A 68-year-old male patient was referred by his general practitioner to the Gastroenterology Outpatient Department, Northampton General Hospital due to on and off symptoms of dyspepsia that started only months after the initiation of aspirin and dipyridamole for a recent lacunar stroke. He experienced occasional heartburn and vomiting for the last year and he also had a few episodes of haematemesis while trying to relieve the reflux symptoms. Shortly after this he had two episodes of melaena. Blood investigations were performed and his urea was raised, but he maintained a satisfactory haemoglobin. His general practitioner initiated an empirical treatment for dyspepsia consisting of the combination of a proton pump inhibitor (PPI) (omeprazole 40 mg) and an H2 receptor antagonist (ranitidine 150 mg b.d.) that settled the symptoms for a short period of time but eventually had to be abandoned due to severe diarrhoea. Aspirin was discontinued by the general practitioner and the patient was free of dyspepsia symptoms. He demonstrated a normal appetite and denied any dysphagia.
When seen at the outpatient department by the gastroenterology team, his physical examination demonstrated a soft and nontender abdomen. Bowel sounds were normal and no masses were identified. The remainder of the physical examination was normal. His past medical history included a duodenal ulcer diagnosed more than 40 years earlier that had led to upper gastrointestinal tract bleeding, and he was interestingly found to be one of the pioneers of the first combination treatment for Helicobacter pylori eradication. He also had hypertension, hypercholesterolemia and was a smoker of 10 cigarettes daily. 10 months prior to his referral he had suffered a left hemisphere lacunar stroke with persistent paraesthesia that was treated with double antiplatelet regime (aspirin + dipyridamole). He had no family history of peptic ulceration or upper gastrointestinal bleeding.
An oesophagogastroduodenoscopy (fig. 1) was performed in an attempt to identify the cause of his symptoms and a middle-sized diverticulum was found in the prepyloric region only a few centimetres from the pyloric opening without causing outflow obstruction. The rest of the examination revealed multiple noncircumferential erosions of the oesophagus, without confluence affecting more than one longitudinal fold and suggestive of reflux oesophagitis. The appearance of the duodenum was normal.
Multiple oesophageal biopsies were taken that showed fragments of stratified squamous epithelium with an inflammatory infiltrate including eosinophils and congested capillaries suggestive of reflux oesophagitis, but there was no evidence of dysplasia or malignancy. In view of his past medical history and the nature of his symptoms, a decision was taken to treat the patient conservatively. An alternative PPI agent was commenced (lansoprazole 30 mg o.d.), but aspirin was not restarted since it was considered that dipyridamole would cover him from any further cerebrovascular events with a reduced risk of gastrointestinal bleeding.
He was not given a follow-up appointment for review at the outpatient clinic, but 6 months after the initiation of the PPI treatment he remains asymptomatic and his general practitioner confirms his steady progress.