Background Acute esophageal necrosis is defined as necrosis of the esophageal mucosa causing diffuse black pigmentation of the esophagus, the so-called black esophagus from its endoscopic findings. The prevalence is only 0.001~0.2%, while its mortality rate is up to 32%. However, most of the cases are fatal by comorbidities. Case presentation A 67-year-old female with diabetes mellitus was transported to the emergency room with hematemesis and disordered consciousness. She had suffered from nausea and epigastralgia for 2 days. The patient’s general status was shock evidenced by vital signs, and she did not respond to rehydration. After intubation, emergency endoscopic examination revealed black pigmentation of the esophageal mucosa, and the condition was diagnosed as acute esophageal necrosis. Antibiotics and plasmapheresis had been started, and the patient gradually stabilized. One week after the admission, esophagus perforation was suspected from the significant increase of the right pleural effusion and free air at the esophagus wall and the mediastinum on CT scan. Emergency thoracoscopy revealed an edematous esophagus which was colored black. Esophagectomy with esophagostomy and enterostomy was performed. On resected specimen, mucosal necrosis was found only on the squamous epithelium, with three perforating areas in the middle to lower thoracic esophagus. No signs of inflammation or ischemia were found on the gastric mucosa of the esophagogastric junction. After the operation, the patient recovered generally well, except for the severe stenosis of the cervical esophagus. Cervical esophagectomy, tracheotomy, and anterior thoracic route reconstruction with free jejunum interposition and gastric tube were performed 9 months after the first surgery. No postoperative complications occurred; on the 37th day after the operation, the patient was eating well and was transferred to continue swallowing rehabilitation. Conclusion It is important to detect the esophagus perforation and mediastinitis early and thereby not to miss the chance of surgical intervention to save the patient’s life. Surgery should be minimized, and reconstruction should be considered next. If the cervical esophagus is also affected, reconstruction surgery should be performed by removing cervical esophagus and anastomosing it to the hypopharynx using a gastric tube and free jejunum interposition as needed.
HighlightsAmyand’s hernia with appendix perforation is an extremely rare condition.Very few cases of Amyand’s hernia with appendix perforation used laparoscope as a therapeutic tool.Laparoscopic approach is diagnostic and enables two stage operation to the perforated cases.
Abstractp16 is generally considered to be a surrogate maker of human papillomavirus (HPV) infection and also a predictive marker of favorable clinical outcome of patients with squamous cell carcinoma of the oropharynx. p16 overexpression is also known to be induced by deregulation of RB1 in neuroendocrine carcinomas. In highly malignant esophageal neoplasms, however, the status of p16 has remained largely unknown. We immunolocalized p16 and Rb1 in 82 surgically resected esophageal high-grade squamous cell carcinomas (46 poorly differentiated and 36 basaloid squamous cell carcinomas) and 15 esophageal small-cell carcinomas in order to clarify the clinical and biological significance of p16. p16 immunoreactivity was detected in 7/82 (9%) high-grade squamous cell carcinomas and 15 (100%) small-cell carcinomas. p16 immunoreactivity was significantly associated with Rb1 protein loss in both groups (P < 0.001). HPV was detected in none of the p16-positive cases examined. Clinical outcome of the p16-positive high-grade squamous cell carcinomas was not different from that of the p16-negative counterparts (P = 0.687) but significantly better than those with the small-cell carcinomas (P = 0.023). p16 was therefore considered to be induced through an inactivation of the RB1 signaling pathway and not through HPV infection in highly malignant esophageal neoplasms. Nevertheless, patients’ clinical outcome of these neoplasms significantly differs; therefore, small-cell carcinomas have to be carefully differentiated from other neoplasms. In addition, p16 overexpression is not predictive of favorable clinical outcome in high-grade squamous cell carcinomas of the esophagus.
Necroptosis is a pivotal process in cancer biology; however, the clinical significance of necroptosis in esophageal squamous cell carcinoma (ESCC) has remained unknown. Therefore, in this study, we aimed to verify the potential involvement of necroptosis in the clinical outcome, chemotherapeutic resistance, and tumor microenvironment of ESCC. Mixed lineage kinase domain-like protein (MLKL) and phosphorylated MLKL (pMLKL) were immunohistochemically examined in 88 surgically resected specimens following neoadjuvant chemotherapy (NAC) and 53 pre-therapeutic biopsy specimens, respectively. Tumor-infiltrating lymphocytes (TILs) were also evaluated by immunolocalizing CD3, CD8, and forkhead box protein 3 (FOXP3) in the residual tumors after NAC. High pMLKL status in the post-NAC resected specimens was significantly correlated with worse prognosis in ESCC patients. Multivariate analysis demonstrated that a high pMLKL status was an independent prognostic factor. In pre-NAC biopsy specimens, a high pMLKL status was significantly associated with a lower therapeutic efficacy. CD8+ TILs were significantly lower in the high-pMLKL group. FOXP3+ TILs were significantly higher in both high-MLKL and high-pMLKL groups. We first demonstrated pMLKL status as an independent prognostic factor in ESCC patients. Our study revealed the possible involvement of necroptosis in the immunosuppressive microenvironment, resulting in the attenuated therapeutic efficacy of NAC and eventual adverse clinical outcomes in ESCC.
