A B S T R A C T Propylthiouracil (PTU) inhibits peripheral deiodination of thyroxine (T4) and triiodothyronine (T3) and decreases the metabolic effectiveness of T4 in animals. To assess the effect of PTU on extrathyroidal conversion of T4 to Ta in man, 15 studies were performed in 7 athyreotic patients treated with 100 or 200 Ag of L-T4 daily for 1 mo before the addition of PTU, 250 mg every 6 h for 8 days. Serum T3, T4, and thyrotropin (TSH) were measured daily by radioimmunoassay; serum TSH response to 500-ig thyrotropin-releasing hormone (TRH) was measured before and on the last day of giving PTU.On the 100-Ag L-T4 dose, serum T3 fell from 120±5 The data suggest that PTU blocks extrathyroidal conversion of To to Ts, thus increasing pituitary TSH secretion and augmenting the TSH response to TRH.
Measurements of serum levels of thyroxine (T4), free T4, 3,5,3'-triiodothyronine (T3), free T3, 3,3',5'-triiodothyronine (reverse T3, rT3), thyroxine-binding globulin capacity (TBGcap), chorionic gonadotrophin (hCG) and thyrotrophin (TSH) were carried out prospectively in eight women with uncomplicated pregnancies, in order to examine interrelationships between the thyroid gland and thyroid stimulating hormones during pregnancy. During pregnancy the levels of T4, free T4, T3, rT3 and TBGcap were significantly elevated, and TSH was decreased. It was noted that the elevation of T4 was maintained from the 8th to the 27th week of gestation while the level of TBGcap progressively increased. The levels of free T4 and rT3 in the first and third trimesters were significantly higher than those of age-matched, non-pregnant women. The levels of hCG showed a biphasic variation, with a peak in the 8th to 15th weeks, followed by a decline in the second trimester and a small, secondary elevation in the 32nd to 39th weeks. This later elevation was positively correlated with changes in free T4 and free T3 levels. The increase of serum T4 accompanied by an increase of free T4 in the first trimester appeared due to augmented secretion of T4, rather than being secondary to the elevated levels of TBGcap.
Sixteen patients with typical signs and symptoms of anorexia nervosa were studied with measurement of serum thyroxine (T4), triiodothyronine (T3) and thyrotropin (TSH), both baseline and stimulated by thyrotropin-releasing hormone (TRH). The results of the patients were compared with those of 16 normal control subjects. Serum T4 (5.8 plus or minus 0.26 mug/100 ml, mean plus or minus SE) and T3 (82 plus or minus 5.7 ng/100 ml) of patients with anorexia nervosa were significantly (P less than 0.001) lower than those of control subjects (T4 7.7 plus or minus 0.32 mug/100 ml and T3 158 plus or minus 4.7 ng/100 ml respectively). Furthermore, the ratio of T3/T4 (1.48 plus or minus 0.243 x 10(-2)) in anorexia nervosa was also lower than that of control subjects (2.21 plus or minus 0.093 x 10(-2)) (P less than 0.001). Basal serum TSH was within normal or below the limits of detection. TSH and T3 rose after administration of TRH. The peak values of TSH were observed after 60 to 12o min, instead of 30 min normally seen after TRH injection.
The physiologic relationships of plasma TSH, T4 and T3 levels measured every 20 min in seven healthy young men and one healthy young woman have been investigated. A nocturnal TSH surge was observed in all subjects on both nights of the 36-48 h baseline observation period. In males the maximum plasma TSH value occurred at 2300 h. The mean peak TSH level was 2.0 +/- 0.3 (se) muU/ml compared with a mean of 1.3 +/- 0.9 muU/ml for the entire baseline records of the 8 subjects. The effect of iv infusion of 32-1000 mug of somatostatin (SRIF) for 1 1/2-3 h was investigated in four of the male subjects during 2 or 4 consecutive nights following the control period. Temporal relationships between the hormonal fluctuations observed throughout the control period and during the nights of SRIF infusion were investigated using time series analysis and Student's t test. Rapid fluctuations of plasma T4 and T3 concentration were noted, even when corrected for changes in total protein concentration, with an average coefficient of variation of 10% for T3 and 12% for T4. No increment of plasma T4 or T3 followed the nocturnal TSH surge nor were the rapid fluctuations of the thyroid hormones altered by the TSH surge. SRIF infusion commencing at 2300 h suppressed the elevated TSH levels (P is less than 0.01) while similar infusions begun at 2100 h blocked the expected nocturnal TSH rise observed during control periods in male subjects. Plasma T4 and T3 levels were not significantly affected by the administration of SRIF. The relationship of the rapid plasma T4 and T3 variations to postural changes was investigated in four euthyroid male subjects. Serum levels of TSH, T4 and T3 and total protein were determined at 15 min intervals while postural changes were carefully monitored. The ratios of T4 and T3 to total protein were relatively stable (3-4% coefficient of variation) when the subjects were kept in a supine and motionless position. A 50 mug bolus infusion of T4 raised the basal T4 level by only 1-2 mug/dl. The data suggest that short-term fluctuation of plasma T4 and T3 result from changes in protein concentration due to hemodynamic responses to alteration of posture and physical activity and not to pulsatile secretion of T4 and T3.
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