Publications by authors named "Nurgün Kandemir"

68 Publications

Urinary bisphenol A levels in prepubertal children with exogenous obesity according to presence of metabolic syndrome.

J Pediatr Endocrinol Metab 2021 Apr 24;34(4):495-502. Epub 2021 Feb 24.

Department of Pediatrics, Faculty of Medicine, Hacettepe University, Ankara, Turkey.

Objectives: Recent studies have shown a potential link between chronic exposure to Bisphenol A (BPA) and exogenous obesity, the prevalence of which has been increasing dramatically in all age groups and particularly among children in the last decades. In this study, we aimed at comparing BPA exposure levels between controls and otherwise healthy, drug-naive, pre-pubertal children having exogenous obesity with/without metabolic syndrome.

Methods: A total of 63 pre-pubertal children with exogenous obesity whom 27 of them having metabolic syndrome attending Hacettepe University Ihsan Dogramaci Children's Hospital were included in this study. The control group consisted of 34 age- and sex-matched healthy children with no significant underlying medical conditions. Urinary BPA levels were measured using LC-MS/MS (high-performance liquid chromatography coupled with tandem mass spectrometry) methodology.

Results: Urinary BPA levels among obese children were significantly higher than those of the control group (median: 22.9 μg/g-creatinine and 6.9 μg/g-creatinine, respectively; p=0.0001). When adjusted with generalized linear models for age, gender and scores of body mass index, obese children having metabolic syndrome had significantly higher urinary BPA levels than obese children without metabolic syndrome and both obese groups had considerably elevated levels of urinary BPA than the controls (estimated marginal mean ± standard error: 42.3 ± 7.4 μg/g-creatinine, 22.6 ± 3.5 μg/g-creatinine and 12.1 ± 2.5 μg/g-creatinine, respectively, p=0.0001).

Conclusions: This study shows much higher BPA exposure among obese children with metabolic syndrome during the prepubertal period.
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http://dx.doi.org/10.1515/jpem-2020-0371DOI Listing
April 2021

Alpha-Melanocyte-Stimulating Hormone is Elevated in Hypothalamic Obesity Associated with Childhood Craniopharyngioma.

Obesity (Silver Spring) 2021 Feb;29(2):402-408

Department of Pediatric Endocrinology, Hacettepe University, Ankara, Turkey.

Objective: The purpose of this study was to investigate the peripheral concentrations of leptin and neuropeptides taking part in the melanocortin pathway in hypothalamic obesity (HO) associated with craniopharyngioma (CP) and to find a peripheral marker for diagnosis.

Methods: Thirty-one patients (52% girls; median age 16 years) with CP were enrolled in the study group. They were grouped as CP with obesity (CP , n = 17) and CP without obesity (CP , n = 14). Two control groups without CP consisted of 27 children with obesity (OC) (55% girls; median age 13.8 years) and 25 children without obesity (normal control [NC]) (72% girls; median age 14.5 years). Obesity was defined as BMI percentile ≥ 95%. Fasting serum concentrations of leptin, brain-derived neurotrophic factor (BDNF), and alpha-melanocyte-stimulating hormone (α-MSH) were measured in the groups.

Results: Leptin and BDNF concentrations were correlated with BMI SD score (SDS) in controls (OC + NC) and CP. However, there was no correlation between α-MSH and BMI-SDS in CP or control groups. After adjusting for age, sex, and BMI-SDS, α-MSH was found to be significantly higher in CP than in other groups, whereas leptin and BDNF were comparable among the four groups.

Conclusions: Serum BDNF, just like leptin, increased with BMI, regardless of hypothalamic damage. On the contrary, α-MSH concentration was significantly high in HO, designating a potential biomarker for HO in CP.
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http://dx.doi.org/10.1002/oby.23087DOI Listing
February 2021

Which parameters predict the beneficial effect of GnRHa treatment on height in girls with central precocious puberty?

Clin Endocrinol (Oxf) 2021 May 7;94(5):804-810. Epub 2021 Feb 7.

Division of Pediatric Endocrinology, Department of Pediatrics, Faculty of Medicine, Hacettepe University, Ankara, Turkey.

Objective: Data about GnRHa on adult height in girls with central precocious puberty (CPP) have shown variable results, ranging from improvement of growth prognosis to lack of any benefit. This study was designed to delineate the criteria to decide which girls with idiopathic CPP (iCPP) will have a height benefit from GnRHa treatment.

Design: Retrospective PATIENTS: 102 girls with iCPP who had reached final height (FH) were included.

Measurements: Auxological, hormonal and radiological findings at treatment onset, and FHs were extracted from records.

Results: Most important factor affecting height gain was chronological age (CA) at treatment onset. All the girls treated ≤6.4 years of age achieved a height gain of ≥1SDS, while none of the girls treated ≥8.3 years of age made the target. 75.6% of patients who started GnRHa between the ages of 6.4 and 8.3 years had a height gain of ≥1SDS. Most important factors affecting height gain in those treated 6.4-8.3 years were advanced bone age (BA), basal estradiol (E ) and pubertal stage (r : 0.906; P < .001). All individuals with BA advancement of ≥2.6 years or E of ≥32.6 pg/ml or pubertal stage of ≥3 had significant height gain, and none of the cases with BA advancement of <2 years or E of <21.5 pg/ml or pubertal stage of <2 had a height gain of ≥1SDS.

Conclusions: Treatment with GnRHa is unquestionably beneficial to improve FH in girls with iCPP when initiated ≤6.4 years of age. GnRHa treatment after 8.3 years of age may not improve FH. Girls between the ages of 6.4 and 8.3 years at presentation can have a better height gain if BA (≥2.6 years over CA) and pubertal findings (pubertal stage ≥3 or E ≥32.6 pg/ml) are well-advanced.
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http://dx.doi.org/10.1111/cen.14420DOI Listing
May 2021

Basal serum thyroxine level should guide initial thyroxine replacement dose in neonates with congenital hypothyroidism.

J Clin Res Pediatr Endocrinol 2020 Dec 30. Epub 2020 Dec 30.

Hacettepe University Faculty of Medicine, Department of Pediatric Endocrinology, Ankara, Turkey.

