This study aimed to determine the association between trajectories of obesity status and prediabetes reversion to normoglycemia or progression to diabetes. The study included 14,452 participants from the National Health Insurance Service-National Health Screening (NHIS-HEALS) cohort who continuously had prediabetes glycemic status during the index period (2002-2008), definedby their fasting plasma glucose. The exposure of the study was the trajectories of obesity (defined by body mass index ≥ 25 kg/m 2 ) generated using latent class growth analysis. The outcomes were reversion to normoglycemia or progression to diabetes, whichever occurred first during the follow-up period (2009-2016). The association between trajectories and changes in prediabetes status were examined using cause-specific hazard regression by obtaining the hazard ratio (HR) with a 95% CI. We identified three distinct trajectories which were “Stable obese”, “Stable non-obese” and “Obese to non-obese”. After a median follow-up of 2years, 51.99% of participants had their glycemic status back to normoglycemia and 32.17% developed diabetes. Compared with participants in the “Stable obese” group, those in “Stable non-obese” and “Obese to non-obese” groups were more likely to have reversion to normoglycemia (HR with a 95% CI = 1.30 [1.23-1.37] and 1.15 [1.07-1.24], respectively) and lower risk of developingdiabetes (0.78 [0.73-0.84] and 0.90 [0.82-0.98], respectively). The findings suggest that maintaining or achieving a non-obese sta-tus is linked to higher reversion to normoglycemia as well as lower risks of developing diabetes.

Purpose: Allgrove syndrome, also known as “triple A” syndrome, is characterized by adrenal insufficiency, achalasia, and alacrimia. When neurological signs are also present, the condition is referred to as “4 A” syndrome. Methods: We conducted a retrospective analysis of three patients with 4 A syndrome confirmed genetically. A complete neurological exam was carried out by an experimented neurologist. Results: Herein, we describe the neurological characteristics often associated with this condition, through the clinical and electrophysiological analysis of three patients. All patients exhibited a mutation in AAAS, the gene coding for ALADIN. While these individuals presented with the classic features of triple-A syndrome, neurological symptoms were not prominent. Conclusion The neurological manifestations of Allgrove syndrome have historically been overlooked and inadequately explored. Due to the condition’s rarity and substantial phenotypic heterogeneity, only recently have a variety of symptoms been recognized and described.