RESUMO
BACKGROUND: Almost all cases of cervical cancer can be attributed to human papillomavirus (HPV) infection. The loop electrosurgical excision procedure (LEEP) is widely used to treat HPV-mediated disease; thus, cervical cancer is highly preventable. However, LEEP does not necessarily clear HPV rapidly and may affect the accuracy of the results of ThinPrep cytology test (TCT) and cervical biopsy due to the formation of cervical scars. CASE SUMMARY: A 40-year-old woman underwent LEEP for cervical intraepithelial neoplasia grade 1 approximately 10 years ago. Subsequent standard cervical cancer screening suggested persistent HPV-52 infection, but TCT results were negative. Cervical biopsy under colposcopy was performed thrice over a 10-year period, yielding negative pathology results. She developed abnormal vaginal bleeding after sexual activity, persisting for approximately 1 year, and underwent hysteroscopy in our hospital. Histopathologic evaluation confirmed adenocarcinoma in situ of the uterine cervix. CONCLUSION: Patients with long-term persistent, high-risk HPV infection and negative pathology results of cervical biopsy after LEEP are at risk of cervical cancer. Hysteroscopic resection of cervical canal tissue is recommended as a supplement to cervical biopsy because it helps define the lesion site and may yield a pathologic diagnosis.
RESUMO
Intrauterine growth restriction (IUGR), when a fetus does not grow as expected, is associated with a reduction in hepatic functionality and a higher risk for chronic liver disease in adulthood. Utilizing early developmental plasticity to reverse the outcome of poor fetal programming remains an unexplored area. Focusing on the biochemical profiles of neonates and previous transcriptome findings, piglets from the same fetus are selected as models for studying IUGR. The cellular landscape of the liver is created by scRNA-seq to reveal sex-dependent patterns in IUGR-induced hepatic injury. One week after birth, IUGR piglets experience hypoxic stress. IUGR females exhibit fibroblast-driven T cell conversion into an immune-adapted phenotype, which effectively alleviates inflammation and fosters hepatic regeneration. In contrast, males experience even more severe hepatic injury. Prolonged inflammation due to disrupted lipid metabolism hinders intercellular communication among non-immune cells, which ultimately impairs liver regeneration even into adulthood. Additionally, Apolipoprotein A4 (APOA4) is explored as a novel biomarker by reducing hepatic triglyceride deposition as a protective response against hypoxia in IUGR males. PPARα activation can mitigate hepatic damage and meanwhile restore over-expressed APOA4 to normal in IUGR males. The pioneering study offers valuable insights into the sexually dimorphic responses to hepatic injury during IUGR.