Evaluating creatine kinase as a biomarker in alcohol-related disorders: promise and constraints.

Alcohol use contributes substantially to global morbidity and mortality, necessitating reliable biomarkers for detection and monitoring. Existing biomarkers, including indirect markers and direct markers, have important limitations related to specificity, sensitivity and temporal detection windows. As a biomarker, creatine kinase (CK) demonstrates strong biological plausibility, as alcohol exerts direct and indirect myotoxic effects through oxidative stress, impaired protein synthesis and metabolic disruption, leading to muscle injury and enzyme leakage. However, its diagnostic specificity is also limited, as CK elevation can result from multiple non-alcohol-related conditions, including trauma, seizures and metabolic disturbances. Despite these limitations, CK shows clinical utility in identifying complications such as rhabdomyolysis, severe withdrawal states and risk of acute kidney injury. It correlates with withdrawal severity and may aid in risk stratification. Overall, CK is best positioned as a supplementary biomarker reflecting alcohol-related complications rather than a primary indicator of alcohol consumption.