Endocrinology Division, Department of Medicine of Federal University of São Paulo, SP, Brazil.
Diabetol Metab Syndr. 2009 Dec 4;1(1):25. doi: 10.1186/1758-5996-1-25.
Type 1A diabetes mellitus (T1ADM) is a progressive autoimmune disease mediated by T lymphocytes with destruction of beta cells. Up to now, we do not have precise methods to assess the beta cell mass, "in vivo" or "ex-vivo". The studies about its genetic susceptibility show strong association with class II antigens of the HLA system (particularly DQ). Others genetics associations are weaker and depend on the population studied. A combination of precipitating events may occur at the beginning of the disease. There is a silent loss of immune-mediated beta cells mass which velocity has an inverse relation with the age, but it is influenced by genetic and metabolic factors. We can predict the development of the disease primarily through the determination of four biochemically islet auto antibodies against antigens like insulin, GAD65, IA2 and Znt8. Beta cell destruction is chronically progressive but at clinical diagnosis of the disease a reserve of these cells still functioning. The goal of secondary disease prevention is halt the autoimmune attack on beta cells by redirecting or dampening the immune system. It is remains one of the foremost therapeutic goals in the T1ADM. Glycemic intensive control and immunotherapeutic agents may preserve beta-cell function in newly diagnosed patients with T1ADM. It may be assessed through C-peptide values, which are important for glycemic stability and for the prevention of chronic complications of this disease. This article will summarize the etiopathogenesis mechanisms of this disease and the factors can influence on residual C-peptide and the strategies to it preservation.
1 型糖尿病（T1ADM）是一种由 T 淋巴细胞介导的进行性自身免疫性疾病，导致β细胞破坏。到目前为止，我们还没有精确的方法来评估β细胞量，无论是“体内”还是“体外”。关于其遗传易感性的研究表明，它与 HLA 系统的 II 类抗原（特别是 DQ）有很强的关联。其他遗传关联则较弱，取决于所研究的人群。在疾病开始时可能会发生一系列诱发事件。存在一种无声的免疫介导的β细胞质量损失，其速度与年龄呈反比，但受遗传和代谢因素的影响。我们可以通过测定针对胰岛素、GAD65、IA2 和 Znt8 等抗原的四种胰岛自身抗体来初步预测疾病的发展。β细胞破坏是慢性进行性的，但在疾病的临床诊断时，这些仍在发挥作用的细胞仍有储备。二级疾病预防的目标是通过重新定向或抑制免疫系统来阻止针对β细胞的自身免疫攻击。这仍然是 T1ADM 的首要治疗目标之一。在新诊断的 T1ADM 患者中，强化血糖控制和免疫治疗药物可能会保留β细胞功能。可以通过 C 肽值来评估，这对于血糖稳定和预防该疾病的慢性并发症很重要。本文将总结该疾病的发病机制以及影响残余 C 肽的因素和保留策略。
