OMED E-Newsletter Issue 7, 2009: Brainteaser/image of the month

This was found in a 60 year old lady presenting with anaemia. She has severe rheumatoid arthritis treated with naproxen, sulphasalazine and methotrexate. She is also hypertensive and takes a beta blocker together with nitroglycerin spray and low dose aspirin. A rapid urea test for H.pylori is negative at the time of her examination and biopsies from the edge of the ulcer does not reveal any evidence of malignancy. The patient is very reluctant to stop her NSAID.

What single treatment option is most likely to benefit the patient?

1. start misoprostol
2. start an H2 antagonist
3. change to a selective Cox-2 inhibitor
4. start a proton pump inhibitors
5. start sucralfate

Explanation

Option D is correct. The average risk of developing a peptic ulcer on NSAID therapy is between 3-4 %. Patients above the age of 65, those with a history of peptic ulcer disease, those with serious co-morbidity, those requiring the prolonged use of maximum recommended doses of standard NSAIDs and patients with heart disease are at even greater risk.

H.pylori and NSAID’s interact to increase the risk of peptic ulceration. Eradicating the HP reduces the risk of ulcer recurrence.  One study found that the risk of ulcer recurrence was lower in patients who had undergone eradication of their HP than in those treated by a PPI.  However, in patients without evidence of H.pylori infection, PPI therapy is the most likely option to prevent a recurrence of gastric ulceration.

H2 antagonists, in standard doses, appear to reduce the risk of duodenal ulceration but not gastric ulceration.

Misoprostol has to be taken in high doses (three times a day) to prevent gastric ulceration.  At these high dosages, it may be more effective than H2 antagonists.  Unfortunately, at this dosage about 30% of patients develop side-effects (diarrhoea and abdominal pain) and have to stop therapy.  In comparison with ranitidine and misoprostol, PPI therapy is associated with higher healing rates of gastric ulcers after 8 weeks treatment.

Sucralfate reduce dyspeptic symptoms but is less effective than misoprostol in preventing ulceration.  In a study of arthritis patients treated with NSAID’s, 32% of those given placebo developed a gastric ulcer compared with 10% of those given misoprostol and 13% of those given a PPI.

The gastric damage by NSAID’s is due to the combined inhibition of both COX- and COX-2.  Thus inhibition of COX-2 would delay healing of her gastric ulcer