Browsing by Author "Nazligul, Yasar"

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Benign Glycogenic Acanthosis Lesions of the Esophagus
(Turkish Soc Gastroenterology, 2012) Nazligul, Yasar; Aslan, Mehmet; Esen, Ramazan; Yeniova, Abdullah Ozgur; Kefeli, Ayse; Kucukazman, Metin; Celik, Yilmaz
Background/aims: Glycogenic acanthosis is described as benign thickening of the esophageal squamous epithelium of unknown etiology. Although its etiology is unknown, it has been reported that glycogenic acanthosis may be related to gastroesophageal reflux and hiatal hernia. The aim of the present study was to review the patients who were diagnosed with glycogenic acanthosis on upper gastrointestinal endoscopy and to determine whether there is any association between glycogenic acanthosis and gastroesophageal reflux and hiatal hernia. Material and Methods: A total of 504 patients who underwent upper gastrointestinal endoscopy for evaluation of non-ulcer dyspepsia were reviewed retrospectively. Results: Glycogenic acanthosis was detected in 143 (28.3%) of those 504 patients. Of the 143 patients, 82 (57.3%) were male and 61 (42.7%) were female. Patients with glycogenic acanthosis were aged 20-83 years. Gastroesophageal reflux was detected in 50 (34.9%) cases with glycogenic acanthosis, while hiatal hernia was detected in 30 (20.9%) cases. Gastroesophageal reflux was detected in 102 (28.2%) control subjects, while hiatal hernia was detected in 50 (13.8%). Hiatal hernia was significantly higher in glycogenic acanthosis patients than in controls subjects (p<0.05). Glycogenic acanthosis patients had higher gastroesophageal reflux than seen in controls subjects, but the difference between groups was not statistically significant (p>0.05). Conclusions: Our results suggest that glycogenic acanthosis is primarily an age-related disease. We demonstrated that glycogenic acanthosis may be associated with gastroesophageal reflux and hiatal hernia. Further studies are necessary to confirm these findings.
The Effect on Serum Myeloperoxidase Activity and Oxidative Status of Eradication Treatment in Patients Helicobacter Pylori Infected
(Pergamon-elsevier Science Ltd, 2011) Nazligul, Yasar; Aslan, Mehmet; Horoz, Mehmet; Celik, Yilmaz; Dulger, Ahmet Cumhur; Celik, Hakim; Erel, Ozcan
Objectives: Myeloperoxidase activity has been investigated after eradication of Helicobacter pylon (H. pylori) in infected patients in previous studies but the results are controversial. The aim of this study was to investigate effect on serum myeloperoxidase activity and oxidative status of eradication treatment in H. pylon-infected patients. Design and methods: Gastric biopsy specimens were obtained from 30 H. pylori infected patients. Serum Myeloperoxidase activity was measured by enzyme-linked immunoassay. Oxidative status was determined using total antioxidant capacity (TAC) and total oxidant status (TOS) measurement and calculation of oxidative stress index (OSI). Results: After 2 weeks of the eradication treatment, serum myeloperoxidase activity, TOS and OSI values were significantly lower (all: p<0.001), while TAC was significantly higher (p<0.001). Conclusions: Our results indicate that eradication treatment in H. pylori-infected patients may affect both oxidative stress and myeloperoxidase activity which is an important biomarker in pathogenesis of atherosclerosis. (C) 2011 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.
Peripheral Lymphocyte Dna Damage and Oxidative Status After Eradication Therapy in Patients Infected With Helicobacter Pylori
(Medycyna Praktyczna, 2011) Dulger, Ahmet C.; Aslan, Mehmet; Nazligul, Yasar; Horoz, Mehmet; Bolukbas, Cengiz; Bolukbas, Fusun F.; Kocyigit, Abdurrahim
Introduction Helicobacter pylori infection has been shown to cause inflammation, increased production of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. However, the effect of eradication treatment on DNA damage in patients infected with H. pylori is unclear. Objectives The objective of this study was to investigate the effect of eradication treatment on peripheral DNA damage and oxidative status in patients wth H. pylori infection. Patients and methods The study involved 42 patients positive for H. pylori (Hp+) and 25 patients negative for H. pylori (Hp-). Peripheral lymphocyte DNA damage was assessed using the alkaline comet assay and plasma oxidative status was determined. Measurements were conducted at baseline and 2 weeks after eradication treatment. Results The total antioxidant status (TAS) was lower in Hp+ patients than in Hp-patients (P <0.05), while the total oxidant status (TOS), oxidative stress index (OSI), and peripheral lymphocyte DNA damage were higher (P <0.001 for all parameters). TOS, OSI, and peripheral lymphocyte DNA damage were significantly lower after eradication treatment (P <0.001 for all parameters), while TAS was significantly higher (P <0.05). There was no correlation between TOS, OSI, peripheral lymphocyte DNA damage, and TAS and the histopathological degree of antral gastric inflammation in the Hp+ group (P >0.05). Conclusions Our results suggest that H. pylori eradication significantly decreases peripheral lymphocyte DNA damage and oxidative stress. Eradication treatment might help prevent the development of gastric cancer in patients with H. pylori infection.
Peripheral Lymphocyte Dna Damage and Oxidative Stress in Patients With Ulcerative Colitis
(Medycyna Praktyczna, 2011) Aslan, Mehmet; Nazligul, Yasar; Bolukbas, Cengiz; Bolukbas, Fusun F.; Horoz, Mehmet; Dulger, Ahmet C.; Kocyigit, Abdurrahim
Introduction Ulcerative colitis (UC) is a fairly common chronic inflammatory disorder. Chronic inflammation may contribute to the risk of colorectal cancer through the accumulation of specific products resulting from DNA damage. Previous studies reported that DNA damage and oxidative stress play a significant role in the pathophysiology of UC, but the results are inconsistent. Objectives In the present study, we investigated peripheral DNA damage and oxidative stress in patients with UC. Patients and methods The study included 20 patients with UC and 20 controls. Peripheral lymphocyte DNA damage was measured using the alkaline comet assay. Plasma total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) were determined. Results DNA damage levels, TOS, and OSI were significantly higher in patients with UC than in controls (P < 0.001 for all para-meters), while TAC was significantly lower (P < 0.001). DNA damage was significantly correlated with TOS, TAC, and OSI (r = 0.604, P < 0.001; r = -0.593, P < 0.001; and r = 0.716, P < 0.001, respectively). Moreover, TAC levels were significantly correlated with TOS and OSI (r = 0.604, P < 0.001; r = -0.399, P < 0.05; and r = -0.513, P < 0.05, respectively). Conclusions Our results show that increased peripheral DNA damage and oxidative stress seem to be associated with decreased antioxidant levels and thus may in part contribute to the development of colorectal cancer associated with UC.