Wiersinga W M, Touber J L
Acta Endocrinol (Copenh). 1980 Nov;95(3):341-9. doi: 10.1530/acta.0.0950341.
Hypergastrinaemia 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.
在24例未经治疗的甲状腺功能亢进患者（格雷夫斯病或结节性甲状腺肿）中，发现11例有高胃泌素血症。7例患者并存（自身免疫性）萎缩性胃炎。其余17例患者中，血浆T3与血浆胃泌素呈正相关，与胃酸分泌呈负相关；胃泌素水平与胃酸分泌之间无相关性。向胃内滴注酸显示酸对胃泌素释放有正常的负反馈作用。16例甲状腺功能亢进患者甲状腺功能正常后再次接受检查。血浆胃泌素从治疗前的171（51 - 1188）ng/l降至治疗后的69（39 - 392）ng/l（P < 0.002），最大胃酸分泌量从1.55（0.00 - 22.75）增加至8.03（0.00 - 26.60）mmol H⁺/h（P < 0.01）（中位数；括号内为范围）。然而，4例治疗前后均完全无胃酸分泌的患者，血浆胃泌素下降程度与有胃酸分泌的患者相同。我们得出结论，甲状腺毒症性高胃泌素血症不能完全用甲状腺功能亢进时胃酸分泌减少来解释。
