OBJECTIVEPancreas size is reduced in patients at type 1 diabetes onset and in autoantibody (AAB)-positive donors without diabetes. We sought to determine whether pancreas volume (PV) imaging could improve understanding of the loss of pancreas size in first-degree relatives (FDRs) of patients with type 1 diabetes. We also examined relationships among PV, AAB status, and endocrine and exocrine functions. RESEARCH DESIGN AND METHODSWe conducted a cross-sectional study that included five groups: AAB 2 control subjects (no diabetes and no firstor second-degree relatives with type 1 diabetes) (N = 49), AAB 2 FDRs (N = 61), AAB + FDRs (N = 67 total: n = 31 with a single positive AAB [AAB + single] and n = 36 with multiple positive AABs [AAB + multiple]), and patients with recent-onset type 1 diabetes (<1 year) (N = 52). Fasting subjects underwent 1.5T pancreatic MRI, and PV and relative PV (RPV) (PV-to-BMI ratio) were analyzed between groups and for correlations with HbA 1c , C-peptide, glucose, and trypsinogen. RESULTSAll FDR groups had significantly lower RPV adjusted for BMI (RPV BMI ) than control subjects (all P < 0.05). Patients with type 1 diabetes had lower RPV BMI than AAB 2 FDR (P < 0.0001) and AAB + multiple (P £ 0.013) subjects. Transformed data indicated that trypsinogen levels were lowest in patients with type 1 diabetes. CONCLUSIONSThis study demonstrates, for the first time, all FDRs having significantly smaller RPV BMI compared with AAB 2 control subjects. Furthermore, RPV BMI was significantly lower in patients with recent-onset type 1 diabetes than in the AAB 2 FDR and AAB + multiple groups. As such, RPV BMI may be a novel noninvasive biomarker for predicting progression through stages of type 1 diabetes risk. This study highlights the potential paracrine relationships between the exocrine and endocrine pancreas in progression to type 1 diabetes in subjects at risk.Despite advances in medical diagnosis and treatment, type 1 diabetes remains one of the costliest diseases in the U.S. in terms of health care dollars spent for diabetesrelated costs (1). Immunotherapy-based intervention trials carried out in patients with new-onset type 1 diabetes have demonstrated potential for short-term benefit (e.g., anti-CD20, anti-CD3, and cytotoxic T-lymphocyte-associated antigen 4 Ig) but have failed to demonstrate long-term efficacy (2,3). The inability to provide long-term preservation of b-cell function or prevent type 1 diabetes may stem from unanswered

Frequency of insulin therapy in youth with T2D was associated with increased disease duration and those with longer duration rarely achieve target HbA1c level. This highlights the aggressive course of T2D in youth and adolescents. Additionally, co-morbidities are not being adequately treated. Follow up data from the PDC will provide additional important information about the natural history of T2D and patterns of gaps in treatment.

Latent autoimmune diabetes in adults (LADA) accounts for 2%-12% of all cases of diabetes. Patients are typically diagnosed after 35 years of age and are often misdiagnosed as type II Diabetes Mellitus (DM). Glycemic control is initially achieved with sulfonylureas but patients eventually become insulin dependent more rapidly than with type II DM patients. Although they have a type II DM phenotype, patients have circulating beta (β) cell autoantibodies, a hallmark of type I DM. Alternative terms that have been used to describe this condition include type 1.5 diabetes, latent type I diabetes, slowly progressive Insulin Dependent Diabetes Mellitus, or youth onset diabetes of maturity. With regards to its autoimmune basis and rapid requirement for insulin, it has been suggested that LADA is a slowly progressive form of type I DM. However, recent work has revealed genetic and immunological differences between LADA and type I DM. The heterogeneity of LADA has also led to the proposal of criteria for its diagnosis by the Immunology of Diabetes Society. Although many workers have advocated a clinically oriented approach for screening of LADA, there are no universally accepted criteria for autoantibody testing in adult onset diabetes. Following recent advances in immunomodulatory therapies in type I DM, the same strategy is being explored in LADA. This review deals with the contribution of the genetic, immunological and metabolic components involved in the pathophysiology of LADA and recent approaches in screening of this distinct but heterogeneous clinical entity.

Hyperglycemic hyperosmolar syndrome (HHS) is a clinical entity not identical to diabetic ketoacidosis (DKA), and with a markedly higher mortality. Children with HHS can also present with concomitant DKA. Patients with HHS (with or without DKA) are profoundly dehydrated but often receive inadequate fluid resuscitation as well as intravenous insulin therapy based on traditional DKA protocols, and this can lead to devastating consequences. In this article, we briefly review HHS along with a report of an adolescent who presented with HHS and DKA and was initially managed as DKA. She went into hypotensive shock and developed severe, multiorgan failure. A thorough understanding of the pathophysiology of HHS and its differences from DKA in terms of initial management is crucial to guide management and improve outcomes. Additionally, fluid therapy in amounts concordant with the degree of dehydration remains the mainstay therapy.

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