Table 3.
Study | N patients | Age | Female (%) |
BMI (kg/m2) |
T2DM (%) |
↑LFTs (%) |
HTN (%) |
DLP (%) | NAFLD (%) |
NASH (%) | Fibrosis % (total/ advanced) |
Cirrhosis (%) |
Independent predictors for NASH |
Independent predictors for fibrosis |
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Dixon et al., 2001 Australia |
105 | 41 ± 11 | 78 | 47 ± 7 | 18 | AST 18 ALT 30 |
38 | 96 | 25 | 25/9 | 1 | HOMA-IR, ↑ALT, HTN | ↑ALT, HTN, ↑ C-peptide | |
Beymer et al., 2003 USA |
48 | 42 ± 10 | 69 | 59.9 ± 12 | 19 | ↑Tg in 23 | 85 | 33 | 35/12 | none | DM (OR 128, CI 5.2–3137) | Severe fibrosis greater in DM than in non-DM (OR 75, CI 7.5–1247) |
||
Spaulding et al., 2003 USA |
48 | 84 | 51 ± 20 | 16 | 18 | 47 | 61 | 90 | 56 | 49/NA | 2 | DM (p=0.029), abnormal LFTs (p=0.029) |
||
Ong et al., 2005 USA |
212 | 42 ± 10 | 80 | 48 ± 9 | 24 | 45 | 30 | 93 | 24 | 23.5/7 | 0.9 | DM, male gender, ↑ALT | Waist/hip ratio, AST, focal necrosis | |
Lima et al., 2005 Brazil |
112 | 40 ± 10 | 74 | 49 ± 8 | 28 | 68 | 40 | 99 | 58 (type 3 and 4 NAFLD) |
21/14 | none | Type 4 NAFLD correlated with T2DM (p=0.018) |
||
Boza et al., 2005 Chile |
127 | 40 ± 11 | 62 | 42 ± 6 | 14 | 41 | 63 | 26 | 22/1.6 | 1.6 | HOMA-IR>5.8, AST>31 | |||
Gholam et al., 2007 USA |
97 | 39 ± 10 | 83 | 55 ± 12 | 24 | 26 AST 12 ALT 23 |
43 | ↑Tg in 35 ↓HDL in 59 |
89 | 36 | 25/NA | none | DM, AST | ALT, HbA1C |
ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMI, body mass index; DLP, dyslipidemia; HDL, high-density lipoprotein; HOMA-IR, homeostatic model assessment of insulin resistance; HTN, hypertension; LFTs, liver function tests; NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis; T2DM, type 2 diabetes mellitus; Tg, triglycerides.
Age, mean ± standard deviation.
Independent predictors for NASH/fibrosis refer to variables that are independently associated with a diagnosis of NASH/fibrosis.
Advanced fibrosis refers to histological fibrosis stages 3 and 4.
Type 3 and type 4 NAFLD refers to the NAFLD classification system proposed by Matteoni et al.: type 1 (steatosis), type 2 (steatosis and lobular inflammation), Type 3 (steatosis, lobular inflammation and hepatocellular ballooning), type 4 (similar to type 3+ fibrosis and/or Mallory's hyaline) (Matteoni et al., 1999).