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Randomized Clinical Trial of Metronidazole Plus Erythromycin to Prevent Spontaneous Preterm Delivery in Fetal Fibronectin–Positive Women

From the Department of Obstetrics and Gynecology, Center for Research in Women’s Health, University of Alabama at Birmingham, Birmingham, Alabama; Department of Obstetrics and Gynecology, University of Tennessee, Memphis, Tennessee; The Biostatistics Center, George Washington University, Rockville, Maryland; Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, Utah; Department of Obstetrics and Gynecology, Wake Forest University School of Medicine, Winston-Salem, North Carolina; The National Institute of Child Health and Human Development, Bethesda, Maryland; Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Obstetrics and Gynecology, Thomas Jefferson University, Philadelphia, Pennsylvania; Department of Obstetrics and Gynecology, University of Chicago, Chicago, Illinois; Department of Obstetrics and Gynecology, University of Miami, Miami, Florida; University of Pittsburgh/Magee-Women’s Hospital, Pittsburgh, Pennsylvania; Department of Obstetrics and Gynecology, Ohio State University, Columbus, Ohio; Department of Obstetrics and Gynecology, University of Texas at San Antonio, San Antonio, Texas; Department of Obstetrics and Gynecology, University of Cincinnati, Cincinnati, Ohio; and Department of Obstetrics and Gynecology, Wayne State University, Detroit, Michigan.

Address reprint requests to: William W. Andrews, PhD, MD, University of Alabama at Birmingham, Department of Obstetrics and Gynecology, 619 19th Street South—OHB 458, Birmingham, AL 35249-7333; E-mail: wandrews{at}uab.edu.

	ABSTRACT

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION APPENDIX REFERENCES

 
OBJECTIVE: To estimate whether antibiotic treatment of asymptomatic women with a positive cervical or vaginal fetal fibronectin test in the second trimester would reduce the risk of spontaneous preterm delivery.

METHODS: Women were screened between 21 weeks 0 days and 25 weeks 6 days of gestation with cervical or vaginal swabs for fetal fibronectin. Women with a positive test (50 ng/mL or more) were randomized to receive metronidazole (250 mg orally three times per day) and erythromycin (250 mg orally four times per day) or identical placebo pills for 10 days. The primary outcome was spontaneous delivery before 37 weeks’ gestation after preterm labor or premature membrane rupture.

RESULTS: A total of 16,317 women were screened for fetal fibronectin, and 6.6% had a positive test; 715 fetal fibronectin test–positive women consented to randomization. Outcome data were available for 703 women: 347 in the antibiotic group and 356 in the placebo group. The antibiotic and placebo groups were not significantly different for maternal age (P = .051), ethnicity (P = .849), marital status (P = .127), education (P = .244), and bacterial vaginosis (P = .236). No difference was observed in spontaneous preterm birth before 37 weeks’ (odds ratio [OR] 1.17, 95% confidence interval [CI] 0.80, 1.70), less than 35 weeks’ (OR 0.92, 95% CI 0.54, 1.56), or less than 32 weeks’ (OR 1.94, 95% CI 0.83, 4.52) gestation in antibiotic-compared with placebo-treated women. Among women with a prior spontaneous preterm delivery, the rate of repeat spontaneous preterm delivery at less than 37 weeks’ gestation was significantly higher in the active drug compared with the placebo group (46.7% versus 23.9%, P = .039).

CONCLUSION: Treatment with metronidazole plus erythromycin of asymptomatic women with a positive cervical or vaginal fetal fibronectin test in the late second trimester does not decrease the incidence of spontaneous preterm delivery.

Preterm birth complicates 11% of all pregnancies and remains the primary cause of perinatal mortality and long-term neurologic morbidity.^1,2 Published literature has strongly linked clinically silent upper genital tract bacterial infection and/or inflammation with preterm birth and adverse pregnancy outcomes.^3–7 Although randomized trials of systemic antibiotics to reduce preterm birth in women with altered vaginal flora have yielded mixed results,^6,8–12 genital tract infections represent a potentially treatable cause of spontaneous preterm delivery.

