Serum 25-hydroxyvitamin D and hyaluronic acid levels as markers of fibrosis in patients with chronic liver disease at the main tertiary referral hospital in Ghana: A case-control study design.
25‐OH vitamin D
CLD
HA
fibrosis
inflammation
markers
Journal
Health science reports
ISSN: 2398-8835
Titre abrégé: Health Sci Rep
Pays: United States
ID NLM: 101728855
Informations de publication
Date de publication:
Feb 2023
Feb 2023
Historique:
received:
26
10
2022
revised:
04
01
2023
accepted:
28
01
2023
entrez:
15
2
2023
pubmed:
16
2
2023
medline:
16
2
2023
Statut:
epublish
Résumé
Liver fibrosis leading to chronic liver disease (CLD) is a major cause of morbidity, mortality and health-care expenditure worldwide. The "gold standard" for diagnosis and staging of liver fibrosis is histological analysis of liver tissue obtained by liver biopsy, an invasive procedure. Therefore, there is the need to identify noninvasive and inexpensive markers for diagnosis and staging of liver fibrosis. This study aimed at evaluating the correlation of hyaluronic acid (HA) and 25-hydroxyvitamin D (25-OH vitamin D) serum levels as markers of fibrosis with histologically staged and graded liver biopsies obtained from CLD patients. This was a case-control study involving 40 CLD patients requiring liver biopsies and 40 controls. Liver biopsies were staged to determine the degree of fibrosis. Serum levels of 25-OH vitamin D and HA were determined using ELISA. Statistical analyses were performed to determine differences in HA and 25-OH vitamin D levels between controls and patients as well as to correlate the biomarkers with the stages of fibrosis. CLD patients showed significant ( CLD patients had significantly reduced serum 25-OH vitamin D and higher HA. Both markers correlated with the degree of liver fibrosis. These findings have major clinical translatable implication in the use of vitamin D supplementation in the management of CLD in Ghana.
Sections du résumé
Background and Aims
UNASSIGNED
Liver fibrosis leading to chronic liver disease (CLD) is a major cause of morbidity, mortality and health-care expenditure worldwide. The "gold standard" for diagnosis and staging of liver fibrosis is histological analysis of liver tissue obtained by liver biopsy, an invasive procedure. Therefore, there is the need to identify noninvasive and inexpensive markers for diagnosis and staging of liver fibrosis. This study aimed at evaluating the correlation of hyaluronic acid (HA) and 25-hydroxyvitamin D (25-OH vitamin D) serum levels as markers of fibrosis with histologically staged and graded liver biopsies obtained from CLD patients.
Methods
UNASSIGNED
This was a case-control study involving 40 CLD patients requiring liver biopsies and 40 controls. Liver biopsies were staged to determine the degree of fibrosis. Serum levels of 25-OH vitamin D and HA were determined using ELISA. Statistical analyses were performed to determine differences in HA and 25-OH vitamin D levels between controls and patients as well as to correlate the biomarkers with the stages of fibrosis.
Results
UNASSIGNED
CLD patients showed significant (
Conclusion
UNASSIGNED
CLD patients had significantly reduced serum 25-OH vitamin D and higher HA. Both markers correlated with the degree of liver fibrosis. These findings have major clinical translatable implication in the use of vitamin D supplementation in the management of CLD in Ghana.
Identifiants
pubmed: 36789398
doi: 10.1002/hsr2.1101
pii: HSR21101
pmc: PMC9919473
doi:
Types de publication
Journal Article
Langues
eng
Pagination
e1101Informations de copyright
© 2023 The Authors. Health Science Reports published by Wiley Periodicals LLC.
Déclaration de conflit d'intérêts
Justice Moses K. Aheto is an Editorial Board member of Health Science Reports and co‐author of this article. He was excluded from editorial decision‐making related to the acceptance of this article for publication in the journal. All other authors declare no conflict of interest.
Références
Hepatol Int. 2010 Jul 25;4(3):634-40
pubmed: 21063488
J Hepatol. 2003;38 Suppl 1:S38-53
pubmed: 12591185
Curr Gastroenterol Rep. 2012 Feb;14(1):67-73
pubmed: 22113744
BMC Infect Dis. 2016 Mar 18;16:130
pubmed: 26987556
Nat Rev Immunol. 2008 Sep;8(9):685-98
pubmed: 19172691
J Pak Med Assoc. 2004 Mar;54(3):146-50
pubmed: 15129876
Dis Markers. 2021 Apr 02;2021:6665893
pubmed: 33884041
Am J Surg Pathol. 1995 Dec;19(12):1409-17
pubmed: 7503362
Eur J Gastroenterol Hepatol. 2003 Sep;15(9):945-50
pubmed: 12923365
J Hepatol. 2013 Dec;59(6):1169-76
pubmed: 23933265
Biomed Pharmacother. 2019 Jan;109:1351-1360
pubmed: 30551386
J Zhejiang Univ Sci B. 2014 Oct;15(10):900-6
pubmed: 25294379
N Engl J Med. 2011 Jan 20;364(3):248-54
pubmed: 21247315
Saudi Med J. 2011 Dec;32(12):1241-5
pubmed: 22159377
Acta Biochim Pol. 2011;58(4):563-6
pubmed: 22140659
Clin Gastroenterol Hepatol. 2007 Apr;5(4):513-20
pubmed: 17222588
Exp Biol Med (Maywood). 2004 Dec;229(11):1136-42
pubmed: 15564440
Gastroenterology. 2010 Nov;139(5):1453-7
pubmed: 20875784
Gut. 2020 Mar;69(3):564-568
pubmed: 31366455
Pol Arch Med Wewn. 2014;124(12):704-12
pubmed: 25394651
J Pediatr Gastroenterol Nutr. 2010 Oct;51(4):500-6
pubmed: 20808246
Endocr Rev. 2005 Aug;26(5):662-87
pubmed: 15798098
Clujul Med. 2016;89(1):24-31
pubmed: 27004022
N Engl J Med. 2007 Jul 19;357(3):266-81
pubmed: 17634462
J Hepatol. 2000 Mar;32(3):447-52
pubmed: 10735615
J Clin Gastroenterol. 2019 May/Jun;53(5):331-341
pubmed: 30702486
PLoS One. 2014 Oct 28;9(10):e111551
pubmed: 25350286