Abstract

Lower oesophageal sphincter pressure has been studied in pernicious anaemia patients and controls using an infused open-tipped system. Resting sphincter pressure was significantly (p < 0·01) lower in the pernicious anaemia patients. After gastric acidification with 0·1 N HCl pressure fell significantly (p < 0·01) in both groups. Following subsequent alkalinization, lower oesophageal sphincter pressure for controls rose significantly (p < 0·001). For pernicious anaemia patients the pressure after alkali was not greater than resting levels. Graded intravenous doses of pentagastrin in controls resulted in a peak pressure change of 38·5 ± 4·9 mm Hg after the 0·8 μg/kg dose. For patients the peak pressure change was only 13·0 ± 5·2 mm Hg and occurred after 0·4 μg/kg. Cholinergic stimulation with edrophonium (10 mg) produced a peak pressure change of 20·6 ± 2·6 mm Hg in controls but only 3·5 ± 1·0 mm Hg in pernicious anaemia patients (p < 0·001). In addition, no change in lower oesophageal sphincter pressure occurred in patients after stimulation with subcutaneous betazole (1·5 mg/kg).

In conclusion, the lower oesophageal sphincter in pernicious anaemia is characterized both by a low resting pressure and a decreased response to endogenous and exogenous stimuli. These results suggest a primary end organ defect and most likely indicate abnormal smooth muscle function in pernicious anaemia. Resting sphincter pressure levels and edrophonium response in age-matched subjects indicate that these changes are not due to aging alone.