Eosinophilic esophagitis (EoE) is a chronic inflammatory disorder of the esophagus characterized by dysphagia and food impaction. Although uncommon, spontaneous esophageal perforation may occur, most frequently involving the distal esophagus and the gastroesophageal junction. These perforations are typically managed with surgical or endoscopic interventions. Early diagnosis and prompt initiation of treatment within the first 24 hours significantly reduce morbidity and mortality. The aim of this report is to demonstrate that gastroesophageal junction perforation secondary to eosinophilic esophagitis can be successfully managed conservatively, even in delayed presentations, and to contribute to the understanding of treatment strategies for this rare but potentially life-threatening complication. We report the case of a 35-year-old male with a 12-year history of EoE who presented to the emergency department with retrosternal pain, dyspnea, and hematemesis. Five days prior to presentation, he developed a sore throat and cherry-colored diarrhea after consuming grilled chicken and self-administered ibuprofen for symptom relief. Contrast-enhanced imaging and upper endoscopy revealed a perforation at the gastroesophageal junction. Due to the location of the lesion, endoscopic stenting or clipping was considered inappropriate. In the absence of signs of acute abdomen, mediastinitis, or significant fluid collection, a conservative management strategy was adopted. The patient was admitted to the intensive care unit and initially treated with intravenous ceftriaxone (2 g/day) and metronidazole (1.5 g/day), which were later changed to piperacillin-tazobactam (4.5 g every 6 hours) following infectious disease consultation. The patient remained clinically stable, and oral intake was initiated on day 6. Antibiotic therapy was discontinued on day 10, and the patient was discharged without complications. At the three-month follow-up, the patient reported recurrent and progressively worsening dysphagia. Control endoscopy performed at the previously visited center revealed a distal esophageal stricture preventing passage of the gastroscope; therefore, a 12-cm fully covered self-expandable esophageal stent was placed. The stent was removed 20 days later, and the patient remained asymptomatic during the subsequent six-month follow-up period. Spontaneous esophageal perforation secondary to EoE is a rare but potentially life-threatening complication. This case highlights that conservative management may be a viable alternative to surgical or endoscopic intervention not only in early-detected cases but also in carefully selected delayed presentations managed in a multidisciplinary setting. Long-term follow-up remains essential for the early detection and treatment of late complications, such as stricture formation.

Advances in systemic therapies have improved survival in metastatic renal cell carcinoma (mRCC), leading to a growing population of long-term survivors who may receive both radiotherapy (RT) and tyrosine kinase inhibitors (TKIs) during their disease course. Both treatments induce vascular and mucosal toxicity, and their biological effects may overlap, increasing the risk of rare but life-threatening complications such as aorto-esophageal fistula (AEF). Herein, we present the case of a 47-year-old man with mRCC treated with nephrectomy and repeated pulmonary metastasectomies, followed by sunitinib, mediastinal stereotactic body radiotherapy (SBRT), and later cabozantinib for hepatic progression. Five years after thoracic RT and shortly after initiating cabozantinib, the patient developed massive hematemesis due to an AEF. Management included thoracic endovascular aortic repair (TEVAR), esophageal stenting, and prolonged antimicrobial therapy. Despite initial stabilization, recurrent fistulization and infections led to progressive deterioration and death 7 months later. This case underscores the catastrophic potential of RT-TKI interaction in long-term survivor patients. Sequential exposure can transform subclinical vascular injury into fatal outcomes. Risk stratification, nonconcurrent scheduling of RT and anti-VEGF therapy, and vigilant long-term monitoring are essential. Integration of multidisciplinary and palliative approaches is necessary to balance treatment efficacy with safety.

