Abstract
To confirm that the organic iodine compounds were not present in saliva or urine a tracer dose of I131-T4 was injected intravenously into patients with various thyroid diseases. The saliva and urine were collected for one hour. Iodine compounds of saliva and urine were extracted with acid-butanol and concentrated using nitrogen. Ascending paperchromatography was applied on the concentrated samples using butanol, acetic acid and water (78 : 5 : 17) as developer. The paper strips were scanned using actigraph, then autoradiograms were performed, and then stained with ceric arsenite reagents. Ascending thin layer chromatography was performed using the same samples and developer as paperchromatography. Then the absorbents were stained with ceric arsenic reagents, were scanned using scintillation counter, and the percentage of radioactivity of each iodine compound was calculated. Columnchromatography utilizing the anion exchange resin Dowex 1 was performed using adjusted acetate buffer to various pH 3.6, 2.2, 1.4, by 0.2 M acetic acid and 0.2 M sodium acetate and 3N-NaBr. Then these samples were scanned. Chemical analysis performed by butanol and Blau' Reasent.
From these results, the presence of a significant amount of organic iodine compounds in urine was confirmed, but a tracer dose of organic iodine compounds in salive was detected.
From these findings, we used the salive to investigate the thyroxine deiodination. There was a high salivary percent-radioactivity in nontreated hyperthyroid patients and a low one in nontreated hypothyroid patients. But these values were normalized with therapy. The s/p ratio (ratio of salivary percent radioactivity in 60 minutes to palsma percent radioactivity at 60 minute) was as follows :
Euthyroid 0.121±0.034
Nontreated hyperthyroid 0.179±0.040 (p<0.01)
Treated hyperthyroid 0.097±0.026
Nontreated hypothyroid 0.070±0.015 (p<0.01)
Treated hypothyroid 0.101±0.011
Simple goiter 0.110±0.027
Next, the early phase of disappearance of intravenous injected I131-T4 from the circulation (acute thyroxine disappearance rate or acute thyroxine half time) was calculated by the next formula.
Acute Thyroxine Half-Time (time in minutes) = 45 log 2/log a -log b a= cpm of 1 ml. serum at 15 min. after intravenous injection of 20 micro C. I131- T4
b = cpm of 1 ml. serum at 60 min. after intravenous injection of 20 micro C.I131-T4
With this method we measured acute thyroxine half-time in patients with various thyroidal diseases. The results were as follows :
Euthyroid 88.0+11.2
Nontreated hyperthyroid 66.3±4.8 (p<0.01)
Treated hyperthyroid 82.3+7.4
Nontreated hypothyroid 120.4±7.3 (p<0.01)
Treated hypothyroid 98.8±4.9
Simple goiter 78.3+9.5
There was no correlation between this acute thyroxine half-time and PBI, RSU, RBCU. But the correlations of PBI, serum cholesterol, RSU, RBCU, BMR to s/p ratio were r=0.61 (p<0.05), r=-0.80 (p<0.05), r=0.86 (p<0.05), r=0.80 (p<0.05), r=0.78 (p<0.05).
Conclusively, these findings suggested that deiodination concerning thyroxine metabolism was accelerated in hyperthyroid and prolonged in hypothyroid, and these states were normalized with therapy.
