi Olguların 45 inde tekrarlayan üriner enfeksiyon 18 inde hidronefroz 18 inde vezikoüreteral reflü 9 unda böbrek taşı 18 inde hipertansiyon saptandı Bu gözlemler atnalı böbrek anomalisi bulunan olgularda genetik ve nefroürolojik izlemenin önemini göstermektedir Anahtar kelimeler: Atnalı Böbrek Üriner Anomaliler Nefrolitiaz Hipertansiyon Horseshoe Kidney

Published
2014

108. Bir Olgu Nedeni İle Nörofibromatoz Tip I ve Renovasküler Hipertansiyon

Author

BAŞ, Firdevs, ALPAY, Harika, NAYIR, Ahmet, EMRE, Sevinç, TANMAN, Faik, and ŞİRİN, Aydan

Abstract

Neurofibromatosis is a multisystemic and autosomal dominant inherited disorder in which vascular anomalies may lead to secondary hypertension Renal artery stenosis is the most common cause of hypertension in such patients A 10 year old male patient with the complaints of headache vomiting vertigo was diagnosed as having neurofibromatosis type I Having observed the presence of hypertension in the patient he was taken under antihypertensive therapy Although there were no abnormalities in the first angiographic evaluation control renal angiography at the end of the first year revealed stenosis in the right main artery and hypovascularisation in the right kidney Nephrectomy was performed after which the patient remained normotensive without any therapy We present this case to show that renovascular hypertension may develop in patients with neurofibromatosis Therefore they should be followed up carefully Key words: Renal Artery Stenosis Neurofibromatosis Hypertension, Multisistemik ve otosomal dominant geçişli bir hastalık olan nörofibromatozda vasküler anomaliler nedeni ile sekonder olarak hipertansiyon ortaya çıkabilmektedir Nörofibromatozlu hastalarda en sık hipertansiyon nedeni renal arter stenozudur Kliniğimize başağrısı kusma başdönmesi yakınmaları ile başvuran 10 yaşındaki erkek hastaya nörofîbromatoz tip I tanısı kondu Antihipertansif tedavi ile kan basıncı kontrol altına alınan hastada ilk yapılan angiografik incelemede vasküler anomali gösterilememesine karşın daha sonra sağana renal arterde belirgin bir stenoz ve sağ böbrekte hipovaskülarizasyon belirlendi Hastaya nefrektomi yapıldı Nefrektomiden sonra antihipertansif ilaçlar kesildi ve hastanın tansiyonu normal sınırlar içinde seyretti Bu olgu nedeniyle nörofibromatozun renovasküler hipertansiyona yol açabileceği bu hastaların sık aralarla izlenmesi gerektiği vurgulandı Anahtar kelimeler: Renal Arter Stenozu Nörofibromatoz Hipertansiyon

Published
2014

109. The Growth Characteristics of Patients with Noonan Syndrome: Results of Three Years of Growth Hormone Treatment: A Nationwide Multicenter Study

Author

Şıklar, Zeynep, primary, Genens, Mikayir, additional, Poyrazoğlu, Şükran, additional, Baş, Firdevs, additional, Darendeliler, Feyza, additional, Bundak, Rüveyde, additional, Aycan, Zehra, additional, Savaş Erdeve, Şenay, additional, Çetinkaya, Semra, additional, Güven, Ayla, additional, Abalı, Saygın, additional, Atay, Zeynep, additional, Turan, Serap, additional, Kara, Cengiz, additional, Can Yılmaz, Gülay, additional, Akyürek, Nesibe, additional, Abacı, Ayhan, additional, Çelmeli, Gamze, additional, Sarı, Erkan, additional, Bolu, Semih, additional, Korkmaz, Hüseyin Anıl, additional, Şimşek, Enver, additional, Çatlı, Gönül, additional, Büyükinan, Muammer, additional, Çayır, Atilla, additional, Evliyaoğlu, Olcay, additional, İşgüven, Pınar, additional, Özgen, Tolga, additional, Hatipoğlu, Nihal, additional, Elhan, Atilla Halil, additional, and Berberoğlu, Merih, additional

Published
2016
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113. Determinants of Increased Aortic Diameters in Young Normotensive Patients With Turner Syndrome Without Structural Heart Disease.

