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Träfflista för sökning "WFRF:(Landin Anders) "

Sökning: WFRF:(Landin Anders)

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  • Åberg, Anders E, et al. (författare)
  • Predictive factors of developing diabetes mellitus in women with gestational diabetes.
  • 2002
  • Ingår i: Acta Obstetricia et Gynecologica Scandinavica. - : Wiley. - 1600-0412 .- 0001-6349. ; 81:1, s. 11-16
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: To investigate which factors during gestational diabetes pregnancies correlate with the risk of developing impaired glucose tolerance or diabetes 1 year postpartum and to compare this risk in women with gestational diabetes and women with a normal oral glucose tolerance test during pregnancy. METHODS: Of 315 women with gestational diabetes, defined as a 2-hr blood glucose value of at least 9.0 mmol/l at a 75-g oral glucose tolerance test, who delivered in Lund 1991-99, 229 (73%) performed a new test 1 year postpartum. We compared maternal and fetal factors during pregnancy with the test value at follow up. A control group of 153 women with a 2-hr test value below 7.8 mmol/l during pregnancy were invited to a new test 1 year postpartum and 60 (39%) accepted. RESULTS: At 1 year follow up, 31% of the women with gestational diabetes but only one of the 60 controls showed pathologic glucose tolerance and one had developed diabetes. The following factors in women with gestational diabetes were identified as predicting impaired glucose tolerance or diabetes at 1 year follow up: maternal age over 40 and--in a multiple regression analysis, independent of each other--a high 2-hr value at oral glucose tolerance test during pregnancy and insulin treatment during pregnancy. CONCLUSION: The risk of developing manifest diabetes after gestational diabetes may be high enough to justify a general screening or diagnostic procedure in all pregnant women to identify women with gestational diabetes and a postpartum follow up program for them. This study did not identify any particular factor during pregnancy with enough precision to predict a later progression to diabetes.
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  • Ahrén, Bo, et al. (författare)
  • Inhibition of dipeptidyl peptidase IV improves metabolic control over a 4-week study period in type 2 diabetes.
  • 2002
  • Ingår i: Diabetes Care. - : American Diabetes Association. - 0149-5992 .- 1935-5548. ; 25:5, s. 869-75
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Glucagon-like peptide-1 (GLP-1) has been proposed as a new treatment modality for type 2 diabetes. To circumvent the drawback of the short half-life of GLP-1, inhibitors of the GLP-1-degrading enzyme dipeptidyl peptidase IV (DPP IV) have been examined. Such inhibitors improve glucose tolerance in insulin-resistant rats and mice. In this study, we examined the 4-week effect of 1-[[[2-[(5-cyanopyridin-2-yl)amino]ethyl]amino]acetyl]-2-cyano-(S)-pyrrolidine (NVP DPP728), a selective, orally active inhibitor of DPP IV, in subjects with diet-controlled type 2 diabetes in a placebo-controlled double-blind multicenter study.RESEARCH DESIGN AND METHODS: A total of 93 patients (61 men and 32 women), aged 64 +/- 9 years (means +/- SD) and with BMI 27.3 +/- 2.7 kg/m(2), entered the study. Fasting blood glucose was 8.5 +/- 1.5 mmol/l, and HbA(1c) was 7.4 +/- 0.7%. Before and after treatment with NVP DPP728 at 100 mg x 3 (n = 31) or 150 mg x 5 (n = 32) or placebo (n = 30), subjects underwent a 24-h study with standardized meals (total 2,000 kcal).RESULTS: Compared with placebo, NVP DPP728 at 100 mg t.i.d. reduced fasting glucose by 1.0 mmol/l (mean), prandial glucose excursions by 1.2 mmol/l, and mean 24-h glucose levels by 1.0 mmol/l (all P < 0.001). Similar reductions were seen in the 150-mg b.i.d. treatment group. Mean 24-h insulin was reduced by 26 pmol/l in both groups (P = 0.017 and P = 0.023). Although not an efficacy parameter foreseen in the study protocol, HbA(1c) was reduced to 6.9 +/- 0.7% in the combined active treatment groups (P < 0.001). Laboratory safety and tolerability was good in all groups.CONCLUSIONS: We conclude that inhibition of DPP IV is a feasible approach to the treatment of type 2 diabetes in the early stage of the disease.
