Lapcević Mirjana
Health Centre, Vozdovac, Belgrade.
Srp Arh Celok Lek. 2005 Oct;133 Suppl 1:84-7. doi: 10.2298/sarh05s1084l.
Autoimmune thyroid disease (ATD) is a multifactorial, genetic disease. It is the sequelae of the impaired immunoregulation, tolerance and poor recognition of one's own proteins, oligopolysaccharides and polypeptides, due to development of somatic lymphocyte mutations. It is manifested by different clinical and morphological entities, inter-related by etiopathogenetic association, i.e., all of them are caused by disorder of immune system regulation. Chronic autoimmune thyroidism (Thyreoiditis lymphocytaria Hashimoto, HT), as well as immunogenic hyperthyroidism (Morbus Graves Basedow, MGB) are frequently associated with autoimmune diseases of other organs, such as: chronic insufficiency of salivary glands (Sy Sjögren), autoimmune hemolytic anemia, megalocytic pernicious anemia, thrombocytopenia, Rheumatoid arthritis, Diabetes mellitus (more often type 2, but also type 1), Morbus Addison, Coeliakia, and other autoimmune diseases such as systemic diseases of connecting tissue (Lupus erythematosus-SLE, Sclerodermia, Vasculitis superficialis). The incidence of autoimmune diseases has been at increase in all age groups of our population. The prevalence of organ-specific and organ-nonspecific antibodies increases with the age. Antigenicity of thyroid epithelial cell may be triggered by different chemical and biological agents (repeated viral infections), repeated stress, and in individuals with genetic propensity. Unrecognized ATD progressively leads to hypothyroidism with hyperlipidemia, blood vessel changes, osteoporosis, deformities, invalidity which substantially reduces the quality of life of patient and requires medical attention and expensive treatment on what account it is medically and socio-economically significant. Multiple diagnostic procedures contribute to faster recognition of this condition. The goal of the primary health care physician (given that preclinical phase of ATD and other associated diseases have different duration) and other specialists is to recognize ATD and, by early diagnosis and multidisciplinary treatment, to take secondary preventive measures of manifestation of above-mentioned associated autoimmune diseases, and in that way, to avoid the development of comorbidity and complications. It is particularly supported by medical doctrine based on evidence of application of corticosteroids, cytostatics, thyro-suppressive and substitution therapy, antilipemics, bisphosphonates and other drugs, significant for autoimmune diseases.
自身免疫性甲状腺疾病(ATD)是一种多因素的遗传性疾病。它是由于体细胞淋巴细胞突变的发生,导致免疫调节、耐受性受损以及对自身蛋白质、寡糖和多肽的识别能力下降的后遗症。它表现为不同的临床和形态学实体,通过病因发病学关联相互联系,即所有这些都是由免疫系统调节紊乱引起的。慢性自身免疫性甲状腺炎(淋巴细胞性甲状腺炎,桥本氏病,HT)以及免疫原性甲状腺功能亢进(格雷夫斯病,MGB)经常与其他器官的自身免疫性疾病相关,例如:唾液腺慢性功能不全(干燥综合征)、自身免疫性溶血性贫血、巨幼细胞性恶性贫血、血小板减少症、类风湿性关节炎、糖尿病(更常见2型,但也有1型)、艾迪生病、乳糜泻以及其他自身免疫性疾病,如结缔组织系统性疾病(红斑狼疮 - SLE、硬皮病、浅表性血管炎)。自身免疫性疾病在我国各年龄组中的发病率一直在上升。器官特异性和器官非特异性抗体的患病率随年龄增长而增加。甲状腺上皮细胞的抗原性可能由不同的化学和生物因子(反复病毒感染)、反复应激以及具有遗传倾向的个体引发。未被识别的ATD会逐渐导致甲状腺功能减退,并伴有高脂血症、血管病变、骨质疏松、畸形、残疾,这会大幅降低患者的生活质量,需要医疗关注和昂贵的治疗,因此在医学和社会经济方面都具有重要意义。多种诊断程序有助于更快地识别这种疾病。初级保健医生(鉴于ATD和其他相关疾病的临床前期阶段持续时间不同)和其他专科医生的目标是识别ATD,并通过早期诊断和多学科治疗,采取二级预防措施以防止上述相关自身免疫性疾病的表现,从而避免合并症和并发症的发生。基于皮质类固醇、细胞抑制剂、甲状腺抑制和替代疗法、抗血脂药、双膦酸盐和其他对自身免疫性疾病有重要作用的药物应用证据的医学理论对此提供了特别支持。