C Torn

Lund University, Lund, Skåne, Sweden

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Publications (8)17.02 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: All newly diagnosed diabetes in Kronoberg during 3 years was registered, with blood samples from 1630/1666 (97.8%) adults. Those positive for GADab and/or ICA and/or C-peptide<0.25nmol/L (0.7%) were classified as type 1 diabetes, the remaining as type 2. Incidence of type 1 in 0-19-year-olds was 37.8(36.1-39.6, 95%CI) and in 20-100 year-olds 27.1(25.6-27.4) per 100 000 and year, it was bimodal with equal peaks in 0-9 year-olds and in 50-80-year-olds. Adults had type 2 incidence 378 (375-380), children 3.1 (2.6-3.6). Among adults 6.9% had type 1 and 93.1% type 2. Among antibodypositive adults (n=101), GADab were present in 90%, ICA in 71%, both GADab and ICA in 61%. Ophthalmology contact as second source was confirmed for 98%. There were no gender differences in type 1 in any age group, small ones in pediatric subgroups. In type 2 men predominated in ages above 40 years. Incidences of type 1 diabetes in both children and adults were very high and as high above age 50 years as in children. Incidence of type 2 was the highest reported from Sweden, to which new diagnostic criteria, a high degree of case-finding, and many elders, may have contributed, but results may also reflect a true increase in incidence of both types of diabetes.
    Diabetes research and clinical practice 10/2008; 82(2):247-55. · 2.74 Impact Factor
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    ABSTRACT: To establish whether children with type 1 diabetes mellitus (T1D) with signs of pronounced beta-cell-specific autoimmunity as reflected by high autoantibody titers or positivity for several beta-cell-specific autoantibodies show a different pattern of month of birth (MOB) compared with children with T1D and low beta-cell autoimmunity and that of the general population. Cosinor analysis was used to analyze MOB rhythmicity in Swedish children with new onset T1D (n = 572), in whom the glutamate decarboxylase autoantibody (GAD65Ab) titer was determined and compared with that in 833 healthy children, and in 505 children with T1D in Berlin, in whom the titers of autoantibodies to insulin, GAD65, and islet antigen-2 were compared with the MOB pattern in the general population (n = 446 571). In both cohorts of children with T1D, we found that children with either a high GAD65Ab titer (above the 80th percentile) or positivity for three beta-cell-specific autoantibodies differed in their pattern of MOB from the healthy population. Our past and present observations support the hypothesis that the autoimmune process leading to childhood T1D is in part triggered in the perinatal period by viral infections in genetically susceptible individuals. The present study suggests that the process is linked to titer levels of autoantibodies.
    Pediatric Diabetes 03/2008; 9(1):46-52. · 2.08 Impact Factor
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    ABSTRACT: The aim was to determine the course of islet cell antibodies [glutamate decarboxylase (GADA), tyrosine phosphatase-like islet antigen 2 (IA-2A) and islet cell (ICA)] after the diagnosis of the diabetic patient. The Diabetes Incidence Study in Sweden (DISS) attempted to prospectively enrol all newly diagnosed diabetic patients aged 15-34 years during 1992 and 1993. C-peptide and autoantibody levels were determined from venous blood samples at diagnosis and again at yearly intervals for 6 years. After the first year, the odds of remaining GADA positive decreased by 9% per year [odds ratio (OR) = 0.91, 95% confidence interval (CI) = 0.85-0.96] while the mean GADA index remained unchanged ( = 0.8, P = 0.37). There was no change in the percentage of subjects testing IA-2A positive after the first year ( = 0.1, P = 0.75). However, the mean index decreased 0.04 per year (95% CI: 0.03-0.05)-a 7.9% decline (95% CI: 5.4-10.4%). The odds of a subject testing positive for ICA decreased by 24% per year (OR = 0.76, 95% CI = 0.70-0.82). The mean ICA levels decreased 0.75 per year (95% CI: 0.66-0.84)-a 16.4% decline (95% CI: 14.1-18.6%). The rate of change in titres for all three autoantibodies was independent of gender, human leucocyte antigen genotype and C-peptide status. GADA levels remained high while ICA levels declined. In contrast to a previous study, we found that the proportion of IA-2A subjects remaining positive did not decrease after the first year, while the average index decreased slightly.
