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Chronic Fatigue Syndrome (CFS): identification of distinct subgroups on the basis of allergy & psychologic variables

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By Borish L, Schmaling K, DiClementi JD, Streib J, Negri J, Jones JF • www.ProHealth.com • August 2, 1998


BACKGROUND: We investigated a role for allergic inflammation
and psychologic parameters in the development of chronic
fatigue syndrome (CFS).

METHODS: The design was a comparison
between subjects with CFS and age- and sex-matched control
cohorts. Studies were performed on CFS subjects (n = 18) and
control cohorts consisting of normal subjects (n = 11),
allergic subjects (n = 14), and individuals with primary
depression (n = 12). We quantified cytokines at baseline as
cell- associated immunoreactive peptides and as transcripts
evaluated by means of semiquantitative RNA-based polymerase
chain reactions. Psychologic evaluations included
administration of the Diagnostic Interview Schedule, the
Structured Clinical Interview, and the Symptom Checklist
90-Revised.

RESULTS: Increases in tumor necrosis factor (TNF)-
alpha were identified in individual subjects with CFS (50.1
+/- 14.4 pg TNF-alpha per 10(7) peripheral blood mononuclear
cells [PBMCs]; mean +/- SEM) and allergic subjects (41.6 +/-
7.6) in comparison with normal subjects (13.1 +/- 8.8) (P <
.01 and P < .05, respectively). Similar trends were observed
for interferon (IFN)-alpha in allergic subjects (3.0 +/- 1.7
pg/10(7) PBMCs) and subjects with CFS (6.4 +/- 3.4) compared
with normal subjects (1.9 +/- 1.4). A significant increase (P
< .05) in TNF-alpha transcripts was demonstrated between
subjects with CFS and depressed subjects. In contrast to these
proinflammatory cytokines, both subjects with CFS (2.6 +/- 1.8
pg/10(7) PBMCs) and allergic subjects (3.4 +/- 2.8) were
associated with a statistically significant (P < .01) decrease
in IL-10 concentrations compared with normal subjects (60.2
+/- 18.2). As shown in other studies, most of our subjects
with CFS were allergic (15 of 18) and therefore presumably
demonstrated cytokine gene activation on that basis. The
seasonal exacerbation of allergy was associated with a further
increase in cellular IFN-alpha (from 2.1 +/- 1.2 to 14.2 +/-
4.5 pg/107 PBMCs; P < .05) but no further modulation of
TNF-alpha or IL-10. Similarly, self- reported exacerbations of
CFS were associated with a further increase in IFN-alpha (from
2.5 +/- 1.0 to 21.9 +/- 7.8; P < .05) and occurred at times of
seasonal exposures to allergens. This linkage does not permit
making any definitive conclusions regarding a causative
influence of either seasonal allergies or the increase in
cellular IFN- alpha with the increase in CFS symptoms. The
close association between atopy and CFS led us to speculate
that CFS may arise from an abnormal psychologic response to
the disordered expression of these proinflammatory and
antiinflammatory cytokines. Psychologic variables were
predictive of immune status within the CFS sample (65.9% of
the variance in immune status; F (3,10) = 6.44, P < .05).
Specifically, the absence of a personality disorder but
greater endorsement of global psychiatric symptoms was
predictive of immune activation.

CONCLUSIONS: Most of our
subjects with CFS were allergic, and the CFS and allergy
cohorts were similar in terms of their immune status. However,
the CFS subjects could be discriminated by the distinct
psychologic profiles among subjects with and without immune
activation. We propose that in at least a large subgroup of
subjects with CFS who had allergies, the concomitant
influences of immune activation brought on by allergic
inflammation in an individual with the appropriate psychologic
profile may interact to produce the symptoms of CFS. In a
psychologically predisposed individual, symptoms associated
with allergic inflammation are recognized as illness.




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