Objective: Initial high-dose Na-L thyroxine (Na-LT4) (10-15 μg/kg/day) replacement for primary congenital hypothyroidism (CH) is recommended in guidelines. However, high-dose Na-LT4 has risks. In this study, we aimed to investigate normalizing effect of varying initial doses of Na-LT4 on serum thyroid hormone levels.

Methods: Fifty-two patients were analyzed retrospectively. The patients were classified into mild (27/51.9%), moderate (11/21.1%) and severe (14/26.9%) CH with respect to initial free thyroxine (FT4) levels. Time taken to achieve target hormone levels was compared within groups.

Results: Initial mean Na-LT4 doses for mild, moderate and severe disease were 6.9±3.3, 9.4±2.2 and 10.2±2 μg/kg/day. Serum FT4 levels reached the upper half of normal range (>1.32 ng/dL) in a median of 16, 13 and 16 days in patients with mild, moderate and severe CH with the mean time from initial treatment to first control visit 14.8 ± 6 days (range 1-36). There was no significant difference in terms of time to achieve target FT4 hormone levels according to disease severity (p=0.478). Seven (25.9%), 8 (72.7%) and 8 (57.1%) patients experienced hyperthyroidism (serum FT4 >1.94 ng/dL) in mild, moderate, severe CH groups in the first visit, respectively (p=0.016).

Conclusion: Not all patients diagnosed with CH require high-dose Na-LT4, initial dose of Na-LT4 may be tailored based on pre-treatment thyroid hormone levels. Some patients with moderate and severe CH, experienced iatrogenic hyperthyroidism even though the dose was close to the lower limit of the recommended range in guidelines; suggesting lower initial doses and closer follow-up within the first week.
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http://dx.doi.org/10.4274/jcrpe.galenos.2020.2020.0194DOI Listing
December 2020

Gender-related differences in etiology of organic central precocious puberty.

Turk J Pediatr 2020 ;62(5):763-769

Division of Pediatric Endocrinology, Department of Pediatrics, Hacettepe University Faculty of Medicine, Ankara, Turkey.

Background: Central precocious puberty (CPP) is idiopathic in 90% of girls and 60% of boys, while some cases are caused by lesions of central nervous system (CNS), a condition often referred to as organic CPP. We aimed to analyze the etiology of organic CPP in a large cohort of girls and boys and determine gender-related differences.

Methods: Medical files of 256 girls and 120 boys diagnosed and treated for CPP in a single center in the last two decades were reviewed. Patients were classified into four groups with respect to previous history and MRI findings: (1) previously established CNS pathology at the time of diagnosis, (2) novel CNS pathology previously asymptomatic, (3) incidentalomas considered to be unrelated to CPP, and (4) completely normal MRI. Group 1 and 2 were considered as organic CPP whereas group 3 and 4 were considered as idiopathic CPP.

Results: Prevalence of CNS pathology was significantly higher in boys than girls (21.7% vs 6.2%). Previous CNS pathologies such as developmental anomaly of CNS, parenchymal injury, necrotic lesions and hydrocephalus were present in 3.5% of girls and 8.3% of boys. Prevalence of novel CNS pathology as determined by imaging among neurologically asymptomatic patients was 2.8% in girls and 14.5% in boys. The most common novel CNS pathologies in boys were hamartomas (5%) and suprasellar arachnoid cysts (3.3%); which were significantly lower in girls (0.8 and 0.8% respectively). Onset of organic CPP was before six years in girls, and seven years in boys.

Conclusions: Organic CPP was 3.5 times more common in boys compared to girls. It is possible to detect an underlying CNS pathology in one out of every five boys with CPP. Frequency and distribution of organic etiology also differ between girls and boys, hypothalamic hamartomas and suprasellar arachnoid cysts being more common in boys than girls. The likelihood of novel intracranial pathology associated with CPP is quite low in girls with an onset after six years of age and in boys with an onset after seven years of age.
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http://dx.doi.org/10.24953/turkjped.2020.05.007DOI Listing
January 2020

Treatment response to long term antiresorptive therapy in osteogenesis imperfecta type VI: does genotype matter?

J Pediatr Endocrinol Metab 2020 Dec 8;33(12):1617-1624. Epub 2020 Oct 8.

Division of Pediatric Endocrinology, Department of Pediatrics, Hacettepe University Medical School, Ankara, Turkey.

Objectives: Osteogenesis imperfecta type VI (OI VI) follows a progressive and severe course, yet unlike other forms of severe OI it has a later onset of fractures, and extra-skeletal findings are not part of the clinical picture. Another difference is that there is an increase in unmineralized osteoid tissue in OI VI, which hinders the effect of bisphosphonates-the current standard of treatment for OI. Therefore, the response to standard treatments in OI VI is not satisfactory. Herein, we report long-term follow-up of two cases with novel mutations, who show great variation in their treatment response to bisphosphonates.

Case Presentation: The first case was given pamidronate at the age of 15 months when he could sit independently, followed a fluctuating course under treatment, fracture rate did not decrease, however he was able to mobilize with walker at the age of 10 years. On the other hand, the second case developed severe deformities and became wheelchair-bound under pamidronate, thus the treatment was switched to denosumab. Unfortunately, there was no improvement under denosumab after 15 months too, and since bone pain increased, denosumab treatment was stopped. He was put on zoledronic acid instead.

Conclusion: transcript amount may be an important factor to explain the variation in response to pamidronate therapy. In OI VI patients, the factors affecting the clinical course should be identified and new or combined treatment options should be established.
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http://dx.doi.org/10.1515/jpem-2020-0260DOI Listing
December 2020

Novel insights into diabetes mellitus due to DNAJC3-defect: Evolution of neurological and endocrine phenotype in the pediatric age group.

Pediatr Diabetes 2020 11 10;21(7):1176-1182. Epub 2020 Sep 10.

Department of Medical Genetics, Hacettepe University, Ankara, Turkey.

Background: A number of inborn errors of metabolism caused by abnormal protein trafficking that lead to endoplasmic reticulum storage diseases (ERSD) have been defined in the last two decades. One such disorder involves biallelic mutations in the gene encoding endoplasmic reticulum resident co-chaperone DNAJC3 (P58 ) that leads to diabetes in the second decade of life, in addition to multiple endocrine dysfunction and nervous system involvement.