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  • Anderberg, Eva, et al. (författare)
  • Prevalence of impaired glucose tolerance and diabetes after gestational diabetes mellitus comparing different cut-off criteria for abnormal glucose tolerance during pregnancy.
  • 2011
  • Ingår i: Acta Obstetricia et Gynecologica Scandinavica. - : Wiley. - 1600-0412 .- 0001-6349. ; 90, s. 1252-1258
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective. To determine the prevalence of diabetes and impaired glucose tolerance after gestational diabetes mellitus in relation to different categories of glucose tolerance during pregnancy. Design. Prospective study. Setting. Four delivery departments and three hospitals in southern Sweden took part in recruitment and follow-up. Population. Women undergoing a 75 g oral glucose tolerance test during pregnancy delivering in 2003-2005. Methods. At first follow-up, 1-2 years after delivery, 29% of eligible women with abnormal glucose tolerance during pregnancy had an oral glucose tolerance test; 160 with gestational diabetes, 309 with gestational impaired glucose tolerance, in addition to 167 control women. Cut-off levels defining gestational diabetes and impaired glucose tolerance were 2-hour capillary blood glucose levels 9.0 and 7.8 mmol/l or plasma glucose 10.0 and 8.6 mmol/l, respectively. Main outcome measures. Frequency of abnormal test results at follow-up. Results: Diabetes was diagnosed in 11% and impaired glucose tolerance in 24% of women with gestational diabetes vs. 4% and 23% in those with gestational impaired glucose tolerance. Combining women with abnormal test results during pregnancy revealed diabetes or impaired glucose tolerance in 29% as compared to 10% among controls; the odds ratio (95% confidence interval) for having abnormal test results was 3.3 (1.8-5.9) in a multivariate logistic regression analysis. Conclusions: Lowering the cut-off level for gestational diabetes to also include the category of impaired glucose tolerance would identify a high percentage of women with diabetes and impaired glucose tolerance postpartum, they constitute target groups for intervention and/or diabetes prevention.
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  • Borg, Henrik, et al. (författare)
  • High levels of antigen-specific islet antibodies predict future beta-cell failure in patients with onset of diabetes in adult age
  • 2001
  • Ingår i: Journal of Clinical Endocrinology and Metabolism. - 1945-7197. ; 86:7, s. 3032-3038
  • Tidskriftsartikel (refereegranskat)abstract
    • It is unclear whether high levels of antigen-specific islet antibodies [GADA (glutamic acid decarboxylase 65 antibodies) and IA2-ab (protein tyrosine phosphatase-like protein antibodies)] predict beta-cell failure in patients with onset of diabetes in adult age. Therefore, GADA and IA2-ab levels at the diagnosis of diabetes were related to fasting plasma C-peptide levels 5 yr later in 148 patients with diabetes onset in adult age (age at onset, 20-77 yr; median, 57 yr). Classical islet cell antibodies (ICA) were also determined. Complete beta-cell failure (undetectable fasting plasma C-peptide) was only present in 4 patients at diagnosis of diabetes, but in 21 patients 5 yr thereafter. At diagnosis, ICA were detected in 20 of 21 (95%) patients with beta-cell failure after 5 yr and in only 7 of 127 (5%) without, whereas GADA and/or IA2-ab (>97.5 percentile of healthy controls) were detected in all 21 (100%) with but also in 23 of 127 (18%) patients without beta-cell failure after 5 yr. Thus, ICA had a higher positive predictive value (74%) than GADA and/or IA2-ab (47%; P < 0.05). With high cutoff values for GADA and IA2-ab, however, GADA and/or IA2-ab were detected in 19 of 21 (90%) patients with beta-cell failure vs. only in 5 of 127 (4%) without, giving a positive predictive value of 79%. Slightly elevated GADA levels in IA2-ab-negative patients were associated with progressive but not complete beta-cell failure within the study period. Hence, high GADA and/or IA2-ab levels predict a future complete beta-cell failure, whereas low GADA levels predict slowly progressive beta-cell insufficiency.
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