Reply to: “Non-invasive prediction of fibrosis in nonalcoholic fatty liver disease”
0
Citation
3
Reference
10
Related Paper
Abstract:
Non-invasive prediction of fibrosis in non-alcoholic fatty liver diseaseJournal of HepatologyVol. 55Issue 2PreviewNon-alcoholic fatty liver disease (NAFLD) is one of the most common causes of liver disease worldwide. It includes a wide spectrum of liver diseases, ranging from pure steatosis to nonalcoholic steatohepatitis (NASH), and eventually to liver cirrhosis with its complications. Full-Text PDF Open Access We would like to address the concerns presented by Dr. Dogru et al. in their letter to the Editor. The first issue commented on pertains to one of the six variables included in the formula of the NAFLD fibrosis score: impaired fasting glucose/diabetes. For that variable, we took the same definition from the original paper by Angulo et al. [[1]Angulo P. Hui J.M. Marchesini G. Bugianesi E. George J. Farrell G.C. et al.The NAFLD fibrosis score: a noninvasive system that identifies liver fibrosis in patients with NAFLD.Hepatology. 2007; 45: 846-854Crossref PubMed Scopus (2048) Google Scholar]. Diabetes was defined as a fasting glucose level ⩾126 mg/dl or a patient who was already under treatment with anti-diabetic drugs; and impaired fasting glucose, as a fasting glucose level ⩾110 mg/dl. We did not perform any glucose tolerance test in our patients. As stated in our paper [[3]Ruffillo G. Fassio E. Alvarez E. Landeira G. Longo C. Domínguez N. et al.Comparison of NAFLD fibrosis score and BARD score in predicting fibrosis in nonalcoholic fatty liver disease.J Hepatol. 2011; 54: 160-163Abstract Full Text Full Text PDF PubMed Scopus (67) Google Scholar], we just retrospectively analyzed data of consecutive patients with biopsy proven NAFLD that had been prospectively collected. One advantage of both, the NAFLD fibrosis score and the BARD score [[2]Harrison S.A. Oliver D. Arnold H.L. Gogia S. Neuschwander-Tetri B.A. Development and validation of a simple NAFLD clinical scoring system for identifying patients without advanced disease.Gut. 2008; 57: 1441-1447Crossref PubMed Scopus (585) Google Scholar], is that they include 6 and 3, respectively, easily available variables. Being a group that is especially interested in research on NAFLD, we had all of these variables available in our database. In fact, at present if we wanted to repeat the analysis of comparison between both scoring systems, data on 182 biopsy proven NAFLD patients would be available (instead of 138 in our published paper). The second concern raises the point about the lack of information on medications that patients could be receiving. We agree that some drugs may influence the serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and we do not have the complete information about medications taken by our patients. Some of them were receiving antihypertensive drugs such as enalapril, or antihyperlipidemic drugs such as statins. However, the pattern of liver enzymes in our NAFLD patients conformed to those commonly found; with a mild to moderate elevation and an ALT predominance. Median ALT was 69 IU/L, interquartile range 50–96.5 IU/L and, in only 4 out of 138 patients (2.9%), levels above 200 IU/L (that is, five times above upper limit of normal) were found (maximal value, 294). AST/ALT ratios in these 4 patients were 0.61, 0.52, 0.78 and 0.55, similar to the whole group of patients. Thus, we might suggest that most of the patients were not showing a drug-induced liver injury able to modify AST or ALT levels. The AST/ALT ratio is a very important variable, strongly associated with the presence of advanced fibrosis in the univariate analysis (with higher odds ratio than other variables) and therefore, is included in both scoring systems, the NAFLD fibrosis score and the BARD score. Furthermore, in the BARD score, an AST/ALT ratio ⩾0.8 sums 2 points while the other two variables, presence of diabetes or body mass index ⩾28, sum only 1 point. However, the information on the list of medications taken by the patients is also lacking in the two original studies [1Angulo P. Hui J.M. Marchesini G. Bugianesi E. George J. Farrell G.C. et al.The NAFLD fibrosis score: a noninvasive system that identifies liver fibrosis in patients with NAFLD.Hepatology. 