BackgroundSeveral studies have shown inconsistent associations between anxiety during pregnancy and adverse pregnancy outcome. This inconsistency may be due to lack of controlling for the timing and type of maternal anxiety. We aimed to isolate a specific type of anxiety - maternal anxiety propensity, which is not directly related to pregnancy, and evaluate its association with adverse pregnancy outcome.MethodsWe conducted a prospective observational study of 512 pregnant women, followed to delivery. The trait anxiety scale of the State-Trait Anxiety Inventories was used in order to detect a propensity towards anxiety. The association between anxiety propensity (defined as trait-anxiety subscale score above 38) and adverse pregnancy outcome was evaluated. Primary outcome was a composite outcome including preterm birth prior to 37 gestational weeks, hypertensive disorders in pregnancy, small for gestational age newborn and gestational diabetes mellitus. Secondary outcomes were each one of the above mentioned gestational complications.ResultsThere were no significant between-group differences in adverse pregnancy outcomes, including the rate of preterm birth, hypertensive disorders, small for gestational age, gestational diabetes or a composite outcome of them all.ConclusionAnxiety propensity is not associated with adverse pregnancy outcome.Electronic supplementary materialThe online version of this article (10.1186/s12884-018-1925-8) contains supplementary material, which is available to authorized users.
Multiple endocrine neoplasia 4 (MEN4) is a rare multiglandular endocrine neoplasia syndrome clinically hallmarked by primary hyperparathyroidism (PHPT), pituitary adenoma (PitAd) and neuroendocrine tumors (NET), clinically overlapping MEN1. The underlying mutated gene, CDKN1B, encodes for the cell-cycle regulator p27. Possible genotype-phenotype correlation in MEN4 have not been thoroughly assessed. Prompted by the findings in three Israeli MEN4 kindreds, we performed literature review on published and unpublished data from previously reported MEN4/CDKN1B cases. Univariate analysis analyzed time-dependent risks for developing PHPT, PitAd, or NET by variant type and position along the gene. Overall, 74 MEN4 cases were analyzed. PHPT risk was 53.4% by age 60 years (mean age at diagnosis age 50.6±13.9 years), for PitAd - 16.2% and NET - 23.2% (34.4±21.4 and 52.9±13.9 years, respectively). The frameshift variant p.Q107fs was the most common variant identified (4/41 [9.7%] kindreds). Patients with Indels had higher risk for PHPT vs. point mutations (Log-Rank, p=0.029). Variants in codons 94-96 were associated with higher risk for PHPT (p<0.001) and PitAd (p=0.031). To conclude, MEN4 is clinically distinct from MEN1, with lower risk and older age for PHPT diagnosis. We report recurrent CDKN1B frameshift variants and possible genotype-phenotype correlations.
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