Chronic Hepatitis C and Diabetes Mellitus

We often see type-2 diabetes mellitus (DM) in the patients admitted to our clinics for chronic hepatitis C. Thereforey, we decide to examine the patients with chronic viral hepatitis (B and C) for DM and the patients with type-2 DM for HBsAg and anti-HCV antibodies. Group-1 was consisted of 72 patients with chronic hepatitis B and 38 patients with chronic hepatitis C between 1990 and 1995 (n=110). The patients who admitted to hospital for type-2 DM second half of 1995 consisted of group-2. In these two group, we searched the transaminases, other biochemical tests and viral hepatitis markers with ELISA method. We found type-2 DM in 34.2% of patients with chronic hepatitis C and 2.7% of chronic B hepatitis group (p<0.001). All of type-2 DM with chronic hepatitis had not any genetic predisposition for DM. Type-2 DM was diagnosed in 2/3 of the patients after chronic hepatitis C was diagnosed. In the patients with type-2 DM, rates of HBsAg and anti-HCV positivity were found 5% and 6% respectively. The prevalence of HBsAg positiveness is the same as general population value of 5 (4-11)%. Percentage (6%) of anti HCV positiveness in diabetics is significantly higher than normal population value of 0.6 (0.2-1)% (p<0,05). As a result, we think that chronic hepatitis C infection might be a risk factor for type-2 DM

Association between single nucleotide polymorphisms in prospective genes and susceptibility to ankylosing spondylitis and inflammatory bowel disease in a single centre in Turkey

To establish the prevalence of the single nucleotide polymorphisms (SNPs) of endoplasmic reticulum aminopeptidase 1 (ERAP1), IL-23 receptor (IL-23R), signal transducer and activator of transcription 3 (STAT-3) and Janus kinase 2 (JAK-2) in ankylosing spondylitis (AS) and inflammatory bowel disease (IBD) in a Turkish population.Materials and Methods: A total of 562 subjects who presented at the Ankara University internal medicine departments of rheumatology and gastroenterology outpatient clinics were recruited in this study, including 365 patients with AS, 197 patients with IBD and 230 healthy controls. ERAP1, IL-23R, STAT-3 and JAK-2) were genotyped in competitive allele-specific polymerase chain reactions. Results: The ERAP1 (rs26653) polymorphism was found to increase the disease risk in patients with AS and IBD compared with the control group (p=0.02 and p=0.01, respectively). In addition, this polymorphism revealed a significant relationship with the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and the Bath AS Functional Index (BASFI) in patients with AS (r=0.829, p&lt;0.001 and r=0.731, p&lt;0.001, respectively). Conclusion: The ERAP1 gene polymorphism might be a risk factor in the pathogenesis of AS and IBD. In contrast, IL-23R gene polymorphisms may serve a protective role in AS and IBDTo establish the prevalence of the single nucleotide polymorphisms (SNPs) of endoplasmic reticulum aminopeptidase 1 (ERAP1), IL-23 receptor (IL-23R), signal transducer and activator of transcription 3 (STAT-3) and Janus kinase 2 (JAK-2) in ankylosing spondylitis (AS) and inflammatory bowel disease (IBD) in a Turkish population.Materials and Methods: A total of 562 subjects who presented at the Ankara University internal medicine departments of rheumatology and gastroenterology outpatient clinics were recruited in this study, including 365 patients with AS, 197 patients with IBD and 230 healthy controls. ERAP1, IL-23R, STAT-3 and JAK-2) were genotyped in competitive allele-specific polymerase chain reactions. Results: The ERAP1 (rs26653) polymorphism was found to increase the disease risk in patients with AS and IBD compared with the control group (p=0.02 and p=0.01, respectively). In addition, this polymorphism revealed a significant relationship with the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and the Bath AS Functional Index (BASFI) in patients with AS (r=0.829, p&lt;0.001 and r=0.731, p&lt;0.001, respectively). Conclusion: The ERAP1 gene polymorphism might be a risk factor in the pathogenesis of AS and IBD. In contrast, IL-23R gene polymorphisms may serve a protective role in AS and IB