Since Cruveilhier1 described the first adenoma of Brunner's glands in 1835, more than 90 patients with hyperplasia of these glands have been reported. Much controversy has arisen as to the etiology of this lesion, the most popular views being hyperstimulation or hamartomatous glandular change. The former hypothesis implicates gastric hyperacidity as the principal cause of the hyperplasia. Recently, we investigated a patient with a circumscribed nodular hyperplasia of Brunner's glands who presented with hypochlorhydria. This led us to study the validity of the hyperacidity theory of etiology.
A review of the English literature disclosed 37 well-documented clinical reports of Brunner's gland hyperplasia. Nineteen of these patients had been studied with gastric analyses. This communication briefly summarizes the pertinent clinical data of these 19 patients, in addition to data on our patient. Analysis of these 20 reports indicates that there is no clear-cut relationship between gastric hyperacidity and hyperplasia of Brunner's
Kaplan EL, Dyson WL, Fitts WT. The Relationship of Gastric Hyperacidity to Hyperplasia of Brunner's Glands. Arch Surg. 1969;98(5):636–639. doi:10.1001/archsurg.1969.01340110128016
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