Impact of sleeve gastrectomy on renal function in patients with morbid obesity: a 1-year prospective cohort study.

PURPOSE: Obesity is an independent risk factor for renal injury. A more favorable metabolic environment following weight loss may theoretically lead to improved renal function. We aimed to evaluate the evolution of renal function one year after sleeve gastrectomy in a large prospective cohort of patients with morbid obesity and assess the influence of fat-free mass (FFM) changes. METHODS: We prospectively included obese patients admitted for sleeve gastrectomy between February 2014 and November 2016. We also included a historical observational cohort of patients undergoing sleeve gastrectomy between January 2013 and January 2014 who had FFM evaluation. Patients were systematically evaluated 1 year after surgery. The estimated glomerular filtration rate (eGFR) was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. The FFM was estimated by analyzing computerized tomography (CT) scan sections from CT systematically performed 2 days and 1 year after sleeve gastrectomy to detect surgery complications. RESULTS: Five hundred sixty-three patients fulfilled the inclusion criteria. The mean age was 41.2 ± 0.5 years. The mean body mass index was 43.5 ± 0.3 kg/m2 and 20.4, 30.5, and 30.7% of the included patients had type 2 diabetes, hypertension, and dyslipidemia, respectively. One hundred fifteen patients were excluded and four hundred forty-eight patients were finally included in the analysis. The eGFR was significantly higher 1 year after sleeve gastrectomy than before surgery (87.8 ± 0.9 versus 86.1 ± 0.9, p < 0.01). There was no difference in terms of post-surgery FFM loss between patients with an improved eGFR and those without (6.7 ± 0.3 kg versus 6.8 ± 0.5 kg, p = 0.9). Furthermore, post-surgery changes in the eGFR did not correlate with the amount of FFM loss (r = 0.1, p = 0.18). CONCLUSION: Renal function assessed by eGFR is significantly improved at 1-year post-sleeve gastrectomy, independent of changes in skeletal muscle mass.

Adaptation of controlled attenuation parameter (CAP) measurement depth in morbidly obese patients addressed for bariatric surgery.

BACKGROUND AND AIM: The controlled attenuation parameter (CAP) using FibroScan (Echosens, Paris, France) M or XL probe has been developed for liver steatosis assessment. However, CAP performs poorly in patients with high body mass index. The aim of our study was to assess whether CAP is overestimated using the standard XL probe in patients with morbid obesity, and in the case of an overestimation, to reprocess the data at a greater depth to obtain the appropriate CAP (CAPa). PATIENTS AND METHODS: We conducted an observational prospective cohort study on a total of 249 severely obese patients admitted to our institution to undergo sleeve gastrectomy. Patients had a liver biopsy performed during the surgery and a CAP measurement during the 15 days preceding biopsy. Patient files were reprocessed retrospectively by an algorithm, blinded to the patients' clinical data. The algorithm automatically assessed the probe-to-capsula distance (PCD) by analysing the echogenicity of ultrasound signals on the time-motion mode. In the case of a distance >35 mm, the algorithm automatically selected a deeper measurement for CAP (CAPa). When PCD was less than 35 mm, the measured CAP was considered as appropriated (CAPa) and no further reprocessing was performed. RESULTS: CAP recording was not performed at a sufficient depth in 130 patients. In these patients, the CAPa obtained at the adapted depth was significantly lower than CAP (298±3.9 versus 340±4.2 dB/m; p< 0.0001) measured at the standard depth (35 to 75 mm). Multiple linear regression analysis revealed that both body mass index and hepatic steatosis were independently correlated with CAP values. After reprocessing the CAP in patients with PCD > 35 mm, steatosis stage was the only parameter independently correlated with CAP values. For the diagnosis of steatosis (S≥1), moderate to severe steatosis (S≥2) and severe steatosis (S = 3), the AUROC curves of CAPa (measured CAP in patients with PCD<35 mm and reprocessed CAP in those with PCD>35 mm) were 0.86, 0.83 and 0.79, respectively. The Obuchowski measure for the diagnosis of steatosis was 0.90±0.013. CONCLUSION: CAP was overestimated in a half of morbidly obese patients using an XL probe, but CAP can be performed correctly in these patients after adapting the measurement depth.

Predictive score of sarcopenia occurrence one year after bariatric surgery in severely obese patients.

