Browsing by Author "Yurekturk, Eyyup"
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Article İndirekt Hiperbilirubinemili Term Yenidoğanların Etiyolojik Değerlendirmesi(2024) Basaranoglu, Murat; Batu, Utku; Aycan, Nur; Yurekturk, Eyyup; Karaman, Serap; Tuncer, OguzAmaç: İndirekt hiperbilirubinemi, yenidoğanlarda sık görülen birçok risk faktörü olan bir hastalıktır. Çalışmamızda, yenidoğan yoğun bakım ünitemize indirekt hiperbilirubinemi tanısı ile yatırılan hastaların öykü, fizik muayene ve tetkiklerinin, hastaların tedavi ve takipleri üzerine olan etkileri incelenmesi amaçlandı. Yöntemler: Kesitsel ve retrospektif olarak yapılan çalışmamıza, miadında doğan, indirekt hiperbilirunemi tanısıyla yatırılan 226 hasta alındı. Hasta dosyalarından öyküleri, fizik muayene ve tetkik verileri değerlendirildi. Bulgular: Çalışmaya alınan 226 hastanın 126’sı (%55,8) erkek, 100’ü (%44,2) kızdı. Gestasyon haftaları ortalama 38,3±0,4 hafta, ortalama doğum ağırlıkları 3146±32 gramdı. Hastaların yatış anındaki ortalama postnatal günleri 4,1±0,1 gün, yatış bilirubinleri 17,1±0,2 mg/dl, fototerapi alma süreleri ise 38,2±1 saat, yatış sırasında tartı kaybı ise %3,7±0,3 olarak görüldü. Hastalardaki en sık tanının ABO uygunsuzluğu (%27,9) olduğu görüldü. Tartı kaybı olan hastaların bilirubin düzeyleri istatiksel açıdan anlamlı yüksekti. Kan uyuşmazlığı ve diğer tanılar karşılaştırıldığında; kan uyuşmazlığı olan hastalarda bilirübin ve hemoglobin düzeyi ve yatış anındaki postnatal yaş istatistiksel açıdan anlamlı daha düşük, yatış süresi ise istatistiksel açıdan anlamlı daha yüksekti. Sonuç: Cinsiyet ve doğum şekli ile yatış total bilirübin ve fototerapi alma süresi arasında anlamlı ilişki görülmedi. Tartı kaybı olan hastaların olmayanlara göre yatış total bilirübin istatistiksel olarak daha yüksekti. Ek olarak ABO uygunsuzluğu olan hastaların yatış sürelerinin de diğer tanılarla yatan hastalara göre istatistiksel açıdan anlamlı daha uzun olduğu görüldü.Article Oxidative and Antioxidative Biomarker Profiles in Neonatal Hypoxic-Ischemic Encephalopathy: Insights for Pathophysiology and Treatment Strategies(int Scientific information, inc, 2024) Aycan, Nur; Demir, Derya Cay; Yurekturk, Eyyup; Basaranoglu, Murat; Karaman, Serap; Tuncer, OguzBackground: Neonatal hypoxic-ischemic encephalopathy (HIE) is a significant cause of perinatal and postnatal morbidity and mortality worldwide. Catalase (CAT) activity detection is used to determine levels of inflammation and oxidative stress. Glutathione (GSH) is the most critical non-enzymatic endogenous antioxidant. Lipid peroxidation levels marked after hypoxia can be detected based on the level of malondialdehyde (MDA). Ischemia-modified albumin (IMA) is considered a biomarker for cardiac ischemia and is known to increase in the liver, brain, and kidney in states of insufficient oxygenation. We aimed to explain the results and relations between the oxidant and antioxidants to detail oxidant-antioxidant balance and cellular mechanisms. Material/Methods: Serum levels of IMA and MDA, as an oxidative stress marker, and CAT and GSH, as antioxidant enzymes, were measured in first blood samples of 59 neonates diagnosed with HIE, with pH <7, base excess >12, and APGAR scores. Results: Neonates who were >= 37 weeks of gestation and had hypoxia were included. Compared with healthy newborns (n=32), CAT was statistically significantly lower in the hypoxia group (P=0.0001), P =0.0001), while MDA serum levels were significantly higher in neonates with hypoxia (P=0.01). P =0.01). There was no difference between hypoxic and healthy neonates in GSH and IMA measurements (P=0.054, P =0.054, P =0.19 respectively). Conclusions: HIE pathophysiology involves oxidative stress and mitochondrial energy production failure. Explaining the pathways between oxidant-antioxidant balance and cell death, which explains the pathophysiology of HIE, is essential to develop treatment strategies that will minimize the effects of oxygen deprivation on other body organs, especially the brain.Article Role of Netrin-1 in Staging Hypoxic Ischemic Encephalopathy(Assoc Medica Brasileira, 2025) Aycan, Nur; Demir, Derya Cay; Yurekturk, Eyyup; Basaranoglu, Murat; Karaman, Serap; Tuncer, OguzOBJECTIVE: The diagnosis and prognosis of neonatal hypoxic-ischemic encephalopathy are established through clinical evidence and laboratory, imaging, and electrophysiological assessments of the nervous system. Netrin-1 was the first axon guidance molecule identified as a critical component of embryonic development in vertebrates and has a solid chemotropic function for angiogenesis, morphogenesis, cell migration, and axonal guidance. It