Aims/hypothesis Low plasma vitamin D concentrations may promote the development of type 1 diabetes. To test this hypothesis, we measured plasma 25-hydroxyvitamin D (25OHD) in young adults with type 1 diabetes. Methods The nationwide Diabetes Incidence Study in Sweden (DISS) covers 15-to 34-year-old people with newly diagnosed diabetes. Blood samples at diagnosis were collected during the 2-year period 1987/1988. Patients with islet antibodies (islet cell antibodies, GAD antibodies or tyrosine phosphatase-like protein antibodies) were defined as having autoimmune type 1 diabetes. Plasma 25OHD was measured in samples taken from 459 patients at the time of diagnosis, and in 138 of these subjects 8 years later. The results were compared with age-and sex-matched control subjects (n=208). Results At diagnosis, plasma 25OHD levels were significantly lower in patients with type 1 diabetes than in control subjects (82.5T1.3 vs 96.7T2.0 nmol/l; p<0.0001). Eight years later, plasma 25OHD had decreased in patients
OBJECTIVE—To estimate the prevalence and severity of diabetic retinopathy (DR) 10 years after diagnosis in a nationwide population-based cohort study of young adult diabetic patients in Sweden.
RESEARCH DESIGN AND METHODS—The Diabetes Incidence Study in Sweden (DISS) aims to register all incident cases of diabetes aged 15–34 years in Sweden. In 1987–1988, 806 cases were reported, and 627 (78%) of them were followed up with regard to retinopathy 8–10 years later. The assessment was based on retinal photographs in most cases (86%).
RESULTS—Ten years after diagnosis, retinopathy was found in 247 patients (39%). The retinopathy was mild in 206 (33%), whereas 30 (4.8%) patients had moderate nonproliferative DR (NPDR) and 11 (1.8%) had proliferative DR (PDR). Patients with retinopathy had worse glycemic control during the years than patients without (HbA1c 8.1 ± 1.5% and 6.8 ± 1.2%, respectively; P < 0.001). In a Cox regression analysis, time to retinopathy was related to high HbA1c (P < 0.001) and high BMI (P = 0.001). Patients with type 2 diabetes had an increased prevalence of severe retinopathy (NPDR or PDR) compared with those with type 1 diabetes (14 of 93 [15%] versus no or mild 24 of 471 [5%], respectively; P < 0.001).
CONCLUSIONS—Despite modern diabetes management, 39% of young adult diabetic patients developed retinopathy within the first 10 years of the disease. Nevertheless, compared with the prevalence of retinopathy (63%), after a similar duration of diabetes before the Diabetes Control and Complications Trial, this prevalence was clearly lower. Current treatment aimed to achieve strict glycemic control has reduced the risk for developing retinopathy.
and an insulin dosage of р0.4 U kg Ϫ1 day Ϫ1 for a minimum of 1 month) in relation to nine biochemical and clinical factors at diagnosis. Results. Sixty-one per cent of the patients entered remission. The duration of remission was longer in males than females (10 Ϯ 12 vs. 2 Ϯ 3 months; P Ͻ 0.01). Male gender, normal serum bicarbonate at onset and a short time of classic symptoms before onset were predictive markers (P Ͻ 0.01; P Ͻ 0.05 and P Ͻ 0.01, respectively) for longer duration of remission. Low serum bicarbonate levels at onset were associated with lower occurrence of remission. Blood glucose, body mass index (BMI), and age at diagnosis did not influence the occurrence or the duration of remission. Conclusions. In most adult patients with new onset of type 1 diabetes remission is induced when using multiple insulin injection therapy. Male patients seem particularly prone to remission, and the length and extent of -cell strain prior to diagnosis strongly influences its course.
In islet antibody-positive Type 1 DM, normal body weight was the strongest factor for entering remission, whilst a low number of islet antibodies was of importance for the duration.
Remissions after diagnosis of Type 1 diabetes were associated with lower proinsulin/C-peptide ratios, suggesting more efficient proinsulin processing, and tended to have lower glucagon release than non-remissions. This indicates that, in remission, the residual islets maintain a secretion of insulin and glucagon of benefit for control of hepatic glucose production.
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