Review of laboratory findings for patients with chronic fatigue syndrome.
Buchwald, D, Komaroff, A L · Reviews of infectious diseases · 1991 · DOI
Quick Summary
This review examined blood test results from many ME/CFS patients and found several patterns in how their immune systems function differently. The most common findings included weaker natural killer cells (which normally help fight infections), unusual antibody levels, and signs of past Epstein-Barr virus infection. These patterns appeared across multiple studies, suggesting they may be important features of the condition.
Why It Matters
This review consolidated evidence that ME/CFS involves measurable immune system abnormalities, providing scientific support for the biological nature of the condition rather than it being purely psychological. Identifying consistent laboratory patterns helps establish ME/CFS as a medical condition and may guide future research into disease mechanisms and potential biomarkers.
Observed Findings
Depressed natural killer cell function and reduced natural killer cell counts reported consistently across studies
Low levels of circulating immune complexes
Reduced antinuclear antibodies and antithyroid antibodies
Altered levels of immunoglobulins
Abnormalities in number and function of lymphocytes
Modestly elevated Epstein-Barr virus-related antibodies (anti-VCA IgG and anti-EA)
Inferred Conclusions
ME/CFS is associated with measurable immune system abnormalities rather than being a purely functional disorder
Natural killer cell dysfunction appears to be a particularly consistent finding across CFS patients
Past Epstein-Barr virus infection may play a role in CFS pathogenesis in some patients
Remaining Questions
Do these immune abnormalities appear before symptom onset or only after illness develops?
Which of these abnormalities, if any, directly cause CFS symptoms versus represent secondary immune dysregulation?
What This Study Does Not Prove
This review does not prove that any single abnormality causes ME/CFS, nor does it establish whether these immune changes are primary triggers or secondary consequences of the illness. The findings are correlational and do not indicate why some patients develop these patterns while others do not, and it cannot determine whether these abnormalities persist, worsen, or improve over time.