黄体酮治疗先兆性流产的临床疗效观察

目的 探讨黄体酮治疗因黄体功能不全而引起的先兆性流产的临床疗效.方法 选取2010-2012年在我院门诊治疗的符合条件的先兆性流产患者128例,采用肌肉注射黄体酮注射液治疗,观察临床治疗效果.结果 肌肉注射黄体酮注射液治疗因黄体功能不全而引起的先兆性流产的有效率为91.4%,不良反应比较轻,并且发生率较低.结论 黄体酮治疗因黄体功能不全而引起的先兆性流产的疗效确切、安全、可靠,可在临床上推广使用.     

孕激素治疗月经期癫痫的临床证据评价

目的 采用循证医学方法评价孕激素治疗月经期癫痫的疗效和药物不良反应,为月经期癫痫提供有循证依据的最佳治疗方案。方法 以月经期癫痫痫（catamenial epilepsy）、药物治疗（drugtherapy）、孕激素（progesterone）、四氢孕酮（allopregnanolone）、系统评价（systematic review）、随机对照试验（randomized controlled trials）等中英文词汇为检索词,分别检索万方数据库、维普期刊资源整合服务平台、中国知网中国知识基础设施工程、英国Cochrane图书馆、美国国立医学图书馆、Google学术搜索等国内外数据库,获得系统评价、随机对照试验、开放性试验、前瞻性或回顾性病例分析研究、病例观察研究和综述等文献,采用Jadad量表质量标准评价文献质量。结果 经筛选共纳入孕激素治疗月经期癫痫相关英文文献18篇,包括系统评价1篇、随机对照试验3篇、开放性试验1篇、前瞻性病例研究2篇、病例随访研究1篇、综述10篇。其中10篇为高质量文献（评分≥4分）,8篇为低质量文献（评分〈4分）。对各项临床试验治疗原则以及疗效和安全性评价显示：（1）孕激素作为抗癫痫药物的添加方案治疗月经期癫痫,可显著减少月经期癫痫发作频率,且安全性和耐受性良好。（2）天然孕激素和人工合成孕激素均可用于月经期癫痫的治疗。（3）孕激素治疗月经期癫痫的方式包括周期性孕激素治疗和抑制治疗,以前者更常用。结论 借助循证医学评价方法可为孕激素治疗月经期癫痫提供最佳临床证据。     

Best Practices for Counseling Adolescents about the Etonogestrel Implant

Among young persons, ease of use, high efficacy, and high acceptability makes the etonogestrel contraceptive implant an important choice for this age group. Adolescent-friendly, patient-centered counseling considers the patient's cognitive development, the influence of friends and family, as well as their own preferences and values. Age-appropriate language, graphics, and models are useful to explain contraceptive options and relevant side effects. Effectiveness, reversibility, safety, noncontraceptive benefits, and side effects are important attributes and should be discussed when teens are choosing a contraceptive method. In this review we describe suggested best practices for counseling adolescents about the etonogestrel implant so they can make informed, prudent decisions about using this contraceptive method.     

Progestins in HRT: Sufferance or desire?

While the benefits of progestins in hormonal replacement therapy are well recognized as far as endometrial protection is concerned the data on breast tissue and the cardiovascular system are contentious. Following the Women's Health Initiative study, the Million Women Study and The Women's International Study of Long-duration (O)estrogen after Menopause the question can be raised: When dealing with optimal hormonal therapy after the menopause, is the progestin component accepted here on sufferance or is it desired? The answer is partly made up by the fact that the recent epidemiological data may have been not only wrongly translated in relation to the clinical settings, but also to the whole class of therapies. The various progestins available for hormonal therapy exert different partial effects at cellular level according to the biochemical composition. Due to the structural differences the progestins result in a variety of tissue transforming changes as well as metabolic and hemostatic changes. Since no single test or algorithm presently serves as golden standard for all desired hormonal effects the least changes or no changes from the premenopausal physiology may often be advantageous. In our opinion targeting this goal includes a sustained desire for an estrogen/progestin combination as optimal future hormone therapy. Moreover the strategy not only includes evaluation of the specific steroidal formula, but also a titration of the dose and choosing the optimal route of administration. With special reference to cardiovascular disease this review therefore makes a plea for differentiating between the array of chemically and functionally distinct progestins used therapeutically after the menopause in combination therapy.     

