自己免疫性甲状腺疾患におけるガストリン値の動態

第1報:甲状腺機能状態とガストリン値

抄録

The relationship between thyroid disorders and gastric pathophysiology has been studied mainly from standpoints of gastric histology and gastric acid output capacity. Though anti-gastric antibody has been thought to play a part in this relationship, there have been no clear conclusions obtained about that. Since blood gastrin levels are easily measurable by radioimmunoassay today, the relationship between thyroid disorders and gastric pathophysiology has drawn attention again from a standpoint of gastrin levels. Seino et al. have reported about hypergastrinemia in hyperthyroidism, speculating that β-adrenergic hyperresponsiveness of gastrin-producing cells could be the mechanism of hypergastrinemia. However, there are other reports which mentioned feedback mechanism between gastrin and gastric acid or interaction of gastrointestinal hormones as the main mechanism of hypergastrinemia.
In this study, the problem of gastrin in Graves' disease and chronic thyroiditis were studied by measurement of fasting serum gastrin levels and gastric juice excretion in view of feedback mechanism between gastrin-producing cells and parietal cells which are the target cells of gastrin.
Following results were obtained.
1) Fasting serum gastrin levels in Graves' disease were 236.2±39.1 (mean±SE) pg/ml for 39 hyperthyroid patients and 126.3±23.9 pg/ml for 35 euthyroid patients. These levels were significantly higher than those of sex and age-matched control subjects with P<0.001 and P<0.05, respectively. Fasting serum gastrin levels in serial studies of 13 patients with Graves' disease were 222.3±56.7 pg/ml before treatment and 167.3±56.6 pg/ml at the time of euthyroid state after a mean observation period of 6.6±1.1 months. Fasting serum gastrin levels at the time of euthyroid state decreased significantly when compared with fasting serum gastrin levels before treatment (P<0.05).
2) Fasting serum gastrin levels in chronic thyroiditis were 160.7±51.1 pg/ml for 24 hypothyroid patients and 96.4±24.7 pg/ml for 31 euthyroid patients. Each of these levels had no significant differences when compared with sex and age-matched control subjects. Fasting serum gastrin levels in serial studies of 10 patients with chronic thyroiditis were 81.1±18.0 pg/ml at the time of hypothyroid state and 91.5±15.2 pg/ml at the time of euthyroid state after a mean observation period of 7.1±2.1 months. Fasting serum gastrin levels before treatment had no significant differences when compared with fasting serum gastrin levels in euthyroid state.
3) Fasting serum gastrin levels in hyperthyroidism did not correlate with any of serum thyroxine levels, serum triiodothyronine levels and free thyroxine indices. Fasting serum gastrin levels did not significantly correlate with any of anti-thyroid microsomal antibody and anti-thyroglobulin antibody titers in both hyperthyroid and euthyroid state.
4) Fasting serum gastrin levels correlated inversely with the maximum acid output in the study of 22 patients with Graves' disease (r=-0.44, P<0.05).
5) Two group were differentiated in serial study of 8 patients with Graves' disease. In one group, fasting serum gastrin levels were decreased and normalized immediately in response to decline and/or normalization of thyroid functions. In the other group, fasting serum gastrin levels decreased rather slowly or retained at high levels with labile fluctuation relatively independently of thyroid functions. These results suggested that Graves' disease could be associated with multiple factors to elevate fasting serum gastrin levels, ie, existence of anti-parietal cell antibody, hyperresponsiveness of β-adrenergic receptors, gastric hypoacidity, interaction of gastrointestinal hormones, etc.