Gang Lin, Xiaoyan Duan, Xiaobo Cai, Liyan Tian, Zhengjie Xu and Jiangao Fan
: potential implications for inflammation and plaque instability. Circulation. 2000; 101: 1372-8.
13. Mazzone GL, Rigato I, Ostrow JD, Bossi F, Bortoluzzi A, Sukowati CH, et al. Bilirubin inhibits the TNFalpharelated induction of three endothelial adhesion molecules. Biochem Biophys Res Commun. 2009; 386: 338-44.
14. Jin X, Yang YD, Chen K, Lv ZY, Zheng L, Liu YP, et al. HDMCP uncouples yeast mitochondrial respiration and alleviates steatosis in L02 and hepG2 cells by decreasing ATP and H2O2 levels: a novel mechanism for NAFLD. J Hepatol
Sher Zaman Safi, Yasmin Badshah, Yasir Waheed, Kaneez Fatima, Sadia Tahir, Alamgir Shinwari and Ishtiaq Qadri
. Hepatology. 1992; 16:293-9.
6. Kanai K, Kako M, Okamoto H. HCV genotypes in chronic hepatitis C virus and response to interferon. Lancet. 1992; 339:1543.
7. Shah H.A, Jafri W, Malik I, Prescott L, Simmonds P. Hepatitis C virus (HCV) genotypes and chronic liver disease in Pakistan. J Gastroenterol Hepatol. 1997; 12: 758-61.
8. Szanto P, Grigorescu M, Dumitru I, Serban A. Steatosis in hepatitis C virus infection. Response to anti-viral therapy. J Gastrointestin Liver Dis. 2006; 15:117-24
9. Marzouk D, Sass J
Sombat Treeprasertsuk, Piyawat Komolmit and Wiriya Tanyaowalak
Ther. 2005; 22(Suppl 2):24-7.
4. 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; 126:586-97.
5. Clouston AD, Jonsson JR, Powell EE. Steatosis as a cofactor in other liver diseases: hepatitis C virus, alcohol, hemochromatosis, and others. Clin Liver Dis. 2007; 11:173-89.
6. Yokoyama H, Hirose H, Ohgo H, Saito I. Inverse association between serum adiponectin level and transaminase
Puth Muangpaisarn, Kanisa Jampoka, Sunchai Payungporn, Naruemon Wisedopas, Chalermrat Bunchorntavakul, Pisit Tangkijvanich and Sombat Treeprasertsuk
Currently, nonalcoholic fatty liver disease (NAFLD) has become a worldwide health concern because its prevalence is rising and it is an emerging etiology of chronic liver diseases [ 1 - 3 ]. Moreover. NAFLD is closely associated with obesity metabolic syndrome, and cardiovascular diseases [ 4 ]. NAFLD can be divided into two groups: simple steatosis and nonalcoholic steatohepatitis (NASH) [ 5 ]. In particular, NASH increases the risk of death compared with the general population, and can progress to cirrhosis and hepatocellular carcinoma [ 5 , 6 ]. Importantly
Non-alcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver disease worldwide. The disease spectrum ranges from fatty liver, non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma.
In general, the definition of NAFLD comprises evidence for fatty infiltration in liver tissue either by histology or imaging and known causes of fat accumulation must be excluded, whereas NASH is classified as steatosis and inflammation with or without fibrosis [ 1 ]. Recent meta-analyses suggest that NAFLD is a precursor of type 2
Background: Severe clinical hepatitis after imatinib treatment has been reported anecdotally. Hepatic tissue of patients with liver matastasis is often fragile and difficult to handle during liver resection from gastrointestinal stromal tumor (GIST).
Objective: Observe hepatic tissue of these patients and examine the detailed histopathology underlying the change in the texture of non-tumorous hepatic parenchyma of these patients.
Materials and methods:We reviewed six GIST patients with liver metastases who underwent hepatic resection at King Chulalongkorn Memorial Hospital between July 2004 and November 2005. Four patients did not have imatinib and two patients received imatinib for four and eight months before liver resection. Preoperative hepatic biochemistry profiles of all patients were unremarkable. We examined histopathology of non-tumorous hepatic parenchyma of these patients using H-E staining, and additional histochemistry for vascular endothelial growth factor and epidermal growth factor receptor using immunohistochemistry staining.
Results: In all patients, common histopathological changes were swelling of hepatocytes, diffuse parenchymal congestion, dilatation of central vein, and infiltration of portal tract by mononuclear cells. However, there was significant zone 3 hepatocytolysis only in patients who received imatinib treatment. Additionally, moderate degree of hepatic steatosis correlated well with the duration of imatinib exposure. Immunohistochemical study could not demonstrate any difference between these two groups.
Conclusion: In two cases of subclinical hepatotoxicity from exposure to imatinib, histopathologic findings were consistent with drug induced liver injury. Imatinib induced liver injury may be more common than obvious clinical hepatitis.
16. Arano T, Nakagawa H, Tateishi R, Ikeda H, Uchino K, Enooku K, et al. Serum level of adiponectin and the risk of liver cancer development in chronic hepatitis C patients. Int J Cancer. 2010;129:2226-35.
17. Baranova A, Jarrar MH, Stepanova M, Johnson A, Rafiq N, Gramlich T, et al. Association of serum adipocytokines with hepatic steatosis and fibrosis in patients with chronic hepatitis C. Digestion. 2011; 83: 32-40.
18. Latif HA, Assal HS, Mahmoud M, Rasheed WI. Role of serum adiponectin level in the development of liver cirrhosis
Sher Zaman Safi, Muhammad Sohail Afzal, Yasir Waheed, Umer Javed Butt, Kaneez Fatima, Yousaf Parvez and Ishtiaq Qadri
additional tools to obtain information from recently diagnosed HIV infected patients. Swiss Med Wkly. 2008; 138:453-8.
5. Ahmed MA, Zafar T, Brahmbhatt H, Imam G, Ul Hassan S, Bareta JC, Strathdee SA. HIV/AIDS Risk Behaviors and Correlates of Injection Drug Use among Drug Users in Pakistan. J Urban Health. 2003; 80: 321-9.
6. Safi SZ, Badshah Y, Waheed Y, Fatima K, Tahir S, Shinwari A, Qadri I. Distribution of hepatitis C virus genotypes, hepatic steatosis and their correlation with clinical and virological factors in Pakistan. Asian Biomed
Chareeporn Akekawatchai, Warisara Sretapunya, Duangnate Pipatsatitpong and Tippawan Chuenchit
patients coinfected with HCV, is associated with hepatic steatosis, a common complication of HCV infection [ 27 , 28 ]. Accumulating evidence suggests that coinfection of HCV accelerates the progression of HCV-related diseases including fibrosis, cirrhosis, and end-stage liver disease in HIV patients, and that treatment with HAART does not seem to improve prognosis of the liver diseases related to HCV infection [ 2 , 29 ]. The current use of antiviral therapy against HCV infection in HCV–HIV coinfected patients seems to delay the progression to chronic liver disease
Thitima Ngoenmak, Julintorn Somran, Chutima Phuaksaman and Jaruwat Khunrat
not specific and lacked of usual morphologic changes, especially microvesicular and macrovesicular steatosis, which have been described in galactosemia [ 13 , 14 ]. Therefore, many potential causes of neonatal hepatitis, including viral infection and metabolic disorders were excluded by investigations.
The appropriate treatment for an infant with galactosemia is to (1) eliminate any lactose-containing formula and breast feeding, and begin a formula such as a soy-based formula that contains no lactose as soon as possible, (2) monitor for signs of sepsis, and (3