Objective: The aim of this study was to define the natural history of this new form of diabetes, especially the course of abnormalities related to glucose metabolism.

Methods: Whole-exome and Sanger sequencing was used to detect DNAJC3 defect in two patients. Detailed analysis of their clinical history as well as biochemical, neurological and radiological studies were carried out to deduce natural history of neurological and endocrine phenotype.

Results: DNAJC3 defect led to beta-cell dysfunction causing hyperinsulinemichypoglycemia around 2 years of age in both patients, which evolved into diabetes with insulin deficiency in the second decade of life, probably due to beta cell loss. Endocrine phenotype involved severe early-onset growth failure due to growth hormone deficiency, and hypothyroidism of central origin. Neurological phenotype involved early onset sensorineural deafness discovered around 5 to 6 years, and neurodegeneration of central and peripheral nervous system in the first two decades of life.

Conclusion: Biallelic loss-of-function in the ER co-chaperone DNAJC3 leads to a new form of diabetes with early onset hyperinsulinemic hypoglycemia evolving into insulin deficiency as well as severe growth failure, hypothyroidism and diffuse neurodegeneration.
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http://dx.doi.org/10.1111/pedi.13098DOI Listing
November 2020

Effect of long-term glucocorticoid therapy on bone mineral density of the patients with congenital adrenal hyperplasia.

Turk J Pediatr 2020 ;62(3):359-366

Division of Pediatric Endocrinology, Department of Pediatrics, Hacettepe University Faculty of Medicine, Ankara.

Background And Objectives: Congenital adrenal hyperplasia (CAH) is characterized by androgen excess which should be treated with life-long glucocorticoid therapy, thus can affect bone mineralization. We aimed to evaluate the bone mineral density (BMD) and determine the factors affecting bone mineralization in patients with CAH.

Method: This prospective case-control study was conducted in children, adolescents and young adults with classical 21-hydroxylase CAH, and age-, sex-, and pubertal stage matched healthy controls. Lumbar1-4 BMD was determined by dual-energy X-ray absorptiometry. BMD z-score was calculated using national standards with respect to height age and was referred as `low BMD` if z-score < -1 SD. Univariate analyses were performed between low BMD and normal BMD groups, and multivariate logistic regression analysis was performed to assess the independent predictors of low BMD. Correlations of Body Mass Index (BMI)-z-score, average serum 17-hydroxyprogesterone level, duration of treatment, average and cumulative glucocorticoid doses with BMD z-score were evaluated with Spearman analyses.

Results: Each group included 37 cases. BMD z-score of patients with CAH [0.47 (-0.04 - 1.56)] was higher than control group [-0.43 (-0.82 -0.05)]; p= < 0.001. Number of patients with low BMD was similar in both groups; [CAH: 6(16.2%), control: 5(13.5%); p= 0.744]. BMI- z-score was higher in patients with CAH when compared to control group; p= < 0.001. BMI z-score was lower in low BMD group as comparison to normal BMD group; p= 0.041. Each 1.0 decrease in BMI z-score, risk of having low BMD was found to increase by 1.79 (%95 CI: 1.03- 3.12, p= 0.040). BMI-z-score, average serum 17-hydroxyprogesterone level, duration of treatment, average and cumulative glucocorticoid doses were not found to be correlated with BMD z-score.

Conclusion: Long-term glucocorticoid therapy did not have negative effect on BMD of patients with CAH. Higher BMI z-score in patients with CAH may have a positive effect on preserving bone health. Precautions should be taken for increased risk of obesity.
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http://dx.doi.org/10.24953/turkjped.2020.03.002DOI Listing
January 2020

Clinical and Molecular Analysis in 2 Families With Novel Compound Heterozygous SBP2 (SECISBP2) Mutations.

J Clin Endocrinol Metab 2020 03;105(3)

Department of Medicine, The University of Chicago, Chicago, Illinois.

Context: Selenocysteine insertion sequence binding protein 2 (SECISBP2, SBP2) is an essential factor for selenoprotein synthesis. Individuals with SBP2 defects have characteristic thyroid function test (TFT) abnormalities resulting from deficiencies in the selenoenzymes deiodinases. Eight families with recessive SBP2 gene mutations have been reported to date. We report 2 families with inherited defect in thyroid hormone metabolism caused by 4 novel compound heterozygous mutations in the SBP2 gene.

Case Descriptions: Probands 1 and 2 presented with growth and developmental delay. Both had characteristic TFT with high T4, low T3, high reverse T3, and normal or slightly elevated TSH. The coding region of the SBP2 gene was sequenced and analysis of in vitro translated wild-type and mutant SBP2 proteins was performed. Sequencing of the SBP2 gene identified novel compound heterozygous mutations resulting in mutant SBP2 proteins E679D and R197* in proband 1, and K682Tfs*2 and Q782* in proband 2. In vitro translation of the missense E679D demonstrated all four isoforms, whereas R197* had only 2 shorter isoforms translated from downstream ATGs, and Q782*, K682Tfs*2 expressed isoforms with truncated C-terminus. Reduction in serum glutathione peroxidase enzymatic activity was also demonstrated in both probands.

Conclusions: We report 2 additional families with mutations in the SBP2 gene, a rare inherited condition manifesting global selenoprotein deficiencies. Report of additional families with SBP2 deficiency and their evaluation over time is needed to determine the full spectrum of clinical manifestations in SBP2 deficiency and increase our understanding of the role played by SBP2 and selenoproteins in health and disease.
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http://dx.doi.org/10.1210/clinem/dgz169DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7034949PMC
March 2020

What is the evidence for beneficial effects of growth hormone treatment beyond height in short children born small for gestational age? A review of published literature.

J Pediatr Endocrinol Metab 2020 Jan;33(1):53-70

Novo Nordisk A/S, Søborg, Denmark.

