Background:Creatine kinase (CK) values are a critical part of the workup of suspected myopathies and are often assessed in patients that develop myalgia on statin therapy. CK elevations may influence the initiation and cessation of statin treatment, and incidentally discovered CK elevation may lead to further testing. A number of factors influence CK levels in healthy patients, but current reference ranges do not incorporate important influencers of CK such as race. Objectives of this study were to evaluate clinical factors associated with CK among healthy individuals and to develop practical reference ranges for important subgroups to improve test interpretation.Methods:CK was evaluated in nonpregnant participants ≥20 years old from the cross-sectional National Health and Nutrition Examination Survey (NHANES) 2011–2014. Linear and logistic regression stratified by sex identified clinical factors associated with CK levels. Adjustment for anthropomorphic measures assessed whether age and race-ethnicity differences in CK were explained by differences in body composition. The 95th and 97.5th percentiles of CK in sex/race-ethnicity subgroups were calculated, excluding patients with recent strenuous exercise.Results:A total of 10,096 nonpregnant adults were studied. Black race was strongly associated with CK. The odds ratio of having an abnormal CK for black women was 5.08 (95% CI 3.65–7.08) and for black men was 8.39 (95% CI 6.11–11.52). CK was substantially lower in older men. Differences in CK by age but not race-ethnicity were largely explained by body composition. Women with low body mass index were less likely to have an elevated CK, and overweight or obese men had an almost 2-fold greater odds of having an elevated CK. The 97.5th percentile of CK was 382 (95% CI 295–469) in white men, 1001 (95% CI 718–1284) in black men, 295 (95% CI 216–374) in white women, and 487 (95% CI 310–664) in black women.Conclusion:CK is substantially higher in men and in black patients. Differences in body size and composition are also important but do not explain racial differences in CK. The 95th and 97.5th percentiles in sex and race-ethnicity subgroups provide a practical guide for clinicians interpreting CK values.

HTLV-1-associated infective dermatitis (HAID) is the main paediatric manifestation of human T-cell lymphotropic virus type 1 (HTLV-1). It is characterised by a chronic exudative eczematous eruption and persistent infection with Staphylococcus aureus (SA) and beta-haemolytic streptococci (BHS). Prevalence is highest in the Caribbean and Brazil; however, cases have been reported in other HTLV-1 endemic regions. Approximately 20 million people worldwide are infected with HTLV-1 and only 5-10% suffer from disease. Other manifestations include adult T-cell leukaemia/lymphoma (ATLL) and tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM). HAID may also progress to ATLL or TSP/HAM. Treatment options are limited to prolonged antibiotic therapy. The aim of this paper is to review existing evidence and propose new theories on the pathogenesis of HAID. The current view is that HTLV-1 infection is required and in susceptible individuals leads to immune dysregulation with subsequent immunosuppression and superinfection with SA and BHS. Evidence suggests that host, environment and genetic factors may play a causative role. Genetic factors within ethnic groups determine host immune response and carrier state or disease manifestation of HTLV-1 infection. Increased IgE levels may contribute to the SA and BHS superinfection in HAID. Additionally, the possible impact of filaggrin, skin proteinase dysregulation, Langerhans cell dysfunction and TH2 chemokines is highlighted. More than 45 years since the discovery of HAID, the exact pathogenesis is still not fully understood. Further research is still needed to clearly elucidate the exact pathogenic mechanism of HAID.