Spontaneous Pharyngeal Perforation After Forceful Vomiting: The Difference from Classic Boerhaave's Syndrome

Boerhaave's syndrome is spontaneous transmural perforation of the esophagus, which occurs most often after forceful vomiting or retching. This commonly occurs in the lower third of the esophagus but spontaneous perforation of the pharynx or cervical esophagus is extremely rare. This case presented a 20-yr-old healthy man with spontaneous pharyngeal perforation after forceful vomiting who had no history of instrumentation, cervical trauma, or having eaten anything sharp. Cervical pain and crepitus were the early symptom and sign of pharyngeal perforation and the rupture was detected on gastrografin swallow and CT examinations. The rupture site was higher than the upper esophageal sphincter, differing from Boerhaave's syndrome. The patient was conservatively managed without significant morbidity and mortality. Although this may resolve without surgical intervention, the pharyngeal rupture should receive early detection and clinical attention for preventing potential morbidity by late diagnosis

Risk Factors and Survival Outcomes for Patients With Anastomotic Leakage After Surgery for Head and Neck Squamous Cell Carcinoma

ObjectivesThis study evaluated the risk factors for anastomotic leakage (AL) and survival outcomes in patients with head and neck squamous cell carcinoma (HNSCC).MethodsPatients with HNSCC who underwent surgery carrying potential AL from 2003 through 2009 were included in this study. Univariate and multivariate analyses were performed and patient survival was calculated by the Kaplan-Meier method.ResultsOf 232 eligible patients, 25 (10.8%) developed AL. Univariate analyses revealed that primary tumor site, salvage surgery, perineural invasion, radiotherapy, chemotherapy, and blood transfusion were significantly associated with the occurrence of AL (P0.1).ConclusionPatients who received salvage surgery and blood transfusion may require careful surveillance for development of AL, which has a tendency toward decreased survival

Chondroradionecrosis of the Larynx: Diagnostic and Therapeutic Measures for Saving the Organ from Radiotherapy Sequelae

ObjectivesChondroradionecrosis (CRN) of the larynx is a rare but fatal complication of radiotherapy. We determined the optimal diagnostic methodology and management of laryngeal CRN in six patients.MethodsWe retrospectively reviewed the records of six patients with Chandler grade IV laryngeal CRN who had received prior radiotherapy (mean total radiation dose, 66.7±4.5 Gy) at a tertiary care hospital. Two patients underwent transoral laser microresection of their laryngeal carcinoma plus postoperative radiotherapy. All patients underwent endoscopy, computed tomography (CT), positron emission tomography (PET), removal of necrotic tissue, biopsy under suspension laryngoscopy, administration of antibiotics, and hyperbaric oxygen therapy (HBO). Their diagnostic and therapeutic results were assessed.ResultsCT showed CRN of the anterior larynx in three patients and CRN of the posterior larynx in three patients, with one patient having a false-positive result on PET. HBO consisted of a mean of 36±6 dives. After early debridement and HBO, five patients showed CRN improvement, but one had aggravation and subsequently underwent total laryngectomy. None of these patients showed local tumor recurrence on pathologic examination or during a mean follow-up of 24 months.ConclusionAlthough CRN of the larynx may be detected by endoscopic and imaging work-ups, detection may require pathologic examination. Early debridement and HBO may effectively treat CRN, saving the functional larynx

Initial Nutritional Status and Clinical Outcomes in Patients With Deep Neck Infection

Objectives The current study aims to determine the correlation between nutritional status upon presentation and disease severity, as well as treatment and survival outcomes. Methods Patients who were diagnosed with deep neck infection, underwent at least one surgical drainage/debridement, and had more than 1 week of hospitalization at a tertiary medical center from 2007 to 2015 were retrospectively included. Thereafter, initial serum albumin, C-reactive protein (CRP), and body mass index (BMI) were reviewed. Results A total of 135 patients were included in the final analysis. Accordingly, the proportion of patients with simultaneous mediastinitis (21.0%), necrotizing fasciitis (12.9%), disease extent >1 cervical level (72.6%), mean CRP (22.4 mg/dL), mean length of hospitalization (25.0 days), and mean 1-week follow-up CRP (7.2 mg/dL) was significantly higher in the hypoalbuminemia group (initial serum albumin 1 cervical level (2.12), initial serum CRP over 20 mg/dL (3.79), hospitalization of more than 14 days (4.10), 1-week follow-up CRP over 5 mg/dL (3.78), and increased duration for an over 50% decrease in initial CRP (2.70) (all P<0.05). Although intravascular albumin replenishment decreased the proportion of patients with hypoalbuminemia after 2 weeks (P<0.05), it did not significantly predict better treatment outcomes. Conclusion Among the markers reflecting an individual’s nutritional state, an initial serum albumin of less than 3.0 g/dL was an independent serologic marker predicting increased disease severity and complications in patients with deep neck infection

