Dimorphic histopathology of long-standing childhood-onset diabetes
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-s...
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| Vydané v: | Diabetologia Ročník 53; číslo 4; s. 690 - 698 |
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| Hlavní autori: | , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
Berlin/Heidelberg
Berlin/Heidelberg : Springer-Verlag
01.04.2010
Springer-Verlag Springer Springer Nature B.V |
| Predmet: | |
| ISSN: | 0012-186X, 1432-0428, 1432-0428 |
| On-line prístup: | Získať plný text |
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| Shrnutí: | 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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| Bibliografia: | http://dx.doi.org/10.1007/s00125-009-1642-y ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
| ISSN: | 0012-186X 1432-0428 1432-0428 |
| DOI: | 10.1007/s00125-009-1642-y |