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Author: search.filters.author.Kinik, Sibel TulgarHas files: No

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    Neonatal Thyrotoxicosis with Severe Supraventricular Tachycardia: Case Report and Review of the Literature
    (2015) Abbasoglu, Aslihan; Ecevit, Ayse; Tugcu, Ali Ulas; Erdogan, Ilkay; Kinik, Sibel Tulgar; Tarcan, Aylin; 0000-0002-2232-8117; 0000-0001-6887-3033; 25153577; AAJ-2305-2021; AAJ-4616-2021; ABB-2220-2021; ABI-2113-2020
    Neonatal thyrotoxicosis is a rare condition caused by the transplacental passage of thyroid stimulating immunoglobulins from mothers with Graves' disease. We report a case of neonatal thyrotoxicosis with concurrent supraventricular tachycardia (SVT). The female infant, who was born by section due to breech delivery and meconium in the amniotic fluid at 36 weeks of gestation, presented with tachycardia on day 7. Her heart rate was between 260 and 300 beats/min, and an electrocardiogram revealed ongoing SVT. Sotalol was effective after two cardioversions in maintaining sinus rhythm. Thyroid function studies revealed hyperthyroidism in the infant, and her mother was found to have Graves' disease. Since symptoms and signs can vary, especially in preterm infants with neonatal hyperthyroidism, we want to emphasize the importance of prenatal care and follow-ups of Graves' disease associated pregnancies and management of newborns after birth.
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    Neuroblastoma Accompanied by Hyperaldosteronism
    (2014) Gulleroglu, Kaan; Bayrakci, Umut; Kinik, Sibel Tulgar; Uslu, Nihal; Atilgan, Alev O. K.; Sarialioglu, Faik; Baskin, Esra; https://orcid.org/0000-0003-1434-3824; https://orcid.org/0000-0002-6733-8669; https://orcid.org/0000-0001-8595-8880; https://orcid.org/0000-0002-8257-810X; https://orcid.org/0000-0003-4361-8508; 25340174; AAJ-8833-2021; ABC-5258-2020; AAK-3333-2021; AAL-7766-2021; B-5785-2018
    Background: Tumors known derived from kidneys which take place in secondary hyperaldosteronism etiology are juxtaglomerular cell tumor and Wilms' tumor. Neuroblastoma presenting with hyperaldosteronism is rare. Case: A 15-month-old girl who had been having diarrhea and fever for 2 weeks presented with a 3 day history of bilious vomiting, metabolic acidosis and severe hypokalemia. She was referred to our hospital with the pre-diagnosis of unknown manifest hypertension etiology, diarrhea, and paralytic ileus after having therapy-resistant hypokalemia and severe resistant acidosis. On her examination after being admitted to our clinic, she was weak, unwell and lethargic with a blood pressure of 140/93 mmHg. Due to the hypertension and severe hypokalemia, the patient was considered to be hyperaldosteronism. Serum aldosterone level, plasma renin activity and cortisol level were elevated. Radiologic findings were compatible with neuroblastoma. The patient underwent an abdominal surgery and the mass excision. The histopathological examination was proved neuroblastoma. Conclusion: Hyperaldosteronism can be presented by unexpected atypical forms as in our patient.
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    Congenital Hyperinsulinism in A Newborn with A Novel Homozygous Mutation (P.Q392H) in The ABCC8 Gene
    (2014) Ince, Deniz Anuk; Sahin, Nursel Muratoglu; Ecevit, Ayse; Kurt, Abdullah; Kinik, Sibel Tulgar; Flanagan, Sarah E.; Hussain, Khalid; Tarcan, Aylin; https://orcid.org/0000-0002-4369-2110; https://orcid.org/0000-0002-8215-0146; https://orcid.org/0000-0002-2232-8117; https://orcid.org/0000-0002-4430-444X; https://orcid.org/0000-0002-8670-6340; 24945427; I-6746-2016; AAA-1266-2019; AAJ-4616-2021; HIU-0129-2022; AFK-0591-2022
    Congenital hyperinsulinism is the most frequent cause of persistent hypoglycemia in infancy. We present the case of a preterm, large-for-gestation-age infant with congenital hyperinsulinism who was found to have a novel p.Q392H homozygous mutation in the ABCC8 gene. The patient had severe brain damage, despite early diagnosis and appropriate management. The new mutations may provide an understanding of the prognosis and treatment of the disease. In addition, the data will help the family make informed decisions about future pregnancies.
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    Evaluation of Serum Leptin and Adiponectin Levels in Obese and Lean Asthmatic Children
    (2015) Koksal, Burcu Tahire; Ozbek, Ozlem Yilmaz; Bayraktar, Nilufer; Kinik, Sibel Tulgar; Yazici, Ayse Canan; 0000-0003-2974-9579; 0000-0002-7886-3688; 0000-0002-3132-242X; 0000-0001-9580-7656; AAJ-2034-2021; Y-8758-2018; AAS-6810-2021; HKW-0623-2023; AAF-2109-2021
    Background: Adipokines have been claimed for the link between obesity and asthma. The aim of the present study was to evaluate the roles of leptin and adiponectin in children with asthma and/or obesity and their effect on pulmonary functions. Methods: Obese (n=71) and lean asthmatics (n=72), obese non-asthmatics (n=46), and lean healthy children (n=49) were included in the study. Serum leptin and adiponectin levels were compared according to groups and sex. Results: Mean leptin levels of obese asthmatics were higher than those of lean asthmatics (13.19.1 vs. 3.7 +/- 4.4; p<0.001). Serum adiponectin levels of lean asthmatics (16 +/- 7.1) were significantly higher than those of obese asthmatics (12.1 +/- 6.9; p<0.001) and of their lean healthy (13.2 +/- 5.9; p<0.05) counterparts. In obese asthmatics, adiponectin levels were positively correlated with the forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) ratio, and serum leptin levels were inversely correlated with forced expiratory flow (FEF25-75). Leptin/adiponectin ratio was inversely correlated with FEV1/FVC ratio in lean and obese asthmatic patients. Conclusions: The present findings suggest that adiponectin may have protective disease modifying effect(s) in asthmatic children. Anti-inflammatory mechanisms regarding adiponectin may work better in girls than in boys.
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    AMH Levels at Central Precocious Puberty and Premature Thelarche: Is It A Parameter?
    (2015) Sahin, Nursel Muratoglu; Kinik, Sibel Tulgar; Tekindal, Mustafa Agah; Bayraktar, Nilufer; 0000-0002-7886-3688; 0000-0002-4060-7048; 0000-0002-8215-0146; 26226120; Y-8758-2018; U-9270-2018; AAA-1266-2019
    Background: The possible difference of antimllrin hormone (AMH) levels at central precocious puberty (CPP) and premature thelarche (PT) has not been properly evaluated. Objective/hypothesis: By evaluating AMH levels in girls with diagnosed CPP and PT, we aim to show the change of AMH levels at the pubertal onset. Subjects: Sixty-five girls who have breast development before the age of 8 years and 25 healthy girls were enrolled in the study. Methods: The subjects were divided into two groups as CPP and PT, according to results of GnRH test. AMH levels were determined in the two groups. Results: The mean AMH levels of the CPP group were significantly lower than those in the PT group (13.57 +/- 9.85 pmol/L and 58.42 +/- 12.78 pmol/L, respectively, p=0.022). Conclusion: These results suggest that the AMH levels decrease in the duration of the hypothalamus-pituitaryovarian axis activation. We thought that AMH might/may be a marker for distinguishing between CPP and PT.