Background An increasing body of evidence supports the view that both an adverse intrauterine milieu and rapid postnatal weight gain in children born small for gestational age (SGA) contribute towards the risk for the development of chronic diseases in adult life. Content The aim of this review was to identify and summarize the published evidence on metabolic and cardiovascular risk, as well as risk of impaired cardiac function, intellectual capacity, quality of life, pubertal development and bone strength among children born SGA. The review will then address whether growth hormone (GH) therapy, commonly prescribed to reduce the height deficit in children born SGA who do not catch up in height, increases or decreases these risks over time. Summary Overall, there are limited data in support of a modest beneficial effect of GH therapy on the adverse metabolic and cardiovascular risk observed in short children born SGA. Evidence to support a positive effect of GH on bone strength and psychosocial outcomes is less convincing. Outlook Further evaluation into the clinical relevance of any potential long-term benefits of GH therapy on metabolic and cardiovascular endpoints is warranted.
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http://dx.doi.org/10.1515/jpem-2019-0098DOI Listing
January 2020

Long-term effects of GnRH agonist treatment on body mass index in girls with idiopathic central precocious puberty.

J Pediatr Endocrinol Metab 2020 Jan;33(1):99-105

Division of Pediatric Endocrinology, Department of Pediatrics, Hacettepe University Medical School, Ankara, Turkey.

Introduction Studies evaluating effects of gonadotropin-releasing hormone agonist (GnRHa) on weight and body-mass-index (BMI) in girls with idiopathic central precocious puberty (iCPP) include short-term effects. The aim of this study is to investigate changes in BMI during and 2 years after completion of GnRHa to determine the factors that may impact BMI in girls with iCPP. Methods Medical files of 138 girls who completed GnRHa were evaluated. All patients had weight and height measurements at the beginning and end of treatment, and 111 patients had anthropometric measurements 2 years after the completion of treatment. Results In the beginning, 82 (59.4%) had normal weight (NW), 42 (30.4%) were overweight (OW), and 14 (10.2%) were obese (OB). Analysis of BMI-standard deviation score (SDS) in the whole group showed an overall increase during GnRHa treatment (0.92 ± 0.74 vs. 1.20 ± 0.51, p < 0.001). Changes in BMI-SDS (ΔBMI-SDS) during GnRHa differed between NW and OW/OB (0.45 ± 0.31 vs. 0.03 ± 0.20, p < 0.001). BMI-SDSs of both groups returned to baseline scores (or initial levels) 2 years after the completion of treatment. Two factors affecting ΔBMI-SDS in multiple linear regression analyses were baseline BMI and Δheight-SDS, both correlated negatively with ΔBMI-SDS. Conclusions The present study is one of the studies evaluating BMI change over a long period of time in girls with CPP. Although BMI-SDS increased during GnRHa in NW girls, it was reversible in follow-up after treatment. However, BMI-SDS did not change during and in follow-up in OW/OB girls. Conserving BMI-SDS in OW/OB girls may be related to the fact that weight management programs were recommended for these patients. Dietary recommendations should be provided for children with NW who undergo GnRHa, as is the case for OW patients.
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http://dx.doi.org/10.1515/jpem-2019-0214DOI Listing
January 2020

Treatment with Depot Leuprolide Acetate in Girls with Idiopathic Precocious Puberty: What Parameter should be Used in Deciding on the Initial Dose?

J Clin Res Pediatr Endocrinol 2020 03 26;12(1):37-44. Epub 2019 Jul 26.

Hacettepe University Faculty of Medicine, Department of Pediatrics, Division of Pediatric Endocrinology, Ankara, Turkey

Objective: Doses of gonadotropin releasing hormone (GnRH) analogues used to treat idiopathic central precocious puberty (iCPP) vary among clinicians. Study aims were to evaluate the efficacy of a monthly 3.75 mg dose of leuprolide acetate (LA) to suppress the hypothalamo-pituitary-gonadal (HPG) axis in girls with iCPP and to determine factors that may have an impact on the supressing dose.

Methods: Study subjects were 220 girls receiving LA for iCPP. LA was started at a dose of 3.75 mg/28 days. Suppression was assessed using the GnRH test at the third month. To assess clinical suppression signs and symptoms of puberty were also evaluated. The dose of LA was increased to 7.5 mg/28 days in those who had a peak luteinising hormone (LH) ≥2 IU/L and in whom adequate clinical suppression of puberty was absent. Receiver operating characteristic curves were used to determine thresholds for clinical and hormonal factors affecting the suppressing dose of LA. Logistic regression analyses were used to investigate thresholds which might differentiate between those requiring high dose for suppression and those in whom lower dose LA was adequate.

Results: Peak stimulated LH <2 IU/L was achieved in 88.6% with a dose of LA of 3.75 mg (0.11±0.03 mg/kg). Significant variables for differentiating the two doses were body weight (Wt) of 36.2 kg and/or body mass index (BMI)-standard deviation scores (SDS) of 1.64 (p<0.001). Multiple logistic regressions showed that Wt and BMI-SDS values above thresholds indicated requirement of LA at a dose of 7.5 mg/28 days (p<0.001).

Conclusion: Monthly injections of 3.75 mg LA is an effective treatment in the majority of girls with iCPP. However, a higher initial dose may be preferred in patients with a Wt ≥36 kg or BMI-SDS ≥1.6 for effective suppression of the HPG axis.
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http://dx.doi.org/10.4274/jcrpe.galenos.2019.2019.0060DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7127887PMC
March 2020

Further expanding the mutational spectrum and investigation of genotype-phenotype correlation in 3M syndrome.

Am J Med Genet A 2019 07 13;179(7):1157-1172. Epub 2019 Apr 13.

Department of Pediatric Genetics, Hacettepe University Faculty of Medicine, Ankara, Turkey.

