Pediatric Diabetes Unit, Department of Pediatrics, University of Pisa Medical School, Pisa, Italy.
Laboratory of Clinical Microbiology, Department of Biotechnology, University of Insubria and Ospedale di Circolo, Varese, Italy.
Pediatr Diabetes. 2018 Aug;19(5):923-929. doi: 10.1111/pedi.12673. Epub 2018 Apr 17.
At the time of the clinical onset of type 1 diabetes (T1D), we investigated 82 pediatric cases in parallel with 117 non-diabetic controls matched by age, geographic area, and time of collection. The occurrence of an enteroviral infection was evaluated in peripheral blood using a sensitive method capable of detecting virtually all human enterovirus (EV) types. While non-diabetic controls were consistently EV-negative, 65% of T1D cases carried EVs in blood. The vitamin D status was assessed by measuring the concentration of 25-hydroxyvitamin D [25(OH)D] in serum. Levels of 25(OH)D were interpreted as deficiency (≤50 nmol/L), insufficiency (52.5-72.5 nmol/L), and sufficiency (75-250 nmol/L). In T1D cases, the median serum concentration of 25(OH)D was 54.4 ± 27.3 nmol/L vs 74.1 ± 28.5 nmol/L in controls (P = .0001). Diabetic children/adolescents showed deficient levels of vitamin D 25(OH)D (ie, 72.5 nmol/L) in 48.8% cases vs 17.9% in non-diabetic controls (P = .0001). Unexpectedly, the median vitamin D concentration was significantly reduced in virus-positive vs virus-negative diabetics (48.2 ± 22.5 vs 61.8 ± 31.2 nmol/L; P = .015), with deficient levels in 58.5% vs 31.0%, respectively. Thus, at the time of clinical onset, EV-positive cases had reduced vitamin D levels compared with EV-negative cases. This could indicate either that the virus-negative children/adolescents had been hit by a non-infectious T1D-triggering event, or that children/adolescents with proper levels of vitamin D had been able to rapidly clear the virus. Thus, it would be important to assess whether adequate vitamin D supplementation before or during the prediabetic phase of T1D may counteract the diabetogenic potential of infectious pathogens.
在 1 型糖尿病（T1D）的临床发病时，我们平行调查了 82 例儿科病例，并与年龄、地理区域和采集时间相匹配的 117 例非糖尿病对照进行了比较。使用一种能够检测几乎所有人类肠道病毒（EV）类型的敏感方法，在外周血中评估肠道病毒感染的发生情况。而非糖尿病对照始终为 EV 阴性，而 65%的 T1D 病例的血液中携带 EV。通过测量血清中 25-羟维生素 D [25(OH)D]的浓度来评估维生素 D 状态。25(OH)D 水平的解释为缺乏（≤50 nmol/L）、不足（52.5-72.5 nmol/L）和充足（75-250 nmol/L）。在 T1D 病例中，血清 25(OH)D 的中位数浓度为 54.4 ± 27.3 nmol/L，而对照组为 74.1 ± 28.5 nmol/L（P =.0001）。糖尿病儿童/青少年中维生素 D 25(OH)D 缺乏（即 72.5 nmol/L）的比例为 48.8%，而非糖尿病对照组为 17.9%（P =.0001）。出乎意料的是，病毒阳性与病毒阴性糖尿病患者的中位维生素 D 浓度显著降低（48.2 ± 22.5 vs 61.8 ± 31.2 nmol/L；P =.015），分别为 58.5%和 31.0%。因此，在临床发病时，EV 阳性病例的维生素 D 水平低于 EV 阴性病例。这可能表明病毒阴性的儿童/青少年受到了非传染性 T1D 触发事件的影响，或者维生素 D 水平正常的儿童/青少年能够迅速清除病毒。因此，评估在 T1D 糖尿病前期阶段之前或期间是否进行充足的维生素 D 补充是否可能抵消感染病原体的致糖尿病潜力非常重要。
