Context: The definition of what constitutes a normal TSH during pregnancy is in flux. Recent studies suggested that the first trimester upper limit of normal for TSH should be 2.5 mIU/liter. Objective: The objective of the study was to evaluate the pregnancy loss and preterm delivery rate in first-trimester thyroid peroxidase antibody-negative women with TSH values between 2.5 and 5.0 mIU/liter. Design: The present study is a component of a recently published large-scale prospective trial that evaluated the impact of levothyroxine treatment on maternal and neonatal complications in thyroid peroxidase-positive women with TSH levels above 2.5 mIU/liter. The present study evaluated 4123 thyroid peroxidase antibody-negative women with TSH levels at or below 5.0 mIU/liter. Women were divided into two groups based on their initial TSH: group A, TSH level below 2.5 mIU/liter, excluding hyperthyroid women defined as an undetectable TSH with an elevated free T₄, and group B, TSH level between 2.5 and 5.0 mIU/liter. Setting: The study was conducted at two ambulatory clinics of community hospitals in southern Italy. Patients: A total of 4123 women were evaluated. Intervention: There was no intervention. Main Outcome Measures: The incidence of pregnancy loss and preterm delivery in group A as compared with group B was measured. Results: The rate of pregnancy loss was significantly higher in group B as compared with group A (6.1 vs. 3.6% respectively, P = 0.006). There was no difference in the rate of preterm delivery between the two groups. Conclusions: The increased incidence of pregnancy loss in pregnant women with TSH levels between 2.5 and 5.0 mIU/liter provides strong physiological evidence to support redefining the TSH upper limit of normal in the first trimester to 2.5 mIU/liter.

Context: Thyroid disease during pregnancy has been associated with multiple adverse outcomes. Whether all women should be screened for thyroid disease during pregnancy is controversial. Objective: The objective of the study was to determine whether treatment of thyroid disease during pregnancy decreases the incidence of adverse outcomes and compare the ability of universal screening vs. case finding in detecting thyroid dysfunction. Design: Women in the first trimester were randomly assigned to the universal screening group or case-finding group. Women in both groups were stratified as high risk or low risk based on risk factors for thyroid disease. All women in the universal screening group, and high-risk women in the case-finding group, were immediately tested for free T₄, TSH, and thyroid peroxidase antibody. Low-risk women in the case-finding group had their sera tested postpartum. Setting: The study was conducted at two ambulatory clinics of community hospitals in southern Italy. Patients: A total of 4562 women were randomly assigned to the universal screening or case-finding group. Intervention: Intervention included levothyroxine in women with a TSH above 2.5 mIU/liter in TPO antibody-positive women and antithyroid medication in women with a undetectable TSH and elevated free T₄. Main Outcome Measure: Total number of adverse obstetrical and neonatal outcomes was measured. Results: No significant differences were seen in adverse outcomes between the case-finding and universal screening groups. Adverse outcomes were less likely to occur among low-risk women in the screening group than those in the case-finding group. Conclusions: Universal screening compared with case finding did not result in a decrease in adverse outcomes. Treatment of hypothyroidism or hyperthyroidism identified by screening a low-risk group was associated with a lower rate of adverse outcomes.

Implantation of the zygote outside the uterine cavity occurs in 2% of all pregnancies. The product of conception can be removed safely by laparoscopic surgery and be submitted for histological examination. The rate of ectopic pregnancies has increased from 0.5% in 1970 to 2% today. The prevalence of ectopic pregnancy in all women presenting to an emergency department with first-trimester bleeding, lower abdominal pain, or a combination of the 2 is between 6% and 16%. DESIGNATION: Workup of all localizations of ectopic pregnancies at a university department of obstetrics and gynecology. Comparison of diagnostic and therapeutic modalities from the surgical laparoscopic approach to nonsurgical, medical options. Tubal pregnancies: (1) to preserve tubal function, salpingotomy, partial salpingectomy followed by laparoscopic anastomosis, or fimbrial milking is performed. (2) Tubectomy or salpingectomy is performed only in severely damaged or ruptured tubes or if the patient does not desire further pregnancies. Nontubal ectopic pregnancies (ovarian pregnancy, ectopic abdominal pregnancy, interstitial or cornual pregnancy/rudimentary horn, intraligamental and cervical pregnancies) all require their own specific treatment. The predominant drug is methotrexate, but other systemic drugs, such as actinomycin D, prostaglandins, and RU 486, can also be applied. Tubal rupture is a complication of late diagnosed tubal pregnancy that is more difficult to treat conservatively and often indicates tubectomy or segmental resection. In 5% to 15% of treated ectopic pregnancy cases, remnant conception product parts may require a final methotrexate injection. This article is a review to aid clinical diagnosis of ectopic pregnancies that now can be diagnosed earlier and treated effectively by laparoscopic surgery.

Genital prolapse is frequent in postmenopausal women; it describes the loss of support to the pelvic organs, resulting in a herniation of these into the vaginal channel. This problem affects 50% of parous women, and at least 50% of all women develop a mild form of genital prolapse after pregnancy. An extensive literature review from 1990 to 2008 was performed on prolapse etiology and its risk factors; analyzing the data, we reviewed the genetic and biological aspects, age-related prolapse, biological tissue modifications, surgical problems, pelvic musculature modifications, and neuropathy. Data suggested that aging, pelvic trauma, and surgery evoke tissue denervation and devascularization, anatomic alterations, and increased degradation of collagen; all of these may lead to a decrease in mechanical strength and predispose an individual to prolapse. It has been demonstrated that there is a reduction in protein content and estrogens in uterosacral ligaments, in the vagina, and in the parametrium of women with prolapse. This is a possible explanation for why many surgical procedures to correct prolapse fail and recurrences after surgical correction are frequent. Even if the etiology of pelvic prolapse is poorly defined and multifactorial, aging risk factors, such as biomechanical abnormalities in connective tissue composition, hormonal deficiency, and irregular tissue metabolism, are nonmodifiable and therefore largely stated in clinical practice. Regardless of future developments, based on the reported findings, prolapse therapy will be more influenced by genetics, biological pelvic changes, changes in tissue homeostasis, and topical hormones, rather than general pelvic corrective surgical anatomy.