Assay of hormones in saliva would be more convenient than assay in blood, but there is no information on the route by which hormones enter saliva, information that would provide insight into the clinical value of such assays. We have examined the mode of entry of various hormones into saliva. The results suggest that unconjugated steroids enter saliva by diffusing through the cells of the salivary glands and that their concentration in saliva does not depend on the rate of saliva production. Conjugated steroids enter saliva via "ultrafiltration" through the tight junctions between the acinar cells, and their concentration in saliva is highly flow-rate dependent. Thyroxin and choriogonadotropin enter saliva via the ultrafiltration route or by contamination of the saliva by plasma or gingival fluid. We conclude that the salivary concentration of unconjugated steroids may usefully reflect the concentration of free (nonprotein-bound) steroids in plasma. Conversely, the concentration of conjugated steroids, thyroxin, and protein hormones such as choriogonadotropin in saliva probably does not reflect their concentration in plasma in any clinically useful way.
The ingestion by normal subjects of 3 g of sodium iopodate, which is widely used in routine oral cholecystography, resulted in significant decreases of serum total and free T3 to a nadir on day 4 which averaged 43% and 40%, respectively, below initial mean values. Total and free rT3 increased markedly to a peak on day 3, 244% and 189%, respectively, above initial mean values. Total and free Ti and free T4 index rose to a maximum on day 4, but these changes were not statistically significant. A marked TSH increase was also seen, most evident on day 3. All these changes reverted to baseline values by day 14 at a time when serum total iodide was still markedly elevated. It is concluded that the changes observed after iopodate were not due to alterations in serum binding proteins nor to an effect on thyroid gland by the large iodine component of iopodate, but were consistent with an effect on the peripheral metabolism of T4. Difficulty in ipterpreting routine thyroid function tests may occur for up to 14 days after oral cholecystography with iopodate. Sodium iopodate is a contrast medium commonly used in oral cholecystography. Its chemical struc¬ ture bears some similarity to that of thyroxine (T4) and 61.4% of its weight consists of iodine. Wu et al. (1978) observed the effects of iopodate ingestion for a week and showed that serum 3, 5, 3' triiodothyronine (T3) decreased, 3, 3', 5' triiodothyronine (rT3) increased and T4 increased in euthyroid subjects. Similar changes were observed in thyrotoxic patients excepting that serum T4 decreased. They concluded that iopodate alters peripheral metabolism of T4 and, in thyrotoxicosis, it may decrease thyroid activity also.Because of its widespread use in clinical practice iopodate may commonly complicate the interpreta¬ tion of routine thyroid function tests. We therefore decided to document the magnitude and duration of such interference by observing the effects of oral iopodate on routine thyroid function tests. We also studied the effects on the serum concentrations of total and free rT3, free T3, free T4, thyroid stimu¬ lating hormone (TSH) and total iodide to help elucidate the mechanism of the interference. Subjects and MethodsSix healthy adult male volunteer subjects were studied whose average age was 25 years. Sodium iopodate was given in 3 separate 1 g oral doses between 09.00 and 12.00 h. Similar studies were conducted on two other healthy volunteers given an equivalent oral dose of iodine in the form of potassium iodide. Blood was sampled by venepuncture at 09.00 h on each day of observation namely 10 and 6 days before iopodate, on the day of taking iopodate and on days 1, 3, 4, 7, 14 and 21 after the doses. Samples were taken with minimal venostasis after the subjects had been sitting for 5 min. Serum was stored in aliquots and analyzed soon after the last sample was collected. All samples from each subject were analyzed in the same batch.Concentrations of total T4, total T3, rT» and the TSH were determined by specific radioimmunoassay (RIA) using second anti...
Summary A gradual increase in spontaneous lymphocyte DNA synthesis was demonstrated in each trimester of pregnancy. Autoradiographic studies indicated that lymphocytes were primarily responsible for this activity. PHA‐induced lymphocyte transformation in both fetal calf serum and autologous serum was significantly reduced in the second and third trimesters of pregnancy. Spontaneous lymphocyte DNA synthesis was significantly reduced in patients with mild pre‐eclampsia. However, no significant differences were seen in patients with severe pre‐eclampsia in the third trimester of pregnancy compared with the normal control subjects. No evidence was adduced to implicate inhibitory humoral factors affecting the peripheral blood lymphocytes in pregnant patients in experiments in which washed lymphocytes were cultured in medium containing heterologous serum. In vitro experiments demonstrated that cortisol, progesterone and HPL caused a significant reduction in lymphocyte DNA synthesis, and HGH and HCG had a variable effect. However, only cortisol was regularly inhibitory at physiological concentrations. The progesterone effect was dose‐related, producing 90 per cent inhibition of activity at a concentration of 10 μg/ml. No synergism could be shown between HPL and progesterone on lymphocyte transformation. The increase in activity of circulating immunoreactive cells during pregnancy and its depression with the onset of pre‐eclampsia is discussed.
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