University of Exeter College of Medicine & Health, Exeter, U.K.
Royal Devon University Healthcare NHS Foundation Trust, Exeter, U.K.
Diabetes Care. 2023 Jun 1;46(6):1156-1163. doi: 10.2337/dc22-2159.
To determine whether presentation, progression, and genetic susceptibility of robustly defined adult-onset type 1 diabetes (T1D) are altered by diagnosis age.
We compared the relationship between diagnosis age and presentation, C-peptide loss (annual change in urine C-peptide-creatinine ratio [UCPCR]), and genetic susceptibility (T1D genetic risk score [GRS]) in adults with confirmed T1D in the prospective StartRight study, 1,798 adults with new-onset diabetes. T1D was defined in two ways: two or more positive islet autoantibodies (of GAD antibody, IA-2 antigen, and ZnT8 autoantibody) irrespective of clinical diagnosis (n = 385) or one positive islet autoantibody and a clinical diagnosis of T1D (n = 180).
In continuous analysis, age of diagnosis was not associated with C-peptide loss for either definition of T1D (P > 0.1), with mean (95% CI) annual C-peptide loss in those diagnosed before and after 35 years of age (median age of T1D defined by two or more positive autoantibodies): 39% (31-46) vs. 44% (38-50) with two or more positive islet autoantibodies and 43% (33-51) vs. 39% (31-46) with clinician diagnosis confirmed by one positive islet autoantibody (P > 0.1). Baseline C-peptide and T1D GRS were unaffected by age of diagnosis or T1D definition (P > 0.1). In T1D defined by two or more autoantibodies, presentation severity was similar in those diagnosed before and after 35 years of age: unintentional weight loss, 80% (95% CI 74-85) vs. 82% (76-87); ketoacidosis, 24% (18-30) vs. 19% (14-25); and presentation glucose, 21 mmol/L (19-22) vs. 21 mmol/L (20-22) (all P ≥ 0.1). Despite similar presentation, older adults were less likely to be diagnosed with T1D, insulin-treated, or admitted to hospital.
When adult-onset T1D is robustly defined, the presentation characteristics, progression, and T1D genetic susceptibility are not altered by age of diagnosis.
确定成人发病的 1 型糖尿病（T1D）的发病年龄是否影响其表现、进展和遗传易感性。
我们比较了前瞻性 StartRight 研究中确诊的 T1D 成人和新发糖尿病成人中发病年龄与表现、C 肽丢失（尿 C 肽肌酐比值的年度变化[UCPCR]）和遗传易感性（T1D 遗传风险评分[GRS]）之间的关系。在两种方法中均定义了 T1D：两种或多种胰岛自身抗体阳性（谷氨酸脱羧酶抗体、IA-2 抗原和锌转运体 8 自身抗体）而不论临床诊断如何（n=385）或一种胰岛自身抗体阳性和临床诊断为 T1D（n=180）。
连续分析显示，对于 T1D 的两种定义，诊断年龄均与 C 肽丢失无关（P＞0.1），在 35 岁之前和之后诊断的患者中，平均（95%CI）每年 C 肽丢失率（用两种或多种阳性自身抗体定义的 T1D 中位数年龄）：2 种或更多种阳性胰岛自身抗体为 39%（31-46）比 44%（38-50），一种阳性胰岛自身抗体和经临床诊断证实的临床诊断为 43%（33-51）比 39%（31-46）（P＞0.1）。基线 C 肽和 T1D GRS 不受诊断年龄或 T1D 定义的影响（P＞0.1）。在由两种以上自身抗体定义的 T1D 中，35 岁之前和之后诊断的患者的发病严重程度相似：体重意外减轻，80%（95%CI 74-85）比 82%（76-87）；酮症酸中毒，24%（18-30）比 19%（14-25）；发病时血糖，21mmol/L（19-22）比 21mmol/L（20-22）（均 P≥0.1）。尽管表现相似，但老年患者更不可能被诊断为 T1D、接受胰岛素治疗或住院治疗。
当明确诊断为成人发病的 T1D 时，发病年龄不会改变其表现特征、进展和 T1D 遗传易感性。
