Demir K, Akyuz F, Ozdil S, Aksoy N, Kaymakoglu S, Poturoglu S, Akyüz Ü, Besisik F, Boztas G, Mungan Z, Cevikbas U, Cakaloglu Y, Okten A

Language: English
References: 18
Page: 92-96
PDF size: 130.67 Kb.

Text Extraction

Background and study aims: Increased alanine aminotransferase (ALT) levels with negative hepatitis B virus (HBV) DNA by hybridization is a common problem in Turkey where is a mild endemic region. We aimed to evaluate the causes of elevated ALT levels in patients who are negative for hepatitis B e antigen (HBeAg) and HBV DNA (by hybridization) for at least 6 months. Patients-methods: Forty-nine patients were enrolled in this study. Histological changes [histological activity index (HAI), and the extent of fibrosis] were assessed according to the Knodell scoring system and steatosis were graded by Brunt’s classification for NAFLD in all patients. Results: A mean age of the patients was 34.9 ± 12.1 years (16-70). 43 (87.8%) of them were male. Mean ALT level was 95 ± 39.7 IU/L (50-258). Hyperglycemia (›100 mg/dL) and hyperlipidemia were found in 12 and 24 patients, respectively. Hepatic steatosis (7 patients grade 1; 5 patients grade 2; and 7 patients grade 3), ground-glass hepatocyte, chronic hepatitis, and Wilson disease were found in liver biopsy in 38.8%, 32.6%, 26.6%, 2%, respectively. Mean HAI was 6.5 ± 3.6 (4-12) in chronic hepatitis. Seven patients (53.9%) were in stage 1 and 2 while 6 patients (46.1%) were in stage 3 and 4. Conclusions: Nonalcoholic fatty liver disease is the most common cause of elevated ALT levels in HBeAg negative/HBV DNA negative patients. Chronic hepatitis B was found in 26.6% of these patients.

REFERENCES

1. Bonino F, Brunetto MR. Chronic hepatitis B e antigen (HBeAg) negative, anti-HBe positive hepatitis B: overview. J Hepatol 2003; 39: S160-163.

2. Knodell RG, Ishak KG, Black WC, Chen TS, Craig R, Kaplowitz N, Kiernan TW, et al. Formulation and application of a numerical scoring system for assessing histological activity in asymptomatic chronic active hepatitis. Hepatology 1981; 1: 431-35.

3. Brunt EM, Janney CG, Di Bisceglie AM, Neuschwander-Tetri BA, Bacon BR. Nonalcoholic steatohepatitis: a proposal for grading and staging the histological lesions. Am J Gastroenterol 1999; 94: 2467-74.

4. Okten A, Demir K, Kaymakoglu S, Cakaloglu Y, Dincer D, Besisik F. Etiologies of chronic hepatitis. Turk J Gastroenterol 1998; 2: 113-15.

5. Bozdayi AM, Bozkaya H, Turkyilmaz AR, Saryodlu M, Cetinkaya H, Karayalcin S, Yurdaydin C, et al. Nucleotide divergences in the core promoter and precore region of genotype D hepatitis B virus in patients with persistently elevated or normal ALT levels. J Clin Virol 2001; 21: 91-101.

6. Brunetto MR, Oliveri F, Coco B, Leandro G, Colombatto P, Gorin JM, Bonino F. The outcome of chronic antiHBe-positive chronic hepatitis B in alpha interferon treated and untreated patients; a long term cohort study. J Hepatol 2002; 36: 263-70.

7. Day CP, James OFW. Hepatic steatosis: innocent bystander or guilty party? Hepatology 1998; 27: 1463-1466.

8. Bellentani S, Saccoccio G, Masutti F, Croce LS, Brandi G, Sasso F, Cristanini G, et al. Prevalance of and risk factors for hepatic steatosis in northern Italy. Ann Intern Med 2000; 132; 112-7.

9. Keeffe EB, Dieterich DT, Han SH, Jacobson IM, Martin P, Schiff ER, Tobias H, et al. A treatment algorithm for the management of chronic hepatitits B virus infection in the United States. Clin Gastroenterol Hepatol 2004; 2: 87-106.

10. Sharma P, Balan V, Hernandez J, Rosati M, Williams J, Rodriguez-Luna H, Schwartz J, et al. Hepatic steatosis in hepatitis C virus genotype 3 infection: does it correlate with body mass index, fibrosis, and HCV risk factors? Dig Dis Sci 2004; 49: 25-29.

11. Lonardo A, Adinolfi LE, Loria P, Carulli N, Ruggiero G, Day CP. Steatosis and hepatitis C virus: Mechanisms and significance for hepatic and extrahepatic disease. Gastroenterology 2004; 126: 586-597.

12. Rubbia-Brandt L, Fabris P, Paganin S, Leandro G, Male PJ, Giostra E, Carlotto A, et al. Steatosis affects chronic hepatitis C progression in a genotype specific way. Gut 2004; 53: 406-412.

13. Adinolfi LE, Gambardella M, Andreana A, Tripodi MF, Utili R, Ruggiero G. Steatosis accelerates the progression of liver damage of chronic hepatitis C patients and correlates with specific HCV genotype and visceral obesity. Hepatology 2001; 33: 1358-1364.

14. Bach N, Thung SN, Schaffner R. The histological features of chronic hepatitis C and autoimmune chronic hepatitis: a comparative analysis. Hepatology 1992: 15: 572-577.

15. Czaja AJ, Carpenter HA, Santrach PJ, Moore B. Host and disease specific factors affecting steatosis in chronic hepatitis C. J Hepatol 1998; 29: 198-206.

16. Wieslaw K, Antoinette U, Magdalena C, Dorota M, Katarzyna P. The significance of hepatic steatosis in chronic hepatitis B and C. J Hepatol 2003; 38: 119.

17. Seppala-Lindroos A, Vehkavaara S, Hakkinen AM, Goto T, Westerbacka J, Sovijarvi A, Halavaara J, et al. Fat accumulation in the liver associated with defects in insulin suppression of glucose production and serum free fatty acids independent of obesity in normal men. J Clin Endocrinol Metab 2002; 87: 3023-3028.

18. Stranges S, Dorn JM, Muti P, Freudenheim JL, Farinaro E, Russell M, Nochajski TH, et al. Body fat distribution, relative weight, and liver enzyme levels: a population-based study. Hepatology 2004; 39: 754-763.