The aim of this study is to investigate the association between oxidative stress and bone mineral density (BMD) according to menopausal status of Korean women. A total of 2,232 women who visited to the health promotion center at Pusan National University Hospital between 2010 and 2014 were included in this cross-sectional study. Laboratory tests, such as uric acid, albumin, total bilirubin, which were evaluated as a natural antioxidants. Homocysteine also was evaluated as a factor associated with oxidative stress. Correlation analyses and partial correlation coefficient between BMD scores and laboratory parameters associated with oxidative stress according to menopausal status were performed with Pearson test. By correlation analysis, uric acid had only positive correlation with femur and lumbar BMD in premenopausal and postmenopausal group. But albumin and bilirubin, which were the other natural antioxidants, had no correlation with BMD except total bilirubin with femur BMD in postmenopausal group. Homocysteine had negative correlation with femur BMD in postmenopausal group. But there were different results in partial correlation coefficient adjusted by age and BMI. In premenopausal group, uric acid was still positive correlation with femur and lumbar BMD, whereas in postmenopausal group homocysteine had no correlation with femur BMD, total bilirubin and uric acid had no correlation with lumbar BMD. At the multiple logistic regressions, only age and menopause status, uric acid had correlation with BMD. In this study, homocysteine had no correlation with BMD. But in natural antioxidant, uric acid had only positive correlation with BMD.

Pregnancy-related osteoporosis is a very rare condition characterized by the occurrence of fracture during pregnancy or the puerperium. Despite its relative rarity, it can be a dangerous condition that causes severe back pain, height loss and disability. Normal physiologic changes during pregnancy, genetic or racial difference, obstetrical history and obstetrical disease, such as preterm labor or pregnancy-induced hypertension, are presumed risk factors of pregnancy-related osteooporosis. However, exact etiology and pathogenesis are uncertain. The management and natural history are still poorly defined. Traditional medications for osteoporosis are calcium/vitamin D and bisphosphonate. Concerns with bisphosphonate include accumulation in bone and fetal exposure in subsequent pregnancies. The newly developed medication, teriparatide, has shown good results. We report six cases of pregnancy-related osteoporosis and spinal fracture with literature review.

To evaluate the effect of tamoxifen on female reproductive organs in women with breast cancer. We retrospectively reviewed the medical records of 309 women with breast cancer who were currently receiving tamoxifen and undergoing regular gynecological examination. We evaluated 92 pre- and 217 postmenopausal women. The prevalence of endometrial thickening was 12% in the pre- and 10.6% in the postmenopausal group. An endometrial biopsy was performed in 43 women and confirmed endometrial cancer in 1, endometrial polyps in 14, and endometrial hyperplasia in 4 women. Transvaginal ultrasonography showed 25 cases of newly developed ovarian cysts. Most ovarian cysts had disappeared during follow-up. Tamoxifen use in women with breast cancer causes few complications and is considered safe for female reproductive organs in case of regular gynecological examination.

Endometriosis is a chronic gynecological disorder characterized by the presence of endometrial-like tissue outside the uterus, leading to inflammation, pain, and infertility. Emerging evidence indicates that endometriotic lesions exhibit cancer-like properties, including metabolic reprogramming marked by increased glucose uptake, enhanced Warburg’s effect, and altered mitochondrial function. These metabolic adaptations support cell survival under hypoxic conditions and contribute to immune evasion and sustained proliferation. This review summarizes current findings on the molecular mechanisms driving metabolic reprogramming in endometriosis, including the roles of mitochondrial dysfunction, hypoxia-inducible factor (HIF) signaling, the PI3K/AKT/mTOR pathway, inflammatory cytokines, and genetic and epigenetic regulators. In addition, we discuss therapeutic strategies targeting glycolytic pathways using both synthetic inhibitors and natural compounds, which represent promising non-hormonal options. Finally, we highlight the need for further preclinical and clinical studies to validate metabolic interventions and improve outcomes for patients with endometriosis.

Shin KH, et al. Ann Lab Med. 2020 Jan;40(1):40-47. https://doi.org/10.3343/alm.2020.40.1.40

Endometriosis is a gynecological disease prevalent in women of reproductive age, and it is characterized by the ectopic presence and growth of the eutopic endometrium. The pathophysiology and diagnostic biomarkers of endometriosis have not yet been comprehensively determined. To discover molecular markers and pathways underlying the pathogenesis of endometriosis, we identified differentially expressed genes (DEGs) in three Gene Expression Omnibus microarray datasets (GSE11691, GSE23339, and GSE7305) and performed gene set enrichment analysis (GSEA) and protein–protein interaction (PPI) network analyses. We also validated the identified genes via immunohistochemical analysis of tissues obtained from patients with endometriosis or healthy volunteers. A total of 118 DEGs (79 upregulated and 39 downregulated) were detected in each dataset with a lower (fold change) FC cutoff (log2|FC| > 1), and 17 DEGs (11 upregulated and six downregulated) with a higher FC cutoff (log2|FC| > 2). KEGG and GO functional analyses revealed enrichment of signaling pathways associated with inflammation, complement activation, cell adhesion, and extracellular matrix in endometriotic tissues. Upregulation of seven genes (C7, CFH, FZD7, LY96, PDLIM3, PTGIS, and WISP2) out of 17 was validated via comparison with external gene sets, and protein expression of four genes (LY96, PDLIM3, PTGIS, and WISP2) was further analyzed by immunohistochemistry and western blot analysis. Based on these results, we suggest that TLR4/NF-κB and Wnt/frizzled signaling pathways, as well as estrogen receptors, regulate the progression of endometriosis. These pathways may be therapeutic and diagnostic targets for endometriosis.