RESUMO
Una de las manifestaciones del síndrome de ovario poliquístico (SOP) es la infertilidad, y hoy es la primera causa de infertilidad por anovulación, representando aproximadamente el 80% de los casos. Las alteraciones del SOP en su mayoría son tratables y el diagnóstico temprano de las pacientes mejora su pronóstico reproductivo. Pese a su alta incidencia e importancia, los mecanismos fisiopatológicos del SOP aún son relativamente desconocidos. Recientemente se han publicado recomendaciones internacionales basadas en evidencia para su tratamiento.
Infertility is one of the main manifestations of the polycystic ovary syndrome (PCOS), and to day PCOS is the main cause of anovulatory infertility accounting for 80% of the cases. The majority of PCOS causes of infertility are treatable, and early diagnosis improves the patient's fertility outcome. In spite of its incidence and importance, the physiopathological mechanisms of PCOS are still relatively unknown. Recently an international evidence base recommendation for treatment have been published.
Assuntos
Humanos , Feminino , Síndrome do Ovário Policístico/complicações , Infertilidade Feminina/etiologia , Indução da Ovulação , Síndrome do Ovário Policístico/diagnóstico , Síndrome do Ovário Policístico/fisiopatologia , Hiperandrogenismo , Infertilidade Feminina/terapia , AnovulaçãoRESUMO
Today health professionals are not only required to know medicine, but scientific reading, interpretation, and communication of new data. The new information about contraception and hormonal therapies must be analyzed by gynecologists to determine whether or not the new data are applicable to their patients and if it has an impact on their health. Recently a new study of hormonal contraceptives and the risk of breast cancer was published. In this study, the investigators found an elevation of the relative risk of breast cancers on the users versus the nonusers of hormonal contraception. After analyzing the publication and other data available, it is our opinion that it is a very low increase of the risk and its impact should be evaluated case by case, not forgetting to take into account the numerous beneficial effects that hormonal contraception have.
Assuntos
Neoplasias da Mama/epidemiologia , Neoplasias da Mama/etiologia , Anticoncepcionais Orais Hormonais/efeitos adversos , Feminino , Humanos , Incidência , RiscoRESUMO
Many pharmacological agents have been investigated to manage preterm labor; we postulate that a combination of tocolytic drugs may achieve a better effect in the prevention of uterine contractions without dose-dependent adverse effects. The aim of this study was to evaluate the inhibitory effect of dual combinations of tocolytics in vitro. Human myometrium was obtained during elective cesarean sections (term without labor; n = 40). Myometrial strips were placed in organ baths for the measurement of isometric tension. Contractile activity was induced by oxytocin (10-8 mol/L), then a concentration-response curve to single or dual combinations of tocolytics was started. All studied tocolytics (nifedipine, ritodrine, nitroglycerin, atosiban, and NS-1619), when used alone, significantly inhibited myometrial contractions. When combined, nifedipine plus ritodrine produced a significantly greater inhibition of contractility than each drug alone in the midrange of concentrations. The combination of nifedipine plus nitroglycerin or nifedipine plus atosiban produced a significantly greater inhibition than nitroglycerin or atosiban alone but not greater than nifedipine. The combination of nifedipine plus NS-1619 (Ca+2-activated K+ [BKCa] channel opener) reduced the inhibitory effect of each drug. We concluded that a selected combination of tocolytics (nifedipine plus ritodrine) produced a significantly greater inhibitory effect on contractility than each drug alone at intermediate concentrations. Thus, specific combinations of tocolytics with different intracellular signaling pathways may have a synergic effect constituting a provocative new option for preterm labor treatment.
Assuntos
Miométrio/efeitos dos fármacos , Nifedipino/farmacologia , Ritodrina/farmacologia , Tocolíticos/farmacologia , Contração Uterina/efeitos dos fármacos , Benzimidazóis/farmacologia , Sinergismo Farmacológico , Feminino , Humanos , Gravidez , Vasotocina/análogos & derivados , Vasotocina/farmacologiaRESUMO
Chlormadinone acetate (CMA) is a progesterone derivative (17α-acetoxy-6-chloro-4,6-pregnadiene-3,20-dione), first synthesized in 1961. It was used as progestin-based hormone replacement therapy; since 1999 it was first used for oral contraception combined with ethinyl estradiol (EE). CMA exerts a potent progestagenic effect, about one third higher than that observed with endogenous progesterone. CMA is also an anti-estrogen, showing no androgenic effects (at birth control dose). Unlike progesterone, it has a mild glucosteroidal effect with no anti-mineralocorticoid effect at all. These biological actions have allowed CMA to have a role for therapeutic use in dysmenorrhea, hyperandrogenism, and as a contraceptive agent. In addition, CMA has exhibited beneficial neuroendocrine effects on women's mood. CMA-EE combination has shown excellent contraceptive efficacy, high tolerability, and compliance due to its risk-benefit profile, having additional benefits on skin and hair, such as reduction of seborrhea and acne. Metabolic tolerance of CMA has been demonstrated in several clinical studies. Currently, CMA is formulated to be taken as oral caplets in a 21 caplets package containing 0.03 mg/EE and 2 mg CMA per pill with/without seven placebo additional pills. Another presentation has 24 caplets containing 0.02 mg/EE and 2 mg CMA plus four placebo pills.