BACKGROUND AND AIM: Sarcopenic obesity is a risk factor of morbidity and mortality. The aim of this study was to generate a predictive score of sarcopenia occurrence one year after bariatric surgery. PATIENTS AND METHODS: We conducted an observational prospective cohort study on a total of 184 severely obese patients admitted to our institution to undergo sleeve gastrectomy. Skeletal muscle cross-sectional area at the third lumbar vertebrae (SMA, cm2) was measured from the routinely performed computed tomography. The skeletal muscle index (SMI) was calculated as follows: SMA/height2 (cm2/m2). Sarcopenia was defined as an SMI < 38.5 cm2/m2 for women and < 52.4 cm2/m2 for men. Measurements were performed at surgery and one year later. RESULTS: Most of the included patients were female (79%), with a mean age of 42±0.9 years and body mass index of 43.2±0.5 kg/m2. Fifteen patients (8%) had sarcopenia before surgery and 59 (32%) at the one-year follow-up. Male gender (p<0.0001), SMA before surgery (p<0.0001), and SMI before surgery (p<0.0001) significantly correlated with the occurrence of sarcopenia one year after surgery by multivariate analysis. Two predictive sarcopenia occurrence scores were constructed using SMA and gender (SS1 score) or SMI and gender (SS2 score). The area under receiver operating characteristic (AUROC) curve of the SS2 score was significantly greater than that of the SS1 score for the diagnosis of postoperative sarcopenia occurrence (0.95±0.02 versus 0.90±0.02; p<0.01). A cut-off value for the SS2 score of 0.53 had a sensitivity of 90%, a specificity of 91%, a positive predictive value of 83%, and a negative predictive value of 95%. In the group of patients without baseline sarcopenia, the SS2 score had still an excellent AUROC of 0.92±0.02. A cut-off of 0.55 predicted development of sarcopenia one year after sleeve gastrectomy in these patients with a sensitivity of 87%, a specificity of 88%, and negative predictive value of 95%. CONCLUSION: The SS2 score has excellent predictive value for the occurrence of sarcopenia one year after sleeve gastrectomy. This score can be used to target early intensification of nutritional and dietetic follow-up to the predicted high-risk population.

Controlled attenuation parameter for diagnosing steatosis in bariatric surgery candidates with suspected nonalcoholic fatty liver disease.

INTRODUCTION: Steatosis in patients with nonalcoholic fatty liver disease (NAFLD) is often benign, but may progress to fibrosis. The accurate diagnosis of hepatic steatosis is therefore important for clinical decision-making and prognostic assessments. The controlled attenuation parameter (CAP), a noninvasive measurement obtained with Fibro-Scan, has been developed for liver steatosis assessment. CAP performs poorly in patients with high BMI. The XL probe was initially developed for measuring liver stiffness in overweight patients. We assessed the diagnostic value of CAP in candidates for bariatric surgery with suspected NAFLD examined with the XL probe. PATIENTS AND METHODS: For the retrospective group, raw ultrasonic radiofrequency signals were stored prospectively in the Fibro-Scan examination file for offline CAP calculation in 194 consecutive obese patients undergoing liver stiffness measurement in the 15 days before liver biopsy. For the prospective group, CAP was calculated automatically and prospectively from the XL probe in 123 obese patients. RESULTS: In the retrospective group, the diagnostic accuracy of CAP was satisfactory for differentiating S3 from S0-S1-S2 (0.79±0.03; 95% confidence interval: 0.71-0.84) and S3 from S0 (0.85±0.05; 95% confidence interval: 0.73-0.92). The Obuchowski measure demonstrated a very good discriminatory performance: 0.87±0.02 in the retrospective group and 0.91±0.02 in the prospective group. CONCLUSION: CAP calculations from XL probe measurements efficiently detected severe steatosis in morbidly obese patients with suspected NAFLD. However, the cutoff values should now be confirmed in a larger prospective cohort.

Transient elastography alone and in combination with FibroTest® for the diagnosis of hepatic fibrosis in alcoholic liver disease.

