While 10% of pregnant individuals report a penicillin allergy, there is no established best practice for penicillin allergy delabeling in pregnancy. To better understand options for penicillin delabeling, we aimed to evaluate two penicillin allergy delabeling protocols in pregnancy regarding efficacy, adverse events, and patient satisfaction.
From July 2019 to December 2022, we completed a two-center prospective cohort study, where each site recruited pregnant patients over 24 weeks gestational age with a reported penicillin allergy. One center offered antepartum amoxicillin oral challenges, either directly or after negative skin testing (i.e., antepartum oral challenge site). Our other centers completed a two-step approach with antepartum penicillin skin testing only and deferred oral challenges to the postpartum period (i.e., postpartum oral challenge site). Our primary outcome was the rate of penicillin allergy delabeling, defined as tolerating an antibiotic challenge with penicillin or amoxicillin. Univariate analyses were completed using chi-squared, Fisher's exact, and Wilcoxon rank tests.
During the study period, 276 pregnant patients were assessed, with 207 in the antepartum oral challenge site and 69 in the postpartum oral challenge site. Among the 204 patients who completed antepartum oral challenges, 201 (98%) passed without reactions. Deferring oral challenges to the postpartum period led to a loss of follow-up for 37/53 (70%) of eligible individuals. Overall, 97% (201/207) of patients at the antepartum oral challenge site were delabeled from their penicillin allergy—compared to 38% (26/69) of patients referred to the postpartum oral challenge site (p < 0.0001). Three antepartum oral challenge reactions were noted, including two mild cutaneous reactions and a case of transient abdominal discomfort.
Antepartum amoxicillin oral challenge is a more effective method to delabel pregnant patients from their penicillin allergy. Deferral of oral challenges to the postpartum period introduces a significant barrier for penicillin allergy delabeling.
Previous studies have established a link between gut microbiota and polycystic ovary syndrome (PCOS), but little is known about their precise causal relationship. Therefore, this study aims to explore whether there are precise causal relationships between gut microbiota and PCOS.
We performed a bidirectional two-sample Mendelian randomization (MR) analysis. Datasets were from the largest published meta-analysis on gut microbiota composition and the FinnGen cohort of the IEU Open Genome-Wide Association Study Project database. Inverse variance weighted (IVW), MR-Egger, constrained maximum likelihood-based Mendelian randomization, weighted median, weighted mode, and simple mode were used. Cochran's Q and MR-Egger intercept tests were employed to measure the heterogeneity.
A total of 211 gut microbiota taxa were identified in MR analysis. Nine taxa of bacteria, including Alphaproteobacteria (0.55, 0.30–0.99, p = 0.04), Bacilli (1.76, 1.07–2.91, p = 0.03), Bilophila (0.42, 0.23–0.77, p < 0.01), Blautia (0.16, 0.03–0.79, p = 0.02), Burkholderiales (2.37, 1.22–4.62, p = 0.01), Candidatus Soleaferrea (0.65, 0.43–0.98, p = 0.04), Cyanobacteria (0.51, 0.31–0.83, p = 0.01), Holdemania (0.53, 0.35–0.81, p < 0.01), and Lachnospiraceae (1.86, 1.04–3.35, p = 0.03), were found to be associated with PCOS in the above MR methods included at least IVW method. Cochran's Q statistics and MR-Egger intercept test suggested no significant heterogeneity. In addition, 69 taxa were shown significant for at least the IVW method in reverse MR analysis, of these, 25 had a positive correlation, and 37 had a negative correlation. Additionally, Alphaproteobacteria and Lachnospiraceae (0.95, 0.91–0.98, p < 0.01; 0.97, 0.94–0.99, p = 0.02, respectively) were shown a bidirected causally association with PCOS.
Our study provides evidence of the bidirectional causal association between gut microbiota and PCOS from a genetic perspective.
Childhood obesity is associated with maternal obesity, but the link to gestational weight gain (GWG) is not fully elucidated. We examined the relationship between early pregnancy maternal body mass index (BMI) and GWG on early childhood growth.
Data from 30 197 mother–child pairs from Uppsala County Mother and Child Cohort were divided into 15 groups according to maternal BMI and GWG, based on World Health Organization classification and Institute of Medicine guidelines, respectively. Postnatal growth patterns were analyzed with linear mixed regression models within maternal BMI groups. Odds ratios of overweight and obesity at 4 years of age were assessed with logistic regression analyses. We treated children of mothers with normal weight and adequate GWG as the reference group, and all analyses were adjusted for potential confounders.
GWG was associated with infant BMI z-score at birth, independent of potential confounding factors. Independent of GWG, we observed an overall decrease in BMI z-score from 18 months to 5 years in children of mothers who were underweight, while an increase in BMI z-score was seen in children of mothers who were overweight or obese. In children of normal- and overweight mothers, the risk of childhood overweight and obesity was associated with excessive compared to adequate GWG (adjusted odds ratio [aOR] 1.17, 95% confidence interval [CI] 1.01–1.36 for normal-weight mothers, and aOR 1.25, 95% CI 1.04–1.51 for overweight mothers, respectively). Children of mothers with obesity and excessive GWG had the highest risk of being overweight or obese at 4 years (aOR 2.88, 95% CI 2.40–3.44, and 4.38, 95% CI 3.37–5.67, respectively). Associations did not differ between children of mothers with obesity class 1 and 2–3 when comparing excessive and adequate GWG (aOR 1.33, 95% CI 0.96–1.85, and 1.12, 95% CI 0.74–1.70, respectively).
Maternal GWG affects infant birth size and growth until 18 months, although maternal BMI is more crucial for childhood growth beyond 18 months. Further, children of mothers who are normal- or overweight and experience excessive GWG have an increased risk of obesity at 4 years.
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