Patients with
Myalgic Encephalomyelitis/
Chronic Fatigue Syndrome (ME/CFS) differ for triggers, mode of start, associated symptoms, evolution, and biochemical traits. Therefore, serious attempts are underway to partition them into subgroups useful for a
personalized medicine approach to the disease. Here, we investigated clinical and biochemical traits in 40 ME/CFS patients and 40 sex- and age-matched healthy controls. Particularly, we analyzed serum levels of some
cytokines,
Fatty Acid Binding Protein 2 (FAPB-2),
tryptophan, and some of its metabolites via
serotonin and
kynurenine. ME/CFS patients were heterogeneous for genetic background, trigger, start mode, symptoms, and evolution. ME/CFS patients had higher levels of
IL-17A (p = 0.018), FABP-2 (p = 0.002), and
3-hydroxykynurenine (p = 0.037) and lower levels of
kynurenine (p = 0.012) and
serotonin (p = 0.045) than controls. Changes in
kynurenine and
3-hydroxykynurenine were associated with increased
kynurenic acid/
kynurenine and 3-hydroxykynurenine/
kynurenine ratios, indirect measures of
kynurenine aminotransferases and
kynurenine 3-monooxygenase enzymatic activities, respectively. No correlation was found among
cytokines, FABP-2, and
tryptophan metabolites, suggesting that
inflammation, anomalies of the intestinal barrier, and changes of
tryptophan metabolism may be independently associated with the pathogenesis of the disease. Interestingly, patients with the start of the disease after
infection showed lower levels of
kynurenine (p = 0.034) than those not starting after an
infection. Changes in
tryptophan metabolites and increased
IL-17A levels in ME/CFS could both be compatible with anomalies in the sphere of energy metabolism. Overall, clinical traits together with serum
biomarkers related to
inflammation, intestine function, and
tryptophan metabolism deserve to be further considered for the development of
personalized medicine strategies for ME/CFS.