Five common areas for error in gastrointestinal prescribing

The comments in this review are didactic and, while mostly well supported by evidence, some are my personal opinion. The use of the term “error” may be too strong for some – one person’s great idea may be another person’s error!

However, this article attempts to provide some quick tips that might help in day-to-day practice. The focus is on prescribing, but obviously diagnostic issues are directly connected with effective treatment choices. Most of the issues are also covered, sometimes in more detail, in previous “Gastroenterology” articles.

A dose of omeprazole 20mg before breakfast effectively treats 70 per cent of patients with reflux, and increasing the dose to 20mg before breakfast and before dinner (not 40mg in the morning) treats the majority of patients. Failure to respond to twice-daily treatment should start a reconsideration of the diagnosis – maybe the diagnosis is functional heartburn or functional dyspepsia.

Relying on the PPI test for diagnosis of reflux (ie, symptom response to PPI) is a mistake. The interpretation is usually difficult because of a strong placebo response. The diagnosis is made from a good history and, if needed, a gastroscopy can be helpful.

There should always be a review of the ongoing need for a PPI. Patients with definite heartburn symptoms on a daily basis are unlikely to get off the PPI unless significant lifestyle changes are made. However, many other patients could manage on antacids or an H₂-receptor antagonist as needed, particularly if the symptoms are more consistent with functional dyspepsia (rather than typical heartburn).

It is worth noting that pantoprazole is less effective on a milligram per milligram comparison. For those who do not respond to pantoprazole, switching to omeprazole (at the same dose) is an option.

It is not enough to suggest a low-FODMAP diet, then leave the patient with no resources or without a long-term dietary plan

The focus of management in IBS should be a confident diagnosis, reassurance, then a discussion of dietary triggers and possibly a low-FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) diet. It is not enough to suggest a low-FODMAP diet, then leave the patient with no resources or without a long-term dietary plan. There should be a plan for reintroduction of foods after a trial of a low-FODMAP diet, otherwise there is the risk of an overly restrictive diet (could be described as a type of eating disorder).

Medications can be helpful, but some common options may actually aggravate symptoms. Antispasmodics such as scopolamine butylbromide (Buscopan) or mebeverine (Colofac) can relieve cramping lower abdominal pain, but daily use may lead to constipation in some patients. The benefit is modest – there can be a reduction in severity of abdominal pain. There are often side effects (dizziness, nausea or feeling generally unwell) that may limit tolerance in the long term.

Failure to distinguish slow-transit constipation from constipation-predominant IBS is a common problem. The distinction is subtle but does direct treatment in different ways. Slow-transit constipation requires increasing doses of osmotic laxatives until the desired effect is achieved. Constipation-predominant IBS can benefit from gentle laxatives – usually low doses. Stimulant laxatives should not be used for IBS because of increased abdominal pain and exaggeration of variable bowel habit.

Diarrhoea-predominant IBS can be treated with low-dose loperamide. Sometimes, even one 2mg capsule has too strong an effect, leading to constipation and new symptoms of abdominal discomfort and bloating. In this case, the 2mg tablet of loperamide is useful as it can be split, giving a lower dose. I suggest taking the medication at night to reduce the usual morning bowel frequency. Taking loperamide after a loose bowel motion, as is often suggested, is too late!

Low-dose tricyclic antidepressants are effective and have the best evidence base of all IBS treatment options. Treatment is better tolerated for diarrhoea-predominant IBS. It is important to start at a low dose and to warn of possible side effects. Patients need to understand the slow onset of effect and the need for treatment to continue for at least one year. I start with amitriptyline 5mg at night if there are sleep issues (more common with IBS) or 5mg nortriptyline if sedation is a potential problem. The effective dose for an individual varies from 5–20mg. Higher doses are not well tolerated.

H. pylori infection is often a “bystander” issue for most patients with dyspepsia. It is a mistake to overpromise a good response to successful H. pylori eradication. Studies show patients who have gastritis only (not peptic ulceration) gain an additional 10 per cent chance of success compared with placebo (generally there is a high placebo response). The problem with emphasising the potential role of H. pylori comes when the initial treatment is unsuccessul.

Treatment should not be given based on H. pylori serology alone. This test has largely been replaced by H. pylori faecal antigen testing, which is very accurate for current infection. Serology remains positive after successful treatment for one to two years and has a high rate of false positives.

Antibiotic resistance is an increasing problem. It is important to maximise the results from the first course of treatment. The standard triple therapy of omeprazole, amoxycillin and clarithromycin should be given for two weeks rather than one week.

Testing for successful eradication should be by an H. pylori faecal antigen test three months after completing antibiotics, with PPIs discontinued for one month before testing. Retreatment of H. pylori should not be with the same triple therapy. The chance of success is 10–15 per cent because of the inevitable development of resistance, mainly to clarithromycin. Second-line treatment options are currently limited in New Zealand. The best option is quadruple treatment – omeprazole, colloidal bismuth subcitrate (De-Nol), tetracycline and metronidazole given for two weeks. This is a difficult regimen, and referral to a gastroenterologist is helpful before considering further treatment.

Functional dyspepsia is the most common cause of upper abdominal discomfort in primary care, but it is not a diagnosis given very often, perhaps because it seems too vague.

Alternative explanations can lead to problems “down the track”. The label of “gastritis” is commonly used but has no supporting evidence. There is a very poor correlation between gastric mucosal inflammation and dyspepsia. Gastric biopsies may appear to support this diagnosis, but often this is an over-interpretation of subtle findings reported on biopsy that are not relevant to the symptoms.

The diagnosis of functional dyspepsia rather than gastritis or reflux helps introduce the patient to the need for lifestyle changes rather than medication. The main conversation should be about reduction of alcohol, stopping smoking, weight loss and avoiding larger meals later in the evening. A focus on medication leads to prescribing of increasing doses of PPI, with frustration at the lack of response by both prescriber and patient. If a trial of PPI is given, there should be an agreement to stop if the results are equivocal. There should be early consideration given to the possible impact of anxiety and depression on symptoms.

Bloating is a symptom that needs to be carefully evaluated. Bloating that is persistent during the day or gradually increasing during the day is most likely to be part of IBS. A sense of fullness and bloating just after meals could be described as “dysmotility-type dyspepsia”. There has been an interest in using domperidone for this symptom complex (post-prandial nausea, fullness and bloating), but the results are often disappointing.

Constipation may be easily managed with general advice and the use of fibre supplements. The next step for patients failing to respond to fibre supplements is more contentious.

I would discourage the use of stimulant laxatives as the next option. While popular with prescribers and patients, there are disadvantages. There is often an increase in cramping abdominal pain, particularly if there is an element of IBS. The dose may need to gradually increase because of a degree of tolerance. The long-term safety of stimulant laxatives is also debated. These drugs are suitable in the postoperative period, for institutional older people and for palliative care, but caution is required in young people with slow-transit constipation who will require long-term laxatives.

For a long time, the main funded option other than stimulant laxatives was lactulose. This is an effective and safe osmotic laxative but does have the disadvantage of bloating, which can be as troublesome as the constipation-related symptoms.

Molaxole sachets are well tolerated and safe in the long term. The dose needs to be titrated for effect – this can be between half to two sachets daily.

Alan Fraser is a gastroenterologist with Auckland Gastroenterology, Mercy Endoscopy and Endoscopy Auckland, and associate professor of medicine at the University of Auckland