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Decreased Sulfation of Serum and Tissue Gastrin in Hypergastrinemia of Antral Origin
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The sulfation of gastrin in serum, antrum and duodenum was studied in 22 normo- and 20 hypergastrinemic patients. The ratio between gastrin-17 and gastrin-3 4 was measured in antrum and duodenum. The degree of sulfation was reduced in the antrum of hypergastrinemic patients (35.3 ± 1.3%, mean ± SEM) compared with 48.0 ± 2.1% in normo-gastrinemic patients (p < 0.001). The degree of sulfation in serum and duodenum was similar to that of the antral gastrins in all patients. The percentage of gastrin-34 in antrum was increased (7.3 ± 0.7%) in hypergastrinemic compared with 4.9 ± 0.3% in normogastrinemic patients (p < 0.01). In the duodenum the percentage of gastrin-34 was similar in normo- and hypergastrinemia. When classified according to clinical diagnosis, sulfation of antral gastrin was normal in duodenal ulcer (47.6 ± 4.5%) but decreased in gastric ulcer (36.7 ± 1.6%, p < 0.01) and pernicious anemia (31.3 ± 1.9%, p < O.OOl) compared with 48.2 ± 2.2% in control patients. In pernicious anemia a larger proportion of antral gastrins occurred as gastrin-34 (8.2 ± 0.9%) compared with 4.8 ± 0.4% in control patients (p < 0.01). Our study suggests that both sulfation and proteolytic processing of the gastrin precursor is diminished in hypergastrinemia of antral origin.
Title: Decreased Sulfation of Serum and Tissue Gastrin in Hypergastrinemia of Antral Origin
Description:
The sulfation of gastrin in serum, antrum and duodenum was studied in 22 normo- and 20 hypergastrinemic patients.
The ratio between gastrin-17 and gastrin-3 4 was measured in antrum and duodenum.
The degree of sulfation was reduced in the antrum of hypergastrinemic patients (35.
3 ± 1.
3%, mean ± SEM) compared with 48.
0 ± 2.
1% in normo-gastrinemic patients (p < 0.
001).
The degree of sulfation in serum and duodenum was similar to that of the antral gastrins in all patients.
The percentage of gastrin-34 in antrum was increased (7.
3 ± 0.
7%) in hypergastrinemic compared with 4.
9 ± 0.
3% in normogastrinemic patients (p < 0.
01).
In the duodenum the percentage of gastrin-34 was similar in normo- and hypergastrinemia.
When classified according to clinical diagnosis, sulfation of antral gastrin was normal in duodenal ulcer (47.
6 ± 4.
5%) but decreased in gastric ulcer (36.
7 ± 1.
6%, p < 0.
01) and pernicious anemia (31.
3 ± 1.
9%, p < O.
OOl) compared with 48.
2 ± 2.
2% in control patients.
In pernicious anemia a larger proportion of antral gastrins occurred as gastrin-34 (8.
2 ± 0.
9%) compared with 4.
8 ± 0.
4% in control patients (p < 0.
01).
Our study suggests that both sulfation and proteolytic processing of the gastrin precursor is diminished in hypergastrinemia of antral origin.
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