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J B Hoekstra

Publications and source records attributed to J B Hoekstra.

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Evaluation of three commercially available C-peptide kits.

Three commercially available methods for the determination of C-peptide in human serum were evaluated. All kits were found to be acceptable with respect to precision and analytical recovery, while differences were observed with respect to sensitivity and cross-reactivity to human proinsulin. Furthermore an intermethod comparison was performed. It is pointed out that, before C-peptide determination on serum from insulin-treated diabetic subjects, a PEG precipitation, to remove antibody-bound proinsulin, should be done.

C-Peptide↗

Humoral immune response to a yeast-derived hepatitis B vaccine in patients with type 1 diabetes mellitus.

The immune response following vaccination with a recombinant hepatitis B vaccine was investigated in 32 patients with Type 1 diabetes mellitus and compared with the outcome in 32 healthy age- and sex-matched volunteers. Participants were vaccinated at 0, 30, and 180 days and in vivo immune response was determined at 30, 60, 90, 180, and 210 days. The number of responders (anti-HBs greater than 1 IU l-1) was significantly lower (p less than 0.05) among patients at 30 (2 vs 11), 60 (17 vs 26), 90 (20 vs 28) and 180 (22 vs 29) days. The number of patients protected (anti-HBs greater than 10 IU l-1) was lower (p less than 0.05) than the number of protected volunteers at 60 (5 vs 14), 90 (10 vs 19), 180 (15 vs 24), and 210 days (24 vs 31). After the complete course of vaccination 8 out of 32 patients were still unprotected against hepatitis B (p less than 0.05). The anti-HBs titre of responders at 210 days was 251 (20, 3162) (geometric mean (-SD, +SD] IU l-1 in patients and 1259 (126, 12589) IU l-1 in control subjects (p less than 0.05). The HLA-antigen DQw1 frequency in the diabetic low responders (anti-HBs less than 100 IU l-1) was 0.27 compared with 0.86 in diabetic adequate responders. No relation between anti-HBs production and concentration of HbA1c could be demonstrated.

Adult↗

C-peptide.

C-peptide is a polypeptide originating from proinsulin after its cleavage in the B-cell. It is secreted equimolarly with the other cleavage product, insulin, into the portal circulation. Only a minimal fraction of C-peptide is extracted by the liver; it is supposed to be mainly removed by the kidney. A small, constant proportion is excreted in the urine. C-peptide is measured in serum and urine by radioimmunoassay. The major sources of error of the assay are related to standard, tracer, antiserum specificity and reactivity with proinsulin, and to degradation of C-peptide. Many secretagogues are used to evaluate the B-cell function, of which glucagon is the most simple. Clinical applications of C-peptide include differentiating between endogenous and exogenous hyperinsulinism and establishing the need of insulin therapy in diabetic patients already treated with insulin. The primary value of C-peptide, however, is in clinical research, where it offers a unique opportunity to follow the B-cell secretion in diabetic subjects and to evaluate the difference that various factors may exert on its activity.

Animals↗

C-peptide reactivity as a measure of insulin dependency in obese diabetic patients treated with insulin.

The C-peptide increase after an oral glucose tolerance test (OGTT) and intravenous glucagon test (GT) was assessed to establish actual insulin dependency in 16 obese diabetic patients treated with insulin for years. The results, compared to five reference groups, showed two types of reaction: first, a negative response in 3 patients with a minimal C-peptide increase after either stimulation (range 0-0.1 ng/ml during GT, 0-0.5 during OGTT), not different from that in the insulin-dependent reference group (GT: 0.1 +/- 0.2, OGTT: 0.1 +/- 0.3. means +/- SD). Second, a positive response in 13 patients with a C-peptide increase, different from that in the insulin-dependent group after glucagon (range 0.7-5.6), and in 6 patients after OGTT (range 0.8-1.8). When insulin treatment was discontinued in two nonresponders, the B-hydroxybutyrate levels and ketobutyrate levels increased to over 2.1 and 0.60 mmol/L within 10 days, proving insulin dependency, and thus type I diabetes. B-hydroxybutyrate and ketobutyrate levels increased to maximal 0.4 and 0.17 after stopping insulin therapy in nine positive responders. No ketoacidosis developed during a 4-wk follow-up, indicating non-insulin dependency (type II diabetes). Measuring C-peptide after glucagon is a simple test that may be a discriminative method to establish insulin dependency in obese diabetic patients treated with insulin.

Adult↗