Latent autoimmune diabetes in adults (LADA) is dead: long live autoimmune diabetes!

Abstract

Latent autoimmune diabetes in adults (LADA) prevails as a name in diabetes research although it was ranked as the second silliest name some years ago [1]. LADA describes a subgroup of patients who develop phenotypic type 2 diabetes but with markers of autoimmunity [2, 3]. In 2005, we tried to describe the background to LADA and establish a definition based on adult age at onset, presence of autoantibodies and lack of requirement for insulin at least 6 months after diagnosis [4]. Both the age and the insulin criteria were soon questioned [1, 5], but they also gained some support [6]. The question of how to define LADA has resulted in numerous articles and debates discussing whether LADA is a disease on its own or just a variant of type 1 diabetes [7–9]. Thus, it could be questioned whether the introduction of the term LADA has been an asset or an obstacle to our understanding of diabetes. The first question we should ask is: what good has the concept of LADA done for science and patients? In defence of LADA we may note that the categorisation has put the existence of autoimmune diabetes in adults on the scientific map. We know that by including LADA in type 1 diabetes, as recommended by the WHO [10], more adults than children are affected by autoimmune diabetes [11]. We know more about cellular and humoral responses [12–15], metabolic traits [16, 17] and genetic background [18] in adult patients with autoimmune diabetes. Thus, the LADA concept has been an efficient tool for studying and communicating different pathophysiological aspects of autoimmune diabetes in adults. Another reason for classifying diabetes is to facilitate studies on treatment and prevention where strict inclusion criteria are needed. It was concluded in a recent Cochrane Review [19] that there were few randomised controlled trials of good quality available to evaluate which treatment is optimal for LADA patients, but using sulfonylurea seemed unfavourable for beta cell function. The review also noted that the definition of LADA was imprecise, which hampered comparison between the studies. Taken together, the scientific use of LADA has up to now been better and more productive than its clinical use. So, what is the problem with the concept of LADA? The main problem is how to define LADA. This leads to futile discussion that does not take our understanding of autoimmune diabetes any further; it might even be an obstacle to our way of thinking. This could be exemplified by studies trying to subgroup LADA, which already is a subgroup. There are manuscripts proposing different kinds of LADA based on the antibody titre, with low-titre and high-titre LADA [20, 21]. We even will have patients who fulfil the age and treatment criteria with T cell reactivity to O. Rolandsson (*) Family Medicine, Department of Public Health and Clinical Medicine, Umea University, Umea, Sweden e-mail: olov.rolandsson@fammed.umu.se