Table 2.
Study | Sample measured | Control | Liver disease | Data as mean ± 95% CI | P |
---|---|---|---|---|---|
Burgunder & Lauterburg 82 | Plasma GSH (mean ± SD μmol l−1) | 9.3 ± 2.4 (n = 8) | 3.6 ± 1.1 (alcoholic cirrhosis n = 8) | Control 9.3 ± 2.0 Alcoholic cirrhosis 3.6 ± 0.9 | P < 0.001 |
Total GSH (mean ± SD μmol l−1) | 16.6 ± 6.2 (n = 8) | 7.1 ± 2.6 (alcoholic cirrhosis n = 8) | Control 16.6 ± 5.2 Alcoholic cirrhosis 7.1 ± 2.2 | P < 0.002 | |
Altomare et al. 83 | Tissue GSH (mean ± SEM μmol g−1 liver) | 4.14 ± 0.1 (n = 15) | 2.77 ± 0.1 (NALD* n = 20) | Control 4.14 ± 0.2 NALD* 2.77 ± 0.2 | P < 0.001 |
2.55 ± 0.1 (ALD n = 35) | ALD 2.55 ± 0.2 | P < 0.001 | |||
Bianchi et al. 70 | Plasma GSH (mean ± SD μmol l−1) | 5.91 ± 1.04 (n = 6) | 1.69 ± 1.06 (alcoholic and HCV cirrhosis n = 10) | Control 5.91 ± 1.09 Alcoholic and HCV cirrhosis 1.69 ± 0.76 | Not significant |
Bernhard et al. 84 | Plasma GSH (mean ± 95%CI μmol l−1) | 14.1 ± 1.3 (n = 19) | 12.5 ± 1.6 (chronic hepatitis C n = 36) | Control 14.1 ± 1.3 Chronic hepatitis C 12.5 ± 1.6 | Not significant |
Van de Casteele et al. 85 | Whole blood GSH (mean ± SEM μmol l−1) | 908 ± 43 (n = 21) | 952 ± 71 (alcoholism without cirrhosis n = 14) | Control 908 ± 90 Alcoholism without cirrhosis 952 ± 153 | Not significant |
823 ± 51 (alcoholic cirrhosis Child‐Pugh A n = 9) | Alcoholic cirrhosis Child‐Pugh A 823 ± 118 | Not significant | |||
909 ± 91 (alcoholic cirrhosis Child‐Pugh B n = 5) | Alcoholic cirrhosis Child‐Pugh B 909 ± 253 | Not significant | |||
500 ± 71 (alcoholic cirrhosis Child‐Pugh C n = 18) | Alcoholic cirrhosis Child‐Pugh C 500 ± 150 | P < 0.05 | |||
520 ± 90 (non‐alcoholic cirrhosis Child‐Pugh C n = 6) | Non‐alcoholic cirrhosis Child‐Pugh C 520 ± 231 | P < 0.05 | |||
Saricam et al. 86 | Erythrocytic GSH (mean ± SD nmol g−1 Hb) | 56.90 ± 5.03 (n = 16) | 34.09 ± 2.19 (NAFLD n = 26) | Control 56.90 ± 2.68 NALFD 34.09 ± 0.88 | P < 0.001 |
Cemek et al. 87 | Whole blood GSH (mean ± SD mg dl−1) | 34.38 ± 1.41 (n = 29) | 3.89 ± 1.59 (acute hepatitis A n = 19) | Control 34.38 ± 0.54 Hepatitis A 3.89 ± 0.77 | P < 0.001 |
Czeczot et al. 88 | Tissue GSH (mean ± SD μmol mg−1 protein) | 5.52 ± 3.27 (n = 15) | 4.62 ± 2.94 (HCC n = 15) | Control 5.21 ± 1.81 HCC 4.62 ± 1.63 | P < 0.05 |
3.45 ± 2.11 (cirrhosis n = 15) | Cirrhosis 3.45 ± 1.17 | P < 0.05 | |||
Kuffner et al. 89 | Plasma GSH (mean ± SD μmol l−1) | 2.17 ± 0.97 (n = 56) | 2.27 ± 0.85 (alcoholic patients, day 3 of detox while taking paracetamol n = 56) | Control 2.17 ± 0.26 Alcoholics taking paracetamol 2.27 ± 0.23 | Not significant |
