Dr John Wright



There is more to heartburn than acid

Dr John P Wright
Updated: 12 June 2011

For most people a burning sensation radiating up into the chest from the epigastrium is usually recognised as being due to acid reflux and the natural reflex is to grab for an alkaline such as milk or antacids. Characteristically this brings rapid relief which may last minutes or hours. More resistant symptoms may well require a H2 antagonist or protein pump inhibitor (PPI) and a consultation with the general practitioner.

The relief obtained with a PPI of the symptoms of acid reflux is quite dramatic and prolonged. The complicating symptoms of acid reflux such as dysphagia and regurgitation usually respond well and the relief from nocturnal heartburn secures patient loyalty to their first PPI.

In some patients however the response is less than satisfactory. The commonest cause of this is under dosing. An increased dose of PPI rather than a change of brand should be the first option. Patients should be reminded to take their first dose 20 min before breakfast and if a second dose is required this should be 20 min before dinner.

If symptoms are persistent or there are alarm symptoms such as dysphagia or onset in the mature patient, a referral to a gastroenterologist for assessment is indicated.

The above is the classic description of acid reflux disease but increasingly a separate group of patients is being recognised. These patients have an eosinophilic infiltrate into the oesophageal mucosa. Usually this is of unknown cause but clearly an allergic component may well be present particularly as this condition appears more commonly in atopic patients. Identifying an allergen is however usually unsuccessful. Most patients are of the male persuasion and can be children or young adults up to the age of 25 years. There is an association with a more generalized eosinophilic infiltrate of the gastrointestinal tract although few have any peripheral blood abnormalities. Celiac disease ( glutenenteropathy) has also been associated.

A confounding factor is that eosinophils are typically present in the mucosa of patients with regular acid reflux and it is only when the eosinophils pack the mucosa (typically more than 20 per high-power field) that the diagnosis of eosinophilic infiltrate is entertained.

Most patients with eosinophilic infiltrate, particularly milder cases, will respond to normal anti-acid therapy. In some a higher dose of PPI will be required. In these non-responders a locally active steroid such as budesonide may be needed. This can be administered by traditional asthma pump with a spacer and the patient swallowing rather than breathing the active agent in.

Patients with eosinophilic infiltrate may be suspected both clinically and endoscopically. Typically these patients present with the major symptom of dysphagia and/or food impaction rather than heartburn. The symptoms may have been quite chronic and seem to come and go of their own accord over the years. To the endoscopist the radial rings and creases in the oesophagus or even linear streaks without many signs of traditional oesophagitis just above the oesophago-gastric junction are suggestive of the diagnosis.

The lessons to be learnt are:

Some patients with heartburn need a higher dose of PPI rather than a change in brand.

Young men with a history of food impaction or poor response to PPIs may have an eosinophilic infiltrate.

A gastroscopy without oesophageal biopsy cannot diagnose eosinophilic infiltrate.

A pathologist who does not count eosinophils cannot diagnose eosinophilic infiltrate.

When the primary physician suspects that the patient may have this condition both the gastroenterologist and pathologist need to be alerted as there is more to heartburn than acid.