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Endometriosis shares similarities with several autoimmune diseases. The human leukocyte antigen (HLA)-C genotype is associated with several human autoimmune diseases. HLA-C is a ligand of killer cell immunoglobulin receptors (KIRs) and is an essential regulator of natural killer cell activity, which is associated with endometriosis progression. Polymorphisms in HLA-C and KIR affect the activity of NK cells and susceptibility to several diseases. Therefore, we attempted to investigate an association between HLA-C genotype and KIR polymorphism and the occurrence of endometriosis. We tested the association of certain KIR and HLA-C combinations and the development of endometriosis by characterizing both KIR and HLA-C genes in 147 women with endometriosis and 117 controls. The HLA-C genotypes and KIR polymorphisms were analyzed via DNA-based method for higher-resolution genotyping. We found that the occurrence of HLA-C*03:03*01 was increased in endometriosis than in control groups. Analysis of various KIR haplotypes revealed differences between the endometriosis and control cohorts. The number of KIR centromeric A/A haplotypes was increased in the endometriosis group than controls. Moreover, the endometriosis cohort was characterized by reduced number of KIR2DS2-positive individuals in the Han Chinese population. Our current findings suggest that the KIR and HLA-C genotypes are associated with the pathogenesis of endometriosis.

The antenatal diagnosis of aortic dissection carries a grave prognosis. Although cases of pregnant women with Marfan syndrome have been encountered that resulted either in sudden death or emergency surgery at diagnosis, cesarean section delivery for patients who survive is associated with the risk of anesthesia and manipulation of the abdomen. Such complications can be avoided if the aortic dissection can be treated conservatively. We report the successful treatment of an aortic dissection with pharmacologic therapy and the birth of a healthy infant.

The physiological changes in endometriosis involving multiple steps of matrix remodeling include abnormal tissue growth, invasion, and adhesion formation. Endometriosis-associated abnormal matrix remodeling is affected by several molecular factors including proteolytic enzymes and their inhibitors, which mediate tissue turnover throughout the reproductive tract to maintain the integrity of the endometrium, and ovarian steroids, which normally regulate reconstruction and breakdown of endometrium in the menstrual cycle. In addition, various growth factors, such as platelet-derived growth factor, transform growth factor β, and epidermal growth factor, direct modulation of growth, activation, and chemotaxis which may facilitate endometrial cell adhesion onto the peritoneal mesothelium during the development of endometriosis. Furthermore, cell adhesion molecules are believed to be critically involved in most cellular-level processes including cellular differentiation, motility, and attachment with the extracellular matrix. The present review focuses on the abnormal matrix remodeling process and its possible regulatory mechanism in association with endometriosis development. As a greater understanding of the cause of endometriosis is achieved, better treatment of the disease and its prevention become possible.

Vanishing fetuses are frequently encountered in pregnancies results from in vitro fertilization. Ultrasound scans taken at the 4-5th weeks showed multiple gestation has occurred, it frequently happens that more than one amniotic sac can be seen in early pregnancy, whereas a few weeks later there is only one to be seen and the other has disappeared. Whereas the triplet pregnancy evolved into a normal twin gestation, and may further evolve into a singleton gestation. These very high resorption rates, which can be explained on the basis of the intense fetal competition for space, nutrition, or other factors during early gestation with frequent loss of the other fetus. Here, we report a case of a vanishing triplet of spontaneous pregnancy, one fetus vanished in the first month of pregnancy while another fetus disappeared at the end of second month. The normal pregnancy of the singleton was followed up until six months.

Intrauterine devices (IUDs) have been plagued by many early and late complications, including uterine perforation and subsequent migration into adjacent structures. Perforation of the uterus by an IUD is a serious complication occurring in approximately 1 of 350 to 1 of 2,500 insertions. It is more common among older women with “lost” IUDs. This case illustrates that unusual phenomenon that a lost IUD can penetrate into the omentum. We herein report a case of acute peritonitis and pneumoperitoneum with perforation of the uterus associated with a lost IUD and perforation of a malignancy of the sigmoid colon. A 68-year-old woman, Gravida 4, Para 4, presented to the emergency department with a 2-hour history of sudden, diffuse lower abdominal pain. Physical examination revealed an acutely ill-appearing patient with unstable vital signs, including a temperature of 37.8 C. The patient’s abdomen was distended with marked rebounding tenderness and varying tympanic sound on percussion. Bowel sounds were sparse. Her family disclosed that the patient had received an insertion of a loop IUD at 30 years previously and had complaints of pelvic pain, difficulty defecating, and mucus and blood in the stool for the past 6 months. Laboratory studies revealed a white blood cell count of 5,400/mL with a neutrophilic shift to the left (segmented: 84%; normal: 55e71%), hemoglobin of 6.8 g/dL (normal: 12e16 g/dL), and a C-reactive protein level of 144 mg/L (normal

Summary Objective Bladder endometriosis is a rare disease with variable symptoms. No definite treatment for this disease has been documented due to its rarity. We present a case of bladder endometriosis mimicking a lower segment uterine adenomyoma. Case Report A 25-year-old woman presented with the complaint of severe dysmenorrhea and suprapubic tenderness of 6 months' duration. Transvaginal ultrasonography showed a lower segment heteroechogenic mass of the uterus. Laparoscopy revealed a mass on the posterior wall of the urinary bladder after dissection of the vesicouterine fold. Cystoscopy confirmed that the lesion was confined to the muscular layer, without involvement of bilateral ureter orifices. Partial cystectomy was performed during exploratory laparotomy. Bladder endometriosis was confirmed by pathology. The patient had an uneventful recovery. The postoperative severity of dysmenorrhea was reduced to half that experienced preoperatively. Conclusions Women with bladder endometriosis may have no symptoms during urination. A high index of suspicion of bladder endometriosis is necessary when a heteroechogenic mass in the anterior lower segment of the uterus is detected on pelvic ultrasound.