Hn. Ho et al., DECREASE IN INTERFERON-GAMMA PRODUCTION AND IMPAIRMENT OF T-LYMPHOCYTE PROLIFERATION IN PERITONEAL-FLUID OF WOMEN WITH ENDOMETRIOSIS, American journal of obstetrics and gynecology, 175(5), 1996, pp. 1236-1241
OBJECTIVE: Our purpose was to verify regional immune modulations and t
o test the effect of gonadotropin-releasing hormone agonist in women w
ith endometriosis. STUDY DESIGN: Concentrations of peritoneal cytokine
s, including interleukin-1 beta, interleukin-2, soluble interleukin-2
receptor, interleukin-6, granulocyte-monocyte colony-stimulating facto
r, interferon gamma, and tumor necrosis factor-alpha were compared in
women with and without endometriosis. Peritoneal cytokine and interleu
kin-2 production were examined by adding various mitogens to peritonea
l fluid mononuclear cells of women with advanced endometriosis before
and after gonadotropin-releasing hormone agonist treatment. RESULTS: A
significant increase in peritoneal interleukin-1 beta, interleukin-6,
and tumor necrosis factor-cc and a decrease in interferon gamma were
noted in women with endometriosis. After gonadotropin-releasing hormon
e agonist treatment interleukin-6 decreased and interferon gamma incre
ased. A significant impairment of interleukin-2 production of peritone
al fluid mononuclear cells by phytohemagglutinin and pokeweed mitogen
stimulation was demonstrated in endometriosis, and production could be
restored after gonadotropin-releasing hormone agonist treatment. CONC
LUSION: These results indicate that regional immunologic dysfunction m
ight be invoked in the disease process of endometriosis.