Seetharaman Sujatha, Sasidharan Pillai Sabitha, Ganta Avani, Millington Kate, Quintos Jose Bernardo, Topor Lisa Swartz, Serrano-Gonzalez Monica
Division of Pediatric Endocrinology and Diabetes, University of California San Francisco, San Francisco, California.
Center for Endocrinology, Diabetes and Metabolism, Children's Hospital Los Angeles, Los Angeles, California.
AACE Clin Case Rep. 2024 Aug 14;10(6):236-239. doi: 10.1016/j.aace.2024.08.003. eCollection 2024 Nov-Dec.
BACKGROUND/OBJECTIVE: Iodine deficiency hypothyroidism is an important cause of neurocognitive and motor impairment in children globally. In the United States, universal salt iodization, which began in the 1920s, led to a dramatic decline in iodine deficiency hypothyroidism. However, iodine deficiency may be reemerging due to increased consumption of noniodized salts, decreased dairy iodine concentrations, and decreased intake of iodine containing foods due to food allergies, dietary preferences such as vegan diets, or restrictive food intake disorders.
We present a case series that challenges the existing clinical paradigm for hypothyroidism and describe 3 patients without underlying thyroid dysfunction who were diagnosed with iodine deficiency hypothyroidism over an 18-month period beginning in February 2021 in Northeastern United States. Prior studies reported 2 additional cases diagnosed in that same time frame at our clinical center.
We report significant heterogeneity in clinical presentation: 3 patients had large goiters, 1 had a mild goiter, and 1 patient had no goiter. Biochemical tests were also variable and included a wide range of thyroid stimulating hormone elevations.
We suggest that a spot urine iodine concentration, combined with an elevated serum thyroglobulin level, can be an alternative to a 24-hour urinary iodine excretion for the diagnosis of iodine deficiency hypothyroidism given the clinical challenges of obtaining the latter. Thyroid function normalized in all patients with iodine supplementation.
背景/目的：碘缺乏性甲状腺功能减退症是全球儿童神经认知和运动障碍的重要原因。在美国，始于20世纪20年代的全民食盐加碘导致碘缺乏性甲状腺功能减退症显著下降。然而，由于未加碘盐消费增加、乳制品碘浓度降低以及因食物过敏、纯素饮食等饮食偏好或限制性食物摄入障碍导致含碘食物摄入量减少，碘缺乏可能正在重新出现。
我们呈现了一系列挑战现有甲状腺功能减退症临床范式的病例，并描述了3例无潜在甲状腺功能障碍的患者，他们于2021年2月开始的18个月内在美国东北部被诊断为碘缺乏性甲状腺功能减退症。此前的研究报告了在同一时间段内我们临床中心另外2例确诊病例。
我们报告了临床表现的显著异质性：3例患者有大甲状腺肿，1例有轻度甲状腺肿，1例患者无甲状腺肿。生化检查结果也各不相同，包括促甲状腺激素升高范围广泛。
鉴于获取24小时尿碘排泄量存在临床挑战，我们建议，结合血清甲状腺球蛋白水平升高的即时尿碘浓度可作为诊断碘缺乏性甲状腺功能减退症的24小时尿碘排泄量的替代方法。所有补充碘的患者甲状腺功能均恢复正常。
