高血圧症における甲状腺機能について

抄録

Studying the thyroid activity in essential hypertension, we have measured serum protein bound iodine (PBI) level and basal metabolic rate (BMR) in patients with hypertensive diseases and normal adults. We have also investigated the effects of thyroid extract on essential hypertension.
Serum PBI is determined by the slightly modified Barker's alkali incineration method.
1) We can not find any marked difference between the serum average PBI level of 20 patients with essential hypertension and of 10 normal adults. But it is interesting that the PBI level is lower in patients with the essential hypertension of group 1 (according to Keifh Wagener's classification-i.e. early stage) than in normal adults. However, the PBI level in group 2, 3 and 4 is higher than normal adults, and then it tends to rise as the hypertention develops.
2) The average of the basal metabolic rates in 20 cases of essential hypertention is higher than that of 9 normal adults.
3) We can not find any corelation between the PBI level and the BMR in essential hypertention. The increase of the BMR in essential hypertension may not always mean the hyperfunction of the thyroid gland.
4) Nine cases of essential hypertension are administered with thyroid extract (0.05-0.1gr. pro day) for 2 to 13 weeks.
Among them in 5 cases of low PBI level at the earlier stage is shown the remarkable response to administration of thyroid extract. It results that serum PBI level rises up and both systolic and diastolic pressure begins to fall. Another 4 cases with high PBI level (1 case of Group 2, 1 case of Group 3 and 1 case of Group 4) do not so clearly respond to administration of thyroid extract as the formers. The PBI level decreases against our expectation. The slight fall of systolic pressuer is observed but diastolic pressure does not fall. 5) The favorable response to thyroid extract in these cases may be ascribed to the existence of the hypofunction of thyroid gland which may be at the early stage of essential hypertension. The reverse response to thyroid extract observed in the late stage of the disease may be the result of the fact that the secretion of thyrotropic hormone may be inhibited by the thyroid extract administered and then the already existing compensative hyperfunction of thyroid gland is diminished.
Although it is not able to conclude that the hypertension occurs from the hypo- or hyper-function of thyroid gland, it may be thought that the interrelation between essential hypertention and thyroid activity may be more complicated than it has been considered up to now.