The rise in allergic disorders over the past three decades has been suggest
ed to be related to the decrease in infectious diseases. Recently, a negati
ve association between tuberculin responses and atopic disorders has also b
een reported, We planned to investigate the effect of natural exposure to M
ycobacterium tuberculosis on atopic status in patients with active tubercul
osis and to compare the findings with the data of patients with inactive di
sease. A total of 97 subjects were divided into two groups. Group 1, patien
ts with proven active pulmonary tuberculosis (n = 66); group 2, subjects wh
o had a history of previous tuberculous disease, with negative bacteriologi
c studies and no clinical and/or roentgenographic evidence of current disea
se (n = 31). Current history of allergic diseases was recorded by a physici
an with the use of a questionnaire adapted from the European Community Resp
iratory Health Survey (ECRHS), and skin-prick rests (SPTs) were performed u
sing a standardized panel. Total IgE and Phadiatop were measured by the Pha
rmacia uniCAP system. The rate of one or more positive SPTs was significant
ly lower in the patients with active tuberculosis than the inactive group (
15% versus 48.4%, p < 0.001). The current history of atopic diseases was 7.
6% and 29% in the active and inactive tuberculosis groups, respectively (p
= 0.002), The rate of positive skin tests to inhalant allergens in patients
with inactive disease was higher than the rate of healthy adult Turkish pe
ople (48.4% versus 25%, p = 0.001). Geometric mean of total IgE levels were
lower in patients with inactive disease than patients with arrive pulmonar
y tuberculosis (74.97 kU/L versus 106.3 kU/L, p = 0.05). The ratios of Phad
iatop positivity were 21% and 38.7% in the active and inactive tuberculosis
groups, respectively (p = 0.008), We found lower atopy rates in patients w
ith active pulmonary tuberculosis than subjects with inactive disease. Alth
ough our data support the hypothesis that M. tuberculosis may prevent the d
evelopment of atopic disorders by inducing the production of cytokines anta
gonistic to Th2 development, we believe prospective and experimental studie
s ore needed before attributing a direct cause-effect link to this associat
ion.