2007; 45: 846-854Crossref PubMed Scopus (2048) Google Scholar, 2Harrison S.A. Oliver D. Arnold H.L. Gogia S. Neuschwander-Tetri B.A. Development and validation of a simple NAFLD clinical scoring system for identifying patients without advanced disease.Gut. 2008; 57: 1441-1447Crossref PubMed Scopus (585) Google Scholar]. The authors declared that they do not have anything to disclose regarding funding or conflict of interest with respect to this manuscript.Keywords:
Steatohepatitis
Steatosis
Стеатоз печени диагностируется при наличии жировых включений более 5% от массы органа. Жировая инфильтрация печени с наличием в ней очагов воспаления выделено в отдельное заболевание - стеатогепатит. Целью исследования явилась оценка жизнеспособности клеточных моделей стеатоза и стеатогепатита линии HepG2 с использованием трет-бутилгидропероксида (tBHP) и олеиновой кислоты in vitro. Добавление олеиновой кислоты приводило к снижению процента живых клеток, увеличению содержания мертвых клеток и росту площади жировых включений в клеточной линии HepG2. Liver steatosis is diagnosed in the presence of fatty inclusions of more than 5% of the organ mass. Fatty infiltration of the liver with the presence of foci of inflammation in it is singled out as a separate disease - steatohepatitis. The aim of the study was to assess the viability of cell models of steatosis and steatohepatitis of the HepG2 line using tert-butyl hydroperoxide (tBHP) and oleic acid in vitro. The addition of oleic acid led to a decrease in the percentage of living cells, an increase in the content of dead cells, and an increase in the area of fatty inclusions in the HepG2 cell line.
Steatohepatitis
Steatosis
Viability assay
Cite
Citations (0)
Steatosis
Steatohepatitis
Cite
Citations (229)
Steatohepatitis
Cite
Citations (0)
Xanthohumol
Steatosis
Steatohepatitis
Nonalcoholic steatohepatitis
Cite
Citations (0)
ENWEndNote BIBJabRef, Mendeley RISPapers, Reference Manager, RefWorks, Zotero AMA Augustyn M, Grys I, Kukla M. Small intestinal bacterial overgrowth and nonalcoholic fatty liver disease. Clinical and Experimental Hepatology. 2019;5(1):1-10. doi:10.5114/ceh.2019.83151. APA Augustyn, M., Grys, I., & Kukla, M. (2019). Small intestinal bacterial overgrowth and nonalcoholic fatty liver disease. Clinical and Experimental Hepatology, 5(1), 1-10. https://doi.org/10.5114/ceh.2019.83151 Chicago Augustyn, Monika, Iwon Grys, and Michał Kukla. 2019. "Small intestinal bacterial overgrowth and nonalcoholic fatty liver disease". Clinical and Experimental Hepatology 5 (1): 1-10. doi:10.5114/ceh.2019.83151. Harvard Augustyn, M., Grys, I., and Kukla, M. (2019). Small intestinal bacterial overgrowth and nonalcoholic fatty liver disease. Clinical and Experimental Hepatology, 5(1), pp.1-10. https://doi.org/10.5114/ceh.2019.83151 MLA Augustyn, Monika et al. "Small intestinal bacterial overgrowth and nonalcoholic fatty liver disease." Clinical and Experimental Hepatology, vol. 5, no. 1, 2019, pp. 1-10. doi:10.5114/ceh.2019.83151. Vancouver Augustyn M, Grys I, Kukla M. Small intestinal bacterial overgrowth and nonalcoholic fatty liver disease. Clinical and Experimental Hepatology. 2019;5(1):1-10. doi:10.5114/ceh.2019.83151.
Cite
Citations (71)
Steatosis
Liver steatosis
Cite
Citations (2)
Transplant surgery
Cite
Citations (0)
Steatohepatitis
Steatosis
Nonalcoholic steatohepatitis
Cite
Citations (0)
Steatosis
Steatohepatitis
Nonalcoholic steatohepatitis
Cite
Citations (2)