Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, United States; Feinstone Department of Molecular Microbiology and Immunology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, United States.
Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Autoimmun Rev. 2014 Apr-May;13(4-5):391-7. doi: 10.1016/j.autrev.2014.01.007. Epub 2014 Jan 13.
Hashimoto thyroiditis (HT), now considered the most common autoimmune disease, was described over a century ago as a pronounced lymphoid goiter affecting predominantly women. In addition to this classic form, several other clinico-pathologic entities are now included under the term HT: fibrous variant, IgG4-related variant, juvenile form, Hashitoxicosis, and painless thyroiditis (sporadic or post-partum). All forms are characterized pathologically by the infiltration of hematopoietic mononuclear cells, mainly lymphocytes, in the interstitium among the thyroid follicles, although specific features can be recognized in each variant. Thyroid cells undergo atrophy or transform into a bolder type of follicular cell rich in mitochondria called Hürthle cell. Most HT forms ultimately evolve into hypothyroidism, although at presentation patients can be euthyroid or even hyperthyroid. The diagnosis of HT relies on the demonstration of circulating antibodies to thyroid antigens (mainly thyroperoxidase and thyroglobulin) and reduced echogenicity on thyroid sonogram in a patient with proper clinical features. The treatment remains symptomatic and based on the administration of synthetic thyroid hormones to correct the hypothyroidism as needed. Surgery is performed when the goiter is large enough to cause significant compression of the surrounding cervical structures, or when some areas of the thyroid gland mimic the features of a nodule whose cytology cannot be ascertained as benign. HT remains a complex and ever expanding disease of unknown pathogenesis that awaits prevention or novel forms of treatment.
桥本甲状腺炎（HT），现在被认为是最常见的自身免疫性疾病，一个多世纪前被描述为一种主要影响女性的明显淋巴性腺肿。除了这种经典形式外，现在还有几种其他临床病理实体被归入 HT 范畴：纤维变体、IgG4 相关变体、青少年形式、桥本甲状腺毒症和无痛性甲状腺炎（散发性或产后）。所有形式在病理学上都以造血单核细胞（主要是淋巴细胞）在甲状腺滤泡间间质中的浸润为特征，尽管在每种变体中都可以识别出特定的特征。甲状腺细胞发生萎缩或转化为更粗胆的富含线粒体的滤泡细胞，称为 Hurthle 细胞。大多数 HT 形式最终会发展为甲状腺功能减退症，尽管在发病时，患者可能是甲状腺功能正常或甚至甲状腺功能亢进。HT 的诊断依赖于在具有适当临床特征的患者中显示循环甲状腺抗原（主要是甲状腺过氧化物酶和甲状腺球蛋白）抗体和甲状腺超声检查回声降低。治疗仍然是对症的，并基于给予合成甲状腺激素来纠正甲状腺功能减退症，根据需要进行。当甲状腺肿大到足以对周围颈部结构造成明显压迫时，或当甲状腺的某些区域模拟结节的特征且细胞学无法确定为良性时，手术会进行。HT 仍然是一种复杂且不断扩展的病因不明的疾病，需要预防或新形式的治疗。