3M syndrome is characterized by severe pre- and postnatal growth retardation, typical facial features, and normal intelligence. Homozygous or compound heterozygous mutations in either CUL7, OBSL1, or CCDC8 have been identified in the etiology so far. Clinical and molecular features of 24 patients (23 patients and a fetus) from 19 unrelated families with a clinical diagnosis of 3M syndrome were evaluated and genotype-phenotype correlations were investigated with the use of DNA sequencing, chromosomal microarray, and whole exome sequencing accordingly. A genetic etiology could be established in 20 patients (n = 20/24, 83%). Eleven distinct CUL7 or OBSL1 mutations, among which eight was novel, were identified in 18 patients (n = 18/24, 75%). Ten patients had CUL7 (n = 10/18, 56%) while eight had OBSL1 (n = 8/18, 44%) mutations. Birth weight and height standard deviation scores at admission were significantly (p < 0.05) lower in patients with CUL7 mutation compared to that of patients with OBSL1 mutation. Two patients with a similar phenotype had a de novo 20p13p deletion involving BMP2. No genetic etiology could be established in four patients (n = 4/28, 17%). This study yet represents the largest cohort of 3M syndrome patients from a single center in Turkey. Microdeletions involving BMP2 may cause a phenotype similar to 3M syndrome with some distinctive features. Larger cohort of patients are required to establish genotype-phenotype correlations in 3M syndrome.
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http://dx.doi.org/10.1002/ajmg.a.61154DOI Listing
July 2019

Bone Parameters in Anorexia Nervosa and Athletic Amenorrhea: Comparison of Two Hypothalamic Amenorrhea States.

J Clin Endocrinol Metab 2018 06;103(6):2392-2402

Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.

Objective: We have reported low bone mineral density (BMD), impaired bone structure, and increased fracture risk in participants with anorexia nervosa (AN) and normal-weight oligoamenorrheic athletes (OAs). However, data directly comparing compartment-specific bone parameters in participants with AN, OAs, and controls are lacking.

Design: A total of 468 female participants 14 to 21.9 years old were included: 269 with AN, 104 OAs, and 95 normal-weight eumenorrheic controls. Dual-energy x-ray absorptiometry was used to assess areal BMD (aBMD) of the whole body less head (WBLH), spine, and hip. High-resolution peripheral quantitative computed tomography was used to assess volumetric BMD (vBMD), bone geometry, and structure at the non-weight-bearing distal radius and weight-bearing distal tibia.

Results: Participants with AN had lower WBLH and hip aBMD z scores than OAs and controls (P < 0.0001). Participants with AN and OAs had lower spine aBMD z scores than controls (P < 0.01). At the radius, total and cortical vBMD, percentage cortical area, and thickness were lower in the AN and OA groups than in controls (P ≤ 0.04); trabecular vBMD was lower in participants with AN than controls. At the tibia, participants with AN had lower measures for most parameters compared with OAs and controls (P < 0.05); OAs had lower cortical vBMD than controls (P = 0.002). Participants with AN and OAs had higher fracture rates than controls. Stress fracture prevalence was highest in OAs (P < 0.0001); nonstress fracture prevalence was highest in participants with AN (P < 0.05).

Conclusion: AN is deleterious to bone at all sites and both bone compartments. A high stress fracture rate in OAs, who have comparable WBLH and hip aBMD measures to controls, indicates that BMD in these women may need to be even higher to avoid fractures.
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http://dx.doi.org/10.1210/jc.2018-00338DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6456997PMC
June 2018

A pheochromocytoma case diagnosed as adrenal incidentaloma.

Turk J Pediatr 2017 ;59(2):200-206

Division of Pediatric Endocrinology Departments of Pediatrics, Hacettepe University Faculty of Medicine, Ankara, Turkey.

Vurallı D, Kandemir N, Clark G, Orhan D, Alikaşifoğlu A, Gönç N, Ekinci S, Özön A. A pheochromocytoma case diagnosed as adrenal incidentaloma. Turk J Pediatr 2017; 59: 200-206. There are two problems that needs to be addressed in cases of an adrenal incidentaloma. The first is to decide whether the adrenal mass is benign or malignant, and the second is to determine whether the mass is hormonally active or not. A 17-year-old male was admitted with the complaint of progressive weight gain. Abdominal ultrasonography was performed for elevation in transaminases which revealed a hypoechoic mass located in the left adrenal gland. Hormonal investigations revealed an increase in fractionated catecholamine and metanephrine levels in 24-hour urine. Surgery was performed and pathological examination was in accordance with pheochromocytoma. Mutation analysis was carried out. This is a rare case of pheochromocytoma presenting as adrenal incidentaloma during adolescence. In view of this case, we review the approach to incidentally discovered adrenal masses and the approach to pheochromocytoma. A mutation analysis should be performed on all cases with pheochromocytoma that are diagnosed below age 20.
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http://dx.doi.org/10.24953/turkjped.2017.02.015DOI Listing
November 2018

Update on endocrine aspects of childhood obesity.

Curr Opin Endocrinol Diabetes Obes 2018 02;25(1):55-60

Pediatric Endocrinology, Massachusetts General Hospital for Children, Boston, Massachusetts, USA.

Purpose Of Review: Although childhood obesity has leveled off in the last decade, 'severe obesity' continues to be on the rise. Various genetic, environmental and hormonal factors contribute to obesity. This article reviews the most current understanding of obesity's multifactorial origin and recent recommendations for its management in childhood and adolescence.

Recent Findings: Epigenetics plays a key role in transmitting obesity risk to offspring. Single-nucleotide polymorphisms at genetic loci for adipokines and their receptors are associated with obesity. Gut microbiota is an important regulator of weight status, and Bifidobacterium species improves metabolic status. The incidence of comorbidities including prediabetes and type 2 diabetes has increased. Novel biomarkers such as alpha-hydroxybutyrate and branched-chain amino acids correlate with insulin sensitivity and predict glycemic control in adolescents. Lifestyle modifications and pharmacotherapy can produce small BMI changes. Bariatric surgery induces substantial weight loss and remission of comorbidities.

Summary: Alterations in genetics, epigenetics and microbiota influence childhood obesity. Lifestyle modification remains the mainstay of management and pharmacotherapy with Food and Drug Administration approved medications is recommended only for patients resistant to lifestyle changes and for comorbidities. Bariatric surgery produces sustained weight loss and cardiovascular benefits and is an effective option for adolescents with severe obesity.
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http://dx.doi.org/10.1097/MED.0000000000000381DOI Listing
February 2018

Long-Term Follow-up of a Case with Proprotein Convertase 1/3 Deficiency: Transient Diabetes Mellitus with Intervening Diabetic Ketoacidosis During Growth Hormone Therapy.

J Clin Res Pediatr Endocrinol 2017 09 7;9(3):283-287. Epub 2017 Jun 7.