Carcinoma ex Pleomorphic Adenoma of the Salivary Glands: Distinct Clinicopathologic Features and Immunoprofiles Between Subgroups According to Cellular Differentiation

In carcinoma ex pleomorphic adenoma (CXPA), pleomorphic adenoma (PA) and diverse carcinoma components showing luminal (ductal) or non-luminal (myoepithelial) differentiation coexist. To elucidate the clinicopathological implications of cellular differentiation in CXPA and the potential role of p53, vascular endothelial growth factor (VEGF), c-erbB-2, c-kit, and glucose transporter 1 (Glut-1) in carcinogenesis, we analyzed 11 CXPAs with luminal differentiation (CXPAs-LD) and 6 CXPAs with non-luminal differentiation (CXPAs-NLD) and compared protein expressions in residual PAs and carcinomas by immunohistochemistry. Among the CXPAs-LD, 5 were invasive and 8 were histologically high-grade tumors. The 5-year survival rate was 72.7%. P53, c-erbB-2, VEGF, and Glut-1 were more immunoreactive in carcinoma components than in PAs (P = 0.008, 0.004, 0.002, and 0.024, respectively); c-erbB-2 overexpression was associated with high histological grade (P = 0.024). Carcinoma components frequently lacked c-kit expression (P = 0.009). CXPAs-NLD were all low-grade and invasive with a larger mean tumor size (5.2 cm) than CXPAs-LD (3.3 cm) (P = 0.040). The patients remained disease-free without significant immunohistochemical expression. The immunoprofiles and clinical course of CXPA differed according to cellular differentiation. Therefore, it is important to report the histological subtype and to assess potential biomarkers in diagnostic and therapeutic trials

Unleashing Ferroptosis in Human Cancers: Targeting Ferroptosis Suppressor Protein 1 for Overcoming Therapy Resistance

Ferroptosis, a recently identified form of regulated cell death characterized by the iron-dependent accumulation of lethal lipid peroxidation, has gained increasing attention in cancer therapy. Ferroptosis suppressor protein 1 (FSP1), an NAD(P)H-ubiquinone oxidoreductase that reduces ubiquinone to ubiquinol, has emerged as a critical player in the regulation of ferroptosis. FSP1 operates independently of the canonical system xc–/glutathione peroxidase 4 pathway, making it a promising target for inducing ferroptosis in cancer cells and overcoming ferroptosis resistance. This review provides a comprehensive overview of FSP1 and ferroptosis, emphasizing the importance of FSP1 modulation and its potential as a therapeutic target in cancer treatment. We also discuss recent progress in developing FSP1 inhibitors and their implications for cancer therapy. Despite the challenges associated with targeting FSP1, advances in this field may provide a strong foundation for developing innovative and effective treatments for cancer and other diseases

SLC7A11 as a Gateway of Metabolic Perturbation and Ferroptosis Vulnerability in Cancer

SLC7A11 is a cell transmembrane protein composing the light chain of system xc−, transporting extracellular cystine into cells for cysteine production and GSH biosynthesis. SLC7A11 is a critical gateway for redox homeostasis by maintaining the cellular levels of GSH that counter cellular oxidative stress and suppress ferroptosis. SLC7A11 is overexpressed in various human cancers and regulates tumor development, proliferation, metastasis, microenvironment, and treatment resistance. Upregulation of SLC7A11 in cancers is needed to adapt to high oxidative stress microenvironments and maintain cellular redox homeostasis. High basal ROS levels and SLC7A11 dependences in cancer cells render them vulnerable to further oxidative stress. Therefore, cyst(e)ine depletion may be an effective new strategy for cancer treatment. However, the effectiveness of the SLC7A11 inhibitors or cyst(e)inase has been established in many preclinical studies but has not reached the stage of clinical trials for cancer patients. A better understanding of cysteine and SLC7A11 functions regulating and interacting with redox-active proteins and their substrates could be a promising strategy for cancer treatment. Therefore, this review intends to understand the role of cysteine in antioxidant and redox signaling, the regulators of cysteine bioavailability in cancer, the role of SLC7A11 linking cysteine redox signaling in cancer metabolism and targeting SLC7A11 for novel cancer therapeutics