Abdulhalim ŞENYİĞİT, Bülent YAPRAK, Timur ORHANOĞLU

Non-Alkolik Yağlı Karaciğer (NAYK) Hastalığının Derecelerinin ve Olası Biyobelirteçlerinin İncelenmesi

Amaç: Çalışmamızda non-alkolik yağlı karaciğer (NAYK) hastalığında ilgili biyokimyasal belirteçleri vebunlar arasındaki ilişkileri incelemeyi amaçladık.Gereç ve Yöntemler: Herhangi bir yakınması olmayıp hastanemize kontrol amacıyla başvurmuş olanbireylerin dosyaları retrospektif olarak incelendi. Ultrasonografide (USG) karaciğerde değişik derecelerdeNAYK tespit edilen 148 (94 kadın, 54 erkek) birey vaka grubu olarak, USG’de NAYK tespit edilmeyen149 (76 kadın, 73 erkek) birey ise sağlıklı kontrol grubu olarak çalışmaya dahil edildi. Toplamda297 hastanın açlık kan glukozu, insülin, HOMA-IR, ürik asit, C-reaktif protein (CRP), trigliserit, LDL, HDL,TSH, D vitamini, AST, ALT, GGT, ALP değerleri ve USG ile belirlenmiş olan NAYK dereceleri incelendi.Bulgular: Cinsiyet karşılaştırılmasında erkeklerde, NAYK prevalansı vaka grubunda sağlıklı gruptakinegöre anlamlı biçimde daha yüksek bulundu (p=0,029). Benzer şekilde serum açlık kan glukozu, insülin,HOMA-IR, ürik asit, trigliserit, HDL, ALT, AST, GGT, CRP değerleri de vaka grubunda anlamlı biçimdedaha yüksekti. HDL, D vitamini düşüklüklerinin NAYK derecesine etkisi saptanmadı. Vaka grubundaNAYK derecesine göre yapılan analizler açlık kan şekeri (AKŞ), HOMA-IR, ALT, AST ve GGT ortalamalarıaçısından NAYK dereceleri arasında istatistiksel olarak anlamlı fark olduğunu gösterdi. NAYK derecesi2 ve 3 olan gruplar birleştirilerek analizler tekrarlandığında NAYK derecesi 1 ve 2 olan iki yeni gruparasında AKŞ, insülin, HOMA-IR, ALT, GGT ortalamaları açısından istatistiksel olarak anlamlı bir farkbulundu. Bu kez AST’deki farklılık azalırken, insülin değeri ortalaması açısından da istatistiksel olarakanlamlı fark olduğu gözlendi.Tartışma ve Sonuç: Çalışmamız görünürde sağlıklı olan bireylerde de NAYK’nin araştırılması gerektiğini,erken tanı ve uygun yönetim ile siroz ve hepatoselüler karsinom gibi komplikasyonların önünegeçilebileceğini düşündürmektedir.

An Investigation of Degrees and Possible Biomarkers of NonAlcoholic Fatty Liver (NAFL) Disease

Aim: In this study, we aimed to investigate the related biochemical markers and their correlations in non-alcoholic fatty liver (NAFL) disease. Materials and Methods: Patient files of individuals who came to our hospital for routine controls without any complaints were reviewed retrospectively. One hundred and forty-eight individuals (94 females; 54 males) whose ultrasonographic examination revealed varying degrees of NAFL disease constituted the patients group and 149 individuals (76 females; 73 males) whose results were clear the healthy controls group. We reviewed the ultrasonographically determined NAFL disease grades and fasting blood glucose, insulin, HOMA-IR, uric acid, C-reactive protein (CRP), triglyceride, LDL, HDL, TSH, vitamin D, AST, ALT, GGT and ALP values of a total of 297 patients. Results: With respect to sex, NAFL prevalence was significantly higher in the patients group than in the healthy controls for males (p=0.029). Similarly, fasting blood glucose, insulin, HOMA-IR, uric acid, triglyceride, HDL, ALT, AST, GGT and CRP levels were also significantly higher in the patients group. No effect of low HDL and vitamin D levels on NAFL disease grade was observed. Analyses based on NAFL disease grade showed statistically significant difference between the subgroups of disease grade of the patients group in terms of fasting blood glucose, HOMA-IR, ALT, AST and GGT mean values. When the analyses were repeated after the grade 2 and 3 subgroups were combined, there was statistically significant difference between the new grade 1 and 2 subgroups in terms of fasting blood glucose, insulin, HOMA-IR, ALT and GGT mean values. This time there was statistically significant difference in terms of mean insulin levels also, while the difference between the AST levels decreased. Discussion and Conclusion: Our study suggests that apparently healthy individuals also be examined for presence of NAFL disease because timely diagnosis and appropriate management could significantly help prevent complications such as cirrhosis and hepatocellular carcinoma.

