Latest data suggest that placental growth factor (PLGF), growth differentiation factor-15 (GDF-15) and hepatic growth factor (HGF) are involved in hepatic fibrogenesis. Diagnostic performance of these markers for non-invasive liver fibrosis prediction was evaluated based on liver histology and stiffness. In total 834 patients were recruited. Receiver-operating-characteristics were used to define cut-offs for markers correlating to fibrosis stages. Odds-ratios were calculated for the presence/absence of fibrosis/cirrhosis and confirmed in the sub-group of patients phenotyped by elastography only. Logistic and uni- and multivariate regression analyses were used to test for association of markers with liver fibrosis stages and for independent prediction of liver histology and stiffness. Marker concentrations correlated significantly (P<0.001) with histology and stiffness. Cut-offs for liver fibrosis (≥F2) were PLGF = 20.20 pg/ml, GDF15 = 1582.76 pg/ml and HGF = 2598.00 pg/ml. Logistic regression confirmed an increase of ORs from 3.6 over 33.0 to 108.4 with incremental (1–3) markers positive for increased liver stiffness (≥12.8kPa; all P<0.05). Subgroup analysis revealed associations with advanced fibrosis for HCV (three markers positive: OR = 59.9, CI 23.4–153.4, P<0.001) and non-HCV patients (three markers positive: OR = 144, CI 59–3383, P<0.001). Overall, serum markers identified additional 50% of patients at risk for advanced fibrosis presenting with low elastography results. In conclusion, this novel combination of markers reflects the presence of significant liver fibrosis detected by elastography and histology and may also identify patients at risk presenting with low elastography values.
The following information is missing from the Funding Section: FL received funding from the Federal Ministry of Education and Research (BMBF LiSyM 031L0051).There is an error in the first sentence of the Patients and methods section. The correct sentence is: Overall, we prospectively recruited 834 consecutive European individuals (age 18-84 years, males n = 510) with viral (n = 559) and non-viral (n = 275) chronic liver diseases.In the Patients and methods section, there is an error in the penultimate sentence under the subheading "Statistical analysis." The correct sentence is: All variables with P < 0.1 in the univariate analyses were then included in the multivariate model.In the Results section, there is an error in the ninth sentence under the subheading "Serum markers discriminate histological fibrosis stages." The correct sentence is: The positive predictive value of presenting with at least one marker positive and having fibrosis stage ! F2 was 89%.In the Results section, there is an error in the seventh sentence under the subheading "Performance of markers with respect to liver stiffness." The correct sentence is: This association was similarly present in patients without HCV infection (one marker: OR = 3.9, CI 1.9-8.2, P<0.001; two markers: OR = 18.3, CI 7.8-42.7, P<0.001; three markers: OR = 144, CI 59-3383, P<0.001).In the Results section, there is an error in the ninth sentence under the subheading "Performance of markers with respect to liver stiffness." The correct sentence is: To address the question whether the presence of positive markers adds information in patients with low TE values (i.e. <9.2 kPa), we used contingency tables.
Benign recurrent intrahepatic cholestasis (BRIC) is a peculiar familial disease caused by mutations of the genes encoding hepatocanalicular flippase for phosphatidylserine (ATP8B1; BRIC type 1) or the bile salt export pump (ABCB11; BRIC type 2). Here, we report on a patient with nasobiliary drainage‐refractory BRIC type 2 who improved under plasma separation and anion absorption therapy. We also suggest that nasobiliary drainage might be an ineffective approach in carriers of severe loss‐of‐function mutations of the bile salt export pump ABCB11. (Hepatology Communications 2018;2:152–154)
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