Abstract
Objectives: Myalgia is under-recognized in meningococcal disease (MCD). In septic shock, myositis is thought to be mediated by pro-inflammatory cytokines such as tumour necrosis factor-α (TNF-α), interleukin-8 (IL-8) and interleukin-6 (IL-6) but this has never previously been studied in MCD. We aimed to demonstrate whether muscle damage mediated via TNF-α and other pro-inflammatory cytokines occurs in MCD, as estimated by creatine kinase skeletal muscle isoenzyme (CK-MM) and cardiac isoenzyme (CK-MB) concentrations.
Methods: A total of 68 children, median age 2.7 years, with a diagnosis of MCD were prospectively studied. Severity of disease was measured using the Glasgow Meningococcal Septicaemia Prognostic Score (GMSPS). Severe disease was defined as a GMSPS of ≥8. TNF-α, IL-8, IL-6 and IL-1Ra concentrations were determined on samples taken on admission.
Results: CK-MM correlated significantly with TNF-α, IL-8 and GMSPS. There was no significant correlation between CK-MB and TNF-α or IL-6, but CK-MB correlated with GMSPS and IL-8. Fifty-six percent of children with MCD had evidence of muscle damage as manifested by elevated CK-MM.
Conclusions: TNF-α and IL-8 may be potential mediators in the pathophysiology of skeletal muscle damage in MCD.
Methods: A total of 68 children, median age 2.7 years, with a diagnosis of MCD were prospectively studied. Severity of disease was measured using the Glasgow Meningococcal Septicaemia Prognostic Score (GMSPS). Severe disease was defined as a GMSPS of ≥8. TNF-α, IL-8, IL-6 and IL-1Ra concentrations were determined on samples taken on admission.
Results: CK-MM correlated significantly with TNF-α, IL-8 and GMSPS. There was no significant correlation between CK-MB and TNF-α or IL-6, but CK-MB correlated with GMSPS and IL-8. Fifty-six percent of children with MCD had evidence of muscle damage as manifested by elevated CK-MM.
Conclusions: TNF-α and IL-8 may be potential mediators in the pathophysiology of skeletal muscle damage in MCD.
Original language | English |
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Pages (from-to) | 17-21 |
Number of pages | 5 |
Journal | Journal of Infection |
Volume | 44 |
Issue number | 1 |
DOIs | |
Publication status | Published - 2002 |