The paper presented by Korkina and colleagues1 on Multiple Chemical Sensitivity (MCS) gives interesting insights into this poorly defined syndrome. The hypothesis that the intolerance is due to genetic defects has been rejected, while altered redox and cytokine patterns in affected subjects suggest an inflammatory, and perhaps autoimmune mechanism. However, the epidemiological design of the study is extremely weak, and this may raise many doubts about the validity of these conclusions. More information should be provided on recruitment methods. A fuller explanation of recruitment criteria is needed with explicit reference to the Authors’ blindness regarding cases and controls. The Authors should make it clear that patients were recruited with the help of patients’ associations and clarify their relationship with these organizations. Patients were selected on the basis of a self-completed symptom scale, the QEESI, in a modified and non-validated Italian version, and Cullen’s clinical criteria2, which explicitly exclude any known organic disease. However, the concurrence of concomitant diseases was obtained only by anamnestic evaluation, and did not lead to the exclusion of patients suffering from other inflammatory or autoimmune diseases. No diagnostic test was performed to exclude any other undiagnosed diseases. Moreover, approximately half of the observed sample did not correspond to the aforementioned, highly inclusive criteria. Selection bias may explain the observed findings.
- Multiple Chemical Sensitivity
- Patient Selection