Presumptive Type 1 Diabetes With Comorbidities and Rapid Progression Despite Numerous Insulin-Positive Islets  

Oleh:

Jacobsen, Laura M. ; Atkinson, Mark A. ; Campbell-Thompson, Martha ; Schatz, Desmond A.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Diabetes Care vol. 39 no. 07 (Jul. 2016), page 1292-1294.
Topik: Type 1 Diabetes; T1D
Fulltext: D05 v39 n7 p1292 kelik2017.pdf (1.15MB)

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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

The subject was a 26-year-old African American female diagnosed with type 1 diabetes at the age of 11 years, treated with insulin injections, who died because of an anoxic brain injury likely secondary to diabetic ketoacidosis. The patient was found with agonal respirations and had acidosis along with severe hyperglycemia on arrival to the emergency department. In the 15 years since being diagnosed with diabetes, she had developed significant signs of cardiovascular disease including cardiomyopathy and congestive heart failure with recent myocardial infarction and stent placement, hypertension, and hyperlipidemia. She was positive for anti–glutamic acid decarboxylase autoantibodies (GADA) and persistent C-peptide (0.48 ng/mL) below the normal range for healthy control subjects but detectible using standard assays. Residual C-peptide secretion of this level is generally detectable in only 3–9% of patients diagnosed prior to 18 years of age after 10–19 years duration (1); however, recent studies using ultrasensitive assays have demonstrated prolonged secretion of small amounts of C-peptide even three to four decades after diabetes onset (2,3). The Diabetes Control and Complications Trial (DCCT) showed that those patients with type 1 diabetes with even low levels of persistent stimulated C-peptide developed fewer microvascular complications (retinopathy, nephropathy) and less severe hypoglycemia (4). Despite the presence of C-peptide, this donor already had significant comorbidities, mentioned above, that were likely attributable to her diabetes and suggest a rapid progression of disease. Thus, we expected to observe significant loss of ß-cells when presented with this severe clinical picture of type 1 diabetes.

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