Recent advances in the understanding of latent autoimmune diabetes in adults (LADA) pathophysiology make it increasingly evident that people with LADA comprise a heterogenous group of patients. This makes the establishment of a standard treatment algorithm challenging. On top of its glucose-lowering action, insulin may exert anti-inflammatory effects, rendering it an attractive therapeutic choice for a type of diabetes in which autoinflammation and beta cell insufficiency play major pathogenetic roles. However, there is growing evidence that other antidiabetic drugs, such as metformin, dipeptidyl peptidase-4 inhibitors, glucagon-like peptide-1 receptor agonists, and thiazolidinediones, might have a role in optimizing glycemic control and preserving beta cell function in individuals with LADA, either alone or in combination with insulin. Although most of these drugs have been routinely used in the daily clinical setting for years, large prospective randomized trials are needed to assess whether they are capable of delaying progression to insulin dependence as well as their effects on diabetic complications. The aim of the present review is to discuss the current state and future perspectives of LADA therapy, emphasizing the need for individualized and patient-centered therapeutic approaches.
近年来对成人隐匿性自身免疫性糖尿病(latent autoimmune diabetes in adults, LADA)的病理生理学认识的研究越来越多地表明, LADA患者是一组具有异质性的患者群体。因此如何制定标准治疗策略非常具有挑战性。自身炎症以及β细胞功能不全是LADA的主要致病因素, 对于这一类型的糖尿病患者来说, 因为胰岛素首先具有降糖作用, 其次还具有抗炎作用, 因此是理想的治疗药物。然而, 越来越多的证据表明, 其他降糖药物, 例如二甲双胍、二肽基肽酶-4抑制剂、胰高血糖素样肽-1受体激动剂和噻唑烷二酮类药物, 单独或联合胰岛素使用, 对于LADA患者来说可能能够优化血糖控制并发挥保护β细胞功能的作用。尽管这些药物中大多数已在日常临床环境中常规使用多年, 但仍需要大规模的前瞻性随机试验来评估它们是否能够延缓胰岛素依赖性的进展以及对糖尿病并发症的影响。本综述旨在讨论LADA治疗的现状与未来前景, 强调需要采用个体化并且以患者为中心的治疗方法。.
Keywords: dipeptidyl peptidase-4 inhibitors; glucagon-like peptide-1 receptor agonists; insulin; latent autoimmune diabetes in adults; oral glucose-lowering agents; thiazolidinediones; 二肽基肽酶-4抑制剂; 口服降糖药; 噻唑烷二酮类; 成人隐匿性自身免疫性糖尿病; 胰岛素; 胰高血糖素样肽-1受体激动剂.
© 2019 Ruijin Hospital, Shanghai Jiaotong University School of Medicine and John Wiley & Sons Australia, Ltd.