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Introduction: Arterio-oesophageal fistulae are a very uncommon cause of severe gastrointestinal bleeding, and mostly result from an aberrant right subclavian artery and mediastinal surgery or prolonged endotracheal/nasogastric intubation., Material and Methods: We present the case of a patient with an oesophageal adenocarcinoma and haematemesis due to a subclavian arterio-oesophageal fistula after mediastinal radiotherapy., Conclusion: We discuss the rare, life-threatening condition of acute erosion of the left subclavian artery caused by an oesophageal tumour and presenting with Chiari's triad., Learning Points: Subclavian arterio-oesophageal fistula is an uncommon, life-threatening cause of gastrointestinal bleeding.Knowledge of Chiari's triad enables early recognition of potentially fatal gastro-intestinal bleeding.A high level of suspicion is essential for prompt diagnosis and referral for surgical treatment especially in patients with malignancies of the upper gastrointestinal tract., Competing Interests: Conflicts of Interests: The Authors declare that there are no competing interests., (© EFIM 2021.)

We discuss the case of a 44-year-old man with a refractory left lower lobe pneumonia progressing to a pulmonary abscess caused by a colobronchial fistula, a rare complication of underlying Crohn's disease. The patient presented with weight loss and signs of a pulmonary consolidation, which responded incompletely to the targeted antibiotic treatment. The causative colobronchial fistula was demonstrated by CT-guided puncture and retrograde injection of contrast medium. After fistula excision, the patient recovered rapidly with a weight gain of 4 kg within a few weeks., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2018. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: TNF-alpha is known to play a decisive role as a pro-inflammatory cytokine in several autoimmune conditions. Its neutralisation by TNF-alpha antagonists such as infliximab (Remicade), a chimeric monoclonal anti-TNF-alpha antibody, may be beneficial in patients with active disease. These anticytokine drugs have been approved and are being increasingly used in the therapy of rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, psoriatic arthropathy and generalised psoriasis after established treatments have failed. Whenever therapy options are few, TNF-alpha antagonists are regarded as an effective, relatively safe and generally well-tolerated alternative, even if there is no detailed knowledge of their safety profile and possible long-term adverse events. In the respiratory tract an increased risk of viral, (myco-)bacterial, fungal and opportunistic infections has been observed. Furthermore, rare cases of severe fibrosing alveolitis in patients with concomitant immunosuppressant therapy or underlying lung disease have been reviewed recently., Case: We present a case of drug-induced alveolitis following infliximab and azathioprine for the treatment of severe, generalised psoriasis and atopic eczema without pre-existing lung disease. Withdrawal of both drugs achieved clinical and functional stabilisation, and the addition of prednisolone resulted in a rapid improvement., Conclusion: As the pathophysiology of the pulmonary insult is unknown and since there are potentially serious adverse effects, we advise caution and close screening before and after initiation of TNF-alpha blockade, especially in patients with an underlying lung disease or with a combination of pneumotoxic agents.

The pulmonary endothelin (ET) system has been implicated in the pathogenesis of chronic lung diseases such as pulmonary hypertension, asthma, chronic obstructive lung disease, idiopathic pulmonary fibrosis, and bronchiolitis obliterans. However, the etiologic role of ET-1 in these diseases has not yet been established. We recently demonstrated that ET-1 transgenic mice, generated using the human prepro-ET-1 expression cassette including the cis-acting transcriptional regulatory elements, had predominant transgene expression in lung, brain, and kidney. We used these mice in the present study to analyze the pathophysiologic consequences of long-term pulmonary overexpression of ET-1. We found that ET-1 overexpression in the lungs did not result in significant pulmonary hypertension, but did result in development of a progressive pulmonary fibrosis and recruitment of inflammatory cells (predominantly CD4-positive cells). Our study provides evidence that a long-term activated pulmonary ET system, without any other stimuli, produces chronic lymphocytic inflammation and lung fibrosis. This suggests that overexpression of ET-1 may be a central event in the pathogenesis of lung diseases associated with fibrosis and chronic inflammation, such as pulmonary fibrosis and bronchiolitis.