Laparoscopic management of pregnancy in a patient with uterus didelphys, obstructed hemivagina, and ipsilateral renal agenesis.

Pregnancy in a rudimentary uterine horn is a rare and potentially lethal condition. The highest risk of rupture is reported to be during the late first and second trimester. The risk of rupture correlates with the thickness of the myometrium surrounding the fetal pole. In 2005, a 20-year-old woman was incompletely diagnosed by imaging studies and laparoscopy to have an absent right kidney, a bicornate uterus with a right rudimentary uterine horn and a single cervix, a transverse vaginal septum with hematocolpos, and endometriosis caused by reflux menstruation. The transverse vaginal septum was excised, and the surgeon observed a single cervix. Oral contraceptives were prescribed as complementary treatment for the endometriosis and associated dysmenorrhea. In 2009, magnetic resonance imaging confirmed resolution of hematocolpos and revealed a right cervix connected to the right horn of a uterus didelphys and covered by a partial longitudinal vaginal septum. The patient had a contraception failure and presented in 2010 at 9(6/7) weeks' gestation. By ultrasonography and subsequent magnetic resonance imaging, the pregnancy was in the right uterus and the corpus luteum was on the left ovary. The myometrium was thinned to 2 to 3 mm atop the gestational sac. Using the Harmonic ACE, laparoscopic excision of the right fallopian tube and a supracervical right hysterectomy with an intact pregnancy was performed. This case supports the Acién hypothesis that the vagina forms from both Müllerian and Wolffian duct elements, and it illustrates the risk for uterine rupture when pregnancy forms in a rudimentary structure; presumed transperitoneal migration of an ovum that was captured by the opposite fallopian tube; and surgical management of the in situ pregnancy by laparoscopic supracervical excision of the rudimentary uterine body.

Elevated early follicular gonadotropin levels in women with unexplained infertility do not provide evidence for disordered gonadotropin-releasing hormone secretion as assessed by luteinizing hormone pulse characteristics.

OBJECTIVE: To determine whether women with rigorously defined unexplained infertility demonstrated altered GnRH secretion, as reflected by serum LH secretion patterns. DESIGN: Prospective observational study. SETTING: National Center for Infertility Research at Michigan. PATIENT(S): Nine women with rigorously defined unexplained infertility and 11 healthy, parous age-matched control women.Gonadotropin-releasing hormone (25 ng/kg) as a bolus injection. MAIN OUTCOME MEASURE(S): Daytime pulse patterns of LH secretion measured every 10 minutes; mean serum concentrations of LH, FSH, E(2), P, PRL, and cortisol; and response to a physiologic dose of GnRH in the early follicular, late follicular, mid-luteal, and late luteal phases of the same menstrual cycle. RESULT(S): Serum LH pulse frequency and pulse amplitude and LH secretion in response to a physiologic bolus of GnRH were not significantly different in unexplained infertility patients at any phase of the cycle. Luteinizing hormone pulse frequency and amplitude, as well as response to GnRH, varied significantly across the cycle. Mean early follicular serum LH and FSH concentrations were significantly higher in unexplained infertility patients than in fertile control subjects (LH: 5.31 +/-.51 vs. 4.03 +/-.33 [mIU/mL +/- SEM]; FSH: 5.81 +/-.63 vs. 3.80 +/-.45) but were not different at any other phase of the cycle. CONCLUSION(S): These data do not support the hypothesis that unexplained infertility is caused by an abnormality in pulsatile GnRH secretion or abnormal pituitary sensitivity to GnRH. However, the results are consistent with a difference in negative feedback from the ovary to the pituitary in unexplained infertility patients that is suggestive of diminished ovarian reserve.

Estrogen raises the sweating threshold in postmenopausal women with hot flashes.

OBJECTIVE: To determine if estrogen ameliorates hot flashes by raising the core body temperature sweating threshold, by reducing core body temperature fluctuations, and/or by reducing sympathetic activation (as measured by plasma 3-methoxy-4-hydroxyphenylglycol). DESIGN: Laboratory physiological study. SETTING: University medical center. PATIENT(S): Twenty-four healthy postmenopausal women reporting frequent hot flashes. INTERVENTION(S): Participants were randomly assigned, in double-blind fashion, to receive 1 mg/d 17beta-estradiol orally or placebo for 90 days. MAIN OUTCOME MEASURE(S): Core body temperature, core body temperature fluctuations, mean skin temperature, sternal sweat rate, laboratory hot flash counts (sternal skin conductance), plasma 3-methoxy-4-hydroxyphenylglycol. RESULT(S): The E(2) group had significant increases in plasma E(2) (8 +/- 2 vs. 132 +/- 22 pg/mL) and core body temperature sweating threshold (37.98 +/- 0.09 vs. 38.14 +/- 0.09 degrees C) and decreases in plasma FSH (58.8 +/- 8.9 vs. 40.1 +/- 7.6 mIU/mL) and hot flashes (1.4 +/- 0.5 vs. 0.6 +/- 0.6). These changes did not occur in the placebo group. There were no significant changes in any other measure. CONCLUSION(S): E(2) ameliorates hot flashes by raising the core body temperature sweating threshold, but does not affect core temperature fluctuations or plasma 3-methoxy-4-hydroxyphenylglycol.