5 research outputs found
Análise retrospectiva do resultado do tratamento com iodo radioativo em 120 pacientes tirotóxicos por doença de Basedow-graves
We studied retrospectively the outcome of radioactive iodine therapy (RAI) in 120 thyrotoxic patients with Graves' disease (96 F/ 24 M) who were primarily treated with anti-thyroid drugs (ATD). The decision to use RAI was due either to relapse after ATD-induced remission, lack of compliance on ATD, goiter larger than 60g, old age or association with severe diseases. ATD were discontinued one week before RAI administration, calculated by the formula: glandular volume (g) vs. effective radiation (80 mCi/g of tissue) divided by 24h thyroid uptake (%). We reexamined the patients for 48 months after RAI. Medians of age, goiter size and 24h thyroid uptake were 34y (17-69), 54.5g (20-210) and 73% (21-99), respectively. After RAI, patients became gradually hypothyroid on a rate of 15%/ 6mo until the first 18mo, followed by a rate of 2-5%/ 6mo until the end of 48mo. The number of patients in thyrotoxicosis decreased continuously, being 52.2% 6mo after RAI, 25% after 18mo and 6.7% after 48mo; at the end of the study 8 patients were still thyrotoxic. The total of patients without thyrotoxicosis at the end of observation, that is, the sum of those in euthyroidism and hypothyroidism on T4 therapy (cure of thyrotoxicosis) reached 46.8% in 6mo, 63.3% in 12mo, 81.7% in 24mo, 87.5% in 36mo and 93.3% in 48mo. Transient hypothyroidism, that is, elevation of TSH higher than 4.5 mU/L until 12mo after RAI, followed by normalization of TSH was found in 7.5% of patients. The following correlations were found in this study: a) initial T3 values and absence of cure of thyroxicosis (p=0.2); b) total RAI doses in relation to time for cure of thyrotoxicosis (p=0.01); c) dose of 131l/thyroid volume in relation to time for cure of thyrotoxicosis (p=0.02). Adverse effects included exarcebation of thyrotoxicosis in 3 patients and pain in the anterior cervical area in one, all reversible and of short duration. Two patients became pregnant after RAI but both gestations and their outcomes were normal.Estudamos retrospectivamente 120 pacientes (96 F/ 24 M) portadores de tirotoxicose por doença de Basedow-Graves submetidos à terapia com iodo radioativo (131I), que receberam inicialmente, para compensação da moléstia, drogas anti-tiroidianas (DAT). A indicação terapêutica posterior de radioiodo deveu-se a uma das seguintes condições clínicas: recidiva após compensação com DAT, falta de compensação devida à baixa aderência às DAT, bócios maiores que 60g, idade avançada ou doença grave associada. As DAT foram suspensas uma semana antes da administração da dose de 131I, calculada pela fórmula: volume glandular (em g) X radiação efetiva (80 mCi/g de tecido) ¸ captação tiroideana de 24hs. Reavaliamos os pacientes por até 48 meses após a radioiodoterapia. As medianas iniciais de idade, bócio e captação tiroideana de 24hs dos 120 pacientes foram, respectivamente, 34 anos (17-69), 54,5g (20-210) e 73% (21-99). A evolução para hipotiroidismo foi gradual, com 15% dos pacientes a cada 6m até o 18º mês, seguidos de 2 a 5% dos pacientes a cada 6m até o 48º mês. O número de pacientes em tirotoxicose decresceu continuamente, representando 52,2% do total inicial após 6m, 25% após 18m e 6,7% após 48m. Ao final, 8 pacientes continuaram em tirotoxicose. O número de pacientes sem tirotoxicose após o tratamento com 131I, ou seja a soma daqueles em eutiroidismo com aqueles em hipotiroidismo com reposição com T4 (denominada por nós de cura da tirotoxicose), alcançou 46,8% dos pacientes em óm, 63,3% em 12m, 81,7% em 24m, 87,5% em 36m e 93,3% em 48m. O número de pacientes que apresentaram hipotiroidismo transitório, ou seja, elevação do TSH acima de 4,5 mU/L até 12m após a dose de 131I, com normalização posterior, foi 7,5%. Correlacionaram-se positivamente: a) valores iniciais de T3 e ausência de evolução para a cura da tirotoxicose (p=0,02); b) doses totais de 131I administradas, únicas ou múltiplas, em relação ao tempo de cura da tirotoxicose (p=0,01); c) dose de 131 l/volume glandular em relação ao tempo de cura da tirotoxicose (p=0,02). Os efeitos adversos incluíram exacerbação da tirotoxicose em 3 pacientes e dor na região cervical anterior em um, com reversão dos quadros em todos. Outras duas pacientes engravidaram após o dose terapêutica de 131I para a tirotoxicose e tiveram gestações sem intercorrência e recém-nascidos normais.Universidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Departamento de MedicinaUNIFESP, EPM, Depto. de MedicinaSciEL
Characteristics of Thyroxine 5'-Deiodination in Cultured Human Placental Cells Regulation by lodothyronines
Human and rat placental homogenates convert L-thyroxine (T4) to 3,5,3'-L-triiodothyronine (T3) via a pathway termed type II iodothyronine deiodination. To study regulation of this pathway, cell dispersions were prepared from human placental chorionicdecidual membrane. Dispersed cells deiodinated T4 and 3,3',5'triiodothyronine (rT3), but not T3, at the 5 ' position. The reaction was only slightly inhibited by 1 mM 6-n-propylthiouracil, enhanced by dithiothreitol, and substantially inhibited by 50 nM iopanoic acid. Incubation of the cells in thyroid hormone-depleted medium induced a near doubling of T4 5'-deiodination in 36-48 h, with a significant rise seen as early as 12 h. Addition of T4, rT3, or T3 to hormone-depleted medium impaired the rise in type II deiodination in a dose-dependent fashion. T4 and rT3 were equipotent in this regard, and T3 was 2-3 times less potent. T4 was effective in physiological concentrations, 6.5-13 nM in medium containing 10 % calf serum, and the effect of T4 was not due to its conversion to either T3 or rT3. In cells with deiodinase activity raised by 48 h incubation in thyroid hormone-depleted medium, addition of T4, T3, or rT3 reversed the increase in 8-24 h. Secretion of prolactin and,thCG by the dispersed cells was not substantially affected by thyroid hormone deprivation. The increase in type II deiodination during thyroid hormone deprivation appears to depend on a signal from the thyroxine molecule, per se, and could potentially defend intracellular, and/or circulating, T3 pools in pathological states of mild-to-moderate hypothyroxinemia