Hvpergastrinaemia was found in 11 out of 24 untreated hyperthyroid patients (Graves' disease or nodular goitre). Seven patients had a co-existent (autoimmune) atrophic gastritis. In the remaining 17 patients plasma T3 was positively related to plasma gastrin, and negatively to gastric acid output; there was no relation between gastrin levels and acid output. Acid instillation into the stomach revealed a normal negative feedback of acid upon gastrin release.
Sixteen hyperthyroid patients were restudied when euthyroid. Plasma gastrin decreased from 171 (51–1188) ng/l before treatment to 69 (39–392 ng/l after treatment (P < 0.002), and maximal acid output increased from 1.55 (0.00–22.75) to 8.03 (0.00–26.60) mmol H+/h (P < 0.01) (median values; range in brackets). However, in 4 patients with complete achlorhydria before and after treatment plasma gastrin decreased to the same extent as in the patients with gastric acid secretion.
We conclude that thyrotoxic hypergastrinaemia cannot be fully explained by the low gastric acid output in hyperthyroidism.
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