Tıp Fakültesi / Faculty of Medicine

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Subject: search.filters.subject.Nasal polyposis

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    Kartagener's Syndrome Presented with Nasal Obstruction: A Case Report
    (2014) Asilsoy, Suna; Kilicaslan, Buket; Ozer, Cem; 0000-0002-6641-5300; ABH-1785-2020; AAW-9958-2021; AAM-7975-2020
    The nasal polyposis is a chronic inflammatory process of the nasal mucosa. Although it is rare in children, there may be also association with cystic fibrosis and primary ciliary dyskinesia. About 50% of primary ciliary dyskinesia patients develop situs inversus and it is known as Kartagener's syndrome. The Kartagener's sydrome is a rare autosomal recessive disorder characterized by sinusitis, bronchiectasis, situs inversus. Clinically, patients present to the otolaryngologist with nasal obstruction. We as pediatricians, should consider nasal polyposis as a rare cause of nasal obstruction in children. In the presence of recurrent upper and lower respiratory tract infections accompanying nasal polyposis, Kartagener's syndrome must be kept in mind as a rare reason.
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    Investigation of SCGB3A1 (UGRP2) Gene Arrays in Patients with Nasal Polyposis
    (2014) Palali, Mehmet; Ozcan, K. Murat; Ozdas, Sibel; Koseoglu, Sabri; Ozdas, Talih; Erbek, Selim S.; Yildirim, Erol; Ensari, Serdar; Dere, Huseyin; https://orcid.org/0000-0003-4825-3499; 24710847; B-7604-2019
    The aim of the current study is to investigate the potential relationship between polymorphisms and nasal polyposis (NP) pathogenesis in the SCGB3A1 (UGRP2) gene, which is a member of the secretoglobin gene super family. Genotypic variations were studied by performing DNA sequencing in blood samples of 80 patients with NP and 70 healthy individuals to evaluate nucleotide changes and their positions that might be in the SCGB3A1 gene (promotor, splicing points, and exon distributions). In the SCGB3A1 gene, three single-nucleotide changes labeled IVS1-89 T > G, c. -183 G > T, IVS1-189 G > A were identified. IVS1-89 T > G and IVS1-189 G > A belong to the first intronic region of the gene, whereas c. -183 G > T was observed in the promoter region of the gene. The IVS1-89 T > G nucleotide change was observed in the patient and control groups, whereas c. -183 G > T and IVS1-189 G > A nucleotide changes were observed in the control group only. SCGB3A1 (IVS1-89) genotype frequencies between patients with NP and control group were not significantly different (p = 0.311). There was a statistically significant difference in the control group in comparison to patients with NP in terms of SCGB3A1 (c. -183 GT) and SCGB3A1 (IVS1-189 GA) frequency (p = 0.0045 and p = 0.009, respectively). The findings of the current study suggest that SCGB3A1-183 T and SCGB3A1 IVS1-189 A alleles might have a protective effect against NP, and that SCGB3A1 (-183 GT and IVS1-189 GA) genotypes should be studied in future population-based studies.