Clinical and experimental evidence indicates that carcinoid tumours of the stomach fundic mucosa represent another example of hormone-dependent neoplasm, gastrin being the hormone involved in tumour induction. In this context hyperplasia of fundic endocrine cells associated with chronic atrophic gastritis (CAG) and hypergastrinaemia is regarded as the most frequent preneoplastic lesion. However, the cell type involved in this hyperplasia has not been clarified. To elucidate this problem fundic endocrine cells were characterized ultrastructurally in 9 patients from which endoscopic gastric biopsies were obtained. ECL cells were the most frequent cell type in 8 cases, in 4 of which they were more numerous than all other cell types taken together. D1 cells were the most frequent type in one case while they were inconspicuous in the other cases. P cells were found with a frequency in each case intermediate between that of ECL cells and that of D1 cells. These results indicate that fundic endocrine cell hyperplasia occurring in hypergastrinaemic CAG is in most cases cytologically similar to that found in other hypergastrinemic conditions, in which the gastrin-dependent ECL cells were already found to prevail. They also explain why fundic carcinoids arising in CAG are mostly composed of ECL cells. The relation between ECL, D1 and P cells, if any, remains obscure.

Polyclonal antibodies have been raised against purified bovine pyrazine-binding protein, a protein that binds the odorant 2-isobutyl-3-methoxypyrazine. These antibodies have been utilized in immunocytochemical experiments to localize the pyrazine-binding protein in bovine nasal mucosa. Tissue fragments, macroscopically identified as olfactory and respiratory mucosa, were fixed in Bouin's fluid and embedded in paraffin. Consecutive serial sections were processed for immunofluorescence studies and restained either with haematoxylin-eosin or with periodic acid Schiff-Alcian Blue. In both olfactory and respiratory mucosa, only seromucous tubulo-acinar glands were specifically labelled. These glands are located in the lamina propria underlying typical respiratory epithelium, even in those tissues that are macroscopically defined as olfactory mucosa.

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Eighteen cases of severe hyperplasia of fundic argyrophil cells observed during routine histologic examination of endoscopic gastric biopsy specimens from unselected patients with upper gastro-intestinal symptomatology were investigated. All patients, except one, were female with a mean age of 57 years. Atrophic gastritis of fundic mucosa with severe hypo- or achlorhydria was present in all cases. Hypergastrinaemia (of antral origin) was found in 15 subjects in which circulating gastrin levels were determined. Pernicious anaemia was seen in 1 patient. At light microscopy, the hyperplastic fundic cells were stained by the Grimelius and the Sevier-Munger silver methods and, in approximately 30% of cases, by lead-haematoxylin. In addition, these cells reacted with anti chromogranin antibodies. In 8 of 9 patients studied by electron-microscopy, enterochromaffin-like (ECL) cells were found to be the more frequent cell type. D₁ cells prevailed in 1 case and were rare in the others. The frequency of P cells was intermediate between that of ECL cells and that of D₁ cells. In conclusion, our observations indicate that: (a) argyrophil cell hyperplasia of atrophic fundic mucosa is prevalently found in women with hypergastrinaemia, and (b) the hyperplastic process involves mostly the ECL type of gastric endocrine cells. It is noteworthy that similar associations have been shown to be present in patients affected by fundic carcinoid tumours and atrophic gastritis.