BACKGROUND & AIMS: The reliability of transient elastography (TE) to assess liver fibrosis is insufficiently validated in alcoholic liver disease (ALD). We aimed to validate the diagnostic utility of TE for liver fibrosis in patients with excessive alcohol consumption and evaluate whether Fibrotest® adds diagnostic value relative to or in combination with TE. METHODS: We conducted a multicentre prospective study on a total of 217 heavy drinkers with high serum aminotransferase levels. Patients underwent liver biopsy, TE, Fibrotest® , PGAA, APRI, FIB-4 and FORNS. The overall diagnostic performance was evaluated by the area under the receiver operating characteristic (AUROC) curves and Obuchowski measures. RESULTS: TE values correlated with fibrosis stage (r=.73; P<.0001) and steatosis stage (r=.19; P<.01). Patients with alcoholic hepatitis had higher TE values than those without alcoholic hepatitis (P<.0001). In an multivariate analysis, fibrosis stage and the presence of alcoholic hepatitis were the only parameters that correlated with liver stiffness. For the diagnosis of advanced fibrosis (F≥3), the AUROC curves were 0.90, 0.85, 0.83, 0.91 and 0.90 for TE, Fibrotest® , PGAA and associations TE-Fibrotest® , TE-PGAA respectively. For the diagnosis of cirrhosis, the AUROC curves were 0.93, 0.88, 0.89, 0.94 and 0.95 respectively. The Obuchowski measures for the diagnosis of fibrosis were 0.94, 0.92, 0.91, 0.95 and 0.94 respectively. The performance of TE was not significantly different than those of Fibrotest® , PGAA and combinations TE-Fibrotest® , TE-PGAA. CONCLUSIONS: TE has excellent diagnostic value for liver fibrosis in alcoholic liver disease. The combined use of TE-Fibrotest® or TE-PGAA does not improve the performance of TE.

Adaptation of liver stiffness measurement depth in bariatric surgery candidates with suspected nonalcoholic fatty liver disease.

BACKGROUND AND AIMS: A thick layer of subcutaneous adipose tissue may lead to an overestimation of liver stiffness by transient elastography. The aim of this study was to assess whether liver stiffness measurement (LSM) was overestimated using an XL probe in patients with severe obesity and, if so, to reprocess the data to the adapted depth to obtain the appropriate LSM (LSMa). METHODS: A total of 152 obese patients prospectively underwent bariatric surgery and needle liver biopsy. Liver stiffness was measured by transient elastography 15 days before. To determine whether the LSM was overestimated, an expert operator retrospectively determined whether the skin-to-capsula distance was greater than 35 mm by analyzing the hyperechogenicity of ultrasound signals and the measured slope between 35 and 75 mm. In the case of an overestimation, a deeper measurement depth was selected to calculate the LSMa. RESULTS: There was an overestimation of the LSM obtained between 35 and 75 mm in 76 patients (50%). Among these patients, the LSMa was obtained between 40 and 75 mm in 49 patients and between 45 and 80 mm in 27 patients. Only the percentage of steatosis was independently and positively correlated with LSM overestimation. The areas under receiver operating characteristic of LSMa was 0.82±0.04 for predicting fibrosis stage F3. The Obuchowski measure was 0.85±0.02. CONCLUSION: The LSM was overestimated in severely obese patients obtained between 35 and 75 mm using an XL probe in 76 patients (50%), but LSM can be performed correctly in these patients after adapting the measurement depth to deeper beneath the patients' skin.

Alcohol withdrawal alleviates adipose tissue inflammation in patients with alcoholic liver disease.

BACKGROUND & AIMS: Patients with alcoholic liver disease (ALD) display inflammation of the subcutaneous adipose tissue (SAT) which correlates with liver lesions. We examined macrophage markers and polarization in the SAT of alcoholic patients and adipokine expression according to liver inflammation; we studied the consequences of alcohol withdrawal. PATIENTS AND METHODS: Forty-seven patients with ALD were prospectively included. SAT and blood samples were collected at inclusion and after 1 week of alcohol withdrawal. Pro-inflammatory cytokines/chemokines, inflammasome components and products, adipokine expression levels, macrophage markers and polarization in liver and SAT samples were assessed by RT-PCR arrays. RESULTS: mRNA expression level of chemokines (IL8, semaphorin 7A) correlated with hepatic steatosis in both liver and SAT. Liver expression of inflammasome components (IL1ß, IL18, caspase-1) and SAT IL6 and CCL2 correlated with liver damage. In patients with mild ALD, 1 week of alcohol withdrawal was sufficient to decrease expression level of total macrophage markers in the adipose tissue, to orient adipose tissue macrophages (ATM) towards an anti-inflammatory M2 phenotype and to decrease the mRNA expression of cytokines/chemokines (IL18, CCL2, osteopontin, semaphorin 7A). In patients with severe ALD, 1 week of abstinence was also associated with an increase in CCL18 expression. CONCLUSIONS: In alcoholic patients, upregulation of chemotactic factors in the liver and SAT is an early event that begins as early as the steatosis stage. The inflammasome pathway is upregulated in the liver of patients with ALD. One week of alcohol withdrawal alleviates macrophage infiltration in SAT and orients ATM towards a M2 anti-inflammatory phenotype; this implicates alcohol in adipose tissue inflammation (ClinicalTrials.gov NCT00388323).