Fetal fibronectin is a placental and membrane protein that is a unique epitope of the fibronectins. When detected in asymptomatic women (those without signs or symptoms of vaginal infection or preterm labor) as early as 23–24 weeks’ gestation, a positive fetal fibronectin test is associated with a 59-fold increased risk of spontaneous preterm delivery at less than 28 weeks’ gestation.¹³ One hypothesis holds that intrauterine infection causes disruption of the extracellular choriodecidual basement membrane, causing leakage of fetal fibronectin into cervical or vaginal secretions, in which it can then be detected.^14–16

Our objective in this study was to estimate whether treatment with metronidazole plus erythromycin of asymptomatic women with a positive cervical or vaginal fetal fibronectin test before 26 weeks’ gestation would reduce the risk of spontaneous preterm delivery.

	MATERIALS AND METHODS

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION APPENDIX REFERENCES

 
Women undergoing routine prenatal care at each of 13 participating centers were screened between 21 weeks 0 days and 25 weeks 6 days of gestation for cervical and vaginal fetal fibronectin. Separate Dacron swab specimens were collected from the exocervix and posterior vaginal fornix with a vaginal speculum without a lubricant and before collection of other specimens. These specimens were immediately stored at 2–8C and shipped overnight to a central laboratory (Adeza Biomedical, Sunnyvale, CA), where fetal fibronectin was determined by an enzyme-linked immunosorbent assay. Based on previously published data,¹⁷ a positive test was defined as a concentration of 50 ng/mL or more in either the cervical or the vaginal swab. Other details of the specimen collection, handling, and assay have been previously published.^13,14 Vaginal smears obtained at screening were evaluated (with Nugent criteria¹⁸) in a central laboratory for the presence of bacterial vaginosis. Women were not selected based on the presence or absence of any specific risk factor (other than a positive fetal fibronectin test) for a spontaneous preterm birth. Exclusion criteria included the following: fetal death, major fetal anomalies, multiple gestation, allergy to study medication, antibiotic use at randomization, use of topical antifungals within 24 hours of screening, vaginal symptoms (unelicited, spontaneously reported vaginal symptoms, including itching, burning, or malodor indicating need for specific treatment), vaginal bleeding (defined as active bleeding at screening, not spotting and not bleeding due to a friable cervix), ethanol abuse, preterm labor, rupture of membranes, tocolytic use, cerclage, preeclampsia, hypertension requiring medication, placenta previa, uterine anomaly, insulin-requiring diabetes mellitus, renal insufficiency, collagen vascular disease, isoimmunization, acquired immunodeficiency syndrome–defining illness, and anticipated prenatal care or delivery at a nonparticipating center.

The study was approved by the institutional review boards at each clinical site, and all women gave written, informed consent before enrollment in the study. Eligible women with a positive fetal fibronectin test were randomized (double-masked) between 21 weeks 0 days and 25 weeks 6 days of gestation to receive either metronidazole 250 mg three times daily plus erythromycin 250 mg four times daily or identical placebo capsules orally for 10 days. The simple urn method of randomization¹⁹ with stratification according to clinical center was used to create a computer-generated random sequence, and study drugs were packaged accordingly in vials for distribution to the participants. Subjects were instructed to take one metronidazole capsule (or identical placebo) three times daily with meals and one erythromycin capsule (or placebo) four times daily (at each meal and at bedtime) for 10 days. Medication was begun on the day of randomization.

One follow-up visit was scheduled 14 days after randomization, at which fetal fibronectin and bacterial vaginosis status were reassessed. Medication compliance was estimated at this visit by examining the pill containers for remaining capsules. Subjects who failed to return the pill container were asked whether any capsules remained. If unconsumed capsules remained, the cervical and vaginal specimens were still obtained, and the women were encouraged to take the remainder of the study medication.

