Objective: Computerized fetal heart rate (FHR) analysis revealed that antenatal corticosteroids transiently suppress multiple parameters of fetal well-being, potentially leading to the erroneous diagnosis of fetal distress and to unnecessary iatrogenic delivery of premature infants. Our aim was to determine whether clinicians who visually analyze FHR tracings detect these suppressive effects, thereby potentially affecting their clinical management decisions. Methods: Singleton pregnancies admitted for preterm labor between 26 and 34 weeks’ gestation received two doses of betamethasone, 24 h apart, and were monitored daily between 16:00 and 19:00 h for 5 days. FHR tracings were randomly coded and presented in a non-consecutive order to four clinicians, who were unaware of the time of steroid administration. FHR baseline, FHR variability, number of accelerations and amplitude of maximal FHR acceleration were determined. Variability was scored semiquantitatively based on a modified Hon score. Analysis of variance (ANOVA) with repeated measures was used for primary analysis and followed up with the Wald test of significance. Corrections for multiple comparisons were made and only p < 0.005 considered significant. ANOVA was also used to assess the uniformity of trend in the interpretation by the four examiners for each given day. Results: Baseline FHR was elevated, FHR variability was decreased, and the number of accelerations decreased on day 1 (p < 0.0001; p < 0.0001; p < 0.0001) and day 2 (p > 0.0001; p < 0.0001; p < 0.0001) in comparison to day 0. On day 3, the FHR baseline, variability and number of accelerations returned to pre-exposure values (p = NS). The maximal amplitude of FHR accelerations showed a trend towards reduction (p = 0.08). Subgroup analysis by gestational age (group I = 26–30 weeks and group II = 30–34 weeks) showed the same response patterns and significance levels for both groups. Conclusions: Betamethasone causes profound, but transient, suppression of FHR parameters, which can mimic fetal distress. This effect is clinically recognized by visual FHR analysis. Clinicians need to be aware of this phenomenon, in order to avoid unwarranted iatrogenic delivery.

Multiple endocrine neoplasia type 1 (MEN‐1) is characterized by hyperfunction and tumor formation of the parathyroids, anterior pituitary and endocrine pancreas. We carried out exon‐specific, PCR‐based DNA sequencing of the coding exons of the MEN1 gene in 8 Israeli MEN1 patients: 4 familial and 4 sporadic. We similarly analyzed Israeli families with a unique phenotype of isolated hyperprolactinemia (HPRL). Four mutations were detected in 4 MEN1 patients: C to T alteration at nucleotide 2608 resulting in R108X, and three intronic insertions/deletions (a 13 basepair (bp) deletion and a 1 bp insertion both in intron 1, and a 2 bp insertion in intron 3) leading to exonic frame shifts as they encompass the splice junctions. An additional patient exhibited a compound mutation: a G to T change at position 7614 resulting in E463X, and insertion/deletion of 9 bp at position 7622‐7630 resulting in EAE466‐468X. Haplotype analysis showed no segregation of phenotype with 11q13 markers in 4 familial HPRL, and no men 1 germline mutations were detected in three representative individuals, from 3 families. Our results confirm that men 1 gene germline mutations occur in the majority of patients with clinically diagnosed MEN1, and that familial HPRL is a genetically distinct disorder. Hum Mutat 16:269, 2000. © 2000 Wiley‐Liss, Inc.

The results suggest that in vitro addition of beta-estradiol can inhibit, to a certain degree, specific activation markers on phytohemagglutinin-stimulated lymphocytes from young men and women. The present study could not define the role of sex differences because of the small number of samples. A comparison between men and women at various ages in a greater number of cases, as well as studies on activation markers after treatments with estrogens, would be useful.