Endometrial polyps with increased plasma cells are associated with chronic endometritis in infertility patients: Hysteroscopic findings and post-polypectomy pregnancy rates.

PURPOSE: The relationship between endometrial polyps (EPs), chronic endometritis (CE), hysteroscopic findings, and antimicrobial in infertility patients was determined. METHODS: We retrospectively enrolled 115 infertility patients with suspected EPs who underwent office hysteroscopy. Patients were divided into 3 groups: 38 with increased plasma cells in EPs (group 1); 31 without increased plasma cells in EPs (group 2); and 46 without EPs (group 3). The 3 groups underwent hysteroscopy with or without polypectomies, and immediately thereafter, an endometrial aspiration biopsy (EAB) was performed. CE was diagnosed based on plasma cell infiltration in the non-polypoid endometrium obtained by EAB. RESULTS: The percentage of CE was 68.4%, 32.2%, and 28.3% in groups 1, 2, and 3, respectively. CE was more frequent in group 1 than group 2 or 3 (P = .01 and P = .002, respectively). The number of polyps was higher in group 1 than group 2. After adjustment for age and assisted reproductive technology, antibiotic therapy was not associated with pregnancy (adjusted odds ratio, 0.44; 95% confidence interval, 0.05-3.57) in patients with EPs and CE. CONCLUSIONS: Group 1 was associated with CE, and hysteroscopic findings were different from group 2. Antibiotic therapy after polypectomy for EPs with CE may not always be necessary.

Oxidized LDL and lysophosphatidylcholine stimulate plasminogen activator inhibitor-1 expression through reactive oxygen species generation and ERK1/2 activation in 3T3-L1 adipocytes.

Plasminogen activator inhibitor-1 (PAI-1) is secreted from adipose tissue and is considered to be a risk factor for both atherosclerosis and insulin resistance. Here we report for the first time that PAI-1 expression is enhanced by oxidized low-density lipoprotein (OxLDL) and its lipid component lysophosphatidylcholine (LPC) in mouse 3T3-L1 adipocytes. In fully differentiated 3T3-L1 cells, OxLDL treatment increased the mRNA expression and protein secretion of PAI-1 in a dose- and time-dependent manner, whereas native LDL had no effect. The addition of an anti-CD36 antibody suppressed OxLDL-stimulated PAI-1 expression by 50%, suggesting that adipose-derived CD36 contributes to roughly half of the PAI-1 expression stimulated by OxLDL. In addition, pharmacological experiments showed that the OxLDL-stimulated enhancement in PAI-1 expression was mediated through the generation of reactive oxygen species (ROS) and phosphorylation of extracellular signal-regulated kinase 1/2. Furthermore, LPC, a major lipid component of OxLDL, was responsible for the enhanced expression of PAI-1 as phospholipase A(2)-treated acetyl LDL, which generates LPC, strongly stimulated PAI-1 expression, whereas acetyl LDL itself had no such activity. These data demonstrate that the uptake of OxLDL and, in particular, its lipid component LPC into adipocytes triggers aberrant ROS-mediated PAI-1 expression, which may be involved in the pathogenesis of metabolic syndrome.