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Abstract Background Macroscopic vascular invasion (MVI) significantly impacts survival in patients with hepatocellular carcinoma (HCC), warranting systemic therapy over locoregional therapy. Despite novel approaches, HCC with MVI has a poor prognosis compared to early-to intermediate-stage HCC. This study aimed to evaluate the safety and efficacy of carbon-ion radiotherapy (C-ion RT) for HCC characterized by MVI. Methods This retrospective cohort study evaluated HCC patients with MVI treated using C-ion RT with a dose of 45.0–48.0 Gy/2 fractions or 52.8–60.0 Gy/4 fractions between 1995 and 2020 at our institution in Japan. We analyzed the prognostic factors and rates of local recurrence, survival, and adverse events. The local recurrence rate was determined using the cumulative incidence function, with death as a competing event. Survival rates were determined using the Kaplan–Meier method. The log-rank test for univariate analysis and the Cox proportional hazards model for multivariate analysis were used to compare subgroups. Results In total, 76 patients with a median age of 71 years (range, 45–86 years) were evaluated. Among them, 68 had Child–Pugh grade A while eight had grade B disease. In 17 patients, the vascular tumor thrombus reached the inferior vena cava or main trunk of the portal vein. Over a median follow-up period of 27.9 months (range, 1.5–180.4 months), the 2-year overall survival, progression-free survival, and local recurrence rates were 70.0% (95% confidence interval [CI]: 57.7–79.4%), 32.7% (95% CI: 22.0–43.8%), and 8.9% (95% CI: 1.7–23.5%), respectively. A naïve tumor and a single lesion were significant prognostic factors for overall survival in the univariate analysis. Albumin-bilirubin grade 1 and a single lesion were independent prognostic factors in the multivariate analysis. Overall, four patients (5%) experienced grade 3 late adverse events, with no observed grade 4 or 5 acute or late adverse events. Conclusions C-ion RT for HCC with MVI showed favorable local control and survival benefits with minimal toxicity.

Infections after obstetric and gynecologic surgery are commonly caused by enterobacteria, commensal vaginal bacteria, or indigenous skin bacteria (primarily Staphylococcus aureus and Streptococcus). Mycoplasma hominis (M. hominis) rarely causes postoperative infection in the field of obstetrics and gynecology and its treatment is generally delayed. This report describes a case report of peritonitis caused by M. hominis after laparoscopic total hysterectomy. A 44-year-old patient (gravida 1, para 1) presented with heavy menstrual bleeding and severe anemia. She was diagnosed as having multiple uterine fibroids and bilateral endometriomas and underwent laparoscopic surgery. She subsequently developed postoperative peritonitis due to M. hominis. This microorganism was identified in the postoperative cultures of the vaginal discharge and the transvaginal drainage fluid by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. The patient was treated successfully with the appropriate antimicrobial agents. It is important to consider M. hominis infection when gynecological postoperative infection persists despite treatment with beta-lactam antibiotics, and no causative organisms are identified by Gram staining.

The case report describes the management of endometriotic cysts in a woman taking adjuvant tamoxifen. A diagnosis of endometriosis was made at the age of 38, and the condition was initially managed with a low-dose estrogen-progestogen combination; the patient then switched to dienogest at the age of 45. Following a diagnosis of breast cancer at the age of 46, dienogest was stopped and adjuvant tamoxifen treatment started. After 4 months the patient was diagnosed with bilateral ovarian cysts and underwent laparoscopic bilateral salpingo-oophorectomy. Endometriosis was diagnosed in both ovaries on histopathological examination. This case report describes progression of endometriosis in a tamoxifen user.

Introduction: Imperforate hymen and transverse vaginal septum are conditions characterized by obstructive defects, typically leading to hematometrocolpos detected around the time of puberty. We encountered a patient who had undergone hymenotomy in infancy to treat pyocolpos due to an imperforate hymen and later developed hematometrocolpos in puberty due to a transverse vaginal septum. Case presentation: A 13-year-old female presented with hypomenorrhea and hematometrocolpos-induced dysmenorrhea. She had a history of pyocolpos with a urinary tract infection at 3 months of age. At that time, no vaginal opening was found on perineal examination, and imperforate hymen was diagnosed. When hymenotomy was performed, the external cervical os was not detected by intravaginal bronchoscopic examination. However, this abnormal finding was not fully investigated. The postoperative course after hymenotomy was free of complications, and the patient remained asymptomatic until menarche. When she presented 3 months after menarche, genital examination revealed a bulging transverse septum inside the vagina, 5 cm from the hymen. Ultrasound and magnetic resonance imaging revealed a distended uterus, distended upper vagina, and collapsed lower vagina. Transverse vaginal septum was considered, and vaginoscopy was performed to exclude vaginal reclosure or adhesion caused by the previous surgery. A diagnosis of transverse vaginal septum was confirmed, and total excision of the septum was performed. The patient underwent regular postoperative follow-ups for stenosis prevention. Conclusion: Considering the rarity of these concurrent conditions, clinicians must always consider the possibility of several complex anomalies. Vaginoscopy using a hysteroscope may be useful for definitive diagnosis and determining appropriate treatments.

Mutations in the complement factor H (CFH) gene are associated with complement dysregulation and the development of atypical hemolytic uremic syndrome (aHUS). Several fusion genes that result from genomic structural variation in the CFH and complement factor H-related (CFHR) gene regions have been identified in aHUS. However, one allele has both CFHR gene duplication and CFH::CFHR1 fusion gene have not been reported. An 8-month-old girl (proband) presented with aHUS and was treated with ravulizumab. Her paternal grandfather developed aHUS previously and her paternal great grandmother presented with anti-neutrophil cytoplasmic antibody-associated vasculitis and thrombotic microangiopathy (TMA). However, the proband’s parents have no history of TMA. A genetic analysis revealed the presence of CFH::CFHR1 fusion gene and a CFHR3-1-4-2 gene duplication in the patient, her father, and her paternal grandfather. Although several fusion genes resulting from structural variations of the CFH–CFHR genes region have been identified, this is the first report of the combination of a CFH::CFHR1 fusion gene with CFHR gene duplication. Because the CFH–CFHR region is highly homologous, we hypothesized that CFHR gene duplication occurred. These findings indicate a novel pathogenic genomic structural variation associated with the development of aHUS.