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1.
Turk J Gastroenterol ; 19(4): 245-9, 2008 Dec.
Article in English | MEDLINE | ID: mdl-19119483

ABSTRACT

BACKGROUND/AIMS: Several lines of evidence suggest that peroxisome proliferator-activated receptor alpha may be involved in hepatocarcinogenesis. L162V polymorphism of the peroxisome proliferator-activated receptor alpha gene enhances the transactivation activity of this transcription factor. The aim of this study was to determine the frequency and clinical correlates of peroxisome proliferator-activated receptor alpha L162V polymorphism in hepatitis virus-induced hepatocellular carcinoma. METHODS: 90 hepatocellular carcinoma patients diagnosed at Ankara University Gastroenterology Clinic between January 2002 and July 2003 and 80 healthy controls with normal body mass index, blood chemistry and with negative viral serology were included. peroxisome proliferator-activated receptor alpha L162V polymorphism was determined by PCR-RFLP. RESULTS: hepatocellular carcinoma etiologies were as follows: 56 HBV, 12 HBV+HDV, 22 HCV. Eighty-seven patients (97%) were cirrhotic, and 60 patients (67.5%) had advanced tumors. In 83 (92%) of 90 hepatocellular carcinoma patients, gene segment including polymorphic region could be amplified by PCR (50 HBV, 12 HBV+HDV, 21 HCV) and 6 of them (7.2%, all infected with HBV) had L162V polymorphism, while 2 (2.5%) of 80 controls had this polymorphism (p=0.162). This trend became more remarkable when only HBV (HBV+HDV)-infected patients were compared with controls (6/62, 9.7% vs. 2/80, 2.5%, respectively, p=0.071). Five of 6 patients with L162V had advanced disease. CONCLUSIONS: Peroxisome proliferator-activated receptor alpha L162V polymorphism tends to occur in HBV-induced hepatocellular carcinoma and is absent in HCV-related hepatocellular carcinoma. These findings may show clues for the existence of different carcinogenesis mechanisms in these two common etiologies. Frequent occurrence of advanced disease in patients with L162V polymorphism suggests a role for this polymorphism in tumor progression.


Subject(s)
Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/virology , Hepatitis B, Chronic/complications , Hepatitis C, Chronic/complications , Liver Neoplasms/genetics , Liver Neoplasms/virology , Peroxisome Proliferator-Activated Receptors/genetics , Polymorphism, Genetic , Case-Control Studies , Female , Humans , Male , Polymerase Chain Reaction , Polymorphism, Restriction Fragment Length
2.
J Investig Med ; 53(7): 353-9, 2005 Nov.
Article in English | MEDLINE | ID: mdl-16297361

ABSTRACT

BACKGROUND: Peroxisome proliferator-activated receptor alpha (PPARalpha) plays important roles in lipid metabolism. A recently discovered L162V polymorphism of the PPARalpha gene is associated with enhanced transcriptional activity. In this study, the frequency of L162V was investigated in nonalcoholic steatohepatitis (NASH) and genotype 1 hepatitis C virus (HCV)-related liver steatosis. METHODS: Seventy-two NASH and 141 HCV-infected patients (54 with steatosis, 87 without steatosis) and 119 healthy controls were included. L162V polymorphism of the PPARalpha gene was analyzed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). RESULTS: PCR and RFLP analysis of the related gene segment was successful in 93%, 96%, and 100% of NASH and HCV-infected patients and controls, respectively. The frequency of the L162V polymorphism was similar in the NASH and HCV-infected patients and controls (5.9%, 3.6%, and 2.5%, respectively). No difference in the frequency of this polymorphism was observed in HCV-infected patients with or without significant liver steatosis. L162V was not associated with obesity, type 2 diabetes mellitus, hypercholesterolemia, or hypertriglyceridemia. CONCLUSIONS: Neither NASH nor genotype 1 HCV-related liver steatosis seems to be associated with the PPARalpha L162V polymorphism. This polymorphism may have no association with the presence of type 2 diabetes mellitus, obesity, or various blood lipid alterations in NASH and HCV-infected patients.


Subject(s)
Fatty Liver/genetics , PPAR alpha/genetics , Adult , Base Sequence , Body Mass Index , Case-Control Studies , DNA/genetics , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/genetics , Fatty Liver/complications , Fatty Liver/pathology , Female , Genotype , Hepacivirus/genetics , Hepatitis C, Chronic/complications , Hepatitis C, Chronic/genetics , Hepatitis C, Chronic/virology , Humans , Hyperlipidemias/complications , Hyperlipidemias/genetics , Male , Middle Aged , Polymorphism, Genetic
3.
Turk J Gastroenterol ; 15(3): 133-6, 2004 Sep.
Article in English | MEDLINE | ID: mdl-15492909

ABSTRACT

BACKGROUND/AIMS: A relation between hepatitis C virus (HCV) infection with lichen planus (LP) has been reported in the literature but remains controversial. To find out the prevalence of HVC infection among patients with LP. METHODS: Forty-one cases of LP diagnosed at the Dermatology Clinic of our hospital between March 1995 and May 1996 were evaluated (22 men and 19 women; mean age 41.6 years). They were screened for the presence of HBsAg, anti HBs, and anti-HCV by ELISA and HCV-RNA by nested polymerase chain reaction (PCR). Blood donors registered in Ankara University Ibni Sina Hospital Blood Bank were used as a control group. RESULTS: Of the 41 LP patients, 2 (4.8%) had anti-HCV positivity together with HCV-RNA positivity. Twelve patients (29.2%) had anti-HBs and 3 patients (7.3%) had HBsAg positivity. In blood donors, anti-HCV positivity prevalence was 2.5%. CONCLUSIONS: The results of this study suggest that no relationship exists between hepatitis C virus infection and lichen planus among Turkish patients.


Subject(s)
Hepatitis C/epidemiology , Lichen Planus/epidemiology , Adult , Blood Donors/statistics & numerical data , Case-Control Studies , Comorbidity , Female , Hepacivirus/isolation & purification , Hepatitis B Antibodies/blood , Hepatitis B Surface Antigens/blood , Hepatitis C/blood , Hepatitis C Antibodies/blood , Humans , Lichen Planus/blood , Male , Prevalence , RNA, Viral/blood
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