Expanding Access to Contraceptive Services in a Family Medicine Residency Clinic: The Rapid Access to Contraception Clinic Model.

BACKGROUND AND OBJECTIVES: Learning to provide long-acting reversible contraception (LARC) during family medicine residency is an important step in building capacity for the primary care workforce to meet the reproductive health care needs of communities. We aimed to measure the impact of adding a contraceptive visit type (CVT) allowing for rapid access to contraception (RAC) on family medicine resident LARC procedure numbers. METHODS: Our program created a CVT in which patients were seen only for contraceptive services. We added the CVT to third-year family medicine resident continuity clinic schedules and a block of CVTs (the RAC clinic) to the third-year gynecology rotation. Residents self-reported LARC procedure numbers performed throughout residency, and the totals were compared for graduating residents from 2023 (post-RAC cohort) to 2022 graduates and 2018-2022 graduates (pre-RAC cohort). RESULTS: Post-RAC cohort residents reported a statistically significant increase in intrauterine device (IUD; P=.015) and contraceptive implant (P=.010) removals compared to the 2022 pre-RAC cohort. Insertions of IUDs and contraceptive implants were unchanged when compared to the pre-RAC cohort. IUD removals (P=.004) and insertions (P=.034), and contraceptive implant removals (P=.028) were significantly increased for post-RAC compared to 2022 graduates, with no difference in contraceptive implant insertions (P=.211). CONCLUSIONS: The addition of the CVT and RAC clinic contributed to an increase in LARC removals in both comparisons, and IUD insertions between 2022 and 2023. This clinic model offers an opportunity for other family medicine residency programs to improve access to contraceptive services and increase resident training in LARC management.

Epithelial myosin light chain kinase activation induces mucosal interleukin-13 expression to alter tight junction ion selectivity.

Intestinal barrier function is reduced in inflammatory bowel disease (IBD). Tumor necrosis factor (TNF) and interleukin (IL)-13, which are up-regulated in IBD, induce barrier defects that are associated with myosin light chain kinase (MLCK) activation and increased claudin-2 expression, respectively, in cultured intestinal epithelial monolayers. Here we report that these independent signaling pathways have distinct effects on tight junction barrier properties and interact in vivo. MLCK activation alters size selectivity to enhance paracellular flux of uncharged macromolecules without affecting charge selectivity and can be rapidly reversed by MLCK inhibition. In contrast, IL-13-dependent claudin-2 expression increases paracellular cation flux in vitro and in vivo without altering tight junction size selectivity but is unaffected by MLCK inhibition in vitro. In vivo, MLCK activation increases paracellular flux of uncharged macromolecules and also triggers IL-13 expression, claudin-2 synthesis, and increased paracellular cation flux. We conclude that reversible, MLCK-dependent permeability increases cause mucosal immune activation that, in turn, feeds back on the tight junction to establish long-lasting barrier defects. Interactions between these otherwise distinct tight junction regulatory pathways may contribute to IBD pathogenesis.

Targeted epithelial tight junction dysfunction causes immune activation and contributes to development of experimental colitis.

BACKGROUND & AIMS: Inflammatory bowel disease (IBD) is a multifactorial disease thought to be caused by alterations in epithelial function, innate and adaptive immunity, and luminal microbiota. The specific role of epithelial barrier function remains undefined, although increased activity of intestinal epithelial myosin light chain kinase (MLCK), which is the primary mechanism of tumor necrosis factor-induced barrier dysfunction, occurs in human IBD. Our aim was to determine whether, in an intact epithelium, primary dysregulation of the intestinal epithelial barrier by pathophysiologically relevant mechanisms can contribute to development of colitis. METHODS: We developed transgenic (Tg) mice that express constitutively active MLCK (CA-MLCK) specifically within intestinal epithelia. Their physiology, immune status, and susceptibility to disease were assessed and compared with non-Tg littermate controls. RESULTS: CA-MLCK Tg mice demonstrated significant barrier loss but grew and gained weight normally and did not develop spontaneous disease. CA-MLCK Tg mice did, however, develop mucosal immune activation demonstrated by increased numbers of lamina propria CD4(+)lymphocytes, redistribution of CD11c+cells, increased production of interferon-gamma and tumor necrosis factor, as well as increased expression of epithelial major histocompatibility complex class I. When challenged with CD4+CD45+Rb(hi) lymphocytes, Tg mice developed an accelerated and more severe form of colitis and had shorter survival times than non-Tg littermates. CONCLUSIONS: Primary pathophysiologically relevant intestinal epithelial barrier dysfunction is insufficient to cause experimental intestinal disease but can broadly activate mucosal immune responses and accelerate the onset and severity of immune-mediated colitis.