No abstract

We examined the role of dietary electrolytes and humoral factors in causing seasonal changes in blood pressure. Normal subjects had no seasonal difference in blood pressure, although urinary sodium and norepinephrine were significantly higher in winter than in summer. In patients with essential hypertension blood pressure, urinary sodium and norepinephrine excretion and plasma norepinephrine concentration were significantly higher in winter. Plasma renin activity, plasma and urinary aldosterone and urinary kallikrein excretion were not significantly different between the two seasons in both normal subjects and hypertensive patients. In conclusions, the blood pressure of patients with essential hypertension has a seasonal variation with higher pressures in the winter than in the summer. Increased sympathetic nervous activity and an increased load of sodium presented to the kidney for excretion may be contributing factors in the rise in blood pressure in winter in patients with essential hypertension.

Postmortem histological examination of the thyroid gland and measurement of serum antithyroid antibodies were performed in 70 patients without overt thyroid disease. Lymphocytic infiltration, antithyroglobulin hemagglutination antibody (TGHA), and antithyroid microsomal hemagglutination antibody (MCHA) were found in 12, 2, and 9 cases, respectively. The incidence of lymphocytic infiltration in females was three times that in males. Ten of the 12 cases with lymphocytic infiltration had positive antibodies (either TGHA or MCHA), while 10 of 11 patients with positive antibodies showed lymphocytic infiltration. Thus, the correlation between morphological and serological findings was highly significant at P less than 0.001. The incidence of a small thyroid gland of less than 15 g in weight was higher in patients with lymphocytic infiltration and/or positive antibodies than in patients with a normal thyroid gland. These data suggest that positive serum antithyroid antibodies in subjects without overt thyroid disease may indicate the existence of lymphocytic infiltration in the thyroid gland, that is presumably subclinical autoimmune thyroiditis.

The effect of pregnancy on the clinical course of Graves' disease was examined by studies on 41 pregnancies in 35 patients with Graves' disease, who were considered to be in a state of remission or near remission and were not receiving antithyroid drugs, during and after delivery. Eighteen of the 41 cases (44%) showed transient increases in the serum free T4 index (FT4 index) during weeks 10--15 of pregnancy, but normal thyroid function in the second and third trimesters. Similar transient increases in the serum free T3 index (FT3 index) were observed in early pregnancy in these patients. These early increases in the FT4 and FT3 indexes were specific to Graves' disease and were not observed in Hashimoto's disease. Two to 4 months postpartum, 32 cases (78%) developed various degrees of thyrotoxicosis, which was divided into 3 types: 1) persistent thyrotoxicosis with high radioactive iodine (RAIU) (10 cases), 2) transient thyrotoxicosis with normal or high RAIU) (10 cases), and 3) destruction-induced thyrotoxicosis with low RAIU (12 cases). An increase in the FT4 index in early pregnancy was significantly (P less than 0.001) associated with relapse of stimulation-induced thyrotoxicosis of either the persistent or transient type. Patients who developed destruction-induced thyrotoxicosis after delivery had significantly higher titers of antithyroid microsomal antibodies (P less than 0.001) and a longer euthyroid period before pregnancy (P less than 0.01) than patients who had recurrent persistent thyrotoxicosis. These data indicate that Graves' disease is aggravated in early pregnancy and after delivery and ameliorates in the latter half of pregnancy. Postpartum relapse of persistent hyperthyroidism could be predicted from an early increase in the FT4 index during pregnancy.