Portal vein aneurysms are rare abnormal dilations of the portal vein and represent less than 3% of all visceral aneurysms. They may be congenital or acquired, symptomatic or asymptomatic, complicated or uncomplicated. Portal vein aneurysms may be fusiform or saccular and this last one has a low prevalence. Due to the small number of cases reported in the medical literature and the lack of specific guidelines, the management and treatment of this condition is still undefined. In this review, we report a case of saccular portal vein aneurysm in a 73-year old man with liver cirrhosis and discuss all cases of portal vein aneurysms reported in literature.

How to cite this article: Paglia A, Angeletti AG, Conte V, et al. Emphysematous cystitis in an elderly male diabetic patient: a case report. A complicated urinary tract infection.

Challenging differential diagnosis Background:Acute esophageal necrosis, or Gurvits syndrome, is a rare clinical process often secondary to a systemic lowflow state. It can be caused by several medical conditions, and it is thought to arise from a combination of impaired mucosal barrier and chemical and ischemic insults to the esophagus. Acute esophageal necrosis usually presents with severe complications due to delayed diagnosis and only rarely has surgical indications. We present a case of Gurvits syndrome, presumably triggered by metabolic acidosis in a diabetic patient. Case Report:A 61-year-old man with history of hypertension and type 2 diabetes mellitus treated with metformin, canagliflozin, glimepiride, and pioglitazone came to our attention with persistent vomiting, odynophagia, chest pain after each meal, and progressive weight loss. Arterial blood analysis showed mild metabolic acidosis, while the first esophagogastroduodenoscopy performed revealed a circumferential black appearance of the esophageal mucosa, as in concentric necrosis of the distal esophagus with possible fungal superinfection. Brushing cytology confirmed the infection by Candida spp. and the patient was treated with intravenous fluconazole. The second esophagogastroduodenoscopy, performed after 2 weeks, showed almost complete healing of the esophageal mucosa; in this case, biopsy confirmed mucosal ischemia and necrosis, without showing deep impairment of the mucosa by fungal agents. Conclusions:Due to its high lethality, often caused by the underlying medical diseases, acute esophageal disease should be considered in the differential diagnosis of digestive symptoms, even without upper gastrointestinal bleeding. Prompt diagnosis and treatment of contextual collateral conditions can help clinicians to avoid the worst outcomes of the disease. Among the causative factors of metabolic acidosis leading to esophageal necrosis we recognized metformin and dapagliflozin.