Evidence of Clinical Pathology Abnormalities in People with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) from an Analytic Cross-Sectional Study. — CFSMEATLAS
Evidence of Clinical Pathology Abnormalities in People with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) from an Analytic Cross-Sectional Study.
Nacul, Luis, de Barros, Barbara, Kingdon, Caroline C et al. · Diagnostics (Basel, Switzerland) · 2019 · DOI
Quick Summary
Researchers tested blood samples from 272 people with ME/CFS and 136 healthy people to look for measurable differences that might help diagnose the condition. They found that people with severe ME/CFS had notably lower levels of an enzyme called creatine kinase (CK) in their blood compared to healthy people and those with milder ME/CFS. This is the first study to report this pattern, suggesting that CK levels might be useful for identifying who has the most severe form of the disease.
Why It Matters
ME/CFS currently lacks a specific diagnostic biomarker, making clinical diagnosis challenging and delayed. Identifying that severe ME/CFS is associated with distinctly lower CK levels offers a potential objective measure to distinguish disease severity and support diagnosis, which could accelerate diagnosis and enable better disease stratification in future research and clinical settings.
Observed Findings
Serum creatine kinase (CK) was significantly lower in severe ME/CFS cases (median 54 U/L) compared to healthy controls (median 101.5 U/L) and non-severe ME/CFS (median 84 U/L), with p < 0.001
The reduced CK association with severe ME/CFS persisted after adjustment for sex, age, BMI, muscle mass, disease duration, and activity levels
Odds ratio for severe ME/CFS versus healthy controls was 0.05 (95% CI 0.02-0.15) for CK concentrations
Odds ratio for severe ME/CFS versus non-severe ME/CFS was 0.16 (95% CI 0.07-0.40) for CK concentrations
Most other haematological and biochemical markers examined were within normal ranges across all groups
Inferred Conclusions
Serum CK concentrations are markedly reduced in severe ME/CFS and warrant further investigation as a potential biomarker for disease severity
The CK reduction in severe ME/CFS appears to be independent of activity levels, muscle mass, and other clinical and demographic confounders
CK may have utility in stratifying ME/CFS patients by disease severity and supporting clinical diagnosis
Remaining Questions
Does serum CK change over time within individuals, and can baseline CK levels predict disease progression or prognosis?
What This Study Does Not Prove
This study does not prove that low CK causes severe ME/CFS or that it can be used alone as a diagnostic test for the condition. The cross-sectional design captures only one moment in time and cannot establish whether CK levels change over the disease course or predict outcomes. Further validation in prospective studies and diverse populations is needed before clinical implementation.
What is the biological mechanism underlying the reduced CK in severe ME/CFS—does it reflect altered muscle metabolism, mitochondrial dysfunction, or other pathophysiology?
Can CK be validated as a diagnostic/prognostic biomarker in prospective studies with diverse geographic and demographic populations?
What are the optimal CK cutoff values for distinguishing disease severity, and how do they compare to other potential biomarkers in sensitivity and specificity?