Peak TSH Levels Research Articles

Plasma thyrotropin, thyroxine, and triiodothyronine relationships in man.

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.

The Influence of the Circadian Thyrotropin Rhythm on the Thyrotropin Response to Thyrotropin-Releasing Hormone in Normal Subjects

200 μg synthetic thyrotropin-releasing hormone (TRH) was administered intravenously to 6 normal men and 5 normal women at 11 a.m. and again at least one week later at 11 p.m. As expected, the basal TSH level was higher at 11 p.m. than at 11 a.m. The absolute peak TSH levels as well as the increases in TSH after TRH stimulation were higher at 11 p.m. than at 11 a.m. A positive correlation between basal TSH level and maximal serum TSH after TRH was found in the 11 a.m. tests as well as in the 11 p.m. tests. When the TSH response was expressed as per cent increase over the low forenoon and the high night basal levels of the circadian cycles, there was no difference in the TSH response to TRH.

Serum thyrotropin and thyroxine concentrations in patients recieving lithium carbonate.

To determine the incidence of thyroid dysfunction in patients receiving therapy with lithium carbonate, serial determinations of serum thyrotropin (TSH) and thyroxine (T4) concentrations were made in 255 patients receiving lithium. The patients were followed for an average of 8 months and the longest period of lithium treatment was 65 months. The mean peak TSH level in the lithium treated patients was 3 times higher than in the control groups; elevated (>8 μU/ml) TSH levels occurred in 29.8% of the patients (76) at some time during treatment. At the time of final testing, 14.1% (36) of the patients had elevated serum TSH levels. The mean peak and final thyroxine concentrations in the lithium treated patients were only slightly lower than those in the control groups. In 15 patients whose final serum TSH levels were over 20 μU/ml, the mean thyroxine concentration was 2.9 μg/100 ml. A significantly higher incidence of positive anti-thyroglobulin antibody tests was found in these patients. Most were considered to have significant hypothyroidism and received thyroid treatment. In 27 patients pretreatment data were available. In these patients mean TSH levels significantly increased within the first 3 months of treatment and remained above pretreatment levels thereafter. Serum thyroxine levels did not change significantly. These results indicate that anti-thyroid effects of lithium, as manifested by elevated serum TSH levels, can be detected at some time in almost one-third of patients receiving it. With continued treatment, the anti-thyroid effect of lithium may either be lessened, with return of TSH levels to normal, or progress to the development of frank hypothyroidism.

L-DOPA suppression of thyrotropin-releasing hormone response in man.

500 μg of thyrotropin releasing hormone (TRH) was injected intravenously into eight Parkinsonian patients being treated with L-DOPA and into five control patients with Parkinsonism who were not receiving L-DOPA. The mean peak serum level of TSH was 10.1 ± 3.0 (S.D.) μU/ml in the L-DOPA treated patients as compared to 28.8 ± 3.5 (S.D.) μU/ml in the control group. There was no overlap in peak serum TSH levels between patients on L-DOPA and controls. Chronic L-DOPA administration results in the inhibition of TSH secretion in response to TRH stimulation; the mechanism is unknown.