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Results for “IODINE, RADIOACTIVE”

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PubMed2000

Radiation exposure from outpatient radioactive iodine (131I) therapy for thyroid carcinoma.

CONTEXT: In May 1997, the US Nuclear Regulatory Commission (NRC) revised its patient release regulations, allowing for outpatient administration of larger activities of sodium iodide 131I than previously permitted. OBJECTIVE: To measure the radiation exposure to household members from patients receiving outpatient 131I therapy for thyroid carcinoma in accordance with the new regulations. DESIGN: Consecutive case series from October 1998 to June 1999. SETTING AND PATIENTS: Thirty patients who received outpatient 131I therapy following thyroidectomy for differentiated thyroid carcinoma were enrolled, along with their 65 household members and 17 household pets. MAIN OUTCOME MEASURE: Radiation exposure to household members and 4 rooms in each home, as monitored with dosimeters for 10 days following 131I administration. RESULTS: The patients received 131I doses ranging from 2.8 to 5.6 GBq (mean, 4.3 GBq). The radiation dose to 65 household members ranged from 0.01 mSv to 1.09 mSv (mean, 0.24 mSv). The dose to 17 household pets ranged from 0.02 mSv to 1.11 mSv (mean, 0.37 mSv). The mean dose to the 4 rooms ranged from 0.17 mSv (kitchen) to 0.58 mSv (bedroom). CONCLUSION: In our study, 131I doses to household members of patients receiving outpatient 131I therapy were well below the limit (5.0 mSv) mandated by current NRC regulations.

Adolescent↗
PubMed1999

The influence of maternal hypothyroidism and radioactive iodine on rat embryonal development: thyroid C-cells.

There have been no works devoted to the study of the influence of (131)I and maternal (131)I-induced hypothyroidism on the state of the C-cells in the thyroid gland of the developing embryos. A study was made on the effect of a dose of 150 microCi (131)I (0.5 Gy) leading to hypothyroidism in rats, on 35 mother rats and 168 newborn pups. The mother rats were divided into control and four treated groups which were injected with (131)I before pregnancy, on gestation days 5, 10, and 16, respectively. Immunohistochemically, the thyroid gland was examined for calcitonin-positive cells. Maternal hypothyroidism induced by (131)I leads to the development of hyperplasia and hyperthrophy of calcitonin-positive cells in the pups at the time of birth. The discovery of separate C-cells in the peripheral zone of the thyroid lobe may be evidence of an unbalance in the development of the medial and lateral source of the thyroid. There is a verifiable increase in the quantity of C-cells per 1 mm(2) field of the localization in the central zone of the gestation days 10 and 16 groups. This might be a compensatory mechanism for regulating the activity of the thyroid gland under induced hypothyroidism. Thus, in cases when there is a breakdown in the normal external regulation of the embryonic morphogenesis, a reduction in the level of maternal thyroid hormones and also direct exposure to (131)I, there is also a change in the foetus' internal regulatory systems. A change in C-cell system could lead to the appearance of endocrinological disorders later in life.

Animals↗