Asymptomatic/pauci‐symptomatic creatine kinase elevations (hyperckemia)

Abstract

Neuromuscular clinicians are frequently asked to evaluate patients referred for asymptomatic elevations in creatine kinase (CK), a catalytic enzyme that combines creatine and ATP to form phosphocreatine and ADP. This reaction is crucial for cellular energy generation and metabolism. This laboratory finding, often referred to in simplified lexicon as asymptomatic hyperCKemia, continues to generate controversy at several levels, including definition, the extent of evaluation, and the yield of diagnostic testing. In this review, we summarize the literature based on series of patients with asymptomatic hyperCKemia and provide a rational clinical approach to reveal identifiable underlying causes.

An assessment by the Statin Muscle Safety Task Force: 2014 update

“…Many aor oligo-symptomatic neuromuscular conditions have been identified as causes of elevated CK levels (for review, see Silvestri and Wolfe). 44 It is the position of this consensus panel that if an underlying neuromuscular disorder is identified, then it is necessary to determine whether a genuine statin-associated muscle adverse event has occurred or whether it can be explained by other mechanisms. The finding of incidental serum CK elevations in the absence of any clinically discernible change in the patient's baseline symptoms does not constitute an adverse event.…”

Asymptomatic elevation of creatine kinase in patients with hyponatremia

“…Hyper-CKemia in settings other than hyponatremia have been associated with normal as well as non-specific findings on EMGs and muscle biopsies. 2 This study has a number of limitations. Data collection was retrospective and subject to the limitations inherent in this study design.…”

“…2 Among electrolyte disorders, hypokalemia and hypophosphatasemia are known to cause myocyte destruction. 3,4 However, less is known of hyponatremia as a cause of skeletal muscle damage.…”

Asymptomatic hyperCKemia during a two-year monitoring period: A case report and literature overview

“…The three isoenzymes involved are CK-MM, which is mainly present in skeletal muscle; CK-MB in cardiac muscle and CK-BB which is predominantly expressed in the brain. The sum of these three isoenzymes quantifies the total serum CK (sCK) levels (1,2). CK levels have been reported based on age, ethnicity and gender and can be stratified in a 'high CK' group among men of African descent with a mean CK value of 237.8 U/l, an 'intermediate CK' group comprising of non-African-American men and women with mean CK levels between 109.3 and 149.7 U/l and a 'low CK' group consisting of Caucasian women with mean CK levels between 64.6 and 79.8 U/l (3).…”

“…sCK (phospho) level elevation sometimes represents an incidental laboratory finding leading to a diagnostic enigma as it can be related to a variety of disorders such as those of neuromuscular, cardiac, metabolic, endocrine and traumatic origin (2,4,6). Other clinical situations that can lead to hyperCKemia include viral infections, toxin accumulation, heavy muscle exercise, surgery, pregnancy, obstructive sleep apnoea, neuroacanthocytosis syndromes, macro-CK, malignant hyperthermia syndrome and medications (4,6).…”