Adjunctive leuprolide therapy does not improve cycle fecundity in controlled ovarian hyperstimulation and intrauterine insemination of subfertile women

Problems arising from controlled ovarian hyperstimulation for intrauterine insemination, such as premature luteinization and asynchronous ovarian follicular development, are identical to those encountered with controlled ovarian hyperstimulation for in vitro fertilization (IVF) and gamete intrafallopian transfer (GIFT). It has been suggested that the adjunctive use of GnRH agonists for controlled ovarian hyperstimulation improves the efficiency of GIFT and IVF cycles. We hypothesized that adjunctive use of leuprolide acetate, a GnRH agonist, would have a similarly beneficial effect on cycle quality and cycle fecundity in subfertile women treated with controlled ovarian hyperstimulation and intrauterine insemination. We randomly assigned the first cycle of controlled ovarian hyperstimulation and intrauterine insemination for each of 97 subfertile women to include either human menopausal gonadotropins (hMGs) alone or hMGs following midluteal pre-treatment with leuprolide. If a pregnancy did not occur in the first cycle, the woman was given the other treatment in the second cycle. Although the cycles that included leuprolide required a larger amount of hMGs and more days of stimulation per cycle, the mean estradiol concentrations and numbers of follicles were not different. Despite prevention of premature luteinization with leuprolide, the cycle fecundity was not different between groups (0.11 with adjunctive leuprolide treatment and 0.22 with hMGs alone). We conclude that in unselected subfertile patients, the adjunctive use of leuprolide for controlled ovarian hyperstimulation and intrauterine insemination does not improve cycle fecundity compared with treatment cycles that do not include adjunctive leuprolide therapy.     

Combination of ABO blood group incompatibility and glucose-6-phosphate dehydrogenase deficiency: effect on hemolysis and neonatal hyperbilirubinemia

The incidence (%) of hyperbilirubinemia (serum bilirubin ≥257 μmol/l) was similar in neonates with a combination of ABO incompatibility and glucose-6-phosphate dehydrogenase (G-6-PD) deficiency (45%), with ABO incompatibility (54%) or G-6-PD deficiency (37%), alone (ns). Carboxyhemoglobin values, corrected for inspired CO, were similarly elevated in all three groups (0.87 ± 0.32%, 0.82 ± 0.29%, 0.76 ± 0.18%, respectively, ns), but correlated with bilirubin only in those with ABO incompatibility alone. ABO-incompatible/G-6-PD-deficient neonates, compared with those with either condition alone, are not at increased risk for hemolysis or hyperbilirubinemia.     

Lactoferrin gene expression is estrogen responsive in human and rhesus monkey endometrium.

We have previously shown that the estrogen responsiveness of the human lactoferrin gene in a transient transfection system is mediated through an imperfect estrogen response element (ERE) and a steroidogenic factor 1 binding element (SFRE) 26 bp upstream from ERE. Reporter constructs containing SFRE and ERE respond to estrogen stimulation in a dose-dependent manner, whereas mutations at either one of the response elements severely impaired the estrogen responsiveness. In this study, we demonstrated that estrogen receptor (ERalpha) binds to the human lactoferrin gene ERE and forms two complexes in an electrophoresis mobility shift assay (EMSA). These complexes could be supershifted by an antibody to ERalpha. We also showed that in normal cycling women, lactoferrin gene expression in the endometrium increases during the proliferative phase and diminishes during the luteal phase. This in-vivo study thus supported the finding from transient transfection experiments that the human lactoferrin gene expression is elevated in an environment with a high level of estrogen. The estrogen effect on lactoferrin gene expression in the rhesus monkey endometrium was studied by Western blotting and immunohistochemistry. The immunohistochemistry results showed that immunoreactive lactoferrin protein was not detectable in the untreated ovariectomized monkey endometrium, was elevated by estrogen treatment, and was suppressed by sequential, combined estrogen plus progesterone treatment. In conclusion, this study has shown that lactoferrin gene expression is responsive to estrogen in primate endometrium.     

Toxicity of Methoxyacetic Acid in Cultured Human Luteal Cells

Ethylene glycol monomethyl ether (EGME) and its proximate metabolite,2-methoxyacetic acid (MAA), increase ovarian luteal cell progesteroneproduction in the female rat in vivo and in cultured rat lutealcells in vitro, respectively. In order to better assess thepotential hazard of EGME and MAA to women, these studies wereconducted to determine whether the same concentrations of MAAincrease progesterone in human luteinized granulosa cells asin rat luteal cells. Human cells were collected from healthyanonymous oocyte donors, washed, plated 25,000 viable cellsper well, and treated with 10 IU hCG and 0–5 mM MAA for6–48 hr. Progesterone in media was significantly elevatedafter 24 hr incubation at 1 mM MAA. MAA had no effect on ATPlevels at 6 or 24 hr. Thus, MAA increased progesterone productionin cultured human luteal cells at the same concentration asMAA increased progesterone in rat luteal cells. The implicationis that EGME has the potential to alter ovarian luteal functionin women. These data should be useful for determining the realhealth hazards and potential risks of EGME exposure.     

Le traitement familial des enfants et des adolescents anorexiques : Des lignes directrices pour le m��decin communautaire

Anorexia nervosa (AN) is a serious life-threatening illness that typically has its onset during the adolescent years. Evidence regarding the optimal treatment of AN in children and teenagers is growing; however, much remains unknown. Although current treatment approaches vary in Canada and elsewhere, the evidence to date indicates that family-based treatment (FBT) is the most effective treatment for children and teenagers with AN. A key component of the FBT model is that the parents are given the responsibility to return their child to physical health and ensure full weight restoration. An understanding of the basic principles and philosophy underlying FBT allows the physician to initiate elements of this evidence-based intervention to young patients with AN and their families.