Author

Tuğrul, Melike, Aydın, Banu, Yıldız, Seher, Baş, Firdevs, Poyrazoğlu, Şükran, Darendeliler, Feyza, Saka, Nurçin, Yılmaz, Yasin, Bundak, Rüveyde, Uçar, A., Erol, Bülent Oğuz, Yekeler, Ensar, Nişli, Kemal, and Şahin, Aylin Yetim

Subjects
TURNER'S syndrome, AORTIC dissection, NATRIURETIC peptides, SOMATOMEDIN C, MAGNETIC resonance
Abstract

Factors associated with aortic dilation and dissection in patients with Turner syndrome (TS) remain unclear. We assessed magnetic resonance imaging-based aortic diameters at nine predefined anatomic positions and examined associations of increased aortic diameters with B-type natriuretic peptide (BNP), A-type NP (ANP), growth hormone treatment, insulin-like growth factor 1 (IGF1), and estrogen status. Forty-seven patients with TS aged 7.3-21 years and 34 healthy peers were enrolled in this study. Aortic diameters were higher in patients with TS at three positions than in controls (p < 0.05). History of GH treatment, pubertal status, and serum estradiol levels were not associated with increased aortic diameters. Patients with TS had higher plasma BNP and ANP levels than controls. BNP and IGF1 were independently associated with the increase in aortic diameters in TS at three positions of the ascending aorta (R2 = 0.361-0.458, p < 0.05 for all). At two positions of the descending aorta, only BNP emerged as an independent variable (R2 = 0.130-0.139, p < 0.05). We conclude that young, normotensive patients with TS had greater aortic diameters at several positions than healthy controls. BNP and IGF1 were independently associated with increased aortic diameters in TS. [ABSTRACT FROM AUTHOR]

Published
2018
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114. Çocuk hastalarda diyabetik ketoz ve ketoasidoz sırasındaki elektrokardiyografik değişiklikler.

Author

Aygün, Deniz, Aygün, Fatih, Nişli, Kemal, Baş, Firdevs, and Çıtak, Agop

Subjects
ACIDOSIS, DIABETIC acidosis, ELECTROCARDIOGRAPHY, ELECTROLYTES, HEART conduction system, INTENSIVE care units, SEVERITY of illness index, CHILDREN, DIAGNOSIS, THERAPEUTICS
Abstract

Copyright of Türk Pediatri Arşivi is the property of Aves Yayincilik Ltd. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2017
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115. Precocious or early puberty in patients with combined pituitary hormone deficiency due to POU1F1gene mutation: case report and review of possible mechanisms

Author

Baş, Firdevs, Abalı, Zehra, Toksoy, Güven, Poyrazoğlu, Şükran, Bundak, Rüveyde, Güleç, Çağrı, Uyguner, Zehra, and Darendeliler, Feyza

Abstract

Central precocious puberty (CPP) or early puberty (EP) is a rare entity in combined pituitary hormone deficiency (CPHD), the latter caused by mutations in pituitary transcription factor genes. The early onset of puberty in two patients with CPHD with POU1F1gene mutation was evaluated. A 3-month-old boy was diagnosed with central hypothyroidism, and l-thyroxine was commenced. He was referred for the evaluation of short stature at 20 months of age. Anthropometric evaluation revealed severe short stature (− 6.1 SDS), and growth hormone (GH) and prolactin deficiencies were diagnosed. Homozygous POU1F1gene mutation (c.731T>G, p. I244S) was also detected. Testicular enlargement and high luteinizing hormone (LH) levels were observed at 7 years and 9 months of age while he was on GH and l-thyroxine treatment. Due to rapid progression of puberty, gonadotropin-releasing hormone analogue (GnRHa) was initiated at 11.3 years of age. This patient recently turned 19.2 years old, and his final height was − 2.3 SDS. The second patient, a 6-month-old boy, was also referred for growth retardation. His height was − 2.7 SDS, and GH and thyroid-stimulating hormone (TSH) deficiencies were diagnosed. He also had homozygous (c.10C>T, p.Q4*) POU1F1gene mutation. Onset of puberty was relatively early, at 10 years, with advanced bone age. He was on GnRHa treatment between 11.5 and 12.5 years of age. Recent evaluation of the patient was at 13.6 years of age, and he is still on levothyroxine and GH treatment. The relationship between the POU1F1genotype and CPP or EP has not as yet been firmly established in humans. Animal studies have revealed that the Pou1f1gene has a major effect on regulation of GnRH receptor function and the Gata2gene.It has also been demonstrated that this gene controls gonadotrope evolution and prevents excess gonadotropin levels. Further studies are, however, needed to elucidate the relation between POU1F1function and CPP.

