Publications of Charline BEGUIN
Bookmark and Share    
Full Text
See detailUse of methotrexate in the treatment of ectopic pregnancies: a retrospective single center study.
BEGUIN, Charline ULiege; Brichant, Géraldine ULiege; DE LANDSHEERE, Laurent ULiege et al

in Facts, views & vision in ObGyn (2020), 11(4), 329-335

INTRODUCTION: The aim of this study was to evaluate the efficacy of methotrexate (MTX) in the treatment of ectopic pregnancies. We identified predictive factors of success or failure and compared our ... [more ▼]

INTRODUCTION: The aim of this study was to evaluate the efficacy of methotrexate (MTX) in the treatment of ectopic pregnancies. We identified predictive factors of success or failure and compared our results with previous studies to make recommendations for its use. MATERIAL AND METHODS: A cohort of 61 patients from a single center was retrospectively analyzed. Inclusion criteria were a diagnosis of ectopic pregnancy and treatment with a single-dose injection of MTX. The need to perform surgery despite MTX was defined as treatment failure while needing a second MTX injection was not. RESULTS: In our cohort, MTX demonstrated a success rate of 80%. This rate rose to 84% when patients with human Chorionic Gonadotropin (hCG ) > 5,000 IU/L were excluded. Twenty percent underwent surgery for pain, increased mass size and/or suboptimal hCG kinetics. Low hCG levels on days 0, 4 and 7 as well as the absence of pain, metrorrhagia and hemoperitoneum were predictive of success. MTX was also efficient in the treatment of persisting pregnancies of unknown location (PUL). CONCLUSION: Our results are consistent with previous studies and emphasize the fact that MTX is less effective above a certain level of hCG. We obtained a cut-off value of 2439 IU/L with a sensitivity of 66.7% and a specificity of 93.9%. MTX should not be used when hCG is higher than 5,000 IU/L and laparoscopic surgery should be performed. Our results bring additional data about the efficacy of MTX in the management of persisting pregnancies of unknown location. [less ▲]

Detailed reference viewed: 47 (15 ULiège)
Full Text
See detailEpithelial RABGEF1 deficiency promotes intestinal inflammation by dysregulating intrinsic MYD88-dependent innate signaling.
El Abbas, Sophie ULiege; Radermecker, Coraline ULiege; Bai, Qiang ULiege et al

in Mucosal Immunology (2019)

Intestinal epithelial cells (IECs) contribute to the regulation of intestinal homeostasis and inflammation through their interactions with the environment and host immune responses. Yet our understanding ... [more ▼]

Intestinal epithelial cells (IECs) contribute to the regulation of intestinal homeostasis and inflammation through their interactions with the environment and host immune responses. Yet our understanding of IEC-intrinsic regulatory pathways remains incomplete. Here, we identify the guanine nucleotide exchange factor RABGEF1 as a regulator of intestinal homeostasis and innate pathways dependent on IECs. Mice with IEC-specific Rabgef1 deletion (called Rabgef1(IEC-KO) mice) developed a delayed spontaneous colitis associated with the local upregulation of IEC chemokine expression. In mouse models of colitis based on Interleukin-10 deficiency or dextran sodium sulfate (DSS) exposure, we found that IEC-intrinsic RABGEF1 deficiency exacerbated development of intestinal pathology and dysregulated IEC innate pathways and chemokine expression. Mechanistically, we showed that RABGEF1 deficiency in mouse IECs in vitro was associated with an impairment of early endocytic events, an increased activation of the p38 mitogen-activated protein kinase (MAPK)-dependent pathway, and increased chemokine secretion. Moreover, we provided evidence that the development of spontaneous colitis was dependent on microbiota-derived signals and intrinsic MYD88-dependent pathways in vivo. Our study identifies mouse RABGEF1 as an important regulator of intestinal inflammation, MYD88-dependent IEC-intrinsic signaling, and chemokine production. This suggests that RABGEF1-dependent pathways represent interesting therapeutic targets for inflammatory conditions in the gut. [less ▲]

Detailed reference viewed: 75 (23 ULiège)
See detailRab guanine nucleotide exchange factor 1 (Rabgef1) restricts intestinal inflammation by limiting pro-inflammatory signals in Intestinal Epithelial Cells (IECs)
El Abbas, Sophie ULiege; BEGUIN, Charline ULiege; Schyns, Joey ULiege et al

in Proceedings: 4th FARAH-DAY (2017, October 13)

Rab guanine nucleotide exchange factor (GEF-)1 (Rabgef1), a multifunctional protein whose in vivo functions remained unknown until recently, is highly expressed in mouse and human epithelial cells. The ... [more ▼]

Rab guanine nucleotide exchange factor (GEF-)1 (Rabgef1), a multifunctional protein whose in vivo functions remained unknown until recently, is highly expressed in mouse and human epithelial cells. The aim of this study is to investigate the role of Rabgef1 in intestinal epithelial cells (IECs) and intestinal homeostasis in mice. We performed conditional deletion of Rabgef1 gene using the cre-lox system to obtain mice lacking Rabgef1 specifically in IECs (Rabgef1IEC-KO), under the wild-type (WT) or the colitis-prone Interleukin-10 (Il-10)-deficient background. In addition, we used the CRISPR-Cas9 technology to obtain a murine IEC line deficient in Rabgef1. Rabgef1IEC-KO mice under the WT background did not develop spontaneous intestinal abnormalities but exhibited an altered intestinal microbial composition associated with minor changes in IEC pro-inflammatory gene expression profile. Moreover, Rabgef1IEC-KO mice exhibited an increased susceptibility to inflammation in a dextran sodium sulfate (DSS)-induced model of colitis under the WT background, as well as in a constitutive model of colitis under the Il-10-¬deficient background. In vitro, we showed that mouse IECs lacking Rabgef1 significantly overexpressed several pro-inflammatory cytokines and chemokines as compared to control cells. Taken together, these results support that Rabgef1 acts as a regulator of intestinal homeostasis and inflammation, and that dysregulated Rabgef1 expression could contribute to intestinal barrier dysfunction in inflammatory conditions of the gut. [less ▲]

Detailed reference viewed: 36 (9 ULiège)