1.90 ± 0.68 (n = 23) | 2.02 ± 0.74 (alcoholic patients, day 3 of detox while taking placebo n = 23) | Control 1.90 ± 0.29 Alcoholics taking placebo 2.02 ± 0.32 | Not significant | ||
Lee et al. 90 | Blood GSH (mean ± SD μmol l−1) | 1294.3 ± 258.0 (n = 137) | 970.5 ± 321.7 (virus‐originated HCC n = 24) | Control 1294.3 ± 43.6 Virus‐originated HCC 970.5 ± 135.8 | P < 0.001 |
Blood GSH : GSSG ratio (mean ± SD) | 20.3 ± 10.2 (n = 137) | 6.7 ± 4.6 (virus‐originated HCC n = 24) | Control 20.3 ± 1.7 Virus‐originated HCC 6.7 ± 1.9 | P < 0.001 | |
Tissue GSH (mean ± SD μmol l−1g−1 protein) | 723.6 ± 215.0 (adjacent cancer‐free tissue n = 24) | 439.8 ± 198.4 (virus‐originated HCC n = 24) | Control 723.6 ± 90.8 Virus‐originated HCC 439.8 ± 83.8 | P < 0.001 | |
Tissue GSH : GSSG ratio (mean ± SD) | 10.5 ± 3.7 (adjacent cancer‐free tissue n = 24) | 4.4 ± 1.9 (virus‐originated HCC n = 24) | Control 10.5 ± 1.6 Virus‐originated HCC 4.4 ± 0.8 | P < 0.001 | |
Das et al. 91 | Tissue GSH (mean ± SD μg mg−1 protein) | 4.08 ± 0.59 (n = 38) | 3.64 ± 0.19 (NAFLD n = 35) | Control 4.08 ± 0.19 NAFLD 3.64 ± 0.07 | P < 0.01 |
3.19 ± 0.58 (ALD n = 38) | ALD 3.19 ± 0.19 | P < 0.001 | |||
Narasimhan et al. 92 | Age adjusted whole blood GSH (mean ± SD μmol g−1 Hb) | 7.5 ± 1.4 (n = 50) | 6.2 ± 1.3 (NAFLD without T2DM n = 50) | Control 7.5 ± 0.40 NAFLD without T2DM 6.2 ± 0.37 | P < 0.05 |
4.0 ± 1.5 (NAFLD with T2DM n = 50) | NALFD with T2DM 4.0 ± 0.43 | P < 0.001 | |||
5.2 ± 1.5 (T2DM without NAFLD n = 50) | T2DM without NAFLD 5.2 ± 0.43 | P < 0.05 | |||
Kaffe et al. 93 | Whole blood GSH (Median [range] μmol l−1) | 1101 [276‐5409] (n = 50) | 475 [4−2743] (AIC n = 49) | – | P ≤ 0.001 |
495 [4‐2743] (AIC without cirrhosis n = 43) | – | P ≤ 0.01 | |||
209 [89‐659] (AIC with cirrhosis n = 6) | – | P ≤ 0.001 | |||
1135 [293‐5409] (n = 41) | 512 [51‐5541] (AIH n = 36) | – | P ≤ 0.01 | ||
511 [88‐2977] (AIH without cirrhosis n = 26) | – | P ≤ 0.01 | |||
293 [51‐5541] (AIH with cirrhosis n = 10) | – | P ≤ 0.001 |
95% CI were calculated from original data in all studies except Bernhard et al., to facilitate comparison between studies.
NALD (non‐alcoholic liver disease) group included patients with chronic active hepatitis n = 7; chronic persisting hepatitis n = 3; steatosis n = 2; and cirrhosis n = 8.
AIC, autoimmune cholestatic liver disease;
AIH, autoimmune hepatitis;
ALD, alcoholic liver disease;
GSH, glutathione;
HCC, hepatocellular carcinoma;
NAFLD, non‐alcoholic fatty liver disease;
P = significance vs. control group;
T2DM, type 2 diabetes mellitus.