Published
2018
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119. Growth curves for Turkish Girls with Turner Syndrome: Results of the Turkish Turner Syndrome Study Group

Author

Darendeliler, Feyza, primary, Yeşilkaya, Ediz, additional, Bereket, Abdullah, additional, Baş, Firdevs, additional, Bundak, Rüveyde, additional, Sarı, Erkan, additional, Küçükemre Aydın, Banu, additional, Darcan, Şükran, additional, Dündar, Bumin, additional, Büyükinan, Muammer, additional, Kara, Cengiz, additional, Mazıcıoğlu, Mümtaz M., additional, Adal, Erdal, additional, Akıncı, Ayşehan, additional, Atabek, Mehmet Emre, additional, Demirel, Fatma, additional, Çelik, Nurullah, additional, Özkan, Behzat, additional, Özhan, Bayram, additional, Orbak, Zerrin, additional, Ersoy, Betül, additional, Doğan, Murat, additional, Ataş, Ali, additional, Turan, Serap, additional, Gökşen, Damla, additional, Tarım, Ömer, additional, Yüksel, Bilgin, additional, Ercan, Oya, additional, Hatun, Şükrü, additional, Şimşek, Enver, additional, Ökten, Ayşenur, additional, Abacı, Ayhan, additional, Döneray, Hakan, additional, Özbek, Mehmet Nuri, additional, Keskin, Mehmet, additional, Önal, Hasan, additional, Akyürek, Nesibe, additional, Bulan, Kezban, additional, Tepe, Derya, additional, Emeksiz, Hamdi Cihan, additional, Demir, Korcan, additional, Kızılay, Deniz, additional, Topaloğlu, Ali Kemal, additional, Eren, Erdal, additional, Özen, Samim, additional, Demirbilek, Hüseyin, additional, Abalı, Saygın, additional, Akın, Leyla, additional, Eklioğlu, Beray Selver, additional, Kaba, Sultan, additional, Anık, Ahmet, additional, Baş, Serpil, additional, Ünüvar, Tolga, additional, Sağlam, Halil, additional, Bolu, Semih, additional, Özgen, Tolga, additional, Doğan, Durmuş, additional, Çakır, Esra Deniz, additional, Şen, Yaşar, additional, Andıran, Nesibe, additional, Çizmecioğlu, Filiz, additional, Evliyaoğlu, Olcay, additional, Karagüzel, Gülay, additional, Pirgon, Özgür, additional, Çatlı, Gönül, additional, Can, Hatice Dilek, additional, Gürbüz, Fatih, additional, Binay, Çiğdem, additional, Baş, Veysel Nijat, additional, Sağlam, Celal, additional, Gül, Davut, additional, Polat, Adem, additional, Açıkel, Cengizhan, additional, and Cinaz, Peyami, additional

Published
2015
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120. Turner Syndrome and Associated Problems in Turkish Children: A Multicenter Study