The diagnostic accuracy of transient elastography for the diagnosis of liver fibrosis in bariatric surgery candidates with suspected NAFLD.

BACKGROUND: Severe obesity and metabolic syndrome have been implicated in the development of nonalcoholic fatty liver disease (NAFLD). We evaluated the diagnostic value of liver stiffness measurement (LSM), by transient elastography (FibroScan®) in bariatric surgery candidates with suspected NAFLD. METHODS: A total of 100 prospectively included consecutive severely obese subjects underwent bariatric surgery with liver needle biopsy. LSM was performed in the 15 days preceding liver biopsy. RESULTS: According to Kleiner's classification, 28 patients had no fibrosis, 50 had stage F1 fibrosis, 13 had stage F2 fibrosis, and nine had stage F3 fibrosis. LSMs were higher in patients with fibrosis stage F ≥2, than in patients with a fibrosis stage below F2 (p < 0.001). Fibrosis stage (p < 0.002), amount of steatosis (%) (p < 0.001), BMI (p < 0.02), and activity score (p = 0.027) were independently correlated with LSM. Homeostasis model assessment (HOMA) index was also significantly and independently correlated with LSM (p < 0.01). The area under the receiver operating characteristic curve (AUROC) generated by FibroScan® was 0.81 ± 0.05 for predicting fibrosis stage F ≥2 and 0.85 ± 0.04 for predicting F3 fibrosis. The decrease in LSM 1 year after bariatric surgery was significantly correlated with changes in HOMA index (r = 0.43, p = 0.01), but not with changes in BMI or weight. CONCLUSION: FibroScan® allows the early diagnosis of fibrosis in severely obese patients. Our results also suggest that FibroScan® could identify a subgroup of NAFLD patients at high risk of progressive liver disease and that LSM could be used as a surrogate marker of insulin resistance. Further studies are required to evaluate the prognostic value of FibroScan®.

Comparison of Fibrotest and PGAA for the diagnosis of fibrosis stage in patients with alcoholic liver disease.

BACKGROUND AND AIMS: The PGAA index was one of the first composite liver fibrosis markers. This study aims, prospectively, to confirm the diagnostic value of PGAA and Fibrotest in patients with alcoholic liver disease and to compare their diagnostic performances. PATIENTS AND METHODS: We prospectively included 200 consecutive patients (159 men and 41 women; mean age: 51±0.7 years).The PGAA index was calculated by combining the results of four laboratory tests (prothrombin time, γ-glutamyl transpeptidase, apolipoprotein A1, and α-2-macroglobulin) scored on a 0-4 scale. The Fibrotest score was computed using the Biopredictive website. The overall diagnostic performances of scores were evaluated in terms of the area under the receiver operating characteristic (AUROC) curve. The Obuchowski measure was assessed taking into account the distribution of fibrosis stages observed in the cohort. RESULTS: For predicting F≥2 fibrosis stage, the AUROC curves of PGAA and Fibrotest were 0.83±0.03 and 0.80±0.03, respectively. For predicting F4 fibrosis stage, the AUROC curves of PGAA and Fibrotest were 0.87±0.03 and 0.86±0.03. There was no difference between the AUROC curves of PGAA and Fibrotest. The Obuchowski measure was 0.92±0.01 for PGAA and Fibrotest. For a value of 10, PGAA had 98% specificity and 97% positive predictive value for the detection of F≥2 fibrosis stage and 80% sensitivity and 92% negative predictive value for F4 stage fibrosis. CONCLUSION: We confirm the comparable diagnostic values of Fibrotest and PGAA. When Fibrotest use is constrained by an increase in unconjugated bilirubin or is not financially viable, PGAA may be an alternative.

Body fat distribution and risk factors for fibrosis in patients with alcoholic liver disease.