Aortic fistulas are rare but life-threatening vascular abnormalities characterized by abnormal communication between the aorta and an adjacent structure secondary to weakening of the vessel wall, such as in the setting of atherosclerosis or prior surgical intervention. Aortic fistulas can arise anywhere along the course of the aorta, with aortoenteric fistula being the most common type. Clinical presentation varies depending on the fistula type but often includes haemorrhagic symptoms such as hypotension, haematemesis, haematuria, and melena. Haemorrhagic shock and sepsis are common and often fatal complications. Prompt diagnosis is critical to reduce morbidity and mortality, and radiology plays a key role in diagnosis. CT angiography is the preferred imaging modality due to its rapid image acquisition and high spatial resolution. Radiologists must be able to recognize direct and indirect signs of aortic fistulas. In addition, differentiating aortic fistulas from mimics such as perigraft infection and inflammatory aortitis is essential for appropriate management.

Myeloid sarcoma is a rare hematologic malignancy defined by the extramedullary proliferation of myeloid blasts. It may occur without concurrent acute myeloid leukemia, creating a significant diagnostic challenge, particularly when it involves uncommon sites such as the gastrointestinal tract. We report the case of a 43-year-old woman with no relevant comorbidities who presented with a two-year history of epigastric pain and heartburn, later complicated by hematemesis. Imaging revealed a large gastric mass with associated hepatic focal lesions, initially raising suspicion for gastric adenocarcinoma with hepatic metastases. Histopathologic examination of the gastric biopsy showed malignant round cells consistent with a hematolymphoid neoplasm, and immunohistochemistry confirmed the diagnosis of myeloid sarcoma, with strong positivity for CD43 and myeloperoxidase and diffuse expression of CD56 and BCL2. Peripheral blood smear, complete blood count, and bone marrow aspirate showed no overt leukemic involvement. A biopsy from one of the hepatic lesions demonstrated similar histopathologic and immunohistochemical features, confirming multifocal disease. The patient was treated with standard induction chemotherapy using the "7 + 3″ regimen consisting of cytarabine and daunorubicin. During treatment, she developed fever, jaundice, and profound pancytopenia, and on day 12 she suffered sudden cardiorespiratory arrest and died. This case underscores the diagnostic complexity of gastrointestinal myeloid sarcoma, highlights the importance of immunohistochemistry in distinguishing it from other malignancies, and emphasizes the aggressive clinical course and poor prognosis that may occur even in non-leukemic presentations.

Esophagitis dissecans superficialis (EDS), also referred to as "sloughing esophagitis," is an uncommon benign condition characterized by the desquamation of the superficial layer of the esophageal squamous mucosa. It is often underdiagnosed due to its rarity and nonspecific clinical presentation. Although several factors such as caustic ingestion, thermal injury, autoimmune disorders, and mechanical trauma have been implicated, medication-induced mucosal injury remains one of the most significant causes. Among these, bisphosphonates - a class of drugs widely prescribed for osteoporosis and other bone-related disorders - have been identified as a potential offending agent. We report the case of a 66-year-old woman with no significant comorbidities who presented with persistent retrosternal burning and pain for 2 months. There was no associated dysphagia, odynophagia, vomiting, hematemesis, weight loss, or history of nonsteroidal anti-inflammatory drug use. Physical and systemic examinations were unremarkable. Despite treatment with double-dose esomeprazole for 8 weeks, her symptoms persisted. Upper gastrointestinal endoscopy revealed a large area of whitish sloughed-off mucosa overlying a superficial ulcer with regular margins, extending from 26 cm to just above the gastroesophageal junction. A detailed drug history subsequently revealed the use of bisphosphonate gel for osteoporosis. Histopathological analysis demonstrated sloughed squamous epithelium with the features of superficial mucosal necrosis, confirming the diagnosis of EDS secondary to bisphosphonate-induced chemical injury. Discontinuation of the bisphosphonate and continuation of proton-pump inhibitor therapy led to complete symptom resolution within 2 weeks. This case underscores the importance of considering drug-induced esophageal injury in patients with refractory retrosternal pain unresponsive to acid suppression therapy. Bisphosphonates, although highly effective in osteoporosis management, may cause significant mucosal damage when not used properly. Clinicians should maintain a high index of suspicion for bisphosphonate-induced EDS, as timely recognition and withdrawal of the offending agent usually result in rapid clinical and endoscopic improvement.