Abstract
Serum Sclerostin and Muscle Strength in Alcoholics
Highlights
Since several years ago it is well known that osteocytes form a tridimensional net within the bone cortex, able to detect changes in load
Serum sclerostin was directly related with Pugh score, among cirrhotics only (ρ = 0.34, p = 0.05), and when a similar score was calculated for all the patients, both cirrhotics and non-cirrhotics (ρ = 0.36, p = 0.002), and inverse correlations were observed with prothrombin activity (ρ = -0.24, p = 0.05) and albumin (ρ = -0.35, p = 0.003)
Serum sclerostin showed a direct correlation with the duration of ethanol consumption (ρ = 0.33, p = 0.008), but not with the amount of ethanol consumed daily Serum sclerostin was directly related with serum creatinine (ρ = 0.29, p = 0.016)
Summary
Since several years ago it is well known that osteocytes form a tridimensional net within the bone cortex, able to detect changes in load. Osteocytes secrete a biochemical mediator that exerts an opposite action, leading to increased bone resorption, namely sclerostin. Load changes on bone are heavily dependent on muscle contraction. In this sense there are several reports underscoring the role of sclerostin in situations of muscle disuse, such as spinal cord injury [2], or situations characterized by muscle unloading, such as prolonged bed rest [3], or, possibly, living in a low gravity environment. Chronic alcoholic myopathy is a common complication of alcoholism, leading to muscle atrophy and reduced muscle strength. Sclerostin inhibits bone synthesis in situations of reduced load, such as prolonged bed rest or spinal cord injury. The aim pf this study is to analyze the behavior of serum sclerostin in chronic alcoholic myopathy
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