Prenatal care utilization in pregnant women who consider but do not have abortions.

BACKGROUND: Over half of all pregnancies in the United States are unintended, and 18% result in termination of pregnancy (TOP). Some women seek TOP, but ultimately continue their pregnancy. Data are limited about their utilization of prenatal care and their perinatal outcomes. Our primary outcome was to investigate differences in guideline-based prenatal care utilization in women who consider but do not have an abortion. METHODS: Retrospective cohort study of patients having obstetrical dating ultrasound (US) from 2011-2018 at a single academic medical center that offers TOP. Contemplators completed US with intention of TOP but instead continued the pregnancy to live birth. A 2:1 group of non-contemplators completed US and continued to live birth. A prenatal care utilization scoring system was used to compare groups. Secondary outcomes investigated differences in adverse pregnancy outcomes and postpartum care. RESULTS: There were 94 contemplators and 183 non-contemplators. Inadequate prenatal care utilization initially was more common in contemplators than non-contemplators (62.8% vs 85.8%, p < 0.01) but was not significant after adjustment (aOR 1.0, 95% CI 0.40 - 2.56). There were no differences in adverse obstetric or neonatal outcomes. Contemplators were significantly more likely to have a postpartum contraceptive method (PPCM) upon hospital discharge (aOR 4.8, 95% CI 1.16 - 20.0) and significantly more likely to use a highly-effective PPCM (aOR 6.4, 95% CI 2.34 - 17.4). CONCLUSIONS: Reversal of intention for TOP is not associated with differences in prenatal care utilization, but is associated with increased uptake of postpartum contraceptive method.

Author Correction: Microbiota therapy acts via a regulatory T cell MyD88/RORγt pathway to suppress food allergy.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Microbiota therapy acts via a regulatory T cell MyD88/RORγt pathway to suppress food allergy.

The role of dysbiosis in food allergy (FA) remains unclear. We found that dysbiotic fecal microbiota in FA infants evolved compositionally over time and failed to protect against FA in mice. Infants and mice with FA had decreased IgA and increased IgE binding to fecal bacteria, indicative of a broader breakdown of oral tolerance than hitherto appreciated. Therapy with Clostridiales species impacted by dysbiosis, either as a consortium or as monotherapy with Subdoligranulum variabile, suppressed FA in mice as did a separate immunomodulatory Bacteroidales consortium. Bacteriotherapy induced expression by regulatory T (Treg) cells of the transcription factor ROR-γt in a MyD88-dependent manner, which was deficient in FA infants and mice and ineffectively induced by their microbiota. Deletion of Myd88 or Rorc in Treg cells abrogated protection by bacteriotherapy. Thus, commensals activate a MyD88/ROR-γt pathway in nascent Treg cells to protect against FA, while dysbiosis impairs this regulatory response to promote disease.

A Review of Multidisciplinary Interventions in Atopic Dermatitis.

Multidisciplinary interventions have been developed for patients with atopic dermatitis (AD) and their families, with the aim of improving outcomes such as disease control, adherence, and quality of life. We reviewed the content of different multidisciplinary approaches to intervention for AD and evidence for their impact on key outcome measures. We also provided data from our multidisciplinary outpatient program for pediatric AD. Studies included in the review suggest benefits of multidisciplinary interventions as models of treatment or adjuncts to standard medical care, with a positive impact on outcomes including disease severity and itching/scratching. There were limitations to existing studies, including heterogeneous methods used to assess quality of life outcomes across studies and lack of controlled studies assessing the outcome of clinical care programs. Further research will be useful in assessing the impact of multidisciplinary interventions on important outcomes such as treatment adherence and sleep, identifying the elements of multidisciplinary interventions that are most critical for improved outcomes, and identifying the best candidates for multidisciplinary intervention approaches.

Fluoxetine modulates breast cancer metastasis to the brain in a murine model.

BACKGROUND: Despite advances in the treatment of primary breast tumors, the outcome of metastatic breast cancer remains dismal. Brain metastases present a particularly difficult therapeutic target due to the "sanctuary" status of the brain, with resulting inability of most chemotherapeutic agents to effectively eliminate cancer cells in the brain parenchyma. A large number of breast cancer patients receive various neuroactive drugs to combat complications of systemic anti-tumor therapies and to treat concomitant diseases. One of the most prescribed groups of neuroactive medications is anti-depressants, in particular selective serotonin reuptake inhibitors (SSRIs). Since SSRIs have profound effects on the brain, it is possible that their use in breast cancer patients could affect the development of brain metastases. This would provide important insight into the mechanisms underlying brain metastasis. Surprisingly, this possibility has been poorly explored. METHODS: We studied the effect of fluoxetine, an SSRI, on the development of brain metastatic breast cancer using MDA-MB-231BR cells in a mouse model. RESULTS: The data demonstrate that fluoxetine treatment increases the number of brain metastases, an effect accompanied by elevated permeability of the blood-brain barrier, pro-inflammatory changes in the brain, and glial activation. This suggests a possible role of brain-resident immune cells and glia in promoting increased development of brain metastases. CONCLUSION: Our results offer experimental evidence that neuroactive substances may influence the pathogenesis of brain metastatic disease. This provides a starting point for further investigations into possible mechanisms of interaction between various neuroactive drugs, tumor cells, and the brain microenvironment, which may lead to the discovery of compounds that inhibit metastasis to the brain.