Transplantační medicína

This video highlights prurigo nodularis (PN) as a systemic disorder driven by neural inflammation and immune dysregulation. Key inflammatory mediators IL-4 and IL-13, along with fibrosis, emerge as central features, emphasizing the need for targeted therapies that address both neural and immune pathways. 

Delay in screening for autoimmune type 1 diabetes (T1D) can increase the risk of diabetic ketoacidosis (DKA) at diagnosis—a critical complication that is potentially life-threatening and may result in long-term poor glycemic control and neurological complications.^1,2 By identifying autoimmune T1D early, you can significantly lower the risk of DKA at diagnosis.^3,4

Individuals who screen positive for ≥1 autoimmune islet cell antibodies need periodic medical monitoring, which includes regular assessments of blood glucose and HbA1c levels. You can also educate them about symptoms of diabetes, diabetic ketoacidosis (DKA), and provide psychosocial support to prepare them for a possible clinical diagnosis for type 1 diabetes (T1D).¹

Autoimmune type 1 diabetes (T1D) is a progressive disease in which the decline in beta cell function usually begins months or sometimes years before clinical symptoms are observed.^1–3 You can identify such patients at risk of developing autoimmune T1D before clinical symptoms are noticed by you or your patient.³