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  • Title: Disseminated intravascular coagulation induced by progesterone in the pregnant rat. Prevention by estogens.
    Author: Stamler FW.
    Journal: Am J Pathol; 1977 Mar; 86(3):603-22. PubMed ID: 65916.
    Abstract:
    Fatal disseminated intravascular coagulation (DIC) was induced in female rats by administration of progesterone in late pregnacy. This prevented parturition, with intrauterine fetal death 2 to 4 days past term and subsequent retention of dead fetuses. Concomitantly with or closely following the intrauterine death of their litters, a large proportion of pregnant rats died with histologically evident DIC. Administration of cortisone, heparin, or disoumarin did not prevent DIC, and xi-aminocaproic acid, acetylsalicylic acid, or an onion-rich diet tended to increase its incidence. Antibiotic regimens gave variable results, with significant decrease in DIC only with a combination of two wide-spectrum penicillins. Neomycin and polymyxin had little effect on susceptible Sprague-dawley derived rats, but polymxin caused a significant increase in DIC in a resistant strain of hooded rats. Fatal maternal DIC was completely prevented only by use of natural or synthetic estrogens concurrently with progesterone, although this did not alter the sequence of abnormally prolonged pregnacy with intrauterine fetal death and retention of dead fetuses. Potencies of estrogens varied greatly, but all compounds tested prevented DIC at adequate dosage levels. Diethylstilbestrol, the most potent drug tested, was completely protective at 1 mug daily given subcutaneously. beta-Estradiol was the most effective natural estrogen, giving complete protection with a 10-mug daily subcutaneous injection. Estrogens were much more potent by subcutaneous injection than by oral ingestion, and toxic side effects were sometimes noted with higher levels of the latter. For estrogen therapy to be effective, it was necessary to begin its use before the expected onset of DIC, and in no instance was there evidence of reversal of this process after signs of illness were observed. Fatal disseminated intravascular coagulation (DIC) was induced in female rats by administration of progesterone in late pregnancy. This prevented parturition, with intrauterine fetal death 2-4 days past term and subsequent retention of dead fetuses. Concomitantly with, or closely following the intrauterine death of their litters, a large proportion of pregnant rats died with histologically evident DIC. Administration of cortisone, heparin, or dicoumarin did nothing to prevent DIC, and epsilon-aminocaproic acid, acetylsalicylic acid,or an onion-rich diet tended to increase its incidence. Antibiotic regimens gave variable results, with significant decrease in DIC only with a combination of 2 wide-spectrum penicillins. Neomycin and polymyxin had little effect on susceptible Sprague-Dawley derived rats, but polymyxin caused a significant increase in DIC in a resistant strain of hooded rats. Fatal maternal DIC was completely prevented only by use of natural or synthetic estrogens concurrently with progesterone, although the sequence of abnormally prolonged pregnancy with intrauterine fetal death and retention of dead fetuses remained. Potencies of estrogens varied greatly, but all compounds tested prevented DIC at adequate dosage levels. Diethylstilbestrol, the most potent drug tested, was completely protective at 1 mcg daily given sc. Bate-estradiol was the most effective natural estrogen, giving complete protention with a 10 mcg daily sc injection. Estrogens were much more potent by sc injection than by oral ingestion, and toxic side effects were sometimes noted with higher levels of the latter. For estrogen therapy to be effective, it was necessary to begin its use before the expected onset of DIC. Reversal of this process once DIC has started is beyond the powers of this therapy.
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