A 66-year-old woman had progressive bilateral optic neuropathy with dense central scotomas and dyschromatopsia. She had been taking oral methotrexate 2.5 mg three times per week for rheumatoid arthritis for the previous 10 months (total intake 322.5 mg) without folic acid supplementation. She had never smoked or abused alcohol and her diet was healthy. Serum folate was reduced at 1.6 ng/mL (normal >4 ng/mL) and vitamin B12 levels were normal. After stopping methotrexate and after administration of oral folic acid, she experienced complete recovery of vision. Serum folate levels returned to normal during folic acid treatment but decreased to below normal once folic treatment was stopped. The persistently low folate level remains unexplained and may reflect a genetic defect in folate metabolism. Methotrexate can cause toxic side effects resulting from folate inhibition but has not been shown definitively to cause a reversible optic neuropathy associated with low serum folate.

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investigations (eg, enteroscopy, gastroscopy and colonoscopy), 52% underwent therapeutic intervention (eg, APC, polypectomy and surgical referral). However, in 30% their management was unchanged. The majority of patients (88.1%) are still under active follow-up today. Conclusion The CE experience at this centre is of a simple, welltolerated investigation which allows definite diagnoses to be made with minimal complications. Higher diagnostic yield compared to previous published data could be explained by the strict inclusion criteria and recent introduction of this new service. This expanding service highlights the need for more resources to reduce waiting and reporting times in line with other GI investigations.

and no further episodes of ventricular fibrillation occurred. Arterial blood gas tensions at this time were pH 7-3, oxygen pressure 50 7 kPa (380 mm Hg), and carbon dioxide pressure 6-4 kPa (48 mm Hg); standard bicarbonate concentration 21-5 mmol(mEq)/l; and base excess -2-5 mmol(mEq)/l.Amiodarone was continued as an intravenous infusion with 600 mg in 5% dextrose over 12 hours and 300 mg in 5% dextrose for a further 24 hours, during which time an electrocardiogram showed varying degrees of heart block and nodal rhythms. His clinical state improved, and he required only intravenous atropine on two occasions for bradycardia. Serum digoxin concentration was above 5 t&g/l on admission, but the sample was not retained for more accurate determination. Digoxin concentrations did not fall into the therapeutic range until day 5, when a concentration of 1-4 ,ug/l was recorded. As the plasma half life in overdosage is about 13 hours3 the peak digoxin concentration would have been over 40 /eg/l.

SummaryWe have measured pepsin output in two patients with Zollinger Ellison Syndrome before and after an intravenous dose of cimetidine. Pepsin output increased after H2 blockade in both patients despite a decrease in both the volume and acidity of secretion. We suggest that nonresponse to cimetidine may be due to increased pepsin secretion when receiving treatment.