Establishment of the gestational age at randomization was determined by the date of the last menstrual period and by ultrasound results with a previously published scheme.^11,12 Preterm birth was defined as delivery before 37 completed weeks’ gestation (259 days), and spontaneous preterm birth was defined as preterm delivery due to the spontaneous onset of preterm labor or spontaneous preterm premature rupture of membranes. The primary outcome was spontaneous delivery before 37 weeks’ gestation after preterm labor or premature membrane rupture. Usual prenatal care was provided at the respective institutions, but enrollment continued until pregnancy outcomes were assessed.

The target sample size of 700 women was calculated assuming a 30% rate of spontaneous preterm delivery before 37 weeks’ gestation in the placebo group and an estimated effect size of a one third reduction of this outcome in the active drug group. A type I error (two-sided) of 5% and a power of 80% was chosen, and an adjustment for a dropout rate of 5% was made.

Continuous variables were compared using the Wilcoxon rank-sum test, and categoric variables were compared using ² and Fisher exact tests. Before the study was started, the group sequential method of Lan and DeMets with the modified O’Brian-Fleming spending function was chosen for adjustment of the significance level in interim analyses.²⁰ An independent data and safety-monitoring committee reviewed the interim results.

	RESULTS

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION APPENDIX REFERENCES

 
A total of 26,203 women were evaluated for a screening examination between July 1996 and May 2000 (Figure 1). Of these, 9886 were either ineligible or refused consent. Thus, 16,317 women agreed to a screening pelvic examination; 1079 of them were determined to be fetal fibronectin positive. A total of 715 women were randomized to either the active drug (353) or placebo (362) groups (Figure 1). Only 15 women (2%) were lost to follow-up. The treatment groups were similar with respect to demographics and socioeconomic indicators (Table 1). A history of a previous spontaneous preterm delivery was significantly more common among placebo-treated compared with antibiotic-treated women (Table 1).

View larger version (28K): [in this window] [in a new window]   Figure 1. Summary of screening for fetal fibronectin and randomization to active drugs or placebo. Andrews. Fetal Fibronectin and Prematurity. Obstet Gynecol 2003.

Stratification by other clinical factors, including the gestational timing of the fetal fibronectin test, intercourse within 24 hours of the fetal fibronectin test, and the interval between obtaining the fetal fibronectin screening test and subsequent randomization, revealed no statistically significant difference in spontaneous preterm delivery before 37 weeks’ gestation between the antibiotic-treated and placebo-treated groups (Table 3). No significant differences in spontaneous preterm delivery between the two groups were observed when the outcomes were stratified by clinical center (data not shown).

The antibiotic- and placebo-treated groups did not differ significantly with respect to the number of admissions to the hospital for preterm labor or premature rupture of membranes (16.3% versus 13.4%, P = .291), use of tocolytic drugs (6.4% versus 6.0%, P = .821), frequency of antepartum bleeding (0.9% versus 1.1%, P = 1.00), occurrence of preeclampsia or gestational hypertension (7.9% versus 8.3%, P = .842), oligohydramnios (5.0% versus 5.2%, P = .911), need for cesarean delivery (15.4% versus 15.9%, P = .868), presence of meconium in labor (20.9% versus 16.4%, P = .134), placental abnormalities (2.3% versus 1.7%, P = .567), or gestational diabetes (3.8% versus 2.6%, P = .360).

The number of women who developed vaginal infections requiring treatment during the pregnancy (14.7% versus 21.3%, P = .025), postpartum endometritis (2.1% versus 5.2%, P = .028), and clinical chorioamnionitis (3.8% versus 6.6%, P = .099) was lower in the antibiotic-than in the placebo-treated group.

Selected neonatal outcomes were also similar in the group treated with active drugs compared with the group treated with placebo (Table 4). Of particular importance in this antibiotic-intervention study, neonatal infection–related morbidities were similar in the antibiotic- and placebo-treated groups, including culture-proven sepsis, pneumonia, and necrotizing enterocolitis (Table 4).

