Vaginal (Crinone 8%) gel vs. intramuscular progesterone in oil for luteal phase support in in vitro fertilization: a large prospective trial.

OBJECTIVE: To compare the efficacy of intravaginal and IMP for luteal phase support in IVF cycles. DESIGN: Prospective trial. SETTING: Tertiary care private practice. PATIENT(S): Women 25-44 years old with infertility necessitating treatment with IVF. From April 1, 2008-April 1, 2009, 511 consecutive patients were enrolled; 474 completed participation, and 37 were excluded for no autologous ET (freeze all, donor recipients, failed fertilization/cleavage). There were no demographic differences between the two treatment groups. INTERVENTION(S): Luteal phase support using either Crinone or P in oil starting 2 days following oocyte retrieval. MAIN OUTCOME MEASURE(S): Pregnancy and delivery rates stratified by patient age. RESULT(S): Overall, patients who received vaginal P had higher pregnancy (70.9% vs. 64.2%) and delivery (51.7% vs. 45.4%) rates than did patients who received IMP. Patients <35 who received vaginal P had significantly higher delivery rates (65.7% vs. 51.1%) than did patients who received IMP. There were no differences, regardless of age, in the rates of biochemical pregnancy, miscarriage, or ectopics. CONCLUSION(S): In younger patients undergoing IVF, support of the luteal phase with Crinone produces significantly higher pregnancy rates than does IMP. Crinone and IMP appear to be equally efficacious in the older patient.

Estrogen replacement enhances EDHF-mediated vasodilation of mesenteric and uterine resistance arteries: role of endothelial cell Ca2+.

Endothelium-derived hyperpolarizing factor (EDHF) plays an important role in the regulation of vascular microcirculatory tone. This study explores the role of estrogen in controlling EDHF-mediated vasodilation of uterine resistance arteries of the rat and also analyzes the contribution of endothelial cell (EC) Ca(2+) signaling to this process. A parallel study was also performed with mesenteric arteries to provide comparison with a nonreproductive vasculature. Mature female rats underwent ovariectomy, with one half receiving 17beta-estradiol replacement (OVX+E) and the other half serving as estrogen-deficient controls (OVX). Uterine or mesenteric resistance arteries were harvested, cannulated, and pressurized. Nitric oxide and prostacyclin production were inhibited with 200 microM N(G)-nitro-l-arginine and 10 microM indomethacin, respectively. ACh effectively dilated the arteries preconstricted with phenylephrine but failed to induce dilation of vessels preconstricted with high-K(+) solution. ACh EC(50) values were decreased by estrogen replacement by five- and twofold in uterine and mesenteric arteries, respectively. As evidenced by fura-2-based measurements of EC cytoplasmic Ca(2+) concentration ([Ca(2+)](i)), estrogen replacement was associated with increased basal and ACh-stimulated EC [Ca(2+)](i) rise in uterine, but not mesenteric, vessels. These data demonstrate that EDHF contributes to endothelium-dependent vasodilation of uterine and mesenteric resistance arteries and that estrogen controls EDHF-related mechanism(s) more efficiently in reproductive vs. nonreproductive vessels. Enhanced endothelial Ca(2+) signaling may be an important underlying mechanism in estrogenic modulation of EDHF-mediated vasodilation in small resistance uterine arteries.

Insulin resistance with hormone replacement therapy: associations with markers of inflammation and adiposity.

OBJECTIVE: This study was undertaken to determine whether insulin resistance associated with combination hormone replacement therapy (HRT) is mediated by changes in serum markers of inflammation or in serum adipocyte hormones. STUDY DESIGN: Forty-five postmenopausal women, aged 55 +/- 7 years, were examined from a randomized, double-blind placebo-controlled trial evaluating the effect of HRT on insulin-stimulated glucose disposal and body composition. Volunteers were randomly assigned to conjugated estrogens 0.625 mg plus medroxyprogesterone acetate 2.5 mg vs placebo for 1 year. At baseline and at 1 year, body composition was assessed by dual photon x-ray absorptiometry scans; body fat distribution was measured by computed tomographic scans at the L4/L5 vertebral disk space; insulin sensitivity was measured by euglycemic hyperinsulinemic clamp; interleukin-6 (IL-6), leptin, and adiponectin were measured by enzyme-linked immunosorbent assay; and c-reactive protein (CRP) was measured by radioimmunoassay. RESULTS: HRT increased CRP by 121% compared with a 32% increase with placebo (P = .03); HRT decreased glucose disposal by 17% compared with no change with placebo (P = .04) as reported previously. HRT did not affect body composition, body fat distribution, IL-6, leptin, or adiponectin. The increase in CRP did not correlate with the decrease in glucose disposal in the HRT group (R = 0.11, P = .65). CONCLUSION: Treatment with HRT for one year increases CRP, but does not alter IL-6, adiponectin, or leptin. The change in CRP was not, however, related to the decrease in glucose disposal with HRT treatment.

Lithopedion: laparoscopic diagnosis and removal.

A lithopedion is an exceedingly rare obstetric phenomenon where the contents of an abdominal pregnancy calcify and become preserved. We present the case of a young woman undergoing laparoscopy for infertility during which a lithopedion was discovered.