Ratzmann K P, Strese J, Rjasanowski I, Witt S, Kohnert K D, Keilacker H, Richter K V, Giebelmann R, Schulz B
Exp Clin Endocrinol. 1985 Dec;86(3):323-34. doi: 10.1055/s-0029-1210505.
Since mumps virus seems to be one of the most likely candidates in viral etiology of insulin-dependent diabetes (IDDM) we studied the possible relationship of glucose tolerance (75 g oGTT), beta cell function, diabetes associated HLA antigens, haptoglobin phenotype, islet cell antibodies (ICA) and islet cell surface antibodies (ICSA) in 125 subjects with antecedent mumps infection. Impaired glucose tolerance (IGT) was diagnosed in 3.2% (n = 4) but onset of diabetes did not appear within 14 months after mumps infection. There was no relationship between glucose tolerance and complications of antecedent mumps infection (e.g. pancreatitis, meningitis, orchitis). The prevalence rate of ICA was 76%. ICSA were detectable in about 36% of children and 62% of the adults tested (p less than 0.01). There was no relationship between ICA/ICSA and diabetes-associated HLA antigens, haptoglobin phenotype or beta cell function (fasting C-peptide and insulin response to 75 g oGTT). However, adults with circulating ICA were characterized by a significantly lower insulin response to glucose. Fifty two "risk" subjects characterized by IGT, diabetes associated HLA antigen(s), ICA or ICSA either alone or combined were studied again 26 months after mumps infection. No symptomatic diabetes appeared and IGT was diagnosed in one case only. ICA and ICSA persisted in more than 50% of subjects in whom ICA or ICSA were present 14 months after mumps infection. Since the used immunological techniques do not clearly distinguish organ-specific from non-organ-specific antibodies the results must be interpreted with caution. To summarize, the preliminary results do not support a close temporal relationship between mumps infection and the onset of IDDM. The pathogenetic role of mumps virus and ICA/ICSA and their possible relation to a slow progressive beta cell destruction has still to be determined.
由于腮腺炎病毒似乎是胰岛素依赖型糖尿病(IDDM)病毒病因中最有可能的候选病毒之一,我们研究了125例既往有腮腺炎感染的受试者的糖耐量(75g口服葡萄糖耐量试验)、β细胞功能、糖尿病相关HLA抗原、触珠蛋白表型、胰岛细胞抗体(ICA)和胰岛细胞表面抗体(ICSA)之间的可能关系。3.2%(n = 4)的受试者被诊断为糖耐量受损(IGT),但在腮腺炎感染后14个月内未出现糖尿病发病。糖耐量与既往腮腺炎感染的并发症(如胰腺炎、脑膜炎、睾丸炎)之间没有关系。ICA的患病率为76%。在约36%的儿童和62%的接受检测的成年人中可检测到ICSA(p<0.01)。ICA/ICSA与糖尿病相关HLA抗原、触珠蛋白表型或β细胞功能(空腹C肽和对75g口服葡萄糖耐量试验的胰岛素反应)之间没有关系。然而,循环中存在ICA的成年人对葡萄糖的胰岛素反应明显较低。对52例以IGT、糖尿病相关HLA抗原、ICA或ICSA单独或联合存在为特征的“风险”受试者在腮腺炎感染后26个月再次进行研究。未出现症状性糖尿病,仅1例被诊断为IGT。在腮腺炎感染后14个月时存在ICA或ICSA的受试者中,超过50%的受试者ICA和ICSA持续存在。由于所使用的免疫技术不能明确区分器官特异性抗体和非器官特异性抗体,因此对结果的解释必须谨慎。总之,初步结果不支持腮腺炎感染与IDDM发病之间存在密切的时间关系。腮腺炎病毒和ICA/ICSA的致病作用及其与β细胞缓慢进行性破坏的可能关系仍有待确定。