ASSOCIATION OF NON-ALCOHOLIC FATTY LIVER DISEASE WITH SERUM URIC ACID
Abstract
Background: Non-alcoholic fatty liver disorder is a clinicopathological condition, characterized by macro vesicular steatosis in hepatic cells and metabolic stress related disorders without other causes of chronic hepatic disease. Uric acid is basically a heterocyclic compound of hydrogen, carbon, oxygen and nitrogen. Uric acid is the metabolic end product of purine metabolism. Hyperuricemia is considered to be related with the causes responsible for the production of metabolic syndrome. It may cause gout, impaired renal function, hypertension, hypertriglyceridemia, obesity and diabetes mellitus. The objective of study is to investigate the association of non-alcoholic fatty liver disease (NAFLD) and serum uric acid level. METHODS: This cross-sectional study was conducted at Ayub Teaching institute Abbottabad. According to predesigned questionnaire and informed consent, 100 subjects between ages 40-50 years were selected for the study. Data collected and analysis done by SPSS version 20. RESULTS: It was observed that 20(40%) subjects developed NAFLD as compared to 30(60%) of the subjects with normal serum uric acid level. Chi-square test was applied and values found to be significant (p=0.013). CONCLUSION: Our study shows association of NAFLD with serum uric acid level.
Keywords: Non-alcoholic fatty liver disease; serum uric acid level; hepatic disorderReferences
Barshop NJ, Sirlin CB, Schwimmer JB, Lavine JE (2008), Review article: epidemiology, pathogenesis and potential treatments of paediatric nonalcoholic fatty liver disease. Aliment Pharmacol Ther, 28:13-24.
Fan JG, Farrell GC, (2009), Epidemiology of non-alcoholic fatty liver disease in China. J Hepatol, 50(1):204-210.
Amarapurkar DN, Hashimoto E, Lesmana LA, Sollano JD, Chen PJ, Goh KL (2007), How common is non-alcoholic fatty liver disease in the Asia-Pacific region and are there local differences? J Gastroenterol Hepatol, 22(6):788-793.
Fracanzani AL, Valenti L, Bugianesi E, Andreoletti M, Colli A, Vanni E, (2008), Risk of severe liver disease in nonalcoholic fatty liver disease with normal aminotransferase Levels: A role for insulin resistance and diabetes. Hepatology, 48:792-798.
Neuschwander-Tetri BA, Caldwell SH. (2003), Nonalcoholic steatohepatitis: summary of an AASLD Single Topic Conference. Hepatology. 37:1202-1219.
Marchesini G, Brizi M, Bianchi G, Tomassetti S, Bugianesi E, (2001), Nonalcoholic fatty liver disease: a feature of the metabolic syndrome. Diabetes. 50:1844-1850.
Marchesini G, Bugianesi E, Forlani G, Cerrelli F, Lenzi M, (2003), Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome. Hepatology. 37: 917-923.
Yoo TW, Sung KC, Shin HS, Kim BJ, Kim BS, (2005), Relationship between serum uric acid concentration and insulin resistance and metabolic syndrome. Circ J. 69:928-933.
Hjortnaes J, Algra A, Olijhoek J, Huisman M, Jacobs J, (2007), Serum uric acid levels and risk for vascular diseases in patients with metabolic syndrome. J Rheumatol, 34:1882-1887
Choi HK, Ford ES. (2007), Prevalence of the metabolic syndrome in individuals with hyperuricemia. Am J Med, 120:442-447
Li Y, Xu C, Yu C, (2009), Association of serum uric acid level with non-alcoholic fatty liver disease: a cross-sectional study. J Hepatol, 50(5):1029-34.
Haq A, Mahmood R, Ahmad Z, Rehman J, Jilani G, (2010), Association of serum uric acid with blood urea and serum creatinine.Pak J Physiol, 6 (2).
Safi AJ, Mahmood R,Khan MA,Haq (2004), AU.Association of Serum Uric Acid with type 2 Diabetes Mellitus.J Pak Med Ins. 18(1):59-63.
Hayden MR, Tyagi SC (2004) Uric acid: A new look at an old risk marker for cardiovascular disease, metabolic syndrome, and type 2 diabetes mellitus: The urate redox shuttle. Nutr Metab (Lond) 1: 10.
Harrison R (2002) Structure and function of xanthine oxidoreductase: where are we now Free Radic Biol Med 33(6): 774-797
Berry CE, Hare JM (2004) Xanthine oxidoreductase and cardiovascular disease: molecular mechanisms and pathophysiological implications. J Physiol 555(Pt 3):589-606
Baskol G, Baskol M, Kocer D (2007) Oxidative stress and antioxidant defenses in serum of patients with non-alcoholic steatohepatitis. Clin Biochem 40(11): 776-780].
De Oliveira EP, Burini RC (2012) High plasma uric acid concentration: causes and consequences. Diabetol Metab Syndr 4: 12.
Petta S, Camma C, Cabibi D, Di Marco V, Craxi A (2011) Hyperuricemia is associated with histological liver damage in patients with non-alcoholic fatty liver disease. Aliment Pharmacol Ther 34: 757-766.
Kono H, Chen CJ, Ontiveros F, Rock KL (2010) Uric acid promotes an acute inflammatory response to sterile cell death in mice. J Clin Invest 120: 1939-1949.
Hoque R, Vodovotz Y, Mehal W (2013) Therapeutic strategies in inflammasome mediated diseases of the liver. J Hepatol 58: 1047-1052.
Shi Y (2010) Caught red-handed: uric acid is an agent of inflammation. J Clin Invest 120: 1809-1811.
Marangella M. (2005) Uric acid elimination in the urine. Pathophysiological implications. Contrib Nephrol, 147:132-48.
Baldwin W, McRae S, Marek G, (2011). Hyperuricemia as a mediator of the proinflammatory endocrine imbalance in the adipose tissue in a murine model of the metabolic syndrome. Diabetes. 60(4):1258-69.
Sautin YY, Nakagawa T, Zharikov S, (2007). Adverse effects of the classic antioxidant uric acid in adipocytes: NADPH oxidase-mediated oxidative/nitrosative stress. Am J Physiol Cell Physiol, 293(2):C584-96
Kang DH, Han L, Ouyang X, (2005). Uric acid causes vascular smooth muscle cell proliferation by entering cells via a functional urate transporter. Am J Nephrol, 25(5):425-33.
Kanellis J, Watanabe S, Li JH, (2003). Uric acid stimulates monocyte chemoattractant protein-1 production in vascular smooth muscle cells via mitogen-activated protein kinase and cyclooxygenase-2. Hypertension, 41(6):1287-93.
Dasarathy S, Dasarathy J, Khiyami A, (2009). Validity of real time ultrasound in the diagnosis of hepatic steatosis: a prospective study. J Hepatol; 51(6):1061-7.
Lanaspa MA, Tapia E, Soto V, (2011). Uric acid and fructose: potential biological mechanisms. Semin Nephrol, 31(5):426-32.
Lim JS, Mietus-Snyder M, Valente A, (2010). The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome. Nat Rev Gastroenterol Hepatol, 7(5):251-64.
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