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Fenkci S, Rota S, Sabir N, Akdag B. Ultrasonographic and biochemical evaluation of visceral obesity in obese women with non-alcoholic fatty liver disease. Eur J Med Res. 2007;12:68–73.
Toledo FG, Sniderman AD, Kelley DE. Influence of hepatic steatosis (fatty liver) on severity and composition of dyslipidemia in type 2 diabetes. Diabetes Care. 2006;29:1845–50.
Ozhan H, Aydin M, Yazici M ve ark. Mean platelet volume in patients with non-alcoholic fatty liver disease. Platelets. 2010;21:29–32.
Kucukazman M, Ata N, Yavuz B ve ark. Evaluation of early atherosclerosis markers in patients with nonalcoholic fatty liver disease. Eur J Gastroenterol Hepatol. 2013;25:147–51.
Nigam P, Bhatt SP, Misra A ve ark. Non-alcoholic fatty liver disease is closely associated with sub-clinical inflammation: a case-control study on Asian Indians in North India. PLoS One. 2013;8:e49286.
Bayard M, Holt J, Boroughs E. Nonalcoholic fatty liver disease. Am Fam Physician. 2006;73:1961–8.
Cosar S. Alkol Bağımlılarında Biyokimyasal Parametrelerin incelemesi ve Karaciğer Hemodinamisinin Doppler Us ile Değerlendirilmesi [Uzmanlık tezi]. Ankara: Gazi Üniversitesi Radyoloji ABD; 2001.
Matteoni CA, Younossi ZM, Gramlich T ve ark. Nonalcoholic fatty liver disease: a spectrum of clinical and pathological severity. Gastroenterology. 1999;116:1413–9.
Teli MR, James OF, Burt AD ve ark. The natural history of nonalcoholic fatty liver: a follow-up study. Hepatology. 1995;22:1714–9.
Angulo P, Keach JC, Batts KP, Lindor KD. Independent predictors of liver fibrosis in patients with nonalcoholic steatohepatitis. Hepatology. 1999;30:1356–62.
Powell EE, Cooksley WG, Hanson R ve ark. The natural history of nonalcoholic steatohepatitis: a follow-up study of forty-two patients for up to 21 years. Hepatology. 1990;11:74–80.
Falck-Ytter Y, Younossi ZM, Marchesini G, McCullough AJ. Clinical features and natural history of nonalcoholic steatosis syndromes. Semin Liver Dis. 2001;21:17–26.
Washington K, Wright K, Shyr Y ve ark. Hepatic stellate cell activation in nonalcoholic steatohepatitis and fatty liver. Hum Pathol. 2000;31:822–8.
Caldwell SH, Oelsner DH, Iezzoni JC ve ark. Cryptogenic cirrhosis: clinical characterization and risk factors for underlying disease. Hepatology. 1999;29:664–9.
Bugianesi E, Leone N, Vanni E ve ark. Expanding the natural history of nonalcoholic steatohepatitis: from cryptogenic cirrhosis to hepatocellular carcinoma. Gastroenterology. 2002;123:134–40.
Ludwig J, Viggiano TR, McGill DB, Oh BJ. Nonalcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease. Mayo Clin Proc. 1980;55:434–8.
Marchesini G, Brizi M, Bianchi G ve ark. Nonalcoholic fatty liver disease: a feature of the metabolic syndrome. Diabetes. 2001;50:1844–50.
Musso G, Gambino R, Bo S ve ark. Should nonalcoholic fatty liver disease be included in the definition of metabolic syndrome? A cross-sectional comparison with Adult Treatment Panel III criteria in nonobese nondiabetic subjects. Diabetes Care. 2008;31:562–8.
Angulo P. GI epidemiology: nonalcoholic fatty liver disease. Aliment Pharmacol Ther. 2007;25:883–9.
Bellentani S, Tiribelli C, Saccoccio G ve ark. Prevalence of chronic liver disease in the general population of northern Italy: the Dionysos Study. Hepatology. 1994;20:1442–9.
Browning JD, Szczepaniak LS, Dobbins R ve ark. Prevalence of hepatic steatosis in an urban population in the United States: impact of ethnicity. Hepatology. 2004;40:1387–95.
Sanyal AJ, American Gastroenterological Association. AGA technical review on nonalcoholic fatty liver disease. Gastroenterology. 2002;123:1705–25.
Brunt EM. Nonalcoholic steatohepatitis: definition and pathology. Semin Liver Dis. 2001;21:3–16