Torsion of the uterine adnexa. Pathologic correlations and current management trends.

OBJECTIVE: To evaluate the clinical and pathologic correlates of specimens removed for the diagnosis of adnexal torsion and to evaluate trends in the management of torsion. STUDY DESIGN: Cases of ovarian or adnexal torsion (N = 104) were identified retrospectively over a period extending from January 1987 to March 1998 by the coding of ovarian, fallopian tube or adnexal torsion. Statistical evaluation was by chi 2 analysis using the Bonferroni inequality correction when appropriate. RESULTS: Neoplastic and functional tumors of the ovary composed > 90% of the diagnoses at microscopic evaluation, with cancer diagnosed in < 1% of cases. Laparoscopy was attempted in 47 (46%) cases, and adnexasparing procedures were performed in 20 (19%) patients. Patients treated in the latter half of the study were not less likely to undergo laparotomy than those treated in the first half; however, conversion from laparoscopy to laparotomy was significantly less common in the latter half. Patients in this study were more likely to receive an adnexa-sparing operation than historical controls, but there was no improvement in this rate from the first to the second half of this study. A history of previous abdominal surgery was the most common associated condition, but 47% of patients had no known risk factors. Ovarian hyperstimulation, previously omitted in series reports, was an antecedent factor in 9% of patients. CONCLUSIONS: Adnexal torsion is most commonly associated with a benign process. A more-conservative approach to the treatment of this process is becoming increasingly common, as seems warranted in light of the low incidence of malignancy. The need for conversion from a laparoscopic to an open approach appears to have been waning over the last decade; that may correlate with an increased comfort level in gynecologists with laparoscopic approaches.

Perinatal bacterial infection: an update.

This article reviews the current trends in the evaluation and management of bacterial infection involving the uterus, placenta, membranes, amniotic fluid, and fetus occurring near the time of birth. The discussion includes information regarding risk, incidence, pathophysiology, bedside diagnosis, interventional options including antibiotics, corticosteroids, fetal monitoring, and delivery, and possible preventive measures which affect the outcome. The adequate evaluation and management of perinatal infection requires a team approach with obstetricians and pediatricians. Clinical screening is useful in developing the diagnosis, but amniotic fluid evaluation remains the proposed gold standard. The role of cytokines is becoming increasingly important, as is seen in the association of IL-6 with positive amniotic fluid cultures and periventricular leukomalacia. Prompt recognition and management of the pregnancy affected by infection can improve perinatal outcomes. A management protocol is presented to help structure the approach to suspected infection. Premature delivery due to perinatal infection may be preventable.

Direct and endothelial cell-mediated effect of cyclosporin A on the proliferation of rat smooth muscle cells in vitro.

Cyclosporin A (CsA) has been suggested to potentiate graft vascular disease by stimulation of smooth muscle cell (SMC) proliferation. Both the in vitro and in vivo data are discordant, showing both stimulatory and inhibitory effects of CsA on vascular SMC proliferation. The direct and endothelial cell-mediated effects of CsA on vascular SMC proliferation were examined in vitro using the incorporation of [3H]thymidine. All experiments were done in serum-free conditions. The exposure of SMC to CsA (0.0001 to 0.1 micrograms/ml) had no effect on proliferation. High doses of CsA (0.5 to 10.0 micrograms/ml) were toxic to the SMC and endothelial cells; 90% of SMC population died within 3 to 6 days of exposure to 10.0 micrograms/ml CsA. In the studies on the endothelial cell-mediated effect of CsA, the endothelial cell-conditioned medium (ECCM) significantly increased SMC proliferation. This stimulatory effect was significantly attenuated when the ECCM was obtained from endothelial cells exposed to CsA. Endothelin (ET) is suggested to be an endothelial-cell-derived growth factor for SMC, and implicated as a possible cause of the uncontrolled proliferation of SMC during development of graft vascular disease. Exposure of SMC to levels of recombinant ET similar to the levels found in the ECCM (0.19 + 0.01 pg/ml) significantly increased SMC proliferation. CsA increased fivefold ET concentration in the ECCM. However, despite this rise in ET levels, there was a 45% decrease in SMC proliferation. In conclusion, CsA does not exert a direct modulatory effect on SMC proliferation in vitro, but may inhibit SMC proliferation indirectly via endothelial cell-derived factors. These unidentified factor(s) inhibit SMC proliferation and abolish the mitogenic effect of ET on SMC.