Arthritis and rheumatism · 1992
Premature death with bladder outlet obstruction and hyperprolactinemia in New Zealand black X New Zealand white mice treated with ethinyl estradiol and 17 beta-estradiol.
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Walker S E, McMurray R W, Besch-Williford C L, Keisler D H
Аннотация
OBJECTIVE: To determine causes of death, estrogen toxicity, and hyperprolactinemia in a murine model of systemic lupus erythematosus (SLE).
METHODS: Female New Zealand Black x New Zealand White (NZB x NZW) mice were implanted with ethinyl estradiol, 17 beta-estradiol, or empty capsules (controls).
RESULTS: Estrogen-treated mice developed striking hyperprolactinemia and died prematurely with genitourinary complications.
CONCLUSION: Implanted estrogens, including 17 beta-estradiol in a dose reported previously to stimulate SLE, contribute to premature death in NZB x NZW mice, through toxic effects. Estrogen therapy increases the level of prolactin, an immunostimulatory hormone.
METHODS: Female New Zealand Black x New Zealand White (NZB x NZW) mice were implanted with ethinyl estradiol, 17 beta-estradiol, or empty capsules (controls).
RESULTS: Estrogen-treated mice developed striking hyperprolactinemia and died prematurely with genitourinary complications.
CONCLUSION: Implanted estrogens, including 17 beta-estradiol in a dose reported previously to stimulate SLE, contribute to premature death in NZB x NZW mice, through toxic effects. Estrogen therapy increases the level of prolactin, an immunostimulatory hormone.