Loviselli A, Bocchetta A, Mossa P, Velluzzi F, Bernardi F, del Zompo M, Mariotti S
Cattedra di Endocrinologia, University of Cagliari, Italy.
Neuropsychobiology. 1997;36(1):37-41. doi: 10.1159/000119358.
Psychiatric patients on long-term lithium (Li) therapy frequently develop goiter and/or hypothyroidism. It has also been suggested that Li may trigger/exacerbate thyroid autoimmunity. Previous studies provided evidence that underlying thyroid diseases represent important predisposing factors for the development of Li-induced thyroid dysfunction. The aim of the present paper was to assess the value of thyroid ultrasound-a simple and reliable tool to detect subtle thyroid abnormalities-in the longitudinal evaluation of 23 Li-treated psychiatric patients without evidence of biochemical thyroid abnormalities before therapy. For this purpose, thyroid ultrasound was associated with a clinical and laboratory (serum thyroxine, serum triiodothyronine, serum TSH, antithyroglobulin (AbTg), antithyroid microsomal (AbM) and antithyroid peroxidase autoantibodies) evaluation prior to and at 6- to 12-month intervals during Li treatment. On the basis of thyroid ultrasound before Li, patients were subdivided into two groups: group A (n = 15, 7 males, 8 females) with a normal echography and group B (n = 8, 5 males, 3 females) with mild ultrasound abnormalities. In group A the development of a small diffuse goiter was confirmed by physical examination during Li therapy; 2 patients displayed a transient increase of serum TSH concentration and none developed detectable serum antithyroid autoantibodies. Beside the small volumetric increase, no other ultrasound abnormalities were observed during the entire follow-up. In all group B patients a mild diffuse goiter was clinically detected before and on Li administration and no significant volumetric changes were observed during follow-up. Two patients developed high titers of AbM and AbTg 12 and 18 months after the beginning of Li, respectively; in 1 a persistent increase of serum TSH concentration was also observed. Thyroid echography before Li displayed different degrees of scattered or diffuse hypoechogenicity and a further decrease in echogenicity was detected during Li therapy in 2 patients. In conclusion, we provided further evidence that long-term Li administration is not associated with de novo appearance of thyroid autoimmune phenomena in humans, but rather with an exacerbation of underlying thyroid autoimmunity. In addition to thyroid autoantibody and TSH measurements, thyroid echography appears to be a sensitive tool in the identification of patients at risk of developing autoimmune hypothyroidism during long-term Li therapy.
长期接受锂盐(Li)治疗的精神科患者经常会出现甲状腺肿和/或甲状腺功能减退。也有观点认为锂盐可能引发/加重甲状腺自身免疫。先前的研究表明,潜在的甲状腺疾病是锂盐所致甲状腺功能障碍发生的重要易感因素。本文的目的是评估甲状腺超声(一种检测细微甲状腺异常的简单可靠工具)在纵向评估23例接受锂盐治疗的精神科患者中的价值,这些患者在治疗前无生化甲状腺异常证据。为此,在锂盐治疗前及治疗期间每隔6至12个月,将甲状腺超声与临床及实验室评估(血清甲状腺素、血清三碘甲状腺原氨酸、血清促甲状腺激素、抗甲状腺球蛋白(AbTg)、抗甲状腺微粒体(AbM)及抗甲状腺过氧化物酶自身抗体)相结合。根据锂盐治疗前的甲状腺超声检查结果,患者被分为两组:A组(n = 15,男性7例,女性8例)超声检查正常;B组(n = 8,男性5例,女性3例)有轻度超声异常。在A组中,锂盐治疗期间体格检查证实出现了小的弥漫性甲状腺肿;2例患者血清促甲状腺激素浓度短暂升高,无患者出现可检测到的血清抗甲状腺自身抗体。除了体积略有增加外,在整个随访期间未观察到其他超声异常。在所有B组患者中,在锂盐治疗前及治疗期间临床均检测到轻度弥漫性甲状腺肿,随访期间未观察到明显的体积变化。2例患者分别在锂盐治疗开始后12个月和18个月出现高滴度的AbM和AbTg;其中1例还观察到血清促甲状腺激素浓度持续升高。锂盐治疗前甲状腺超声显示不同程度的散在或弥漫性低回声,2例患者在锂盐治疗期间检测到回声进一步降低。总之,我们提供了进一步的证据表明,长期服用锂盐与人类甲状腺自身免疫现象的新发无关,而是与潜在的甲状腺自身免疫加重有关。除了检测甲状腺自身抗体和促甲状腺激素外,甲状腺超声似乎是识别长期锂盐治疗期间有发生自身免疫性甲状腺功能减退风险患者的敏感工具。