Role of Renin-Angiotensin-converting Enzyme Level and ACE Gene Polymorphism in Patients with Nonalcoholic Fatty Liver Disease.

INTRODUCTION: In this study, we aimed to investigate the histological and clinical effect of angiotensin-converting enzyme (ACE) and ACE gene polymorphism in nonalcoholic fatty liver disease (NAFLD) and their roles in the progression of the disease. MATERIALS AND METHODS: Liver function tests, body mass index, waist circumference, lipid parameters, fasting blood glucose (FBG), hemoglobin A1c (HbA1c), homeostasis model assessment-IR (HOMA-IR), ACE, and ACE gene polymorphism were evaluated in the NAFLD group and control group. The study group was evaluated by dividing the group into four subgroups by ACE gene polymorphism (D/D homozygous, I/I homozygous, D/I heterozygous, I/D heterozygous). Liver biopsies were evaluated according to Brunt Classification. RESULTS: A total of 31 patients who were diagnosed with NAFLD and 40 healthy individuals were included in the study. The ACE level was found to be 11.69 ± 1.99 in the NAFLD group and 11.52 ± 1.72 in the control group (p = 0.70). There was a negative correlation between ACE levels and HOMA-IR levels (p = 0.008, r= -0.512). Biochemical parameters were not different among ACE gene polimorphism subgroups, except FBG (between D/D, I/D and D/I, I/D; p = 0.02). When the ACE levels were compared in terms of grade and stage, no significant difference was found (for stage and grade p = 0.68). The ACE gene polymorphism subgroups did not differ by histopathologic findings; grade and stage (for grade p = 0.42, for stage p = 0.92). CONCLUSION: In this study, we could not find a correlation of ACE and ACE gene polymorphism with metabolic risk factors and the disease severity in NAFLD. HOW TO CITE THIS ARTICLE: Tekatas DD, Bahcecioglu IH, Ispiroglu M, Sahin A, Ilhan N, Yalniz M, Demirel U. Role of Renin-Angiotensin-converting Enzyme Level and ACE Gene Polymorphism in Patients with Nonalcoholic Fatty Liver Disease. Euroasian J Hepato-Gastroenterol 2016;6(2):137-142.

Carotenoids and non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is a growing health problem around the world, especially in developed countries. NAFLD includes all cases of fatty liver disease from simple steatosis to cirrhosis, without excessive alcohol intake, use of steatogenic medication or hereditary disorders. Pathogenesis is associated with dietary high fat intake, decreased free fatty acid (FFA) oxidation, increased hepatic lipogenesis and lipolysis from the adipose tissue. These metabolic alterations contribute to the hepatic fat accumulation. Consequently, stimulated oxidative stress and inflammation play a major role in hepatocellular damage. Therefore, antioxidant and anti-inflammatory agents may have a role in the prevention of this disease. Carotenoids are potent antioxidant and anti-inflammatory micronutrients, which have been investigated in the prevention and treatment of NAFLD. The main sources of the carotenoids are fruits and vegetables. In this article we review the potential role and possible molecular mechanism of carotenoids in NAFLD.

Orally administered lycopene attenuates diethylnitrosamine-induced hepatocarcinogenesis in rats by modulating Nrf-2/HO-1 and Akt/mTOR pathways.

Hepatocarcinogenesis is one of the most prevalent and lethal cancers. We studied the mechanisms underlying the inhibition of diethylnitrosamine (DEN)-induced hepatocarcinogenesis by lycopene in rats. Hepatocarcinogenesis was induced by an intraperitoneal injection of DEN followed by promotion with phenobarbital for 24 successive wk. The rats were given lycopene (20 mg/kg body weight) 3 times a week orally for 4 wk prior to initiation, and the treatment was continued for 24 consecutive wk. Lycopene reduced incidence, number, size, and volume of hepatic nodules. Serum alanine transaminase, aspartate aminotransferase, total bilirubin, and malondialdehyde (MDA) considerably increased and hepatic antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase) and glutathione decreased in DEN-treated rats when compared with the control group. Lycopene significantly reversed these biochemical changes and increased the expression of NF-E-2-related factor-2)/heme oxygenase-1, and it decreased NF-κB/cyclooxygenase-2, inhibiting the inflammatory cascade and activating antioxidant signaling (P < 0.05). Lycopene also decreased DEN-induced increases in phosphorylated mammalian target of rapamycin (p-mTOR), phosphorylated p70 ribosomal protein S6 kinase 1, phosphorylated 4E-binding protein 1, and protein kinase B (P < 0.05). Lycopene is an active chemopreventive agent that offers protection against DEN-induced hepatocarcinogenesis by inhibiting NF-κB and mTOR pathways.

Is inflammatory bowel disease a risk factor for early atherosclerosis?

OBJECTIVES: Chronic inflammatory diseases are associated with an accelerated atherosclerotic process. Recent studies have discussed whether inflammatory bowel diseases (IBDs) can predict early atherosclerosis. We investigated this possibility. METHODS: The study consisted of IBD cases (group 1, n = 40) and healthy persons (group 2, n = 40). The IBD group was selected so as not to have vascular disease or the presence of established major cardiovascular risk factors. RESULTS: Group 1 cases showed a significant increase in carotid intima media thickness (cIMT; P = .01). Carotid artery stiffness was impaired in group 1 (P = .03) and high-sensitivity C-reactive protein (hsCRP), homeostasis model assessment of insulin resistance (HOMA-IR), and homocysteine (Hyc) were higher in group 1 patients (P = .02, P = .03, P = .05). CONCLUSIONS: Inflammatory bowel disease patients have an increased risk of early atherosclerosis as shown by greater values of cIMT, carotid artery stiffness, Hyc, hsCRP, and insulin resistance.

Clinical review of 23 patients with tuberculous peritonitis: presenting features and diagnosis.

OBJECTIVE: To better identify which clinical, laboratory, radiological and invasive procedures were most useful in diagnosing tuberculous peritonitis and to assess the methods in order to reach the diagnosis in future cases. METHODS: Tuberculous peritonitis cases diagnosed between 2000 and 2006 were reviewed retrospectively. Their clinical presentation, physical examination, laboratory and diagnostic methods were evaluated. RESULTS: Twenty-three cases oftuberculous peritonitis were diagnosed. The mean age of the patients were 30 +/- 11 years and 16 were women. The mean duration of symptoms prior to diagnosis was 3.6 months. All patients presented with abdominal pain. Abdominal swelling (91.3%), loss of appetite (87%) and weight loss (82.6%) were the other commonest symptoms. The major physical findings were ascites (78.3%) and fever (60.9%). The serum ascites albumin gradient was < 1.1 g/dL in all. An ascites fast bacilli smear was positive in 12 (52.2%) patients. Skin tests with purified protein derivative, adenosine deaminase and polymerase chain reaction were performed in seven, four and five patients, respectively. The tuberculous culture was positive in only two. The most common radiological findings were ascites (100%) and omental involvement (65.2%). A laparoscopy was performed in nine of 23 patients. A total of 22 patients completed anti-tuberculous therapy successfully and were cured, except one with cirrhosis. CONCLUSION: Tuberculous peritonitis may be fatal but is medically cured if diagnosed in a timely fashion. Although both non-invasive and invasive tests have additional benefits, clinician suspicion is still the first step for the diagnosis of tuberculous peritonitis.