BACKGROUND: Only a small proportion of alcoholic patients develop advanced liver disease, suggesting that factors other than alcohol intake may influence alcoholic liver disease (ALD) progression. We have shown that body mass index (BMI) is an independent risk factor for fibrosis in alcohol-induced liver disease and that adipose tissue inflammation is correlated with liver lesions in alcoholic patients. The aim of this study was to determine whether visceral adipose tissue, as assessed by abdominal height measurement, affected individual susceptibility to fibrosis in alcoholic patients. METHODS: We included 127 consecutive alcoholic patients with abnormal liver test findings for whom liver histology data were available. Abdominal height was measured with a Holtain-Kahn abdominal caliper. We carried out univariate comparisons followed by multivariate regression analysis, to investigate the relationship between abdominal height and fibrosis score. RESULTS: Abdominal height (p < 0.005), waist circumference (p < 0.05), fasting blood glucose concentration (p < 0.05), serum triglyceride concentration (p < 0.05), serum bilirubin (p < 0.005), and BMI (p = 0.05) were higher, whereas high-density lipoprotein (HDL) cholesterol level (p < 0.01) was lower in the 72 patients with significant (F2-F4) fibrosis than in the 55 patients with F0-F1 fibrosis. In multivariate regression analysis, only abdominal height (ß = 7.2, p < 0.002) was independently and positively correlated with fibrosis score, which was also negatively correlated with HDL cholesterol level (ß = -1.04, p < 0.05). CONCLUSIONS: We provide the first demonstration that abdominal height may be a predictor of significant fibrosis in patients with ALD. Our findings support a role for visceral fat accumulation, independent of BMI and of metabolic syndrome criteria, in the onset of alcoholic liver damage.

Housekeeping gene variability in the liver of alcoholic patients.

BACKGROUND: Quantification of gene expression using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) requires normalization to an endogenous reference gene termed housekeeping gene (HKG). Many of the commonly used HKGs are regulated and vary under experimental conditions and disease stages. Alcoholic liver disease (ALD) is associated with several different liver histological lesions that may modulate HKG expression. We investigated the variability of commonly used HGKs (18S, ß-actin, glyceraldehyde-3-phosphate [GAPDH], and arginine/serine-rich splicing factor [SFRS4]) in the liver of patients with ALD. METHODS: Fifty consecutive patients at different stages of ALD underwent liver biopsy. The stability of HKG was assessed according to liver histological lesions. RESULTS: ß-actin had the highest coefficient of dispersion (COD) (23.9). ß-actin tended to decrease with steatosis and to increase with alcoholic hepatitis; ß-actin also increased in patients with both alcoholic hepatitis and cirrhosis. GAPDH and SFRS4 COD were 2.8 and 2.1, respectively. GAPDH was decreased with steatosis and increased with alcoholic hepatitis and fibrosis. 18S had the lowest COD (1.4). Both 18S and SFRS4 levels were not significantly modified with respect to all alcohol-induced liver histological lesions. CONCLUSIONS: In patients with ALD, the most constantly expressed HKGs are 18S and SFRS4. These genes are appropriate reference genes for normalization of RT-qPCR in the liver of patients with ALD. The use of other HKGs such as ß-actin or GAPDH would lead to misinterpretation of the results.

Harmful effect of adipose tissue on liver lesions in patients with alcoholic liver disease.

BACKGROUND & AIMS: Adipose tissue is an important source of cytokines. Excess weight is an independent risk factor for steatosis, acute alcoholic hepatitis (AAH), and cirrhosis in patients with alcoholic liver disease (ALD). In this study, we investigated the role of adipose tissue in human ALD. PATIENTS AND METHODS: Fifty patients with ALD underwent liver and abdominal subcutaneous adipose tissue biopsies and supplied blood samples for the investigation of cytokine gene expression and secretion, as well as liver histology. RESULTS: The levels of TNF-alpha and IL-10 in adipose tissue were higher in patients with AAH. IL-10 level in adipose tissue was also correlated with fibrosis score. TNF-alpha gene expression in adipose tissue was correlated with Maddrey score, blood C-reactive protein (CRP) concentration and liver IL-6 concentration. IL-6 production levels in the liver were higher in patients with AAH and correlated with AAH score, liver histological lesions, liver TNF-alpha concentration, Maddrey score, and blood CRP concentration. Plasma concentrations of soluble forms of TNF-receptor were correlated with inflammatory lesions in the liver, Maddrey score and fibrosis score. CONCLUSION: In patients with ALD, inflammation occurs not only in the liver, but also in the adipose tissue. Adipose tissue inflammation is correlated with the severity of pathological features in the liver. Our findings may account for the harmful interactions between body mass index, AAH, fibrosis, and cirrhosis in alcoholic patients.

