Plasma level of D-dimer accompanying different types of gynecologic surgery and effects of prophylactic subcutaneous injection of heparin calcium

Background: The standard range of D-dimer level associated with each type of gynecologic surgery is required to note the occurrence of bleeding or thromboembolism.Methods: Plasma levels of D-dimer of patients who underwent different types of gynecologic surgery were measured on the Day of Preoperative Examination (DPE) and the first postoperative day (POD-1). Patients were classified by surgery type: hysterectomy for benign diseases or cervical intraepithelial neoplasia; hysterectomy for uterine cancer; surgery for ovarian cancer; laparoscopic surgery for a benign adnexal mass; laparotomy for a benign adnexal mass; laparotomic myomectomy; cervical conization; transcervical resection of an intrauterine mass; vaginal surgery for prolapse of a pelvic organ.Results: In each type of gynecologic surgery, plasma levels of D-dimer on POD-1 were higher than those on the DPE. Prophylactic subcutaneous injection of heparin calcium for patients who underwent surgery for endometrial cancer showed no significant difference in the plasma level of D-dimer on the sixth postoperative day (POD-6) and the plasma level of D-dimer on POD-6 was in the same level as those on POD-1.Conclusions: Plasma levels of D-dimer on POD-1 were higher than those on the DPE in each type of gynecologic surgery. The D-dimer level remained high even on POD-6, and not changed by prophylactic subcutaneous injection of heparin calcium.

Vulvar microinvasive squamous cell carcinoma arising in vulvar intraepithelial neoplasia 3 complicated by genital warts and systemic lupus erythematosus: a case report

A patient suffering from long-term systemic lupus erythematosus attended with a complaint of recurrent genital warts. Perineal white-colored skin and a peri-anal papillary protrusion adjacent to the genital warts were biopsied and determined to be vulvar intraepithelial neoplasia (VIN) 3 and microinvasive squamous cell carcinoma (SCC), respectively. These lesions were locally excised. Human papillomavirus (HPV)-6 was detected in these lesions, including in the genital warts, while HPV-56 was detected only in the perineal VIN3 and peri-anal microinvasive SCC.

Necrostatin-1 protects against reactive oxygen species (ROS)-induced hepatotoxicity in acetaminophen-induced acute liver failure

Excessive acetaminophen (APAP) use is one of the most common causes of acute liver failure. Various types of cell death in the damaged liver are linked to APAP-induced hepatotoxicity, and, of these, necrotic cell death of hepatocytes has been shown to be involved in disease pathogenesis. Until recently, necrosis was commonly considered to be a random and unregulated form of cell death; however, recent studies have identified a previously unknown form of programmed necrosis called receptor-interacting protein kinase (RIPK)-dependent necrosis (or necroptosis), which is controlled by the kinases RIPK1 and RIPK3. Although RIPK-dependent necrosis has been implicated in a variety of disease states, including atherosclerosis, myocardial organ damage, stroke, ischemia–reperfusion injury, pancreatitis, and inflammatory bowel disease. However its involvement in APAP-induced hepatocyte necrosis remains elusive. Here, we showed that RIPK1 phosphorylation, which is a hallmark of RIPK-dependent necrosis, was induced by APAP, and the expression pattern of RIPK1 and RIPK3 in the liver overlapped with that of CYP2E1, whose activity around the central vein area has been demonstrated to be critical for the development of APAP-induced hepatic injury. Moreover, a RIPK1 inhibitor ameliorated APAP-induced hepatotoxicity in an animal model, which was underscored by significant suppression of the release of hepatic enzymes and cytokine expression levels. RIPK1 inhibition decreased reactive oxygen species levels produced in APAP-injured hepatocytes, whereas CYP2E1 expression and the depletion rate of total glutathione were unaffected. Of note, RIPK1 inhibition also conferred resistance to oxidative stress in hepatocytes. These data collectively demonstrated a RIPK-dependent necrotic mechanism operates in the APAP-injured liver and inhibition of this pathway may be beneficial for APAP-induced fulminant hepatic failure