Induction of Therapeutic Abortion in Early Pregnancy With Mifepristone in Combination With Prostaglandin Pessary

Rodger, Mary W.; Dt, Baird

doi:10.1016/s0140-6736(87)91126-3

Cited by 107 publications

(29 citation statements)

References 19 publications

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“…19 This is supported by recent reports of improved success rates with the use of antiprogesterones in combination with various prosta-glandins. 20,21 The administration-to-expulsion time for sulprostone in the present study compares favorably with those reported elsewhere. 10,16,18 Complete expulsion in ouopr patients occurred in 39% of the patients given sulprostone compared with 70 to 80% cited in the literature.…”

Section: Discussionsupporting

confidence: 88%

Management of Intrauterine Fetal Death After 12 Weeks of Gestation: Comparison of Two Prostaglandins

Kidess

Ba’aqeel

1990

Ann Saudi Med

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The efficacy of the uteroselective prostaglandin analogue 16-phenoxy-w-tetranor PGE 2 methylsulfonylamide (sulprostone) given intramuscularly was studied in 18 patients who had had intrauterine fetal death after 12 weeks of gestation and the results compared with those of the widely used 15-methyl PGE 2 analogue (dinoprostone) which was given as vaginal tablets to 17 patients. Expulsion of the uterine contents in the sulprostone group was successful in 100% of the cases at all stages of gestation but was achieved in only 29% of the dinoprostone group (P < 0.001), mostly in those who were beyond their 28th week of gestation. The mean time that elapsed between induction and expulsion was 10.7 hours for sulprostone and 37.9 hours for dinoprostone (P < 0.001). Complete expulsion occurred in 39% of the patients given sulprostone and in 80% of the patients given dinoprostone (P = 0.3). In addition to its demonstrated efficacy, sulprostone does not require vaginal manipulations, which is desirable in a culture where patients are reluctant to submit to vaginal procedures. The management of fetal death during the first trimester of pregnancy is safely and effectively dealt with by means of surgical evacuation of the uterus (dilatation and curettage). However, fetal death in the second or early third trimesters poses a difficult management problem, with surgical treatment hazardous. Until recently, treatment consisted of waiting for the spontaneous onset of uterine contractions and expulsion, which was observed to occur in 90% of cases by three weeks after intrauterine death.1 Drawbacks to this approach include increased risk of coagulopathies, 2 infection, 1 and the psychological impact on the mother of carrying a dead fetus for a prolonged period.3 This conservative approach was dictated by the lack of effective and safe methods of evacuating the uterus sooner.The management of intrauterine fetal death has changed dramatically with the advent of prostaglandins. Improved efficacy and reduced side effects from prostaglandins were achieved through the development of newer analogues. [4][5][6][7][8][9][10][11][12][13][14][15][16][17] The aim of this study was to compare the efficacy of the analogue 16-phenoxy-w-tetranor PGE 2 methylsulfonylamide (sulprostone) administered intramuscularly and the widely used 15-methyl PGE 2 analogue (dinoprostone) administered as vaginal tablets in cases of intrauterine fetal death occurring after 12 weeks of

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Section: Discussionsupporting

confidence: 88%

Management of Intrauterine Fetal Death After 12 Weeks of Gestation: Comparison of Two Prostaglandins

Kidess

Ba’aqeel

1990

Ann Saudi Med

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“…GC inhibit macrophage functions, including cytotoxic functions, processing, and presentation of antigen to T cells, inhibit the production of IL-2 and IFN-3, in T lymphocytes (3), shift T cell responses from the Thl to the Th2 type (4), decrease the activity of NK cells, induce programmed cell death in a variety of different immunologically relevant cells, including immature T and B cell precursors (for reviews see references 5, 6) and mature T cells (7), and inhibit the synthesis of a variety of proimflammatory cytokines (IL-1, IL-6, and TNF-o 0 (8). Immune activation frequently is associated with an in- crease in ACTH and GC secretion, and the susceptibility of certain animal strains to develop autoimmune diseases is linked to a deficient GC-mediated inhibition of immune function (2, 9-12).Recently, a synthetic steroid, KU-38486 (RU486, mifepristone), with potent antiprogestational and antiglucocorticoid activity has become available for clinical use as an abortifacient agent (13,14) and for treatment of gestagen-dependent tumors and hypercortisolism (15). In the present study, we investigated the effect of RU-38486 on T cell activation in vivo.…”

mentioning

confidence: 99%

“…Recently, a synthetic steroid, KU-38486 (RU486, mifepristone), with potent antiprogestational and antiglucocorticoid activity has become available for clinical use as an abortifacient agent (13,14) and for treatment of gestagen-dependent tumors and hypercortisolism (15). In the present study, we investigated the effect of RU-38486 on T cell activation in vivo.…”

mentioning

confidence: 99%

Glucocorticoid-mediated control of the activation and clonal deletion of peripheral T cells in vivo.

