Fall in C-Peptide During First 4 Years From Diagnosis of Type 1 Diabetes: Variable Relation to Age, HbA1c, and Insulin Dose  

Oleh:

Wei Hao ; Gitelman, Steven ; DiMeglio, Linda A. ; Boulware, David ; Greenbaum, Carla J.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Diabetes Care vol. 39 no. 10 (Oct. 2016), page 1664-1670.
Topik: Type 1 Diabetes; T1D
Fulltext: D05 v39 n10 p1664 kelik2017.pdf (1.01MB)

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Perpustakaan FK Nomor Panggil: D05.K Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

OBJECTIVE We aimed to describe the natural history of residual insulin secretion in Type 1 Diabetes TrialNet participants over 4 years from diagnosis and relate this to previously reported alternative clinical measures reflecting ß-cell secretory function. RESEARCH DESIGN AND METHODS Data from 407 subjects from 5 TrialNet intervention studies were analyzed. All subjects had baseline stimulated C-peptide values of =0.2 nmol/L from mixed-meal tolerance tests (MMTTs). During semiannual visits, C-peptide values from MMTTs, HbA1c, and insulin doses were obtained. RESULTS The percentage of individuals with stimulated C-peptide of =0.2 nmol/L or detectable C-peptide of =0.017 nmol/L continued to diminish over 4 years; this was markedly influenced by age. At 4 years, only 5% maintained their baseline C-peptide secretion. The expected inverse relationships between C-peptide and HbA1c or insulin doses varied over time and with age. Combined clinical variables, such as insulin-dose adjusted HbA1c (IDAA1C) and the relationship of IDAA1C to C-peptide, also were influenced by age and time from diagnosis. Models using these clinical measures did not fully predict C-peptide responses. IDAA1C =9 underestimated the number of individuals with stimulated C-peptide =0.2 nmol/L, especially in children. CONCLUSIONS Current trials of disease-modifying therapy for type 1 diabetes should continue to use C-peptide as a primary end point of ß-cell secretory function. Longer duration of follow-up is likely to provide stronger evidence of the effect of disease-modifying therapy on preservation of ß-cell function.

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