The main purpuse of our study was to determine the levels of both cortisol and
dehydroepiandrosterone (DHEA) in serum samples from patients suffering from Plamodium
falciparum malaria. Since cortisol is potentially immunesupressive, and, conversely, DHEA is
inherently immunopotentiating, we sought to assess the possible association between serum
levels of these steroids and patient's clinical conditions. We enrolled to participate in this study
24 patients aged 12 to 47 years, of whom 18 were male and 6 female, suffering from
uncomplicated P. falciparum malaria. All patients lived in areas of the Amazon were malaria is
endemic. Half of them were found to be primo-infected, whereas the others were being reinfected
by P. falciparum when recruited for this investigation. Blood samples were obtained from each
patients as follows: at 20-minutes intervals during the pre-treatment phase (i. e. on day 0, D0), 24
hours after starting drug therapy (D1) and at the 8th day of follow-up (D7), when patients were
asymptomatic. All patients at D7 presented with negative parasitemia. Serum levels of cortisol
and DHEA were measured on D0, Dl and D7 and D0 and D7, respectively. In addition, the
determination of IgG antibodies to both P. falciparum and P. vivax was performed only on D0.
Our results indicated that levels of cortisol in serum samples collected on D0 were significantly
higher than those of D1 and D7. High levels of cortisol on D0/D1 and significant parasitemia on
D1 led us to postulated that this corticosteroid may interfere with the initial response of P.
falciparum-infected patients to treatment. The cortisol levels did not correlate with the intensity
of fever, duration of illness and the levels of IgG antibories to P. falciparum. These findings
suggest that temperature does not interfere with the cortisol levels, and these, on the other land,
do not significantly ralate to either antibody response or the duration of illness. The DHEA
levels were found to be significantly more elevated on D0 than on D7, even though patients were
already symptomatic for more than one day when first serum samples was taken. The
progressive decrease in the DHEA levels is therefore likely to be mediated by a continuous
stimulus from the hypothalamic-pituitary-adrenal (HPA) axis. Similarly to cortisol, the DHEA
levels on D0 correlated significantly with D1 parasitemia. Thus, it is suggested that in cortisol
levels paralels that for DHEA. Of interest, the DHEA serum levels seem to inversely correlate
with the duration of illness, in spite of high levels of this steroid detected at the pre-treatment
phase. A not significant correlation has been noted if cortisol and DHEA serum levels are
compared with temperature. This clinical parameter, however, was found to directly interfere
with the correlation that exist between both cortisol and DHEA levels. It is known that fever
reflects the occasion when erythrocytes disrupt from the schizogony, with release of cytokines ,
which act as an acute stimulating factor for the HPA axis. It would therefore be proposed that
liberation of both hormones has a commom mechanism. The lack of significant interrelationships
between DHEA levels and IgG antibodies indicates that this hormone does not seem to interfere
with the production of antibodies by P. falciparum infected patients.
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