Hacettepe University Faculty of Medicine, Department of Pediatric Endocrinology, Ankara, Turkey

Proprotein convertase 1/3 (PC1/3) deficiency is a very rare disease characterized by severe intractable diarrhea in the first years of life, followed by obesity and several hormonal deficiencies later. Diabetes mellitus requiring insulin treatment and diabetic ketoacidosis have not been reported in this disorder. We herein present a girl with PC1/3 deficiency who has been followed from birth to 17 years of age. She developed deficiencies of all pituitary hormones over time as well as diabetes mellitus while receiving growth hormone (GH) therapy. She was complicated with diabetic ketoacidosis during dietary management of diabetes mellitus, thus insulin treatment was initiated. Insulin requirement to regulate hyperglycemia was short-lived. Repeat oral glucose tolerance test five years later was normal. The findings of this patient show that diabetes mellitus can develop at any time during follow-up of cases with proportein convertase 1/3 deficiency especially under GH therapy.
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http://dx.doi.org/10.4274/jcrpe.3986DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5596812PMC
September 2017

Clinical and laboratory parameters predicting a requirement for the reevaluation of growth hormone status during growth hormone treatment: Retesting early in the course of GH treatment.

Growth Horm IGF Res 2017 06 10;34:31-37. Epub 2017 May 10.

Hacettepe University, Faculty of Medicine, Department of Pediatric Endocrinology, Ankara, Turkey.

Objective: We aimed to define the predictive criteria, in the form of specific clinical, hormonal and radiological parameters, for children with growth hormone deficiency (GHD) who may benefit from the reevaluation of GH status early in the course of growth hormone (GH) treatment.

Design And Methods: Two hundred sixty-five children with growth hormone deficiency were retested by GH stimulation at the end of the first year of GH treatment. The initial clinical and laboratory characteristics of those with a normal (GH≥10ng/ml) response and those with a subnormal (GH<10ng/ml) response were compared to predict a normal GH status during reassessment.

Results: Sixty-nine patients (40.6%) out of the 170 patients with isolated growth hormone deficiency (IGHD) had a peak GH of ≥10ng/ml during the retest. None of the patients with multiple pituitary hormone deficiency (MPHD) had a peak GH of ≥10ng/ml. Puberty and sex steroid priming in peripubertal cases increased the probability of a normal GH response. Only one patient with IGHD who had an ectopic posterior pituitary without stalk interruption on MRI analysis showed a normal GH response during the retest. Patients with a peak GH between 5 and 10ng/ml, an age at diagnosis of ≥9years or a height gain below 0.61 SDS during the first year of treatment had an increased probability of having a normal GH response at the retest.

Conclusion: Early reassessment of GH status during GH treatment is unnecessary in patients who have MPHD with at least 3 hormone deficiencies. Retesting at the end of the first year of therapy is recommended for patients with IGHD who have a height gain of <0.61 SDS in the first year of treatment, especially those with a normal or 'hypoplastic' pituitary on imaging. Priming can increase the likelihood of a normal response in patients in the pubertal age group who do not show overt signs of pubertal development.
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http://dx.doi.org/10.1016/j.ghir.2017.05.003DOI Listing
June 2017

Combined pituitary hormone deficiency due to gross deletions in the POU1F1 (PIT-1) and PROP1 genes.

J Hum Genet 2017 Aug 30;62(8):755-762. Epub 2017 Mar 30.

Hospital for Children and Adolescents, Division of Pediatric Endocrinology, University of Leipzig, Leipzig, Germany.

Pituitary development depends on a complex cascade of interacting transcription factors and signaling molecules. Lesions in this cascade lead to isolated or combined pituitary hormone deficiency (CPHD). The aim of this study was to identify copy number variants (CNVs) in genes known to cause CPHD and to determine their structure. We analyzed 70 CPHD patients from 64 families. Deletions were found in three Turkish families and one family from northern Iraq. In one family we identified a 4.96 kb deletion that comprises the first two exons of POU1F1. In three families a homozygous 15.9 kb deletion including complete PROP1 was discovered. Breakpoints map within highly homologous AluY sequences. Haplotype analysis revealed a shared haplotype of 350 kb among PROP1 deletion carriers. For the first time we were able to assign the boundaries of a previously reported PROP1 deletion. This gross deletion shows strong evidence to originate from a common ancestor in patients with Kurdish descent. No CNVs within LHX3, LHX4, HESX1, GH1 and GHRHR were found. Our data prove multiplex ligation-dependent probe amplification to be a valuable tool for the detection of CNVs as cause of pituitary insufficiencies and should be considered as an analytical method particularly in Kurdish patients.
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http://dx.doi.org/10.1038/jhg.2017.34DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5537413PMC
August 2017

Clinical, genetic, and structural basis of congenital adrenal hyperplasia due to 11β-hydroxylase deficiency.

Proc Natl Acad Sci U S A 2017 03 22;114(10):E1933-E1940. Epub 2017 Feb 22.

Division of Adrenal Steroid Disorders, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY 10029;

Congenital adrenal hyperplasia (CAH), resulting from mutations in , a gene encoding 11β-hydroxylase, represents a rare autosomal recessive Mendelian disorder of aberrant sex steroid production. Unlike CAH caused by 21-hydroxylase deficiency, the disease is far more common in the Middle East and North Africa, where consanguinity is common often resulting in identical mutations. Clinically, affected female newborns are profoundly virilized (Prader score of 4/5), and both genders display significantly advanced bone ages and are oftentimes hypertensive. We find that 11-deoxycortisol, not frequently measured, is the most robust biochemical marker for diagnosing 11β-hydroxylase deficiency. Finally, computational modeling of 25 missense mutations of revealed that specific modifications in the heme-binding (R374W and R448C) or substrate-binding (W116C) site of 11β-hydroxylase, or alterations in its stability (L299P and G267S), may predict severe disease. Thus, we report clinical, genetic, hormonal, and structural effects of gene mutations in the largest international cohort of 108 patients with steroid 11β-hydroxylase deficiency CAH.
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http://dx.doi.org/10.1073/pnas.1621082114DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5347606PMC
March 2017

Impact of low-weight severity and menstrual status on bone in adolescent girls with anorexia nervosa.