Author

Yeşilkaya, Ediz, primary, Bereket, Abdullah, additional, Darendeliler, Feyza, additional, Baş, Firdevs, additional, Poyrazoğlu, Şükran, additional, Aydın, Banu Küçükemre, additional, Darcan, Şükran, additional, Dündar, Bumin, additional, Büyükinan, Muammer, additional, Kara, Cengiz, additional, Sarı, Erkan, additional, Adal, Erdal, additional, Akıncı, Ayşehan, additional, Atabek, Mehmet Emre, additional, Demirel, Fatma, additional, Çelik, Nurullah, additional, Özkan, Behzat, additional, Özhan, Bayram, additional, Orbak, Zerrin, additional, Ersoy, Betül, additional, Doğan, Murat, additional, Ataş, Ali, additional, Turan, Serap, additional, Gökşen, Damla, additional, Tarım, Ömer, additional, Yüksel, Bilgin, additional, Ercan, Oya, additional, Hatun, Şükrü, additional, Şimşek, Enver, additional, Ökten, Ayşenur, additional, Abacı, Ayhan, additional, Döneray, Hakan, additional, Özbek, Mehmet Nuri, additional, Keskin, Mehmet, additional, Önal, Hasan, additional, Akyürek, Nesibe, additional, Bulan, Kezban, additional, Tepe, Derya, additional, Emeksiz, Hamdi Cihan, additional, Demir, Korcan, additional, Kızılay, Deniz, additional, Topaloğlu, Ali Kemal, additional, Eren, Erdal, additional, Özen, Samim, additional, Abalı, Saygın, additional, Akın, Leyla, additional, Eklioğlu, Beray Selver, additional, Kaba, Sultan, additional, Anık, Ahmet, additional, Baş, Serpil, additional, Ünüvar, Tolga, additional, Sağlam, Halil, additional, Bolu, Semih, additional, Özgen, Tolga, additional, Doğan, Durmuş, additional, Çakır, Esra Deniz, additional, Şen, Yaşar, additional, Andıran, Nesibe, additional, Çizmecioğlu, Filiz, additional, Evliyaoğlu, Olcay, additional, Karagüzel, Gülay, additional, Pirgon, Özgür, additional, Çatlı, Gönül, additional, Can, Hatice Dilek, additional, Gürbüz, Fatih, additional, Binay, Çiğdem, additional, Baş, Veysel Nijat, additional, Fidancı, Kürşat, additional, Polat, Adem, additional, Gül, Davut, additional, Açıkel, Cengizhan, additional, Demirbilek, Hüseyin, additional, Cinaz, Peyami, additional, and Bondy, Carolyn, additional

Published
2015
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123. Molecular analysis of PROP1, POU1F1, LHX3, and HESX1 in Turkish patients with combined pituitary hormone deficiency: a multicenter study

Author

Baş, Firdevs, primary, Uyguner, Z. Oya, additional, Darendeliler, Feyza, additional, Aycan, Zehra, additional, Çetinkaya, Ergun, additional, Berberoğlu, Merih, additional, Şiklar, Zeynep, additional, Öcal, Gönül, additional, Darcan, Şükran, additional, Gökşen, Damla, additional, Topaloğlu, Ali Kemal, additional, Yüksel, Bilgin, additional, Özbek, Mehmet Nuri, additional, Ercan, Oya, additional, Evliyaoğlu, Olcay, additional, Çetinkaya, Semra, additional, Şen, Yaşar, additional, Atabek, Emre, additional, Toksoy, Güven, additional, Aydin, Banu Küçükemre, additional, and Bundak, Rüveyde, additional

Published
2014
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126. Clinicopathological Characteristics of Papillary Thyroid Cancer in Children with Emphasis on Pubertal Status and Association with BRAFV600E Mutation.