L-norgestrel and progesterone have different influences on plasma lipoproteins

Twenty-six postmenopausal women who had been on cutaneous oestradiol treatment for 3-6 months were given either 120 micrograms of 1-norgestrel (n = 13) or 300 mg of progesterone (n = 13) sequentially for another 6 months. The concentrations of cholesterol, phospholipids and triglycerides were determined in plasma and in the HDL, HDL2, HDL3, LDL and VLDL fractions before and after one, three and six cycles of progestin treatment. Already after 11 days on 1-norgestrel, the mean HDL cholesterol and the mean HDL phospholipid concentrations were reduced by 15%. The reduction of the HDL-lipids was mainly confined to the HDL2 fraction which was decreased by 25-30%. L-norgestrel also reduced the mean TG concentration both in the VLDL and the combined LDL + HDL fractions. Progesterone gave only minor changes of the plasma lipids and lipoproteins. Reduced HDL, especially HDL2, concentration, as induced by 1-norgestrel, might increase the risk for ischaemic heart disease. Therefore, it seems that, as regards the effects on the lipoproteins, progesterone might be more suitable than the 19-nortestosterone derivative 1-norgestrel for postmenopausal sequential hormonal therapy.     

Hormonal approaches to male contraception: approaching reality

The ‘pre-testicular’ suppression of gonadotrophins is the most likely approach for reversible therapeutic male fertility control to reach imminent clinical application. Maintenance of spermatogenesis depends on adequate gonadotrophin and intratesticular testosterone concentrations. Hormonal contraception for men interrupts this physiological axis by various means of gonadotrophin suppression; this interferes with spermatogonial differentiation and meiosis entry resulting in reversible azoospermia or severe oligozoospermia in virtually all men. Clinical trials have confirmed that high contraceptive efficacy, similar to female hormonal contraceptives, can be reliably attained with few side effects. However, the simultaneous suppression of Leydig cell steroidogenesis mandates the requirement for testosterone replacement in hormonal male contraception. Combination regimens of new synthetic progestins and androgens at various stages of development are being investigated with the lead products poised to go into phase III trials. Heterogeneity in response to spermatogenesis suppression has been observed within and between population; the mechanisms are unclear. This new method of reversible and effective contraception has registered high acceptability in surveys of both men and women. The recent entry of pharmaceutical companies into this area of research and development has considerably enhanced the prospects of translating years of academic efforts into new products which provide added family planning choice for many couples.     

Relative in vitro seasonal effects of vasotocin and isotocin on ovarian steroid hormone levels in the catfish Heteropneustes fossilis

In the present investigation, catfish (Heteropneustes fossilis) ovarian tissues were incubated in vitro with vasotocin (VT) or isotocin (IT) to demonstrate their effects on estradiol-17β (E₂), progesterone (P₄), 17α-hydroxy-4-pregnene-3, 20-dione (17-P) and 17α, 20β-hydroxy-4-pregnen-3-one (17, 20β-DP). Parallel incubations with human chorionic gonadotropin (hCG) alone or in combination with VT were used for a comparison. In pre-vitellogenic phase (preparatory phase, GSI—0.48 ± 0.03%), both VT and hCG stimulated E₂ significantly, VT in a biphasic manner and hCG in a dose-dependent manner. In pre-spawning (post-vitellogenic, GSI—9.05 ± 0.11%) and spawning (post-vitellogenic, GSI—8.01 ± 0.12%) phases, both hormones decreased E₂ levels in a dose- and duration-dependent manner; the VT effect being biphasic in the spawning phase. The co-incubation with VT + hCG stimulated E₂ in the preparatory phase but inhibited it in the pre-spawning and spawning phases. The incubations with VT or hCG increased P₄ levels in a dose- and duration-dependent manner, the magnitude of the effect was higher in the pre-spawning and spawning phases. The co-incubation with VT + hCG stimulated P₄ without any additive effect. The P₄ derivatives (17-P and 17, 20β-DP) showed similar changes except 17-P in the spawning phase which decreased at 16 h of the incubation. The incubations with IT produced similar but low responses. In conclusion, like hCG, VT has differential effects on ovarian steroidogenesis and may be involved directly or indirectly in ovarian functions, as a paracrine/autocrine factor or a neurohormone.