Background Lymph node metastasis is one of the pivotal factors of the clinical outcomes of patients with esophageal cancer receiving neoadjuvant chemoradiation therapy (NACRT). Both the nuclear factor‐erythroid 2‐related factor 2 (Nrf2) signaling pathway and heme oxygenase‐1 (HO‐1) are frequently upregulated in various human malignancies and associated with resistance to chemoradiation therapy, subsequently resulting in adverse clinical outcomes. However, the Nrf2 and HO‐1 status in lymph node metastasis and their differences between primary and metastatic lesions are unknown. Aims To examine the levels of Nrf2 signaling proteins and HO‐1 in primary and metastatic lesions of patients with esophageal squamous cell carcinoma using immunohistochemistry. Methods and Results We immunolocalized Nrf2 signaling proteins in 69 patients with lymph node metastases, who received NACRT with 5‐fluorouracil and cisplatin before esophagectomy. We also compared the findings between primary and metastatic lesions. Residual lymph node metastases were detected in 30 patients and among them, both primary and metastatic lesions were available for evaluation in 25 patients. Subsequently, we correlated the results with patients' survival. Nrf2, HO‐1, and the Ki‐67 labeling index were all significantly lower in the patients with lymph node metastases than in those with primary tumors. Carcinoma cells with high HO‐1 levels were significantly associated with pathological resistance to NACRT. These results suggested that overall and disease‐free survival of esophageal squamous cell carcinoma were significantly associated with both pN2 and high HO‐1 levels, respectively. Conclusions Protein expression in the Nrf2 pathway was significantly lower in patients with lymph node metastases than in those with primary lesions. HO‐1 levels in lymph node metastases could be used to predict the eventual clinical outcome of patients with esophageal cancer receiving NACRT.
The tumor microenvironment is considered to play a pivotal role in various human malignancies. Neuroendocrine and non-neuroendocrine neoplasms are considered to have different tumor microenvironments. However, owing to differences in the systemic and/or local immune statuses, tumor microenvironments in different patients may be difficult to compare. Mixed neuroendocrine non-neuroendocrine neoplasms (MiNENs), although rare, could be useful for exploring the effects of neuroendocrine differentiation on the tumor microenvironment, because both neuroendocrine and non-neuroendocrine components are present in the same tumor. Here, we examined 33 cases of histologically confirmed MiNENs and evaluated the influence of neuroendocrine differentiation on the tumor microenvironment by comparing tumor-infiltrating lymphocytes, tumor-associated macrophages, and other relevant factors in the two components the same tumor. The immunoreactivity of those examined above was evaluated quantitatively. The values of vasohibin-1-positive density (p < 0.0001) and immunoreactivity (p < 0.0001) (representing the neoangiogenesis status) were significantly higher in neuroendocrine as compared to non-neuroendocrine areas of the same tumors. In addition, the Foxp3/CD8 (p = 0.0717) and the PD-1/CD8 ratios (p = 0.0176) (representing tumor immunity suppression) tend to increase in neuroendocrine carcinomas. Immunoreactivity of CD163, a marker of M2-like macrophages, was also higher in the neuroendocrine areas. Our findings indicate that neuroendocrine and non-neuroendocrine tumors differ from each other with respect to the characteristics of both tumor cells and the tumor microenvironment.
Sclerosing encapsulating peritonitis is a rare chronic inflammatory condition often with unknown origins. We report a case of an abdominal cocoon or sclerosing encapsulating peritonitis, which was suspected to be a result of bowel obstruction. Tuberculosis peritonitis was also suspected. However, the exact diagnosis was unclear, and it was diagnosed as an idiopathic abdominal cocoon. The patient’s history is of clear relevance in this diagnosis, and this report will be of interest to clinicians attending to cases of bowel obstruction.
A number of elderly esophageal cancer patients who have eligibility for radical esophagectomy are increasing. However, we have no clearly evidence of treating strategy for these population because mostly high evidential clinical studies doesn’t include over 75-year-old patients. In this study, we retrospectively assessed efficacy of neoadjuvant chemotherapy using CDDP +5-FU in over 75-year-old patient in our hospital. We extracted total 105 over 75-year-old esophageal cancer patients who underwent radical esophagectomy from 2007 to 2020 in our hospital. We classified them Group A (surgery alone) and Group B (neo-FP(±RT) + surgery) and analyzed perioperative surgical risk, surgical outcomes, and adverse events or effectiveness for neoadjuvant therapy. Furthermore, long-term survival was assessed by using matched cohort from propensity score matching. Preoperative risk score calculated by E-pass scoring system was significantly higher in group A while surgical score was similar between two groups. Among group B, 86% of patients were underwent neoadjuvant chemotherapy (NAC) and its completion rate was 78.9%. Number of the patients occurred adverse events during NAC were 8/7/12/3 in the G1/2/3/4 respectively. Postoperative complications decided by Clavien-Dindo classification weren’t seen significant difference between two groups. Postoperative in hospital days were significantly shorter in group A. Survival analysis showed significantly worse overall survival and disease-free survival in group A in both all cohort and matched cohort. The level of preoperative risk score was different between two different treatment strategies. Although this study has several limitations including low number population, difference of preoperative risk, and short follow up period, neoadjuvant therapy using FP may safety and effective treatment for elderly esophageal cancer patients.
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