was hypothesized that Netrin-1 will differ at different hypoxic-ischemic encephalopathy stages. METHODS: This study included 75 hospitalized hypoxic-ischemic encephalopathy newborns and 48 healthy newborns born at the same hospital and followed up only by their mothers. Demographic, laboratory, and Netrin-1 data were evaluated for all hypoxic-ischemic encephalopathy stages. RESULTS: Serum Netrin-1 concentrations were significantly greater in patients with moderate and severe hypoxic-ischemic encephalopathy who underwent therapeutic hypothermia than in controls and patients with severe hypoxic-ischemic encephalopathy. However, serum Netrin-1 concentrations were not significantly greater in patients with mild hypoxic-ischemic encephalopathy than in controls. In 75 hypoxic-ischemic encephalopathy patients, correlations of Netrin-1 with lactate, uric acid, and lactate dehydrogenase were statistically significant (p=0.0001, 0.008, and 0.043, respectively). CONCLUSION: Netrin-1 significantly increased in moderate and severe patients. Therefore, this marker could be a biomarker for staging hypoxicischemic encephalopathy and therapeutic hypothermia and predicting the prognosis of neonatal hypoxic-ischemic encephalopathy patients.Article Serum Prolidase and Ischemia-Modified Albumin Levels in Neural Tube Defects: a Comparative Study of Myelomeningocele, Meningocele, and Myeloschisis(int Scientific information, inc, 2025) Zengin, Irfan; Akyol, Mehmet Edip; Arslan, Mustafa; Arabaci, Ozkan; Yurekturk, Eyyup; Cetin, Eyup; Demir, HalitBackground: Neural tube defects (NTDs) are congenital malformations resulting from incomplete neural tube closure, leading to severe neurological impairments. Despite advances in prenatal screening and surgical interventions, the biochemical mechanisms underlying NTDs remain unclear. Prolidase, an enzyme involved in collagen metabolism, and ischemia-modified albumin (IMA), a marker of oxidative stress, may play roles in NTD pathogenesis. This study aimed to compare serum prolidase and IMA levels in infants with NTDs and healthy controls to assess their potential contribution to NTD development. Material/Methods: A case-control study was conducted, including 45 infants diagnosed with NTDs (myelomeningocele, meningocele, and myeloschisis) and 45 age-and sex-matched healthy controls. Serum prolidase and IMA levels were measured using validated spectrophotometric methods. Statistical analyses were performed to compare biomarker levels between groups and among NTD subtypes. Results: Serum prolidase levels were significantly elevated in NTD patients (2.21 +/- 0.06 IU/L) compared to controls (1.07 +/- 0.04 IU/L, p<0.001). Similarly, serum IMA levels were higher in NTD patients (0.40 +/- 0.01 ABSU) than in controls (0.22 +/- 0.01 ABSU, p<0.001). No significant differences were observed in biomarker levels among the different NTD subtypes (p>0.05). Conclusions: Elevated prolidase and IMA levels in NTD patients suggest a potential role in NTD pathogenesis, possibly through impaired collagen metabolism and oxidative stress. Further research is needed to explore their diagnostic and therapeutic implications in neural tube defect management.Article Wiskott-Aldrich Syndrome: Two Case Reports With a Novel Mutation(Taylor & Francis inc, 2017) Kamuran, Karaman; Cetin, Mecnun; Geylan, Hadi; Karaman, Serap; Demir, Nihat; Yurekturk, Eyyup; Tuncer, OguzBackground: The Wiskott-Aldrich syndrome (WAS) is X-linked recessive disorder associated with microplatelet thrombocytopenia, eczema, infections, and an increased risk of autoimmunity and lymphoid neoplasia. The originally described features of WAS include susceptibility to infections, microthrombocytopenia, and eczema.Aim: In this case report, we present our experience about two cases diagnosed with a new mutation.Methods: We report phenotypical and laboratory description of two cases with WAS.Results: We, for the first time, detected a new hemizygote mutation of WAS gene (NM_000377.2 p.M393lfs(*)102 (c.1178dupT)) in two patients. The first case was an 11-month-old boy presenting with complaints of recurrent soft tissue infection, ear infection, anemia, and thrombocytopenia with a low platelet volume. The second case was a 2-month-old boy presenting with thrombocytopenia and a low platelet volume. Both cases were the first-degree relatives: they were cousins and their mothers were sisters.Conclusion: Herein, we report two cases of WAS and a new gene mutation which would disrupt the WAS protein function within the Polyproline (PPP) domain. This report adds to the growing number of mutations which cause complex clinical manifestations associated with WAS.