Endometrial cancer is one of the most frequently diagnosed gynecological neoplasms in developed countries and its incidence is rising. Usually, it is diagnosed in the early stages of the disease and has a good prognosis; however, in later stages, the rate of recurrence reaches up to 60%. The discrepancy in relapse rates is due to the heterogeneity of the group related to the presence of prognostic factors affecting survival parameters. Increased body weight, diabetes, metabolic disturbances and estrogen imbalance are important factors for the pathogenesis of endometrial cancer. Even though prognostic factors such as histopathological grade, clinical stage, histological type and the presence of estrogen and progesterone receptors are well known in endometrial cancer, the search for novel prognostic biomarkers continues. Adipose tissue is an endocrine organ involved in metabolism, immune response and the production of biologically active substances participating in cell growth and differentiation, angiogenesis, apoptosis and carcinogenesis. In this manuscript, we review the impact of factors secreted by the adipose tissue involved in the regulation of glucose and lipid metabolism (leptin, adiponectin, omentin, vaspin, galectins) and factors responsible for homeostasis maintenance, inflammatory processes, angiogenesis and oxidative stress (IL-1β, 6, 8, TNFα, Vascular endothelial growth factor (VEGF), Fibroblast growth factors (FGFs)) in the diagnosis and prognosis of endometrial cancer.

The current stratification model of aneurysm rupture seems to be insufficient in some clinical cases. In our study, we determined the differences in wall structure between ruptured and unruptured aneurysms. We obtained computed tomography angiograms and categorized them into the following three groups, consisting of 49 patients each: the group with ruptured abdominal aortic aneurysms (rAAA), symptomatic (sAAA), and asymptomatic (aAAA). The three-dimensional AAA anatomy was digitally reconstructed for each patient through semi-automatically obtained segmentation, and each aneurysm was distinguished by the following three parameters: AFL (aneurysm flow lumen), ILT (intraluminal thrombus), and calcifications. The AFL volume was greater in rAAA compared with aAAA (p = 0.004), the ILT volume was greater in aAAA than in rAAA (p = 0.013), and the AFL/ILT surface ratio was bigger in rAAA than in aAAA (p < 0.001), sAAA than in aAAA (p = 0.033), and rAAA than in sAAA (p = 0.016). AFL/ILT surface*100 was defined as an independent predictive factor of rAAA to aAAA (OR 1.187; 95% CI 1.099–1.281), to sAAA (OR 1.045; 95% CI 1.004–1.087), and in sAAA vs. aAAA (OR 1.067; 95% CI 1.017–1.119). Consequently, the wall of rAAA differs significantly from unruptured aneurysms. The AFL/ILT surface ratio might indicate an increased risk of aneurysm rupture and the occurrence of symptoms in AAA.

Type II endoleak is one of the most common and problematic complications after endovascular aneurysm repair. It has been suggested that the inferior mesenteric artery (IMA) embolization could prevent further adverse events and postoperative complications. This article is a systematic review and meta-analysis following PRISMA guidelines. The Medline, PubMed, Embase, and Cochrane databases were used to identify studies that investigated the effect of IMA embolization on the occurrence of type II endoleaks and secondary interventions in a group of patients with abdominal aortic aneurysm who underwent EVAR compared with results after EVAR procedure without embolization. A random effects meta-analysis was performed. Of 3510 studies, 6 studies involving 659 patients were included. Meta-analysis of all studies showed that the rate of secondary interventions was smaller in patients with IMA embolization (OR, 0.17; SE, 0.45; 95% CI, 0.07 to 0.41; p < 0.01; I2 = 0%). The occurrence of type II endoleaks was also smaller in the embolization group (OR, 0.37; SE, 0.21; 95% CI, 0.25 to 0.57; p < 0.01; I2 = 16.20%). This meta-analysis suggests that IMA embolization correlates with lower rates of type II endoleaks and secondary interventions.