During pregnancy, steroids are usually used in maternal diseases such as adrenal failure or other autoimmune diseases, e.g. idiopathic thrombocytopenic purpura (ITP), Crohn’s disease, systemic lupus erythematosus, dermatomyositis, scleroderma, Addison’s disease and hyperemesis gravidarum, HELLP syndrome. Endogenous or exogenous maternal steroids are metabolized by the placental enzyme 11 beta-hydroxy steroid dehydrogenase type 2. Prednisolone and methylprednisolone are highly sensitive to this enzyme, while dexamethasone and betamethasone are less well metabolized. Steroids which can cross the placental barrier are administered in cases like fetal lupus, congenital adrenal hyperplasia and for enhancement of fetal lung maturation, whereas steroids used in maternal diseases are usually the ones with low affinity to the placenta; however, in case of long-term use or in high doses, placental enzyme saturation occurs and thus, resulting in fetal adrenal suppression. Antenatal steroids can lead to low birth weight, as observed in our patient. Here, we report a case with fetal adrenal suppression due to maternal methylprednisolone use presenting with early hypoglycaemia and late hyponatremia in neonatal period and requiring three-month replacement therapy. Conflict of interest:None declared.

Childhood obesity is a common and significant public health problem all over the world. As a well-known fact obese children have an increased risk of obesity-associated comorbidities, including obstructive sleep apnea, diabetes, and cardiovascular disorders at an earlier age compared to their normal weight peers. They also have an increased risk of poor self-esteem, greater body dissatisfaction, and increased peer teasing that lead to a lower health-related quality of life. While the presence of adenoid hypertrophy and increased rate of obstructive sleep apnea frequently co-exists in majority of cases. We have limited knowledge about the effect of adenotonsillar hypertrophy on development of childhood obesity. In this study, we aimed to investigate the association between obesity, presence of adenotonsillar hypertrophy and the quality of life parameters in obese children as measured by the OSA-18 quality of life questionnaire. Fifty obese children aged between 3 and 18 years and 50 age- and gender-matched otherwise children were enrolled to the study. All subjects were routinely examined by the otolaryngologist before enrollment. The size of adenoid hypertrophy was measured using lateral cephalometric radiographs. The tonsils were also graded using the schema recommended by Brodsky et al. We used OSA-18 questionnaires to evaluate the subjects' quality of life issues. We found, 34 % of obese group had tonsillar hypertrophy while the rate was 6 % in control group. Similarly 16 % of obese group had tonsillar hypertrophy compared to only 4 % in non-obese group. It was also noted that total OSA-18 scores of obese group were significantly higher than those of non-obese group. In subgroup analysis of obese group, total OSA-18 score of obese subjects with either adenoid and/or tonsillar hypertrophy was significantly higher than that of obese subjects without adenoid or tonsillar hypertrophy. As the related literature suggests that the impact of adenotonsillar size on OSA symptoms is prominent especially in children under 7 years of age, but its impact on the development of childhood obesity is still controversial. Our results revealed a possible relation between adenotonsillar hypertrophy and obesity rates. Further studies on larger populations should be planned to better define the real impact of adenotonsillar hypertrophy in obese children.

Radioactive iodine (RAI) is used effectively in the treatment of hyperthyroidism and thyroid cancer, but it is contraindicated during pregnancy. RAI treatment during pregnancy can lead to fetal hypothyroidism, mental retardation and increased malignancy risk in the infant. Pregnancy tests must be performed before treatment in all women of reproductive age. However, at times, RAI is being used before ruling out pregnancy.We herein present a male newborn infant with congenital hypothyroidism whose mother was given a three-week course of methimazole therapy for her multiple hyperactive nodules and subsequently received 20 mCi RAI during the 12th week of her pregnancy. The patient was referred to our neonatology unit at age two weeks when his thyrotropin (TSH) level was reported to be high in the neonatal screening test. Physical examination was normal. Laboratory investigations revealed hypothyroidism (free triiodothyronine 1.55 pg/mL, free thyroxine 2.9 pg/mL, TSH 452 mU/L, thyroglobulin 20.1 ng/mL). The thyroid gland could not be visualized by ultrasonography. L-thyroxine treatment was initiated. Conflict of interest:None declared.

