Makarewicz Jacek, Lewiński Andrzej, Karbownik-Lewińska Małgorzata
Department of Oncological Endocrinology, Chair of Endocrinology and Metabolic Diseases, Medical University of Lodz, Poland.
Thyroid Res. 2010 Oct 6;3(1):7. doi: 10.1186/1756-6614-3-7.
Radioiodine (131I) therapy is widely accepted as an essential part of therapeutic regimens in many cases of differentiated thyroid cancer. Radiation-induced oxidative damage to macromolecules is a well known phenomenon. Frequently examined process to evaluate oxidative damage to macromolecules is lipid peroxidation (LPO), resulting from oxidative damage to membrane lipids. The aim of the study was to examine serum LPO level in hypothyroid (after total thyroidectomy) cancer patients subjected to ablative activities of 131I.
The study was carried out in 21 patients (18 females and 3 males, average age 52.4 ± 16.5 years) after total thyroidectomy for papillary (17 patients) or follicular (4 patients) thyroid carcinoma. Hypothyroidism was confirmed by increased TSH blood concentration (BRAHMS, Germany), measured before 131I therapy. Activity of 2.8 - 6.9 GBq of 131I was administered to the patients orally as sodium iodide (OBRI, Poland). Concentrations of malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA), as an index of LPO (LPO-586 kit, Calbiochem, USA), were measured in blood serum just before 131I administration (day "0") and on the days 1-4 after 131I therapy. Sera from 23 euthyroid patients served as controls. Correlations between LPO and TSH or 131I activity were calculated.
Expectedly, serum LPO level, when measured before 131I therapy, was several times higher (p < 0.00001) in cancer patients than in healthy subjects, which is probably due to hypothyroidism caused by total thyroidectomy. However, we did not observe any differences between LPO levels after and before 131I therapy. LPO did not correlate with TSH concentration. In turn, negative correlation was found between 131I activity and LPO level on the day "2" after radioiodine treatment.
Radioiodine remnant ablation of differentiated thyroid cancer does not further increase oxidative damage to membrane lipids, at least early, after therapy.
放射性碘(131I)治疗在许多分化型甲状腺癌病例中被广泛接受为治疗方案的重要组成部分。辐射诱导的大分子氧化损伤是一种众所周知的现象。用于评估大分子氧化损伤的常见检测过程是脂质过氧化(LPO),它是由膜脂质的氧化损伤引起的。本研究的目的是检测接受131I消融治疗的甲状腺功能减退(全甲状腺切除术后)癌症患者的血清LPO水平。
本研究对21例患者(18例女性和3例男性,平均年龄52.4±16.5岁)进行,这些患者因乳头状(17例)或滤泡状(4例)甲状腺癌接受全甲状腺切除术后。在131I治疗前通过检测血液中促甲状腺激素(TSH)浓度升高(德国BRAHMS公司产品)确诊甲状腺功能减退。以碘化钠形式向患者口服给予2.8 - 6.9GBq的131I活性(波兰OBRI公司产品)。在131I给药前(“0”天)以及131I治疗后的第1 - 4天,检测血清中丙二醛 + 4 - 羟基烯醛(MDA + 4 - HDA)的浓度,作为LPO的指标(美国Calbiochem公司LPO - 586试剂盒)。选取23例甲状腺功能正常的患者血清作为对照。计算LPO与TSH或131I活性之间的相关性。
不出所料,在131I治疗前检测时,癌症患者的血清LPO水平比健康受试者高出数倍(p < 0.00001),这可能是由于全甲状腺切除导致的甲状腺功能减退。然而,我们未观察到131I治疗前后LPO水平存在任何差异。LPO与TSH浓度无相关性。相反,在放射性碘治疗后第“2”天,发现131I活性与LPO水平呈负相关。
分化型甲状腺癌的放射性碘残留消融至少在治疗早期不会进一步增加对膜脂质的氧化损伤。