No abstract

Publication of findings from clinical trials is a necessary step in the research continuum, to provide a record of the work done, convey information to the community, and support translation of research into clinical practice. Systematic reviews of randomized controlled trials are now widely regarded as the highest level of evidence in determining the effect of an intervention on an outcome. They largely depend on internationally accessible, published reports of all trials undertaken. Investigators and their institutions or organizations have responsibility for reporting their clinical trials accurately and completely, including disclosure of potential conflicts of interest. To ensure evidencebased health care, issues relating to accessibility and accountability of clinical trial results require immediate action.

The objective was to investigate whether cases of fetal trisomy 18 and Turner syndrome with and without hydrops were associated with alterations in the second‐trimester levels of maternal serum inhibin A. Twenty‐one cases of trisomy 18, 10 cases of Turner syndrome without hydrops and 12 cases of Turner syndrome with hydrops were identified. Five control samples were matched to each case for date of sample collection and completed week of gestation. Inhibin A levels were modestly, but significantly reduced in cases of trisomy 18 (median=0·88 MoM) and Turner syndrome without hydrops (median=0·64 MoM). In contrast, inhibin A levels were markedly increased in cases of Turner syndrome with hydrops (median=3·91 MoM). These data for Turner syndrome are similar to those for human chorionic gonadotropin (hCG). The addition of inhibin A to multiple marker screening (alpha‐fetoprotein, unconjugated oestriol and hCG) resulted in a median increase in the Down syndrome risk of 2·6‐fold in cases of Turner syndrome with hydrops. The addition of inhibin A to multiple marker Down syndrome screening programmes will be likely to enhance the detection of fetal Turner syndrome with hydrops, but will not contribute substantially to the detection of fetal trisomy 18. Copyright © 1998 John Wiley & Sons, Ltd.