Duodenal Ulcer

Like gastric ulcers, duodenal ulceration is  a descriptive term for damage to the lining of the duodenal lining that leads to destruction of the delicate epithelium ( cells a little like skin which line the inside of the gut) of the duodenum. An ulcer is conventionally a descriptive term for a hole in this epithelium which is larger than 3mm. The term erosion is used for holes which are less than 3mm. The process leading to both these events is often similar.

 

Ulcers may arise as a result of damage to or dysfunction the protective layer of mucous that covers the epithelium, or as a consequence of noxious substances, such as excess gastric acid, alcohol or chemicals that cause damage to the epithelium in spite of the protective barrier, or a failure of the normal processes of repair. Sometimes damage arises as a result of a combination of these factors.

 

Common causes of duodenal ulceration include H.pylori infection, which may disrupt the mucosal barrier or lead to excess acid production, Non steroidal anti-inflammatory (NSAIDs include brufen and diclofenac) use, which disrupts the mucosal barrier or exposure to infection or excess alcohol. H.pylori infection has historically accounted for over 85% of all duodenal ulcers. Non-steroidal use either with or without H. pylori co-infection accounts for the majority of the remainder.

 

Ulcers are often asymptomatic (cause no symptoms) unless they bleed, in which case they may cause haematemesis or melaena or both. On occasion they may cause epigastric pain, nausea, or weight loss and early satiety.

 

Ulcers are usually treated by eradication of H. pylori. In those where non-steroidals are a factor avoidance of these drugs is required. Rarely other drugs or tumours may cause excess gastric acid production and consequent duodenal ulceration (gastrinoma/ neuro-endocrine tumours).