Author

Poyrazoğlu, Şükran, Bundak, Rüveyde, Baş, Firdevs, Yeğen, Gülçin, Şanlı, Yasemin, and Darendeliler, Feyza

Subjects
THERAPEUTIC use of iodine compounds, RADIOPHARMACEUTICALS, ADOLESCENCE, CHI-squared test, FISHER exact test, GENETIC mutation, PROBABILITY theory, PUBERTY, T-test (Statistics), THYROID gland tumors, RETROSPECTIVE studies, PAPILLARY carcinoma, DATA analysis software, DESCRIPTIVE statistics, KRUSKAL-Wallis Test, CHILDREN, THERAPEUTICS
Abstract

Objective: Papillary thyroid cancer (PTC) may behave differently in prepubertal children as compared to pubertal children and adults. BRAF gene activating mutations may associate with PTC by creating aberrant activation. We aimed to evaluate the clinicopathological characteristics of PTC patients with emphasis on the pubertal status and also to investigate the association of BRAFV600E mutation with disease characteristics. Methods: The medical records of 75 patients with PTC were reviewed retrospectively. BRAFV600E mutation status was available only in the medical records of 56 patients. Results: Mean age at diagnosis was 12.4±3.8 years. There was no difference in sex, initial signs, tumor histopathology, and pathological evidence of tumor aggressiveness between prepubertal and pubertal children. Although not statistically significant, lateral neck nodal metastasis and lung metastasis at diagnosis were more prevalent in prepubertal children. After excluding patients with microcarcinoma, prepubertal children were found to require lateral neck dissection and further doses of radioactive iodine more frequently than pubertal patients. Recurrence was also more frequent in prepubertal children (p=0.016). Frequency of BRAFV600E mutation was similar in prepubertal and pubertal patients. BRAFV600E mutation was found in 14/56 (25%) patients and was high in the classic variant PTC (p=0.004). Multicentricity was high in BRAFV600E mutation (p=0.01). There was no relation between BRAFV600E mutation and lymph node and pulmonary metastasis at diagnosis, or between BRAFV600E mutation and pathological evidence of tumor aggressiveness. Conclusion: PTC is more disseminated in prepubertal children. BRAFV600E mutation does not correlate with a more extensive or aggressive disease. BRAFV600E mutation is not the cause of the differences in the biological behavior of PTC in prepubertal and pubertal children. [ABSTRACT FROM AUTHOR]

Published
2017
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127. Ergenlik Döneminde D ve B12 Vitamin Eksikliklerinin Sıklığıc.

Author

YETİM, Aylin, TIKIZ, Ceyhun, and BAŞ, Firdevs

Abstract

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Published
2017
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131. Adherence to Growth Hormone Therapy: Results of a Multicenter Study

Author

Aydın, Banu Küçükemre, primary, Aycan, Zehra, additional, Şıklar, Zeynep, additional, Berberoğlu, Merih, additional, Öcal, Gönül, additional, Çetinkaya, Semra, additional, Baş, Veysel Nijat, additional, Kendirci, Havva Nur Peltek, additional, Çetinkaya, Ergun, additional, Darcan, Şükran, additional, Gökşen, Damla, additional, Evliyaoğlu, Olcay, additional, Şükür, Mine, additional, Baş, Firdevs, additional, and Darendeliler, Feyza, additional

Published
2014
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132. Pelvic ultrasound findings in prepubertal girls with precocious adrenarche born appropriate for gestational age

Author

Uçar, Ahmet, primary, Erol, Oğuz Bulent, additional, Yekeler, Ensar, additional, Yildiz, Ismail, additional, Bozlak, Serdar, additional, Saka, Nurçin, additional, BaŞ, Firdevs, additional, Poyrazoğlu, Şükran, additional, Bundak, Rüveyde, additional, Kubat Uzum, Ayse, additional, Gul, Nurdan, additional, and Darendeliler, Feyza, additional

Published
2013
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133. Netherton Syndrome Associated with Growth Hormone Deficiency

Author

Aydın, Banu Küçükemre, primary, Baş, Firdevs, additional, Tamay, Zeynep, additional, Kılıç, Gürkan, additional, Süleyman, Ayşe, additional, Bundak, Rüveyde, additional, Saka, Nurçin, additional, Özkaya, Esen, additional, Güler, Nermin, additional, and Darendeliler, Feyza, additional

Published
2013
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137. Ergenlik ve Sosyal Çalışma.

