Search results for: M. Toygar
Commenced in January 2007
Frequency: Monthly
Edition: International
Paper Count: 2

Search results for: M. Toygar

2 The Relation Between Oxidative Stress, Inflammation, and Neopterin in the Paraquat-Induced Lung Toxicity

Authors: M. Toygar, I. Aydin, M. Agilli, F. N. Aydin, M. Oztosun, H. Gul, E. Macit, Y. Karslioglu, T. Topal, B. Uysal, M. Honca

Abstract:

Paraquat (PQ) is a well-known quaternary nitrogen herbicide. The major target organ in PQ poisoning is the lung. Reactive oxygen species (ROS) and inflammation play a crucial role in the development of PQ-induced pulmonary injury. Neopterin is synthesized in macrophage by interferon g and other cytokines. We aimed to evaluate the utility of neopterin as a diagnostic marker in PQ-induced lung toxicity. Sprague Dawley rats were randomly divided into two groups (sham and PQ), administered intraperitoneally 1 mL saline and PQ (15 mg/kg/mL) respectively. Blood samples and lungs were collected for analyses. Lung injury and fibrosis were seen in the PQ group. Serum total antioxidant capacity, lactate dehydrogenase (LDH), and lung transforming growth factor-1 (TGF-1) levels were significantly higher than the sham group (in all, p< 0.001). In addition, in the PQ group, serum neopterin and lung malondialdehyde (MDA) levels were also significantly higher than the sham group (in all, p 1/4 0.001). Serum neopterin levels were correlated with LDH activities, lung MDA, lung TGF-1 levels, and the degree of lung injury. These findings demonstrated that oxidative stress, reduction of antioxidant capacity, and inflammation play a crucial role in the PQ-induced lung injury. Elevated serum neopterin levels may be a prognostic parameter to determine extends of PQ-induced lung toxicity. Further studies may be performed to clarify the role of neopterin by different doses of PQ.

Keywords: paraquat, inflammation, oxidative stress, neopterin, lung toxicity

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1 Still Hepatocellular Carcinoma Risk Despite Proper Treatment of Chronic Viral Hepatitis

Authors: Sila Akhan, Muge Toygar, Murat Sayan, Simge Fidan

Abstract:

Chronic viral hepatitis B, C, and D can cause hepatocellular carcinoma (HCC), cirrhosis and death. The proper treatment reduce the risk of development of HCC importantly, but not to zero point. Materials and Methods: We analysed retrospectively our chronic viral hepatitis B, C and D patients who attended to our Infectious Diseases policlinic between 2004-2018. From 589 biopsy-proven chronic hepatitis patients 3 have hepatocellular carcinoma on our follow up. First case is 74 years old patient. His HCV infection diagnosis was made 8 years ago. First treatment was pegylated interferon plus ribavirin only 28 weeks, because of HCV RNA breakthrough under treatment. In 2013 he was retreated with telaprevir, pegylated interferon plus ribavirin 24 weeks. But at the end of the therapy HCV RNA was found 1.290.000 IU/mL. He has abdominal ultrasonography (US) controls and alpha-fetoprotein (AFP) at 6 months intervals. All seemed normal until 2015 then he has an abdominal magnetic resonance imaging (MRI) and found HCC by chance. His treatment began in Oncology Clinic after verified with biopsy of HCC. And then sofosbuvir/ledipasvir was given to him for HCV 24 weeks. Sustained virologic response (SVR) was obtained. He is on cure for HCV infection and under control of Oncology for HCC. Second patient is 36 years old man. He knows his HBV infection since 2008. HBsAg and HBeAg positive; HDV RNA negative. Liver biopsy revealed grade:4, stage 3-4 according modified Knodell scoring system. In 2010 tenofovir treatment was began. His abdominal US and AFP were normal. His controls took place at 6 months intervals and HBV DNA negative, US, and AFP were normal until 2016 continuously. AFP found 37 above the normal range and then HCC was found in MRI. Third patient is 57 years old man. As hepatitis B infection was first diagnosed; he has cirrhosis and was began tenofovir as treatment. In short time he has HCC despite normal AFP values. Conclusion: In Mediterranian countries including Turkey naturally occurring pre-S/S variants are more than 75% of all chronic hepatitis B patients. This variants may contribute to the development of progressive liver damage and hepatocarcinogenesis. HCV-induced development of HCC is a gradual process and is affected by the duration of disease and viral genotype. All the chronic viral hepatitis patients should be followed up in 6 months intervals not only with US and AFP for HCC. Despite they have proper treatment there is always the risk development of HCC. Chronic hepatitis patients cannot be dropped from follow up even treated well.

Keywords: HCC, HCV, HBV, DAA

Procedia PDF Downloads 108