LAUSR

© BMJ Publishing Group Limited 2022. No commercial reuse. See rights and permissions. Published by BMJ. DESCRIPTION A man in his 30s presented with a 4 day history of severe epigastric pain, described as a 7/10, with dorsal irradiation and progressive dysphagia for solids. He denied vomiting, altered gastrointestinal transit, gastrointestinal bleeding, fever and loss of weight. He denied any previous gastrointestinal complaints. Regarding previous medical history, he was prescribed an oral filmcoated alendronate tablet, 70 mg/month, after an atraumatic vertebral fracture 2 years ago with the diagnosis of osteoporosis of unidentified aetiology. He had taken the oblongshaped pill, with around 13 per 8 mm of size, 2 days before the onset of symptoms, with some water and recumbent position immediately after. He denied any other medications. Family history was unremarkable. On clinical examination, his vital signs were normal, and he had epigastric abdominal tenderness without peritoneal irritation signs. The laboratorial findings showed elevation of the inflammatory parameters (leucocyte count: 19.7×10/L, n: 4–10, and C reactive protein: 3.85 mg/dL, n<0.5). Thoracoabdominal radiography did not show mediastinal enlargement or evidence of perforation. Electrocardiogram and myocardial necrosis markers showed no cardiac ischaemic changes. Abdominal ultrasound was normal. As he maintained the complaints, he was referred to our unit and underwent upper endoscopy, revealing, as shown in figure 1A,B, a circumferential ulceration of almost all oesophageal mucosa, except for a small portion of the proximal oesophagus, with extensively desquamation and friability. Additionally, a deeper longitudinal ulceration was seen in the middle third of the organ (figure 1C). No gastroduodenal lesions were observed. The patient was admitted due to food intolerance. He was started on twice daily intravenous proton pump inhibitor therapy and four times daily oral sucralfate. Due to prolonged food intolerance, parenteral nutritional support was needed. The diagnostic workup excluded infectious aetiology by herpes simplex virus, cytomegalovirus, EpsteinBarr virus, varicellazoster virus, HIV and mycobacterium tuberculosis. Cervicothoracic computed tomography showed some enlarged lymph nodes near the esophagogastric junction, without any suspicious lesions, pneumomediastinum or pneumothorax. The histological analysis revealed, as shown in figure 1D, an extensively ulcerated mucosa with fibrinopurulent debris, without microorganisms, or neoplastic cells. Immunofixation for herpes simplex virus and cytomegalovirus were negative. When asked directly, the patient revealed an inadequate way of taking the alendronate pill, with minimal water ingestion and supine position afterwards. The patient was released 15 days after admission, without complaints and tolerating solid diet. He was referred to a rheumatology consultation and maintains intravenous alendronate. Figure 1 (A) Upper endoscopy revealing an extensive oesophageal injury with an easily sliding fibrinopurulent exudate and a friable mucosa. (B) Lower oesophagus with an extensively desquamation of the mucosa. (C) Middle third of the oesophagus with a deeper longitudinal ulceration. (D) Oesophageal biopsies showed a wide ulceration with a dense inflammatory infiltrate and fibrinopurulent exudate, compatible with pillinduced esophagitis. No microorganisms, dysplasia or neoplastic cells were identified.