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RISS 인기검색어
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- 저자 : ( RK Dhiman ) (검색결과 2 건)
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( Ajay Duseja ),( Kiran K Thumburu ),( Ashim Das ),( Rk Dhiman ),( Yk Chawla ) 대한소화기학회 2007 SIDDS Vol.9 No.-
Background/Aims: There is no effective non-invasive method to differentiate patients with or without histological NASH among patients with NAFLD. Aim of this study was to determine if presence of metabolic syndrome could be used as a predictor of histological NASH in patients with NAFLD. Methods: Fifty eight patients with NAFLD (July 2001-Jan 2007) (mean age 38.2±8.0 years, M:F=41:17) were histologically classified into Class I-IV as per Matteoni et al (Gastroenterology 1999:116;1413-1419). Those having NASH (Class III&IV) were further graded and staged as per Brunt et al (Am J Gastroenterol 1999:94:2467-2474). Differences in age, gender, BMI, waist, waist-hip ratio, serum insulin, insulin resistance (HOMA-IR), liver enzymes (AST, ALT)and presence of metabolic syndrome were studied between those with and without histological NASH. Metabolic syndrome (≥3 criteria) was defined as per adult treatment panel (ATP) III criteria with modified waist for Asian patients. Results: Twenty nine (50%) patients had class I or II (without histological NASH) disease and other 29 (50%) had class III or IV (histological NASH) disease. Overall metabolic syndrome was present in 25 (45.5%) patients with NAFLD. Fifteen (51.7%) patients in class I or II disease (without histological NASH) had metabolic syndrome in comparison to 10 (38.5%) patients in class III or IV (with histological NASH) (p=0.8). Other studied parameters were not different amongst two groups. Conclusion: Presence of metabolic syndrome can not be used as a predictor of histological NASH in patients with NAFLD.
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( Ajay Duseja ),( Kiran K Thumburu ),( Nitin Saini ),( Ashim DAS ),( RK Dhiman ),( YK Chanwla ) 대한소화기학회 2007 SIDDS Vol.9 No.-
Background/Aims: Experimental data suggests role of adipokine leptin in hepatic fibrosis. Human data on this issue is controversial. Aim of this study was to measure serum leptin levels in patients with nonalcoholic fatty liver disease (NAFLD) and chronic hepatitis C (CHC) and correlate its levels with hepatic fibrosis. Methods: serum leptin levels were assessed by ELISA (DRG Diagnostics, Germany) in 40 patients with NAFLD (liver biopsy=29)(mean age 39.8±10.8 years, men 29), 23 patients with CHC (liver biopsy=20) (mean age 37.7±6.7, men 22) and 15 healthy controls (normal BMI, LFT and ultrasound abdomen), (mean age 32.2±9.2 years, men 13). Histological analysis was done as per Matteoni et al (Gastroenterology 1999) and Brunt et al (Am J Gastroenterol 1999) in patients with NAFLD and as per Ishak et al (J Hepatol. 1995) in patients with CHC. Correlation of serum leptin was studied with age, gender, BMI, waist, waist-hip ratio, ALT, insulin resistance, class of NAFLD (NASH vs. no NASH) and hepatic necro-inflammation and fibrosis. Results: Patients with CHC had higher serum leptin levels in comparison to healthy controls (12.6±3.4 ng/ml vs. 5.0±5.2 ng/ml, p=0.002) and NAFLD patients (12.6±3.4 ng/ml vs. 5.9±3.3 ng/ml, p=0.05). There was no difference between serum leptin levels of NAFLD patients and healthy controls. Serum leptin showed no correlation with age, gender, BMI, waist, waist hip ratio, ALT and insulin resistance in both the patient groups. There was no correlation of serum leptin with either class of NAFLD (NASH vs. no NASH) (p=0.75) and with grade of the disease and stage of hepatic fibrosis in both NAFLD (p=0.44) and CHC groups (p=0.59). Conclusions: Patients with CHC have higher serum leptin levels in comparison to NAFLD. Serum leptin levels do not correlate with hepatic fibrosis in patients with NAFLD and CHC.
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