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。