By design, all women were positive for fetal fibronectin at the randomization visit. The frequency of a positive result for fetal fibronectin overall was substantially lower at the follow-up visit (19.5%). The frequency of a positive fetal fibronectin test at the follow-up visit was significantly higher in the active drug group than in the placebo group (22.9% versus 16.2%, P = .040).

	DISCUSSION

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION APPENDIX REFERENCES

 
In this randomized, clinical trial, treatment of asymptomatic women with a positive cervical or vaginal fetal fibronectin test between 21 and 25 weeks’ gestational age with metronidazole plus erythromycin did not decrease the risk of spontaneous delivery and did not result in improved neonatal outcomes. The ineffectiveness of the intervention was observed despite the use of a prolonged course of broad-spectrum combination antibiotics. Rationale for this treatment regimen was derived from a prior study, in which treatment of more than a week with this same combination of antibiotics was associated with a lower rate of spontaneous preterm birth among high-risk women with asymptomatic bacterial vaginosis.⁹ Additionally, the combination of both metronidazole and erythromycin seemed best suited to cover the major organisms typically isolated from the upper genital tract among women with a spontaneous preterm delivery.⁵

Compliance with the study medication was good according to verbal reports by participants and capsule counts conducted by study personnel. One objective measure of compliance was the frequency of bacterial vaginosis detected at the follow-up visit, which was observed to be significantly lower in the women who took active drugs (including metronidazole) compared with those given placebo capsules. Some adverse effects were more commonly reported by women taking active drug compared with placebo-treated women. Also, the primary reason given by subjects for not completing the treatment course was the occurrence of one or more adverse effects. However, the percentage of women who completed 7 or more days of treatment was almost identical in both groups. Therefore, noncompliance in the groups assigned to metronidazole plus erythromycin compared with the group assigned to placebo did not explain the failure of the active intervention to reduce spontaneous preterm delivery.

The assumptions used to calculate the sample size for this investigation were based on extensive data collected during the Preterm Prediction Study, an observational study of 2929 pregnant women previously conducted by the National Institute of Child Health and Human Development Maternal–Fetal Medicine Units Network.¹³ Based on this study, we assumed that an approximate 30% rate of spontaneous preterm delivery before 37 weeks’ gestation would occur in the placebo group.¹³ Instead, we observed a much lower incidence of spontaneous preterm delivery, 13.7% overall. Therefore, it could be argued that this study lacked sufficient statistical power and that a significantly lower incidence of spontaneous preterm birth might have been observed if the sample size had been larger. However, given the almost identical percentage of spontaneous preterm delivery observed in the active drug and placebo groups (14.4% and 12.4%, respectively) providing no suggestion of even a trend toward a lower incidence of the primary outcome in either group, this seems highly unlikely. Nevertheless, explanation for the lower incidence of spontaneous delivery before 37 weeks’ gestation observed in this investigation compared with that observed in the Preterm Prediction Study remains speculative.

Although the frequency of a positive fetal fibronectin test at the follow-up visit was significantly higher in the active drug group than in the placebo group, the magnitude of this difference does not likely explain the failure to observe a benefit to antibiotic treatment. It is difficult to speculate as to whether or not the antibiotic treatment actually increased choriodecidual matrix disruption, leading to higher rate of fetal fibronectin leakage from the upper to the lower genital tract. Notably, the fetal fibronectin test was negative in 80% of the women at the follow-up visit.

