Comparison of the value of T3, T4 and TSH in sera of animals treated with low and high dose concentrated potassium iodine solutions

Abstract

Etiopathogenesis of the most frequent endocrinopathy, Hashimoto thyroiditis (HT) is not clear. Our investigations dating from 1990 on an experimental model for examination of thyroiditis in Wistar rats show morphological changes in the rat thyroid evoked by potassium iodine (KJ) administration. KJ is used as a drug in therapy of numerous diseases such as Erythema Nodosum, Vasculitis Nodularis, Sweet’s Syndrome, as well as tuberculosis and granulomatosis. This study examined the effect of the maximal dose of potassium iodine on the thyroid gland and status of T3, T4 hormones and TSH in Wistar rats. We have groups of Wistar rats: treated with low iodine dose (LKI = 22,5 µg/g b.w.), and with high iodine dose (HKI = 225 µg/g b.w.) of KI, solutions (n=10). Untreated nonimmunised animals served as controls. Solutions were administered daily intraperitonealy during a period of 26 consecutive days. Histological changes within the gland in HKI treated group were the infiltration of the mononuclear cells associated with destruction of tissue architecture, formation of macrofolicules and proliferation of connective tissue significantly higher than in LKI treated rats. Rats injected with LKI had depletion of the serum amount of T3 and T4, as HID injected rats. The early iodide induced cell necrosis and inflammation in the nonimunised animals not carrying a genetic susceptibility, is in fact a new experimental model of the LT.

Etiopatogeneza najčešće endokrinopatije, Hašimotovog tiroiditisa (HT) nije razjašnjena. Naša istraživanja imunomodulirajućeg efekta kalijum jodida (KJ), započeta 1990. godine, jasno pokazuju da KJ izaziva eksperimentalni tiroiditis (ET) na dozno zavistan način u funkciji vremena, bez prethodne imunizacije. KJ se primenjuje u ljudskoj ishrani za jodiranje soli, za terapiju vaskulitisa malih krvnih sudova, erythema nodosum, vaskulitisa nodularisa, Sweet-ovog sindroma, kao i tuberkuloze i granulomatoze. Pacovima Wistar soja ubrizgavan je KJ intraperitonealno u niskoj i visokoj koncentraciji (NKJ - 225 µg/g i VKJ - 675 µg/g) tokom 26 dana. Kontrolna grupa životinje tretirana je fiziološkim rastvorom. Na histološkom preparatu štitnjače pacova tretiranih NKJ naziru se ostaci folikula bez koloida i tireocita, infiltracija mononuklearnim ćelijama i proliferacija vezivnog tkiva, a u onih tretiranih VKJ vidi se proliferacije veziva, gubitka folikularne građe i infiltraciju mononuklearnim ćelijama. Zapaljenjske promene su znatno izraženije kod pacova tretiranih VKJ. Praćenjem hormonskog statusa (T4, T3,TSH ) i morfoloških promena štitaste žlezde, ustanovljeno je da terapijske doze KJ koji se primenjuje za lečenje, indukuju nastanak eksperimentalnog tiroiditisa kod genetski neosetljivih životinja, po tipu hroničnog destruktivnog Hašimoto tiroiditisa kod ljudi. Nekroza i zapaljenje pokrenute jodidom u neimunzovanih životinja, bez genske osetljivosti nov je, originalan, eksperimentalni model tiroiditisa.