Serum sclerostin in hepatitis C virus infected patients

González‐Reimers, Emilio; López-Prieto, J.; Pelazas-González, Ricardo; Alemán-Valls, Remedios; Martín-González, M. Candelaria; Jorge-Ripper, Carlos; Pérez-Hernández, Onán; Fernández-Rodríguez, C.; Martı́nez-Riera, Antonio; Santolaria-Fernández, Francisco

doi:10.1016/j.ejim.2013.08.207

Cited by 4 publications

(4 citation statements)

References 22 publications

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“…Apart from population differences, decreased hepatic sclerostin clearance, secondary to advanced cirrhosis, may be the leading cause of controversy between our and the aforementioned studies [19,20], although the specific route of metabolism or clearance of sclerostin is yet unknown. In a third study, similar sclerostin levels were reported between hepatitis C-infected patients and controls [21]. There were significant population differences between our and this study: in the latter 11 of 40 patients consumed ethanol in significant amounts (>80 g/day) and 14 were also coinfected by human immunodeficiency virus, the effect of which on sclerostin is currently unknown.…”

Section: Discussionsupporting

confidence: 84%

Circulating sclerostin and Dickkopf-1 levels in patients with nonalcoholic fatty liver disease

et al. 2015

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There is increasing evidence for bone-liver interplay. The main aim of this study was to determine serum sclerostin and Dickkopf (DKK)-1 levels in patients with nonalcoholic fatty liver disease (NAFLD) and their association with the disease severity. Patients with biopsy-proven NAFLD, 13 with nonalcoholic simple steatosis (SS) and 14 with steatohepatitis (NASH), and 20 gender-, age-, body mass index- and waist circumference-matched controls were enrolled. Serum sclerostin, DKK-1, bone turnover markers, vitamin D, insulin and standard biochemical and hematologic parameters were measured; lumbar spinal dual-energy X-ray absorptiometry was performed. We observed that there was a progressive decline in serum sclerostin levels from the controls (76.1 ± 6.8) to SS (53.5 ± 6.4) and NASH (46.0 ± 8.1 pmol/l) patients (p = 0.009); in adjusted pairwise comparisons, sclerostin was significantly higher in the controls than in NASH patients (p = 0.012). Although serum DKK-1 did not differ between groups (p = 0.135), there was a trend toward U-shaped distribution (controls 35.8 ± 2.8; SS 27.3 ± 2.9; NASH 36.8 ± 4.4 pmol/l). Higher DKK-1 levels were independently associated with NASH. Regarding specific histological lesions, DKK-1 levels were marginally lower in NAFLD patients with lower (≤33 %) than higher (>33 %) steatosis grade (27.7 ± 3.1 and 38.8 ± 4.7 pmol/l, respectively; p = 0.049). No other significant difference was observed within histological lesions. In conclusion, serum sclerostin levels were lower in NASH patients than in controls. DKK-1 levels were independently associated with NASH in NAFLD patients. The potential importance of these findings indicates a possible bone-liver interaction and warrants further investigation.

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Section: Discussionsupporting

confidence: 84%

Circulating sclerostin and Dickkopf-1 levels in patients with nonalcoholic fatty liver disease

et al. 2015

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“…[32,33,45,67]. Whether all of the circulating sclerostin is biologically active remains to be determined, especially in patients with liver and kidney diseases [32,33,45,67]. Most intriguing is the reported inverse relationship between serum sclerostin levels and mortality [22].…”

Section: Key Pointsmentioning

confidence: 99%

Sclerostin

Honasoge

Rao

2014

Current Opinion in Endocrinology, Diabetes &Amp; Obesity

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Since the discovery of Wnt signaling pathway and sclerostin's association with high bone mass, there has been a remarkable progress. Clinical trials with fracture endpoints, already underway, should expand osteoanabolic therapeutic horizon in the very near future. Measurement of sclerostin levels in a number of conditions has advanced our knowledge about pathophysiology of skeletal and nonskeletal disorders in an altogether new light.

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“…17 The mechanism linking steatosis to hepatitis C may include host factors leading to insulin resistance and interactions between lipid metabolism pathways and the HCV core protein. 18 Several studies demonstrated that viral eradication with DAA therapy is associated with the attenuation of liver stiffness and steatosis assessed using TE or magnetic resonance imaging. [19][20][21] However, in this study, 31.9% hepatitis C patients with advanced fibrosis Alcohol consumption has been reported as a risk factor of persistent ALT elevation in patients with SVR12 after DAA treatment and accounted for 23% of patients with persistently altered liver tests.…”

Section: Current American Association For the Study Of Liver Diseases...mentioning

confidence: 99%

Persistent liver inflammation in chronic hepatitis C patients with advanced fibrosis after direct-acting antivirals induced sustained virological response

Hsieh

Lee

et al. 2021

Journal of the Chinese Medical Association

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Background: Direct-acting antivirals (DAA) improve sustained virological response (SVR) rates with normalization of liver enzymes in patients with hepatitis C. However, liver inflammation may persist despite virus eradication. We aimed to investigate the rate and risk factors for persistent elevated aminotransferase levels in patients with advanced fibrosis after DAA-induced SVR. Methods: From January 2017 to April 2018, chronic hepatitis C patients with advanced fibrosis and SVR after DAA treatment at the Taipei Veterans General Hospital were prospectively enrolled. Persistent liver inflammation after SVR was defined as an increase in levels of alanine aminotransferase (ALT) (>40 U/L) at SVR12. Results: A total of 461 patients were included (57.9% females, mean age 64 years, 69.6% genotype 1b, 46.4% cirrhosis). At SVR12, there was a decline in ALT levels (90.5 ± 80.8 U/L to 25.3 ± 26.5 U/L) from baseline levels. Persistent liver inflammation at SVR12 was detected in 45 patients (9.8%). The presence of cirrhosis, markers of impaired liver functions, history of interferonbased therapy, steatosis, and elevated ALT levels at baseline was associated with persistent liver inflammation after SVR12. Results of multivariate analysis indicated that levels of baseline serum total bilirubin (odds ratio [OR]: 2.605, 95% CI: 1.158-5.858), international normalized ratio (OR: 14.389, 95% CI: 1.754-118.049), ALT (OR: 1.006, 95% CI: 1.003-1.009), and the presence of steatosis (OR: 3.635, 95% CI: 1.716-7.698) were independent predictors of persistent liver inflammation at SVR12. Conclusion: Persistent liver inflammation is not uncommon in chronic hepatitis C patients with advanced fibrosis after DAAinduced SVR. It is associated with impaired baseline liver function and steatosis. Long-term follow-up is required to assess the implication of liver inflammation on disease progression.

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Serum sclerostin in hepatitis C virus infected patients

Cited by 4 publications

References 22 publications

Circulating sclerostin and Dickkopf-1 levels in patients with nonalcoholic fatty liver disease

Circulating sclerostin and Dickkopf-1 levels in patients with nonalcoholic fatty liver disease

Sclerostin

Persistent liver inflammation in chronic hepatitis C patients with advanced fibrosis after direct-acting antivirals induced sustained virological response

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