Int J Eat Disord 2017 Apr 2;50(4):359-369. Epub 2017 Feb 2.

Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.

Clinicians currently use different low-weight cut-offs both to diagnose anorexia nervosa (AN) and to determine AN severity in adolescent girls. The purpose of this study was to evaluate the clinical utility of existing cut-offs and severity criteria by determining which are most strongly associated with risk for low bone mineral density (BMD). Height adjusted BMD Z scores were calculated for 352 females: 262 with AN and 90 healthy controls (controls) (12-20.5 years), using data from the BMD in Childhood Study, for the lumbar spine, whole body less head, and total hip. For most cut-offs used to define low weight (5th or 10th BMI percentile, BMI of 17.5 or 18.5, and 85 or 90% of median BMI), AN had lower BMD Z scores than controls. AN at >85 or >90% expected body weight for height (EBW-Ht) did not differ in BMD Z scores from controls, but differed significantly from AN at ≤85 or ≤90% EBW-Ht. Among AN, any amenorrhea was associated with lower BMD. AN had lower BMD than controls across DSM-5 and The Society for Adolescent Health and Medicine (SAHM) severity categories. The SAHM moderate severity classification was differentiated from the mildly malnourished classification by lower BMD at hip and spine sites. Amenorrhea and %EBW-Ht ≤ 85 or ≤ 90% are markers of severity of bone loss within AN. Among severity categories, BMI Z scores (SAHM) may have the greatest utility in assessing the degree of malnutrition in adolescent girls that corresponds to lower BMD.
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http://dx.doi.org/10.1002/eat.22681DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5386816PMC
April 2017

Novel and prevalent CYP11B1 gene mutations in Turkish patients with 11-β hydroxylase deficiency.

J Steroid Biochem Mol Biol 2017 01 5;165(Pt A):57-63. Epub 2016 Mar 5.

Hacettepe University, Pediatric Metabolism Unit, Institute of Child Health, Ankara, Turkey.

11β-Hydroxylase deficiency is the second most frequent type of congenital adrenal hyperplasia and is more common in those of Turkish descent than in other populations. The purpose of this study is to examine the spectrum of CYP11B1 gene mutations in Turkish patients with 11β-hydroxylase deficiency. Twenty-eight patients from 24 families, ages ranging from 0.1 to 7 years, were included in the study. Clinical diagnosis was based on virilization and high levels of 11-deoxycortisol. Twenty-six cases exhibited the classical and 2 cases the non-classical form. Mutation screening of 9 CYP11B1 exons was performed by direct DNA sequence analysis, specifically amplifying CYP11B1 gene fragments while avoiding simultaneous amplification of homologous CYP11B2 gene sequences. Seventeen different mutations were detected, 6 of which are novel (p.Gln189Hisfs*70, p.Glu198Gly, p.Thr318Lys, p.Gly446Ser, IVS8+5G>C and exon 3-5 del). All of the identified mutations resulted in the classical form with severe virilization, except for the p.Gly446Ser mutation, which caused a late-onset type of 11β-hydroxylase deficiency. The c.954G>A;p.Thr318Thr mutation was the most common in our cohort, with an allele frequency of 14.6%.Of the CYP11B1 gene mutations detected, 75% were found in exons 3, 5 and 7 and the half of the mutations were nonsense, splice site, deletion or insertion mutations, causing severe virilization in female patients. The findings are important for genetic counseling and the prenatal diagnosis of Turkish patients with 11β-hydroxylase deficiency.
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http://dx.doi.org/10.1016/j.jsbmb.2016.03.006DOI Listing
January 2017

Severe Undervirilisation in a 46,XY Case Due to a Novel Mutation in HSD17B3 Gene.

J Clin Res Pediatr Endocrinol 2015 Sep;7(3):249-52

Hacettepe University Faculty of Medicine, Department of Pediatrics, Division of Pediatric Endocrinology, Ankara, Turkey Phone: +90 312 305 11 24 E-mail:

17-β-hydroxysteroid dehydrogenase type 3 (17β-HSD3) is an important enzyme involved in the final steps of androgen synthesis and is required for the development of normal male external genitalia. 46,XY individuals with deficiency of this enzyme present a wide clinical spectrum from a female appearance of the external genitalia through ambiguous genitalia to a predominantly male genitalia with micropenis or hypospadias. This paper reports a one-year-old 46,XY patient with 17β-HSD3 deficiency who presented with female external genitalia and bilaterally palpable gonads in the inguinal region. The low T/Δ4 ratio after human chorionic gonadotropin (hCG) stimulation suggested 17β-HSD3 deficiency. A homozygous mutation, c.761_762delAG, was determined at the intron 9/exon 10 splice site of the HSD17B3 gene. To the best of our knowledge, this mutation has not been reported thus far, but its localization and type would imply a complete disruption of the 17β-HSD3 which may explain the phenotype of our patient.
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http://dx.doi.org/10.4274/jcrpe.2069DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4677563PMC
September 2015

Hyperthyroidism After Allogeneic Hematopoietic Stem Cell Transplantation: A Report of Four Cases.

J Clin Res Pediatr Endocrinol 2015 Dec;7(4):349-54

Hacettepe University Faculty of Medicine, Department of Pediatrics, Ankara, Turkey Phone: +90 312 305 11 68 E-mail:

Hematopoietic stem cell transplantation (HSCT) is the only curative treatment for many hematological disorders, primary immunodeficiencies, and metabolic disorders. Thyroid dysfunction is one of the frequently seen complications of HSCT. However, hyperthyroidism due to Graves' disease, autoimmune thyroiditis, and thyrotoxicosis are rare. Herein, we report a series of 4 patients who were euthyroid before HSCT but developed hyperthyroidism (3 of them developed autoimmune thyroid disease) after transplantation.
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http://dx.doi.org/10.4274/jcrpe.2295DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4805214PMC
December 2015

Growth Hormone Deficiency in a Child with Neurofibromatosis-Noonan Syndrome.

J Clin Res Pediatr Endocrinol 2016 Mar 18;8(1):96-100. Epub 2015 Dec 18.