Gonzalo

González–García

Martı́nez

et al. 1993

The Journal of Experimental Medicine

162

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SummaryPoly-and oligodonal T cell stimuli like anti-CD3e monoclonal antibody or Staphylococcus aureus enterotoxin B (SEB), injected at doses that per se are not lethal, provoke acute death within less than 24 h, provided that endogenous glucocorticoids (GC) are depleted by adrenalectomy or by injection of saturating amounts of the GC receptor antagonist RU-38486 (mifepristone). Pharmacological doses of the GC agonist dexamethasone (DEX) alter the in vivo response of splenic V38 + T cells to SEB, thus impeding the expansion of such cells and causing their rapid (3 d) clonal deletion. In contrast, coadministration of RU-38486 counteracts a SEB-induced early (12 h) reduction of V38+CD4 + and V38+CD8 + spleen cells. In vivo T cell stimulation by injection of bacterial superantigen induces a rapid (peak at 90-120 rain) increase in corticosterone serum levels, suggesting that endogenous GC might control early T cell activation. Accordingly, kinetic studies revealed that RU-38486 has to be administered within 2 h after superantigen administration to exert its lethal effect. Similarly, exogenous GC must be injected during this critical phase (2 h) to rescue animals from acute death induced by coinjection of SEB and D-galactosamine (GAIN). Adrenalectomy, injection of RU-38486 and priming with GaIN per se provoke the programmed death of peripheral CD4 + and CD8 + T cells. Thus, three manipulations that sensitize mice for the lethal effect of T cell stimulation also exert a proapoptotic effect on peripheral T cells. In synthesis, endogenous and exogenous GC regulate T cell responses and determine the propensity of peripheral T cells to undergo apoptosis. SYnthetic glucocorticoid (GC) 1 agonists are used for therapy of a broad spectrum of organ-specific and generalized autoimmune diseases. In the same way, endogenous GC secreted by the adrenal glands may act as immunosuppressive and antiinflammatory agents that contend lifethreatening overreactions of the immune system, as well as autoaggressive responses (for reviews see references 1, 2). GC inhibit macrophage functions, including cytotoxic functions, processing, and presentation of antigen to T cells, inhibit the production of IL-2 and IFN-3, in T lymphocytes (3), shift T cell responses from the Thl to the Th2 type (4), decrease the activity of NK cells, induce programmed cell death in a variety of different immunologically relevant cells, including immature T and B cell precursors (for reviews see references 5, 6) and mature T cells (7), and inhibit the synthesis of a variety of proimflammatory cytokines (IL-1, IL-6, and TNF-o 0 (8). Immune activation frequently is associated with an in- crease in ACTH and GC secretion, and the susceptibility of certain animal strains to develop autoimmune diseases is linked to a deficient GC-mediated inhibition of immune function (2, 9-12).Recently, a synthetic steroid, KU-38486 (RU486, mifepristone), with potent antiprogestational and antiglucocorticoid activity has become available for clinical use as an abortifacient agent (13,14) an...

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“…Surgical abortion is one of the most frequently performed operations in the world, and ap proximately 2% of all women in the reproductive age have induced abortions each year [1], Medical termina tion of pregnancy (medical abortion) as an alternative to surgical abortion has many advantages since it does not require anesthetics and there is no risk of cervical lacera tion or uterine perforation. Mifepristone (RU 486), a potent antiprogestin, is the first practical medical abortifacient [2], but when administered alone, termination of pregnancy is incomplete in 20% or more [3], The efficacy of prostaglandins to complement the effect of mifepris tone is well established [4,5], Mifepristone is approved in France, the UK but not in Turkey. Fortunately, metho trexate and intravaginally administered misoprostol, which is available in our country have been shown to be effective for early abortion with minimal side effects [6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Efficacy of Methotrexate and Misoprostol for Early Abortion

Özeren¹,

Çorakçi²,

Yücesoy³

et al. 1997

Gynecol Obstet Invest

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Background: Medical termination of pregnancy (medical abortion) as an alternative to surgical abortion has many advantages since it does not require anesthetics and there is no risk of cervical laceration or uterine perforation. In the present study, we evaluated the efficacy of methotrexate and intravaginally administered misoprostol for early abortion. Methods: The study population consisted of 32 women seeking abortion of a normal intrauterine pregnancy of 8 weeks or less documented by ultrasound. The dose of methotrexate was 50 mg/m² intramuscularly and the dose of misoprostol was 800 µg intravaginally. The final outcome of treatment was evaluated on day 14 or 16, and an abortion was considered successful if pregnancy was terminated without a surgical procedure. Results: Abortion occurred in only 23 (71.8%) of 32 women. There were 9 failures (28.1%); 3 were ongoing pregnancies (9.3%) and 6 were incomplete abortions (18.7%) requiring suction curettage. After the exclusion of treatment failures, the mean duration of vaginal bleeding was 16.3 ± 2 days. No serious side effects occurred as a result of methotrexate and misoprostol treatment. Conclusion: The use of methotrexate and intravaginal misoprostol for the termination of pregnancy requires larger studies to determine the safety and efficacy of this medical abortion, a comparison with RU 486 in prospective controlled randomized trials is necessary.

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Induction of Therapeutic Abortion in Early Pregnancy With Mifepristone in Combination With Prostaglandin Pessary

Cited by 107 publications

References 19 publications

Management of Intrauterine Fetal Death After 12 Weeks of Gestation: Comparison of Two Prostaglandins

Management of Intrauterine Fetal Death After 12 Weeks of Gestation: Comparison of Two Prostaglandins

Glucocorticoid-mediated control of the activation and clonal deletion of peripheral T cells in vivo.

Efficacy of Methotrexate and Misoprostol for Early Abortion

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