An intriguing finding was the nearly two-fold higher risk of spontaneous preterm delivery observed in the active drug group compared with the placebo group among women with a history of a spontaneous preterm delivery in a previous pregnancy. Interpretation of this observation must be guided by caution because this is a secondary analysis of data, and the explanation remains a subject of speculation. It is unclear whether antibiotic treatment actually increased the risk of preterm delivery in this subset of women by altering the vaginal flora or by some other mechanism. However, this observation is consistent with an increased risk of preterm delivery in certain subgroups of women treated with antibiotics during pregnancy (Hauth JC, Cliver SP, Hodgkins P, Andrews WW, Schwebke JR, Hooke EW, et al. Mid-trimester metronidazole and azithromycin did not prevent preterm birth in women at increased risk: A double-blind trial [abstract]. Am J Obstet Gynecol 2001;185: S86).^6,9,12 Such data underscore the need for clinical caution and argue against the indiscriminate use of antibiotics to prevent preterm birth.

Although vaginal infections and postpartum endometritis were less common in the active drug group compared with the placebo group, these observations are secondary outcomes of this study and do not, in our view, warrant a recommendation for second trimester fetal fibronectin screening and antibiotic treatment solely to reduce the risk of these outcomes. Despite the previously reported performance of the fetal fibronectin test to identify women at increased risk for subsequent spontaneous preterm delivery,^13,14 based on the results of this trial, we discourage the practice of cervical or vaginal fetal fibronectin screening to direct an antibiotic intervention for preterm birth prevention.

	APPENDIX

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION APPENDIX REFERENCES

 
Other members of the National Institute of Child Health and Human Development Maternal–Fetal Medicine Units Network are as follows: University of Alabama at Birmingham, R. Goldenberg, A. Northen, R. Cooper, C. Morgan; University of Tennessee at Memphis, R. Ramsey; George Washington University Biostatistics Center, L. Leuchtenburg, A. Das, M. Fisher; University of Utah, E. Taggart; Wake Forest University, M. Swain, A. Luper; National Institute of Child Health and Human Development, M. Klebanoff, C. Spong; University of Texas Southwestern Medical Center, J. McCampbell, M. L. Sherman; Thomas Jefferson University, M. Di-Vito, A. Sciscione; University of Chicago, P. Jones, G. Mallet, D. Scott, M. R. Brinson, M. Brown; University of Miami, S. Beydoun, C. Alfonso, F. Doyle, R. Washington, G. Diaz; University of Pittsburgh/Magee-Women’s Hospital, M. Cotroneo, T. Kamon, E. Daugherty, P. Heine; Ohio State University, M. Landon, C. Latimer, S. Meadows, F. Johnson; University of Texas San Antonio, S. Nicholson, S. Barker, D. Skiver; University of Cincinnati, H. How; Wayne State University, Y. Sorokin, G. Norman.

	Footnotes

 
Supported by grants from the National Institute of Child Health and Human Development (U10-HD27869, U10-HD21414, U10-HD36801, U10-HD34208, U10-HD27860, U10-HD34116, U10-HD34136, U10-HD27861, U10-HD34122, U10-HD21410, U10-HD27915, U10-HD34210, U10-HD27905, and U10-HD27917). Fetal fibronectin assays were performed at no cost to the project by Adeza Biomedical, Sunnyvale, California.

^* For other members of the Network, see the Appendix.

doi:10.1016/S0029-7844(03)00172-8

Received January 21, 2003. Received in revised form February 7, 2003. Accepted February 13, 2003.

	REFERENCES

TOP ABSTRACT MATERIALS AND METHODS RESULTS DISCUSSION APPENDIX REFERENCES

 
1. Hack M, Fanaroff AA. Outcomes of children of extremely low birthweight and gestational age. Semin Neonatol 2000;5:89–106.[Medline]

2. Ventura SJ, Martin JA, Curtin SC, Mathews TJ. Report of final natality statistics, 1995. Monthly vital statistics report, vol 45, no 11 supplement. Hyattsville, Maryland: National Center for Health Statistics, 1997:1–81.

