No abstract

The aim of this study was to evaluate the prognostic and predictive efficacy of the human epididymis secretory protein 4 (HE4) and serum amyloid-A (S-AA) together with the other tumor markers (CA 125, CA 15-3, CEA, and CA 19-9) in endometrial cancer patients. The study group consisted of 64 patients with defined stage and grade of endometrial cancer and 60 women with benign uterine diseases. Thirty-four healthy women were defined as the control group. Fasting blood samples were collected prior to surgery and tumor marker levels were determined in blood samples by E170 autoanalyzer. S-AA concentrations were measured by particle-enhanced immunonephelometry. Preoperative serum HE4 and S-AA levels were significantly higher in endometrial cancer patients than in controls, whereas the other measured parameters were not significantly different. Serum levels of HE4 were related to both the stage and grade of tumor. The best cutoff point for HE4 was determined to be 59.7 pmol/L; with 75 % sensitivity and 65.5 % specificity. For S-AA, the cutoff point was 8.8 U/mL, with 68.7 % sensitivity and 58.6 % specificity. The combination of HE4, CA 125, CEA, and S-AA raised the sensitivity to 84 %. Preoperative measurement of serum HE4 and S-AA may be of help in early detection of endometrial cancer. Preoperative screening with these markers may provide important information about the patient's outcome and prognosis.

This study was designed to determine the activities of superoxide dismutase and glutathione peroxidase and some of the lipid peroxidation indices (malondialdehyde and total sulfhydryl groups) in eutopic and ectopic endometria of patients with endometriosis. Ectopic endometrial tissues (ovarian cysts; n = 22) were obtained laparoscopically during the preovulatory period. Statistical analyses were made using the Wilcoxon signed-rank test. The levels of malondialdehyde and total sulfhydryl groups were similar in the eutopic and ectopic endometria, whereas the superoxide dismutase activity was found to be significantly higher in the latter (1,893 ± 780 vs. 3,512 ± 1,502 U/g protein; p = 0.002). Although the glutathione peroxidase activity was slightly lower in the ectopic than in the eutopic tissues, the difference was not found to be statistically significant. The malondialdehyde levels were positively correlated with the plasma 17β-estradiol concentrations in the ectopic endometria (r = 0.683, p = 0.001). No such correlation was seen in the eutopic tissue. It is suggested that various factors, such as cytokines released by activated macrophages in the peritoneal fluid and 17β-estradiol itself synthesized by the ovaries, may locally affect the oxidant status of ectopic endometria.

Our biochemical and morphological findings suggest a different organisation of collagen fibres in tissues of patients with USI+POP, when compared with both the controls and the POP patients.

Fetuin-A is synthesized in the liver and is secreted into the bloodstream. Clinical studies suggest involvement of fetuin-A in metabolic disorders such as visceral obesity, insulin resistance, diabetes, and fatty liver. Curcumin is extracted from the rhizome Curcuma longa and has been shown to possess potent antioxidant, anticarcinogenic, anti-inflammatory, and hypoglycemic properties. In this study, we investigated the effect of curcumin treatment on serum fetuin-A levels as well as hepatic lipids and prooxidant-antioxidant status in rats fed a high-fat diet (HFD). Male Sprague-Dawley rats were divided into six groups. Group 1 was fed control diet (10 % of total calories from fat). Groups 2 and 3 were given curcumin (100 and 400 mg/kg bw/day, respectively ) by gavage for 8 weeks and were fed control diet. Group 4 was fed with HFD (60 % of total calories from fat). Groups 5 and 6 received HFD together with the two doses of curcumin, respectively. Curcumin treatment appeared to be effective in reducing liver triglycerides and serum fetuin-A levels. These findings suggest that the reduction of fetuin-A may contribute to the beneficial effects of curcumin in the pathogenesis of obesity.