Biomedical subjects

R M Colzani

Publications and source records attributed to R M Colzani.

4 recordsLinked to original sources

PubMed2001

Hyperthyroidism is associated with lengthening of ventricular repolarization.

OBJECTIVE: Lengthened ventricular repolarization, as assessed by the QT interval on electrocardiogram (ECG), can predispose to an increased risk of cardiac dysrhythmias; no data are available on QT corrected for heart rate (QTc) in hyperthyroidism in vivo. DESIGN: QT and RR intervals from 24 h ambulatory ECG Holter recording were measured in patients with hyperthyroidism and again following pharmacological achievement of stable euthyroidism for at least 2 months. PATIENTS: We enrolled a total of 16 hyperthyroid patients with Graves' disease, six males and 10 females (mean age 47 +/- 4 years, mean +/- SEM); 13 healthy age- and sex-matched subjects were utilized as a control group. MEASUREMENTS: The QT analysis was carried out by a computerized algorithm (QTc was corrected by the heart rate by Bazett's formula). Serum total T4, total T3, free T4, free T3 and TSH concentrations were measured by a fully automated immunoenzymometric assay; plasma norepinephrine by automatized high-pressure liquid chromatography, potassium and chloride by a potentiometric method, magnesium and calcium by a colourimetric method. RESULTS: The 24-h average QTc in the hyperthyroid patients was significantly prolonged compared to controls (458 +/- 7 vs. 431 +/- 6 ms, P = 0.01) and it returned to normal after treatment of thyrotoxicosis (432 +/- 6 ms, P < 0.05 vs. time H, NS vs. controls). QTc positively correlated with FT3 (r = 0.63, P < 0.001) and with FT4 (r = 0.481, P < 0.02). Conversely, QTc did not correlate with plasma basal norepinephrine levels, nor with electrolytes. CONCLUSIONS: Hyperthyroidism is associated with prolonged QTc that normalizes once the patient becomes euthyroid. The strong positive correlation between FT3 and QTc supports the hypothesis of an important role of thyroid hormone on modulation of QTc lengthening.

Adrenergic beta-Antagonists↗

PubMed1999

Effects of iodine repletion on thyroid morphology in iodine and/or selenium deficient rat term fetuses, pups and mothers.

It has been suggested that selenium deficiency aggravates the iodine-induced thyroid inflammation and necrosis in iodine-deficient Wistar rats and possibly in man. Studies were carried out to determine whether large amounts of iodine given to iodine-deficient pregnant Sprague-Dawley rats with or without selenium deficiency would induce inflammation and necrosis in their term fetal thyroids. Iodine deficiency was induced in the dams by a low iodine diet or perchlorate in the drinking water and iodine excess was achieved by iodinated drinking water during pregnancy or daily subcutaneous injections of iodine from days 20 to 22 of pregnancy, 1 day after perchlorate was discontinued. Studies were also carried out in 30-day-old pups whose nursing mothers were iodine-deficient (perchlorate) with or without selenium deficiency from conception onward. The administration of iodine restored the morphologic changes in the thyroid induced by iodine deficiency, irrespective of selenium status, toward normal without inflammatory changes or necrosis. Possible explanations for these unexpected findings are discussed.

Animals↗

PubMed1999

The oral administration of human thyroglobulin does not affect the incidence of lymphocytic thyroiditis in the biobreeding Worcester rat.

Oral tolerization with the appropriate antigen(s) to ameliorate autoimmune diseases in humans and in experimentally induced animal models, including experimentally autoimmune thyroiditis in mice, has been reported to be efficacious. Spontaneous and iodine induced (0.05% iodine in the drinking water) lymphocytic thyroiditis (LT) occurs in the diabetes mellitus (DM)-prone BioBreeding/Worcester (BB/Wor) rat. The present study was carried out to determine whether the oral administration of human thyroglobulin (hTg) would decrease the incidence of spontaneous and iodine-induced LT in the BB/Wor rat. Low iodine content hTg or bovine serum albumin (BSA) were given orally every 2 days for six doses beginning at age 50 days to BB/W rats, half of whom also received iodine in their drinking water. No effect or orally administered hTg was observed on thyroid weight, the incidence of LT or DM, or on serum thyroglobin antibodies (TgAb), thyrotropin (TSH), thyroxine (T4), and triiodothyronine (T3) concentrations when rats were killed at 100 days of age. In a second experiment, the oral administration of iodine rich hTg or BSA every 2 days for six doses beginning at 30 days of age to iodine-treated BB/Wor rats again did not affect the high incidence of LT or DM or serum TgAb, TSH, T4, and T3 concentrations. The present study suggests that oral tolerization with hTg does not affect spontaneous or iodine-induced lymphocytic thyroiditis or serum thyroglobulin antibodies in the BB/Wor rat.

Animals↗

PubMed1998

The effect of recombinant human thyrotropin (rhTSH) on thyroid function in mice and rats.

The vast majority of studies to determine the biological activity of recombinant human thyrotropin (rhTSH) have been carried out in the mouse. We have recently reported that 0.1 mg of rhTSH IM (one-ninth the dose given in thyroid cancer patients) given to normal subjects elicits a brisk rise in serum thyroxine (T4), triiodothyronine (T3), and thyroglobulin (Tg) concentrations. In contrast, in initial studies in the rat, a low dose of rhTSH failed to increase serum T4 or T3 concentrations. The present study was, therefore, carried out to determine the biological activity of rhTSH in euthyroid and in T3-treated, TSH-suppressed rats and mice. Doses of rhTSH based on body weight were used and resulted in similar serum human thyrotropin (hTSH) concentrations in the two species. Euthyroid and TSH-suppressed mice responded briskly to rhTSH administration. In contrast, serum T4 did not increase after rhTSH administration in euthyroid rats. In TSH-suppressed rats, the increase in serum T4 was similar to that observed in TSH suppressed mice. These observations suggest that rhTSH more readily displaces endogenous TSH from the mouse than from the rat thyroid TSH receptor, because equal responses were observed when endogenous TSH was suppressed.

Animals↗