Dimorphic histopathology of long-standing childhood-onset diabetes - PubMed (original) (raw)
doi: 10.1007/s00125-009-1642-y. Epub 2010 Jan 9.
M Campbell-Thompson, S A Sarkar, C Wasserfall, A Pugliese, J M Solis, S C Kent, B J Hering, E West, A Steck, S Bonner-Weir, M A Atkinson, K Coppieters, M von Herrath, G S Eisenbarth
Affiliations
- PMID: 20062967
- DOI: 10.1007/s00125-009-1642-y
Dimorphic histopathology of long-standing childhood-onset diabetes
R Gianani et al. Diabetologia. 2010 Apr.
Erratum in
- Diabetologia. 2010 Aug;53(8):1811-2
Abstract
Aims/hypothesis: Childhood diabetes is thought to usually result from autoimmune beta cell destruction (type 1A) with eventual total loss of beta cells. Analysis of C-peptide in children characterised at diabetes onset for autoantibodies shows heterogeneous preservation of insulin secretion in long-standing diabetes. The aim of this study was to characterise the pancreases of childhood-onset diabetes in order to define the pathological basis of this heterogeneity.
Methods: We evaluated 20 cadaveric organ donor pancreases of childhood-onset long-term patients for disease heterogeneity and obtained corresponding C-peptide measurements.
Results: Pancreases from the majority of cadaveric donors contained only insulin-deficient islets (14 of 20). The remaining six patients (30%) had numerous insulin-positive cells within at least some islets, with two different histological patterns. Pattern A (which we would associate with type 1A diabetes) had lobular retention of areas with 'abnormal' beta cells producing the apoptosis inhibitor survivin and HLA class I. In pattern B, 100% of all islets contained normal-appearing but quantitatively reduced beta cells without survivin or HLA class I.
Conclusions/interpretation: Our data demonstrate that C-peptide secretion in long-standing diabetic patients can be explained by two different patterns of beta cell survival,possibly reflecting different subsets of type 1 diabetes.
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