Objective:Childhood obesity is related to subclinical atherosclerosis. Carotid intima-media thickness (CIMT) and hepatosteatosis are parameters that reflect subclinical atherosclerosis and are shown to be associated with obesity. However, their relation with the corrected QT interval (QTc) has not been thoroughly studied in children. Here, we aimed to research the relation between QTc, hepatic steatosis, and CIMT among obese children.Methods:Fifty-three obese and 53 age- and sex-matched non-obese children aged 6–16 years were included in this prospective cross-sectional study. The QTc of each subject was accordingly obtained from lead II on a 12-lead resting electrocardiogram. Thus, CIMT measurement and abdominal ultrasonographic examination were performed. The data for obese and non-obese children were analyzed and compared.Result:The age and gender distribution of the subjects were statistically similar. The CIMT value of the obese group was higher than that of the non-obese group (p<0.001). The obese group had a higher frequency of hepatosteatosis at grade 1 or 2 than the non-obese group (p<0.001). The QTc values were also found to be more prolonged in the obese group than in the other group (p<0.001). With Student’s t-test and Mann-Whitey U test accordingly.Conclusion:We demonstrated that obese children had higher CIMT and QTc values as well as more frequent hepatosteatosis, and that the presence of hepatosteatosis or increased CIMT had an association with prolonged QTc values in obese children. Therefore, with the aim of detecting cardiovascular effects of obesity, it may be beneficial to perform the measurements of QTc in the presence of hepatosteatosis and/or increased CIMT among obese children.

Neonatal hemochromatosis (NH) is a form of neonatal liver failure caused by maternal-fetal alloimmune injury to hepatocytes. The etiology of neonatal hemochromatosis is not exactly understood. However, according to one theory neonatal hemochromatosis is believed to be an alloimmune disorder causing liver injury in the fetus. In order to diagnose neonatal hemochromatosis there are some criteria that should be taken into account, such as positive family history, high serum ferritin levels, high serum alpha-fetoprotein levels and siderosis demonstrated by histology or with magnetic resonance.We present a case of a monochorionic newborn twin who applied to our hospital with sepsis clinical symptoms like clinics, was diagnosed with NH and immediately treated with antioxidant therapy while the other twin with same clinical symptoms did not respond to therapy and passed away. NH should be considered in the differential diagnosis of cases with sepsis-like clinical symptoms that do not respond to antibiotics; early antioxidant therapy in these cases is lifesaving.

Aim: Iodine deficiency is one of the most important causes of congenital hypothyroidism. In addition to thyroid hormone replacement, iodine supplementation is also given to newborns with congenital hypothyroidism due to iodine deficiency. We aimed to determine whether it is beneficial to administer iodine supplementation in addition to the L-thyroxine (L-T₄) treatment of newborns with congenital hypothyroidism due to iodine deficiency. Materials and Methods: Of 51 newborns, 26 who were diagnosed with congenital hypothyroidism due to iodine deficiency were treated with L-T₄. The remaining 25 cases were given L-T₄ plus 100 μg/day of oral iodine. Free triiodothyronine (fT₃), free thyroxine (fT₄), thyroid-stimulating hormone (TSH), thyroglobulin (TG), thyroid volume, urine iodine and breast milk iodine levels were measured in the first and third months of treatment, and the data were compared between the two groups. Results: First- and third-month values of fT₃, fT₄, TSH, TG and thyroid volume for both groups were statistically similar. There was no significant difference between the two groups in respect to falling levels of fT₃ and TSH, the rate of increase of fT₄ levels or the shrinkage rate of thyroid volume. Conclusion: In this study, the addition of oral iodine to L-T₄ treatment provided no benefit compared to treatment with L-T₄ alone.

The use of antiseptics-containing iodine for mothers before and after birth and for newborns, especially for umbilical cleansing, can lead to iodine loading and hypothyroidism. If transient hypothyroidism develops within this period, then it may not be detected promptly. This can later lead to retardation in psychomotor development and disorder in learning skills during the childhood period.

Congenital hypothyroidism (CH) is the most common endocrine pathology in neonates. Inappropriate treatment of CH is complicated by irreversible brain damage or low IQ score. Hormone replacement therapy with L-thyroxine (L-T4) is sufficient for a very large proportion of patients. However, during treatment, the patient needs to be carefully monitored for presence of factors which might affect the absorption or bio-availability of the drug as well as its dose. Herein, we report a preterm newborn with CH who presented with gastrointestinal problems mimicking necrotizing enterocolitis. The clinical course was also complicated by cholestasis. The L-T4 replacement treatment was switched from oral route to parenteral. After resolution of the cholestasis, L-T4 treatment was continued successfully by the oral route.