## Pathological Features of Type 1 Diabetes Mellitus ### Characteristic Lesions **Key Point:** Type 1 DM is an autoimmune destruction of pancreatic beta cells, NOT an amyloidosis of islets. | Feature | Present in T1DM | Notes | |---------|-----------------|-------| | Insulitis | Yes | Lymphocytic infiltration of islets; hallmark lesion | | CD8+ T cell-mediated beta cell destruction | Yes | Primary mechanism of beta cell loss | | Amyloid deposition (amylin/IAPP) | **No** | Characteristic of Type 2 DM, not Type 1 | | Islet fibrosis and hyalinization | Yes | End-stage finding; loss of normal islet architecture | | Reduced islet number | Yes | Progressive loss of islets over time | ### Why Amyloid Deposition is NOT a Feature of T1DM **High-Yield:** Amylin (islet amyloid polypeptide, IAPP) aggregation and amyloid deposition within islets is a **hallmark of Type 2 Diabetes Mellitus**, not Type 1. In T2DM, amylin is co-secreted with insulin by beta cells; in conditions of chronic hyperinsulinemia and insulin resistance, amylin misfolds and deposits as amyloid fibrils within and around islets, contributing to beta cell dysfunction and loss. In Type 1 DM, the beta cells are destroyed by immune-mediated mechanisms (insulitis, CD8+ T cell infiltration, autoantibodies) before they have a chance to accumulate amyloid. ### Pathogenesis Timeline in T1DM 1. **Autoimmune activation** → CD8+ T cells and autoantibodies (anti-GAD, anti-IA-2, anti-insulin) target beta cells 2. **Insulitis** → Lymphocytic infiltration of islets; selective beta cell destruction 3. **Progressive beta cell loss** → Hyperglycemia emerges when ~90% of beta cells are destroyed 4. **End-stage fibrosis** → Islets become fibrotic, hyalinized, and depleted of beta cells **Clinical Pearl:** Amyloid deposition in islets is so characteristic of T2DM that its presence on pancreatic biopsy or autopsy strongly suggests T2DM rather than T1DM. [cite:Robbins 10e Ch 24]
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