Author

GÜDEK, Kemal, YETİM, Aylin, BAŞ, Firdevs, and KILIÇ, Ayşe

Abstract

Copyright of Journal of the Child / Çocuk Dergisi is the property of Journal of Child and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2016
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138. Clinical and Laboratory Characteristics of Children Referred for Early Puberty: Preponderance in 7-8 Years of Age

Author

Kılıç, Ayşe, primary, Durmuş, Mehmet Sait, additional, Ünüvar, Emin, additional, Yıldız, İsmail, additional, Küçükemre Aydın, Banu, additional, Uçar, Ahmet, additional, Bundak, Rüveyde, additional, Baş, Firdevs, additional, Darendeliler, Feyza, additional, Oğuz, Fatma, additional, Sıdal, Müjgan, additional, and Yekeler, Ensar, additional

Published
2012
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141. The Exon 3-Deleted/Full-Length Growth Hormone Receptor Polymorphism and Response to Growth Hormone Therapy in Growth Hormone Deficiency and Turner Syndrome: A Multicenter Study

Author

Baş, Firdevs, primary, Darendeliler, Feyza, additional, Aycan, Zehra, additional, Çetinkaya, Ergun, additional, Berberoğlu, Merih, additional, Şıklar, Zeynep, additional, Öcal, Gönül, additional, Timirci, Özlem, additional, Çetinkaya, Semra, additional, Darcan, Şükran, additional, Gökşen Şimşek, Damla, additional, Bideci, Aysun, additional, Cinaz, Peyami, additional, Böber, Ece, additional, Demir, Korcan, additional, Bereket, Abdullah, additional, Turan, Serap, additional, Atabek, M. Emre, additional, Tütüncüler, Filiz, additional, İsbir, Turgay, additional, Bozkurt, Nilüfer, additional, Kabataş Eryılmaz, Sema, additional, Uzunhan, Ozan, additional, Küçükemre Aydın, Banu, additional, and Bundak, Rüveyde, additional

Published
2012
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147. CYP21A2 Gene Mutations in Congenital Adrenal Hyperplasia: Genotype-phenotype correlation in Turkish children

Author

Baş, Firdevs, primary, Kayserili, Hülya, additional, Darendeliler, Feyza, additional, Uyguner, Oya, additional, Günöz, Hülya, additional, Yüksel Apak, Memnune, additional, Atalar, Fatmahan, additional, Bundak, Rüveyde, additional, Wilson, Robert C., additional, New, Maria I., additional, Wollnik, Bernd, additional, and Saka, Nurçin, additional

Published
2011
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148. An easily missed diagnosis: 17-alpha-hydroxylase/17,20-lyase deficiency.

Author

Küçükemre-Aydın, Banu, Öğrendil-Yanar, Özlem, Bilge, Ilmay, Baş, Firdevs, Poyrazoğlu, Şükran, Yılmaz, Alev, Emre, Sevinç, Bundak, Rüveyde, Saka, Nurçin, and Darendeliler, Feyza

Abstract

The CYP17A1 gene encodes the enzyme P450c17, which mediates both 17α-hydroxylase and 17,20-lyase activities and is essential for production of cortisol and sex steroids. Loss-of-function mutations of this gene cause 17α-hydroxylase/17,20-lyase deficiency, characterized by hypertension, hypokalemia and sexual infantilism. A 6-year-old phenotypically female patient presented with hypertension and hyperpigmentation. Her blood test results showed low cortisol and high adrenocorticotropic hormone (ACTH), progesterone, deoxycorticosterone and gonadotropin levels and were consistent with the diagnosis of 17α-hydroxylase/17,20-lyase deficiency. Her karyotype was 46XY. Genetic studies of the patient revealed a novel homozygous point mutation, c.1307G>A, within the coding sequence of the CYP17A1 gene. 17α-hydroxylase/17,20-lyase deficiency should be considered in the differential diagnosis of hypertension in children and adolescents, and physical examination of these patients should be done very carefully. [ABSTRACT FROM AUTHOR]

Published
2015

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