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Aim: Several studies have investigated leptin and neuropeptide Y (NPY) levels in children, but the information for newborns in the literature is limited. The purpose of this study was to determine leptin and NPY levels in 14-to 28-day-old newborns. Materials and methods: This prospective study was performed in Atatürk University Medical Faculty Research Hospital Neonatal Clinic, Erzurum, Turkey between July and December, 2014. Sixty-two 14-to 28-day-old neonates, 26 female and 36 male, were included. Age, height, and body weight of the patients were recorded. Feeding status was also recorded. The newborns were divided into two groups -those receiving breastfeeding only and those receiving breastfeeding and formula. Plasma leptin levels were measured using enzyme amplified sensitivity immunoassay (EASIA). Results:The mean leptin level in 14-to 28-day-old female neonates was 4.25±3.08 ng/mL, and the mean NPY level was 24.79±9.87 ng/mL. The mean leptin level in 14-to 28-day male neonates was 3.49±2.52 ng/mL, and the mean NPY level was 25.80±9.58 ng/mL. No significant difference was determined between leptin (p = 0.228) or NPY (p = 0.144) in terms of feeding status. No significant difference was also observed between the sex in terms of leptin or NPY levels (leptin p = 0.775 and NPY p = 0.687). Conclusion: There were no differences in terms of feeding status and sex in leptin and NPY levels in the neonatal period. Keywords: leptin; neuropeptide Y; newborn.What's known on this subject? Several studies have investigated leptin and neuropeptide Y levels in children, but the information for newborns in the literature is limited. What this study adds?This is the first study to investigate leptin and neuropeptide Y levels in healthy newborns. We describes that leptin and neuropeptide Y values of 3rd, 10th, 25th, 50th, 75th, 90th, and 97th percentiles.

Our results indicate that HGF protein and gene may play an important role in the etiopathogenesis of RA. However, further studies are required for a better understanding of mechanisms related to the disease process.

ÖZETAtaksi, arefleksi ve oftalmopleji ile karakterize Miller-Fisher sendromu (MFS), ilk kez 1956 yı-lında farklı bir klinik antite olarak tanımlandı. MFS, Guillain-Barre Sendromu (GBS)'nun bir varyantı olarak kabul edilir ve GBS olgularının %5-10'nunu oluşturur. Hastalığın klinik seyrinde ataksi, oftalmopleji, arefleksi, pitoz, diplopi, midriyazis, fasial paralizi, hipoestezi ve nadiren kuadriparezi görülebilir. MFS klinik bir tanı olmasına rağmen etkilenen birçok hastada Anti-GQ1b antikorunun pozitif olmasıyla da serolojik olarak doğrulanabilir. Biz bu makalede yutma güçlüğü ile gelen atipik bir MFS olgusu sunduk.Anahtar Kelimeler: Ataksi; arefleksi; oftalmopleji; yutma. ABSTRACT Miller-Fisher syndrome (MFS); characterized by ataxia, areflexia, and ophthalmoplegia, was first recognized as a distinct clinical entity in 1956. MFS is considered a variant of Guillain-Barre syndrom(GBS), accounting for 5 to 10% of GBS cases. Ataxia, ophthalmoplegia, areflexia , ptosis, diplopia, mydriasis, facial paralysis, hypoesthesi and rarely quadriparesis can occur in the clinical presentation of the disease. Although MFS is a clinical diagnosis, serological confirmation is possible by identifying the Anti-GQ1b antibody found in most of the affected patients. We prensented an atypical MFS case which is come with swallowing difficulties.