Hacettepe University Faculty of Medicine, Department of Pediatric Endocrinology, Ankara, Turkey, E-mail:

Neurofibromatosis-Noonan syndrome (NFNS) is a distinct entity which shows the features of both NF1 (neurofibromatosis 1) and Noonan syndrome (NS). While growth hormone deficiency (GHD) has been relatively frequently identified in NF1 and NS patients, there is limited experience in NFNS cases. The literature includes only one case report of a NFNS patient having GHD and that report primarily focuses on the dermatological lesions that accompany the syndrome and not on growth hormone (GH) treatment. Here, we present a 13-year-old girl who had clinical features of NFNS with a mutation in the NF1 gene. The case is the first NFNS patient reported in the literature who was diagnosed to have GHD and who received GH treatment until reaching final height. The findings in this patient show that short stature is a feature of NFNS and can be caused by GHD. Patients with NFNS who show poor growth should be evaluated for GHD.
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http://dx.doi.org/10.4274/jcrpe.2070DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4805056PMC
March 2016

Surgical and clinical strategies in the management of thyroid medullary carcinoma in children with and without ret proto-oncogene mutations.

Turk J Pediatr 2016 ;58(4):436-441

Department of Pediatric Surgery, Hacettepe University, Faculty of Medicine, Ankara, Turkey.

Medullary thyroid carcinoma (MTC) may arise sporadically or in familial manner. We presented sporadic and familial cases with MTC in order to raise awareness on management of such patients. Three medullary thyroid carcinoma (MTC) cases were presented. Case 1 had RET634 mutation; managed with total thyroidectomy (TT) and cervical lymph node dissection (CLND). Case 2 had RET804 mutation; managed with prophylactic TT. Case 3 had thyroid nodule; managed with TT and CLND. Case 1 had micro-carcinomatosis foci, Case 2 had normal thyroid tissue in histopathological examination and Case 3 had medullary thyroid carcinoma with tumor negative surgical borders. Case 1 was re-operated for persisting focus of disease. Follow-up of cases were uneventful. Clinicians and surgeons should be aware of critical timing for surgery and various surgical and clinical strategies in the management of MTC in children.
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http://dx.doi.org/10.24953/turkjped.2016.04.017DOI Listing
July 2017

Evidence of hypothalamic-pituitary-adrenal axis suppression during moderate-to-high-dose inhaled corticosteroid use.

Eur J Pediatr 2015 Nov 9;174(11):1421-31. Epub 2015 Aug 9.

Department of Pediatric Allergy, Faculty of Medicine, Hacettepe University, Sıhhıye, 06100, Ankara, Turkey.

The possible risk of adverse effects due to regular use of inhaled corticosteroids (ICS) is a real concern. Our aim was to describe the factors that have an impact on hypothalamic-pituitary-adrenal axis suppression (HPA-AS) in children and adolescents taking ICS regularly. The HPA axis status of patients who were on moderate-to-high-dose ICS [>176 and >264 μg/day fluticasone propionate-hydrofluoroalkane (FP-HFA) for patients 0-11 and ≥12 years, respectively] was investigated. Various types of ICS were converted to FP-HFA equivalent according to National Asthma Education and Prevention Program (NAEPP) guidelines. Participants with a baseline (8 a.m.) serum cortisol <15 μg/dL underwent a low-dose ACTH stimulation test (LDAT) to diagnose HPA-AS. Among 91 patients, 60 (75.9 %) participants underwent LDAT, and seven (7.7, 95 % CI 3.5-15.3 %) were diagnosed with HPA-AS. Ciclesonide was more frequently used by the participants with HPA-AS compared to patients with a normal HPA axis (42.9 vs. 4.8 %, p = 0.009). Use of ICS at moderate-to-high doses for at least 7 months distinguished participants with HPA-AS from those with a normal HPA axis. Among the duration, type, and dose of ICS, solely the use of ICS with a body mass index (BMI)-adjusted daily dose of ≥22 μg FP was found to increase the risk for HPA-AS (odds ratio (OR) 7.22, 95 % confidence interval (CI) 1.23-42.26, p = 0.028). The receiver operating characteristics (ROC) curve analysis revealed a cutoff value of 291 μg/day FP (area under the curve (AUC) = 0.840, p = 0.003) for predicting HPA-AS Conclusion: The prevalence of HPA-AS was found to be 7.7 % in children taking not only high-dose ICS but also moderate-dose ICS. Dose alone was found to be an actual risk factor for HPA-AS.
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http://dx.doi.org/10.1007/s00431-015-2610-9DOI Listing
November 2015

Variable Phenotype of Diabetes Mellitus in Siblings with a Homozygous PTF1A Enhancer Mutation.

Horm Res Paediatr 2015 14;84(3):206-11. Epub 2015 Jul 14.

Department of Pediatric Endocrinology, Hacettepe University, Ankara, Turkey.

Neonatal diabetes is a rare form of diabetes, characterized by onset in the first 6 months of life. A number of cases are due to pancreas agenesis. Recently, PTF1A enhancer mutations have been shown to cause neonatal diabetes associated with pancreatic agenesis. Herein, we report the clinical features of two siblings with PTF1A enhancer mutations, one of whom had neonatal diabetes, whereas the elder sister had a milder form of the disease with onset of diabetes at 9 years of age.
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http://dx.doi.org/10.1159/000435782DOI Listing
June 2016

Prevalence of nasal carriage of methicillin-resistant Staphylococcus aureus in children with diabetes mellitus: Trends between 2005 and 2013.

Am J Infect Control 2015 09 3;43(9):1015-7. Epub 2015 Jun 3.

Pediatric Infectious Disease Unit, Department of Pediatrics, Hacettepe University Faculty of Medicine, Ankara, Turkey.

The aim of this prospective study was to establish the methicillin-resistant Staphylococcus aureus (MRSA) colonization rates in pediatric outpatients with type 1 diabetes mellitus, while also evaluating changes in colonization rates over time. There was no significant difference between 2005 and 2013 patients in terms of demographic and clinical findings. MRSA colonization rates were 0.7% (in 101 patients) and 0.9% (in 134 patients) (P = .84). Although increased MRSA colonization has become a significant problem worldwide, it does not seem to be a major issue in our diabetic outpatient population.
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http://dx.doi.org/10.1016/j.ajic.2015.04.206DOI Listing
September 2015