Neutrophil gelatinase-associated lipocalin serum level: A potential noninvasive biomarker of endometriosis?

Neutrophil gelatinase-associated lipocalin (NGAL, also known as lipocalin-2) is an acute-phase protein expressed in many tissues and plays a role in cell proliferation, regulation, and epithelial-mesenchymal transformation. Therefore, this study aimed to investigate serum NGAL levels and endometrioma tissue expression in women with endometriosis. This cross-sectional study was conducted at a university hospital. The endometrioma group included 36 women who underwent ovarian cystectomy for endometrioma, which was compared with a control group (n = 36) of women who underwent ovarian cystectomy due to benign persistent cysts (follicle cyst, theca lutein cyst, and serous cystadenoma). NGAL levels were analyzed using both serum enzyme-linked immunosorbent assay analysis and immunohistochemical tissue staining. Serum C-reactive protein and CA-125 levels were also evaluated. NGAL serum levels were significantly higher in the endometrioma group than in the control group (P < .05). C-reactive protein and CA-125 levels were also significantly higher in the endometrioma group (P < .05) and were correlated with NGAL levels. Immunohistochemical staining for NGAL was also higher in the endometrioma group (P < .001). NGAL may be considered a potential noninvasive biomarker of endometriosis.

The role of ERK-1 and ERK-2 gene polymorphisms in PCOS pathogenesis.

BACKGROUND: Ovulation is regulated by extracellular signal-regulated kinase-1 (ERK-1) and ERK-2 signaling mechanisms, and ERK-1/2 kinases modulates the function of most of the LH-regulated genes. Defective ERK kinase signaling that is secondary to a genetic problem contributes to both ovulatory dysfunction and metabolic problems in polycystic ovary syndrome (PCOS). We planned to investigate ERK-1 and ERK-2 gene polymorphisms in PCOS for the first time in the Turkish population. METHODS: One hundred two PCOS patients and 102 healthy controls were recruited for this patient control study. HOMA-IR, Ferriman-Gallwey score (FGS), waist-to-hip ratio (WHR), and body mass index (BMI) were assessed. Lipid profile levels, CRP, and total testosterone were determined. ERK-2 rs2276008 (G > C) and ERK-1 rs11865228 (G > A) SNPs were analyzed with a real-time PCR system. RESULTS: ERK-1 and ERK-2 genotypes were found to differ between the PCOS and control groups. In patients with PCOS, ERK-1 GA and ERK-2 GC genotypes were different in terms of BMI, FGS, HOMA-IR, CRP, total testosterone, and total cholesterol levels. CONCLUSIONS: ERK-1 and ERK-2 genes are involved in PCOS pathogenesis. BMI, FGS, HOMA-IR, and CRP levels are related to the heterozygote polymorphic types of ERK-1 and ERK-2 genes.

Endotrophin as a novel marker in PCOS and its relation with other adipokines and metabolic parameters: a pilot study.

BACKGROUND: Polycystic ovary syndrome is known to be the most common hormonal disorder in women of reproductive age. Current evidence shows that regulatory proteins secreted from the adipose tissue called adipokines may have a role in polycystic ovary syndrome. We planned to investigate the role of endotrophin that has never been researched in polycystic ovary syndrome before and its correlation with other metabolic parameters and adipokines such as adiponectin and ghrelin in patients with polycystic ovary syndrome. METHODS: Forty-three women (n: 43) with polycystic ovary syndrome and 43 (n: 43) women as a control group were enrolled in this cross-sectional study. Serum levels of endotrophin, adiponectin, and ghrelin levels were measured with the enzyme-linked immunosorbent assay method. High-density lipoprotein cholesterol, low-density lipoprotein cholesterol, total cholesterol levels, luteinizing hormone/follicle-stimulating hormone ratio, total testosterone, and triglyceride levels were measured. Homeostasis model assessment for insulin resistance index, body mass index, Ferriman Gallwey Score, and waist-to-hip ratio were also evaluated. RESULTS: Total testosterone, homeostasis model assessment for insulin resistance, C-reactive protein, luteinizing hormone/follicle-stimulating hormone ratio, and triglyceride levels were higher in patients with polycystic ovary syndrome (p < 0.01). No difference was detected between the groups in terms of body mass index, Ferriman Gallwey Score, waist-to-hip ratio, total cholesterol, low-density lipoprotein, and high-density lipoprotein levels (p > 0.05). We did not observe any significant difference in adiponectin and ghrelin levels between the groups (p > 0.05). Patients with polycystic ovary syndrome had significantly higher endotrophin levels (p < 0.01). According to our regression analyses [area under the curve: 0.973 (0.935-1.000), 95% confidence interval, 95.2% sensitivity, and 100% specificity], it was shown that endotrophin greater than 92 ng/ml and homeostasis model assessment for insulin resistance greater than 2.5 might be good predictors for polycystic ovary syndrome diagnosis. CONCLUSION: We demonstrated that endotrophin level is higher in patients with polycystic ovary syndrome and may have predicted polycystic ovary syndrome with increased homeostasis model assessment for insulin resistance index. There was no significant difference in adiponectin and ghrelin levels in the polycystic ovary syndrome group. Endotrophin may have a role in polycystic ovary syndrome etiology rather than other adipokines.