    Diabetic Medicine 12/2007; 24(11):1221-8. · 3.24 Impact Factor
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    ABSTRACT: Autoantibodies to insulin (IAA) are one of the first markers of the autoimmune process leading to type 1 diabetes (T1D). While other autoantibodies in T1D have been studied extensively, relatively little is known about IAA and their binding specificities, especially after insulin treatment is initiated. We hypothesize that insulin antibodies (IA) that develop upon initiation of insulin treatment differ in their epitope specificities from IAA. We analysed insulin antibody binding specificities in longitudinal samples of T1D patients (n = 49). Samples were taken at clinical diagnosis of disease and after insulin treatment was initiated. The epitope specificities were analysed using recombinant Fab (rFab) derived from insulin-specific monoclonal antibodies AE9D6 and CG7C7. Binding of radiolabelled insulin by samples taken at onset of the disease was significantly reduced in the presence of rFab CG7C7 and AE9D6. rFab AE9D6 competed sera binding to insulin significantly better than rFab CG7C7 (P = 0.02). Binding to the AE9D6-defined epitope in the initial sample was correlated inversely with age at onset (P = 0.005). The binding to the AE9D6-defined epitope increased significantly (P < 0.0001) after 3 months of insulin treatment. Binding to the CG7C7-defined epitope did not change during the analysed period of 12 months. We conclude that epitopes recognized by insulin binding antibodies can be identified using monoclonal insulin-specific rFab as competitors. Using this approach we observed that insulin treatment is accompanied by a change in epitope specificities in the emerging IA.
    Clinical & Experimental Immunology 10/2006; 146(1):9-14. · 3.41 Impact Factor
  • Clinical Immunology - CLIN IMMUNOL. 01/2006; 119.
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    ABSTRACT: Autoantibodies to insulin are often the first autoantibodies detected in young children with type 1 diabetes and can be present before the onset of clinical diabetes. These autoantibodies and their epitopes are, however, not well characterized. We explored the use of monoclonal antibodies and their recombinant Fab as reagents for epitope analysis. In this study we cloned and characterized the recombinant Fab of the insulin-specific monoclonal antibody CG7C7. We found the epitope of this antibody to be located predominantly at the A-chain loop of the insulin molecule. The recombinant Fab was then used to compete for insulin binding against insulin autoantibodies present in sera from patients with type 1 or type 1.5 diabetes. In competition experiments with sera positive for autoantibodies to insulin the recombinant Fab significantly reduced the binding to [125I]-insulin by sera of type 1 (n = 35) and type 1.5 diabetes [latent autoimmune diabetes in adults (LADA)] (n = 14) patients (P < 0.0001). We conclude that competition between insulin-specific monoclonal antibodies or their recombinant Fab and insulin autoantibodies should prove useful in the epitope analysis of autoantibodies to insulin.
    Clinical & Experimental Immunology 06/2005; 140(3):564-71. · 3.41 Impact Factor
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    ABSTRACT: This study presents a 2-yr follow-up of 281 patients, aged 15-34 yr, diagnosed with diabetes between 1992 and 1993. At diagnosis, 224 (80%) patients were positive for at least one of the following autoan- tibodies: islet cell antibodies (ICAs), glutamic acid decarboxylase an- tibodies (GADAs), or tyrosine phosphatase antibodies (IA-2As); the remaining 57 (20%) patients were negative for all three autoantibod- ies. At diagnosis, C-peptide levels were lower (0.27; 0.16 - 0.40 nmol/L) in autoantibody-positive patients compared with autoantibody- negative patients (0.51; 0.28 - 0.78 nmol/L; P , 0.001). After 2 yr, C-peptide levels had decreased significantly in patients with auto- immune diabetes (0.20; 0.10 - 0.37 nmol/L; P 5 0.0018), but not in autoantibody-negative patients. In patients with autoimmune dia- betes, a low initial level of C-peptide (odds ratio, 2.6; 95% confidence interval, 1.7- 4.0) and a high level of GADAs (odds ratio, 2.5; 95% confidence interval, 1.1-5.7) were risk factors for a C-peptide level below the reference level of 0.25 nmol/L 2 yr after diagnosis. Body mass index had a significant effect in the multivariate analysis only when initial C-peptide was not considered. Factors such as age, gen- der, levels of ICA or IA-2A or insulin autoantibodies (analyzed in a subset of 180 patients) had no effect on the decrease in b-cell function. It is concluded that the absence of pancreatic islet autoantibodies at diagnosis were highly predictive for a maintained b-cell function during the 2 yr after diagnosis, whereas high levels of GADA indicated a course of decreased b-cell function with low levels of C-peptide. In autoimmune diabetes, an initial low level of C-peptide was a strong risk factor for a decrease in b-cell function and conversely high C- peptide levels were protective. Other factors such as age, gender, body mass index, levels of ICA, IA-2A or IAA had no prognostic importance. (J Clin Endocrinol Metab 85: 4619 - 4623, 2000)
    Journal of Clinical Endocrinology & Metabolism - J CLIN ENDOCRINOL METAB. 01/2000; 85(12):4619-4623.
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    ABSTRACT: A new, relatively simple tetra-acid ligand derived from acetophenone was synthesized and its luminescence properties when forming Eu(III) and Tb(III) chelates were evaluated in aqueous and methanol solutions. The titled compound displayed excellent quantum yields of triplet sensitization of lanthanide luminescence (0.20–0.25 for Eu3+ and 0.95–1.00 for Tb3+). Results suggested that the metal and the cromophore should be in close contact and that the iminodiacetic arms isolate very well the metal from the surrounding OH oscillators which normally quench lanthanide luminescence.
    Journal of Luminescence 01/1998; 79(2). · 2.14 Impact Factor