Serum Sclerostin in Alcoholics: A Pilot Study

González‐Reimers, Emilio; Martín-González, Candelaria; Vega-Prieto, Marı́a José de la; Pelazas-González, Ricardo; Fernández-Rodríguez, C.; López-Prieto, J.; Alvisa-Negrín, Julio; Santolaria-Fernández, F.

doi:10.1093/alcalc/ags136

Cited by 40 publications

(31 citation statements)

References 36 publications

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“…Serum sclerostin was higher in patients with advanced liver cirrhosis (Child-Pugh classes B or C) than healthy controls or Child-Pugh grade A cirrhosis [19]; most patients (85 %) had chronic hepatitis B and none NASHrelated cirrhosis in this study. Likewise, others reported higher sclerostin levels in alcoholic cirrhosis (11 of 31 also infected by hepatitis C) than controls; notably, patients with advanced liver cirrhosis (Child-Pugh classes B or C) also had higher sclerostin than those with Child-Pugh grade A cirrhosis [20]. 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.…”

Section: Discussionmentioning

confidence: 94%

“…Likewise, others reported higher sclerostin levels in alcoholic cirrhosis (11 of 31 also infected by hepatitis C) than controls; notably, patients with advanced liver cirrhosis (Child-Pugh classes B or C) also had higher sclerostin than those with Child-Pugh grade A cirrhosis [20]. 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].…”

Section: Discussionmentioning

confidence: 94%

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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: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 94%

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

et al. 2015

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“…However, serum sclerostin positively correlated with lumbar and hip BMD, suggesting that the increased sclerostin may be reflective of increased osteocyte number (10). Increased serum sclerostin has been reported in other liver conditions, including alcoholism (60) and advanced liver cirrhosis (61), although this appears to be due to impaired liver function and metabolism. It is unclear whether the sclerostin detected by IHC is reflective of cholangiocyte- or osteocyte-derived sclerostin, and whether the presence of sclerostin staining in the bile duct may be the result of impaired liver function in these patients; however, the fact that liver from these patients also exhibited increased SOST mRNA suggests the sclerostin is derived from a local site.…”

Section: Other Tissues and Pathologies Impacted By Sclerostinmentioning

confidence: 99%

Sclerostin expression and functions beyond the osteocyte

Weivoda

Youssef

Oursler

2017

Bone

110

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Sclerostin, the product of the SOST gene, is a secreted inhibitor of Wnt signaling that is produced by osteocytes to regulate bone formation. While it is often considered an osteocyte-specific protein, SOST expression has been reported in numerous other cell types, including hypertrophic chondrocytes and cementocytes. Of interest, SOST/sclerostin expression is altered in certain pathogenic conditions, including osteoarthritis and rheumatic joint disease, and it is unclear whether sclerostin plays a protective role or whether sclerostin may mediate disease pathogenesis. Therefore, as anti-sclerostin antibodies are being developed for the treatment of osteoporosis, it is important to understand the functions of sclerostin beyond the regulation of bone formation.

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“…Therefore, high sclerostin levels should be associated with decreased bone mass and bone turnover, but this is not always the case. Only some preliminary results are available for sclerostin among alcoholics, showing an increase among these patients, an inverse correlation with osteocalcin, but a direct one with telopeptide suggesting a role in bone breakdown 26 .…”

Section: Increased Breakdown: Cytokines and The Opg/rank-l Systemmentioning

confidence: 97%

Bone changes in alcoholics: A review

Gonzlez-Reimers¹,

Santolaria-Fernndez²,

Alvisa-Negrn³

2013

OA Alcohol

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IntroductionAlcoholism may damage the skeleton. In addition to a direct effect of ethanol, many other mechanisms are involved which should be considered in the clinical evaluation of alcoholic patients. We will review the mechanism and clinical consequences of bone alterations observed in alcoholics. ConclusionOsteoporosis is the main metabolic disease observed in alcoholic patients. The main factors involved in its pathogenesis are: a direct effect of ethanol, associated malnutrition, liver disease, altered hormone profile and cytokine pattern, and alcoholic myopathy. Osteoporosis may lead to bone fracture. It improves with ethanol withdrawal.

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Serum Sclerostin in Alcoholics: A Pilot Study

Cited by 40 publications

References 36 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 expression and functions beyond the osteocyte

Bone changes in alcoholics: A review

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