3. Andrews WW, Goldenberg RL, Hauth JC. Preterm labor: Emerging role of genital tract infections. Infect Agents Dis 1995;4:196–211.[Medline]

4. Gibbs RS, Romero R, Hillier SL, Eschenbach DA, Sweet RL. A review of premature birth and subclinical infection. Am J Obstet Gynecol 1992;166:1515–28.[Medline]

5. Goldenberg RL, Hauth JC, Andrews WW. Intrauterine infection and preterm delivery. N Engl J Med 2000;342: 1500–7.[Free Full Text]

6. Andrews WW, Hauth JC, Goldenberg RL. Infection and preterm birth. Am J Perinatol 2000;17:357–65.[Medline]

7. Kimberlin DF, Andrews WW. Bacterial vaginosis: Association with adverse pregnancy outcome. Semin Perinatol 1998;22:242–50.[Medline]

8. Morales WJ, Schorr S, Albritton J. Effect of metronidazole in patients with preterm birth in preceding pregnancy and bacterial vaginosis: A placebo-controlled, double-blind study. Am J Obstet Gynecol 1994;171:345–7.[Medline]

9. Hauth JC, Goldenberg RL, Andrews WW, DuBard MB, Copper RL. Reduced incidence of preterm delivery with metronidazole and erythromycin in women with bacterial vaginosis. N Engl J Med 1995;333:1732–6.[Abstract/Free Full Text]

10. McDonald HM, O’Loughlin JA, Vigneswaran R, Jolley PT, Harvey JA, Bof A, et al. Impact of metronidazole therapy on preterm birth in women with bacterial vaginosis flora (Gardnerella vaginalis): A randomized, placebo controlled trial. Br J Obstet Gynaecol 1997;104: 1391–7.[Medline]

11. Carey JC, Klebanoff MA, Hauth JC, Hillier SL, Thom EA, Ernest JM, et al. Metronidazole to prevent preterm delivery in pregnant women with asymptomatic bacterial vaginosis. N Engl J Med 2000;342:534–40.[Abstract/Free Full Text]

12. Klebanoff MA, Carey JC, Hauth JC, Hillier SL, Nugent RO, Thom EA, et al. Failure of metronidazole to prevent preterm delivery among pregnant women with asymptomatic Trichomonas vaginalis infection. N Engl J Med 2001;345: 487–93.[Abstract/Free Full Text]

13. Goldenberg RL, Mercer BM, Meis PJ, Copper RL, Das A, McNellis D. The Preterm Prediction Study: Fetal fibronectin testing and spontaneous preterm birth. Obstet Gynecol 1996;87:643–8.[Abstract]

14. Lockwood CJ, Senyei AE, Dische MR, Casal D, Shah KD, Thung SN, et al. Fetal fibronectin in cervical and vaginal secretions as a predictor of preterm delivery. N Engl J Med 1991;325:669–74.[Abstract]

15. Feinberg RF, Kliman HJ, Lockwood CJ. Is oncofetal fibronectin a trophoblast glue for human implantation? Am J Pathol 1991;138:537–43.[Abstract]

16. Goldenberg RL, Thom E, Moawad AH, Johnson F, Roberts J, Caritus SN, et al. The Preterm Prediction Study: Fetal fibronectin, bacterial vaginosis and peripartum infection. Obstet Gynecol 1996;87:656–60.[Abstract]

17. Goepfert AR, Goldenberg RL, Andrews WW, Hauth JC, Mercer B, Iams J, et al. The Preterm Prediction Study: Quantitative fetal fibronectin values and the prediction of spontaneous preterm birth. Am J Obstet Gynecol 2000; 183:1480–3.[Medline]

18. Nugent RP, Krohn MA, Hillier SL. Reliability of diagnosing bacterial vaginosis by a standardized method of Gram stain interpretation. J Clin Microbiol 1991;29: 297–301.[Abstract/Free Full Text]

19. Wei LJ, Lachin JM. Properties of the urn randomization in clinical trials. Control Clin Trials 1988;9:345–64.[Medline]

20. Lan KKG, DeMets DL. Discrete sequential boundaries for clinical trials. Biometrika 1983;70:659–63.[Abstract/Free Full Text]

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