Predictive factors for pure steatosis in alcoholic patients.

BACKGROUND: Bearing in mind the mechanisms involved in nonalcoholic fatty liver disease, this study aims to verify whether metabolic syndrome or its various individual components are independent predictive factors for steatosis > or =10% in alcoholic patients. METHODS: This study included 281 consecutive alcoholic patients with abnormal liver tests and either normal liver histology or steatosis <10% (n = 119) or steatosis > or =10% (n = 162). Logistic regression analysis was used to study the relationship between metabolic syndrome components and various risk factors and the presence of steatosis > or =10%. We assessed apolipoprotein A1 (ApoA-1) levels, a major protein component of plasma high-density lipoprotein (HDL), rather than HDL-cholesterol levels. RESULTS: Plasma ApoA-1 levels (p < 0.01), body mass index (BMI) (p < 0.01), and waist circumference (p < 0.05) were significantly higher in patients with steatosis > or =10% than in patients with normal liver histology or steatosis <10%. A higher percentage of patients with steatosis > or =10% had high blood pressure (p = 0.003) than patients with normal liver histology or steatosis <10%. In the logistic regression, ApoA-1 [odds ratio (OR) = 1.57 (1.10-2.22)], BMI [OR = 1.10 (1.01-1.23)], and high blood pressure [OR = 1.84 (1.10-3.06)] were positively and independently correlated with the presence of steatosis > or =10%. In the multivariate regression high blood pressure was independently and positively correlated with steatosis score (r = 0.55 +/- 0.26; p < 0.05). On the other hand, when the presence of high blood pressure was the dependent variable, the presence of steatosis > or =10% positively and independently correlated with it [OR = 1.82 (1.05-3.15)]. CONCLUSION: In alcoholic patients without fibrosis, ApoA-1, BMI, and high blood pressure on the next morning after the admission were predictive of steatosis > or =10%. High blood pressure was the only metabolic syndrome component associated with the presence of alcoholic steatosis >/=10% and was not correlated with other metabolic syndrome components. These findings suggest that steatosis mechanisms are different in alcoholic and nonalcoholic fatty liver.

Diagnostic and prognostic values of noninvasive biomarkers of fibrosis in patients with alcoholic liver disease.

FibroTest has been validated as a biomarker of fibrosis in patients with chronic viral hepatitis, with a similar prognostic value as biopsy. The aim of the study was to compare the diagnostic and prognostic values of FibroTest versus the recently patented biomarkers, FibrometerA, and Hepascore. A total of 218 consecutive patients with ALD and available liver biopsy examination were included. Biomarkers were compared using univariate area under the ROC curves (AUROC) and multivariate analysis (logistic regression and Cox). The median follow-up was 8.2 years. Eighty-five patients died, including 42 deaths related to liver complications. The diagnostic values of FibrometerA and Hepascore did not differ from that of FibroTest for advanced fibrosis (all AUROC = 0.83 +/- 0.03) and cirrhosis (FibroTest and FibrometerA = 0.94 +/- 0.02, Hepascore = 0.92 +/- 0.02), and were significantly greater than those of nonpatented biomarkers (APRI, Forns, FIB4; P < 0.01). In multivariate analysis the most significant was FibroTest (P = 0.001), without independent diagnostic value for FibrometerA (P = 0.19), and Hepascore (P = 0.40). The prognostic values of FibroTest (AUROC for survival or non liver disease-related death = 0.79 +/- 0.04), FibrometerA (0.80 +/- 0.04), Hepascore (0.78 +/- 0.04), did not differ from that of biopsy fibrosis staging (0.77 +/- 0.04). In multivariate analysis the most significant were FibroTest (P = 0.004) and biopsy (P = 0.03), without independent prognostic values for FibrometerA (P = 0.41) and Hepascore (P = 0.28). In patients with alcoholic liver disease, FibrometerA and Hepascore did not improve the diagnostic and prognostic values of FibroTest.