Display options
Cite
El Sagheer GM, Ahmad AK, Abd-ElFattah AS, et al. A study of the circulating fibroblast growth factor 21 as a novel noninvasive biomarker of hepatic injury in genotype-4 chronic hepatitis C: Egyptian patients and their response to direct-acting antiviral agents. Clin Exp Gastroenterol. 2018;11:415-422doi: 10.2147/CEG.S173484.
El Sagheer, G. M., Ahmad, A. K., Abd-ElFattah, A. S., Saad, Z. M., & Hamdi, L. (2018). A study of the circulating fibroblast growth factor 21 as a novel noninvasive biomarker of hepatic injury in genotype-4 chronic hepatitis C: Egyptian patients and their response to direct-acting antiviral agents. Clinical and experimental gastroenterology, 11415-422. https://doi.org/10.2147/CEG.S173484
El Sagheer, Ghada M, et al. "A study of the circulating fibroblast growth factor 21 as a novel noninvasive biomarker of hepatic injury in genotype-4 chronic hepatitis C: Egyptian patients and their response to direct-acting antiviral agents." Clinical and experimental gastroenterology vol. 11 (2018): 415-422. doi: https://doi.org/10.2147/CEG.S173484
El Sagheer GM, Ahmad AK, Abd-ElFattah AS, Saad ZM, Hamdi L. A study of the circulating fibroblast growth factor 21 as a novel noninvasive biomarker of hepatic injury in genotype-4 chronic hepatitis C: Egyptian patients and their response to direct-acting antiviral agents. Clin Exp Gastroenterol. 2018 Oct 24;11:415-422. doi: 10.2147/CEG.S173484. eCollection 2018. PMID: 30425548; PMCID: PMC6204854.
Copy Download .nbib Format: NLM
Share it on

Clin Exp Gastroenterol. 2018 Oct 24;11:415-422. doi: 10.2147/CEG.S173484. eCollection 2018.

A study of the circulating fibroblast growth factor 21 as a novel noninvasive biomarker of hepatic injury in genotype-4 chronic hepatitis C: Egyptian patients and their response to direct-acting antiviral agents.

Clinical and experimental gastroenterology

Ghada M El Sagheer, Asmaa K Ahmad, Aliaa S Abd-ElFattah, Zienab M Saad, Lamia Hamdi

Affiliations

  1. Internal Medicine Department, Endocrinology Unit, [email protected].
  2. Hepatology Department.
  3. Clinical Pathology Department, Minia University, El-Minia, Egypt.

PMID: 30425548 PMCID: PMC6204854 DOI: 10.2147/CEG.S173484

Abstract

BACKGROUND: Fibroblast growth factor (FGF) 21 was reported to be induced by different injurious agents, including chronic hepatitis C (CHC) virus, affecting the liver. The aims of this study were to evaluate the FGF21 levels in CHC patients before and after the treatment with direct-acting antiviral agents (DAAs) in comparison to that in control subjects and to correlate these levels with insulin resistance (IR), lipid profile, and fibrosis stages.

PATIENTS AND METHODS: We studied 75 naive CHC patients and 40 age- and gender-matched healthy control subjects. Patients were divided into five groups based on the severity of fibrosis as detected by Fibroscan as follows: F0, n=2; F1, n=13; F2, n=23; F3, n=16; F4, n=21. We estimated the FGF21 levels at the start of the study for all the participants and for the patients only at the end of treatment with simisipivir (SIM) and sofosbuvir (SOF). These levels were compared between the patients and the control subjects and also for the patients before and after the treatment with DAAs. The FGF21 levels were correlated to IR, lipid profile, and stages of liver fibrosis

RESULTS: The FGF21, fasting blood sugar (FBS), fasting insulin, and homeostasis model of IR (HOMA-IR) were significantly higher in CHC patients compared to control (5.04±0.75 vs 4.7±0.52, 20.15±5.13 vs 13.15±4.2, 4.49±1.28 vs 2.72±0.87, and 123.7±52.6 vs 21.8±8.8;

CONCLUSION: Besides its metabolic modulator role, FGF21 strongly introduced itself as a novel biomarker of hepatic injury in Egyptian, genotype-4, CHC patients.

Keywords: direct-acting antiviral agents; fibroblast growth factor 21; hepatitis C

Conflict of interest statement

Disclosure The authors report no conflicts of interest in this work.

References

  1. Clin Chem. 1972 Jun;18(6):499-502 - PubMed
  2. Expert Opin Ther Targets. 2014 Nov;18(11):1305-13 - PubMed
  3. PLoS One. 2013 Jun 26;8(6):e67160 - PubMed
  4. Virology. 2009 Sep 1;391(2):257-64 - PubMed
  5. Scand J Gastroenterol. 2012 Sep;47(8-9):1037-47 - PubMed
  6. Diabetes. 2008 May;57(5):1246-53 - PubMed
  7. BMC Gastroenterol. 2013 Apr 17;13:67 - PubMed
  8. Horm Mol Biol Clin Investig. 2016 Jun 20;30(1):null - PubMed
  9. Genes Dev. 2012 Feb 1;26(3):271-81 - PubMed
  10. Mol Endocrinol. 2010 Oct;24(10):2050-64 - PubMed
  11. PLoS One. 2011 Mar 18;6(3):e17868 - PubMed
  12. Diabetes Res Clin Pract. 2008 Nov;82(2):209-13 - PubMed
  13. Toxicol Appl Pharmacol. 2016 Jan 1;290:43-53 - PubMed
  14. Eur J Pharmacol. 2013 Feb 28;702(1-3):302-8 - PubMed
  15. Diabetes. 2009 Jan;58(1):250-9 - PubMed
  16. Biochimie. 2013 Apr;95(4):692-9 - PubMed
  17. Scand J Gastroenterol. 2013 Feb;48(2):252-3 - PubMed
  18. Biochimie. 2014 Mar;98:63-74 - PubMed
  19. J Hepatol. 2010 Nov;53(5):934-40 - PubMed
  20. Sci Rep. 2016 Aug 08;6:31026 - PubMed
  21. Endocrinology. 2009 Sep;150(9):4084-93 - PubMed
  22. Eur J Gastroenterol Hepatol. 2013 Sep;25(9):1076-81 - PubMed
  23. Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14379-84 - PubMed
  24. Nat Rev Drug Discov. 2009 Mar;8(3):235-53 - PubMed
  25. Biomed Res Int. 2017;2017:9729107 - PubMed
  26. J Clin Invest. 2005 Jun;115(6):1627-35 - PubMed
  27. Endocrinology. 2012 Jun;153(6):2689-700 - PubMed

Publication Types