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Sökning: WFRF:(Ivarsson Sten A)

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1.
  • Resic-Lindehammer, Sabina, et al. (författare)
  • Temporal trends of HLA genotype frequencies of type 1 diabetes patients in Sweden from 1986 to 2005 suggest altered risk
  • 2008
  • Ingår i: Acta Diabetologica. - 0940-5429 .- 1432-5233. ; 45:4, s. 231-5
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The aim of this study was to compare the frequency of human leukocyte antigen (HLA) genotypes in 1-18-year-old patients with type 1 diabetes newly diagnosed in 1986-1987 (n = 430), 1996-2000 (n = 342) and in 2003-2005 (n = 171). We tested the hypothesis that the HLA DQ genotype distribution changes over time. Swedish type 1 diabetes patients and controls were typed for HLA using polymerase chain reaction amplification and allele specific probes for DQ A1* and B1* alleles. The most common type 1 diabetes HLA DQA1*-B1*genotype 0501-0201/0301-0302 was 36% (153/430) in 1986-1987 and 37% (127/342) in 1996-2000, but decreased to 19% (33/171) in 2003-2005 (P \ 0.0001). The 0501-0201/0501-0201 genotype increased from 1% in 1986-1987 to 7% in 1996-2000 (P = 0.0047) and to 5% in 2003-2005 (P &gt; 0.05). This study in 1-18-year-old Swedish type 1 diabetes patients supports the notion that there is a temporal change in HLA risk.</p>
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2.
  • Resic-Lindehammer, Sabina, et al. (författare)
  • Temporal trends of HLA genotype frequencies of type 1 diabetes patients in Sweden from 1986 to 2005 suggest altered risk
  • 2008
  • Ingår i: Acta Diabetologica. - 0940-5429 .- 1432-5233. ; 45:4, s. 231-235
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The aim of this study was to compare the frequency of human leukocyte antigen (HLA) genotypes in 1-18-year-old patients with type 1 diabetes newly diagnosed in 1986-1987 (n = 430), 1996-2000 (n = 342) and in 2003-2005 (n = 171). We tested the hypothesis that the HLA DQ genotype distribution changes over time. Swedish type 1 diabetes patients and controls were typed for HLA using polymerase chain reaction amplification and allele specific probes for DQ A1* and B1* alleles. The most common type 1 diabetes HLA DQA1*-B1*genotype 0501-0201/0301-0302 was 36% (153/430) in 1986-1987 and 37% (127/342) in 1996-2000, but decreased to 19% (33/171) in 2003-2005 (P \ 0.0001). The 0501-0201/0501-0201 genotype increased from 1% in 1986-1987 to 7% in 1996-2000 (P = 0.0047) and to 5% in 2003-2005 (P &gt; 0.05). This study in 1-18-year-old Swedish type 1 diabetes patients supports the notion that there is a temporal change in HLA risk.</p>
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3.
  • Carlsson, Annelie, et al. (författare)
  • Low risk HLA-DQ and increased body mass index in newly diagnosed type 1 diabetes children in the Better Diabetes Diagnosis study in Sweden.
  • 2012
  • Ingår i: International Journal of Obesity. - Nature Publishing Group. - 1476-5497. ; 36, s. 718-724
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective:Type 1 diabetes and obesity has increased in childhood. We therefore tested the hypothesis that type 1 diabetes human leukocyte antigen DQ (HLA-DQ) risk genotypes may be associated with increased body mass index (BMI).Design:The type 1 diabetes high-risk HLA-DQ A1(*)05:01-B1(*)02:01/A1(*)03:01-B1(*)03:02 genotype along with lower risk DQ genotypes were determined at the time of clinical onset by PCR and hybridization with allele-specific probes. BMI was determined after diabetes was stabilized.Subjects:A total of 2403 incident type 1 diabetes children below 18 years of age were ascertained in the Swedish national Better Diabetes Diagnosis (BDD) study between May 2005 to September 2009. All children classified with type 1 diabetes, including positivity for at least one islet autoantibody, were investigated.Results:Overall, type 1 diabetes HLA-DQ risk was negatively associated with BMI (P<0.0008). The proportion of the highest risk A1(*)05:01-B1(*)02:01/A1(*)03:01-B1(*)03:02 genotype decreased with increasing BMI (P<0.0004). However, lower risk type 1 diabetes DQ genotypes were associated with an increased proportion of patients who were overweight or obese (P<0.0001). Indeed, the proportion of patients with the low-risk A1(*)05:01-B1(*)02:01/A1(*)05:01-B1(*)02:01 genotype increased with increasing BMI (P<0.003). The magnitude of association on the multiplicative scale between the A1(*)05:01-B1(*)02:01/A1(*)05:01-B1(*)02:01 genotype and increased BMI was significant (P<0.006). The odds ratio in patients with this genotype of being obese was 1.80 (95% confidence interval 1.21-2.61; P<0.006). The increased proportion of overweight type 1 diabetes children with the A1(*)05:01-B1(*)02:01 haplotype was most pronounced in children diagnosed between 5 and 9 years of age.Conclusions:Susceptibility for childhood type 1 diabetes was unexpectedly found to be associated with the A1(*)05:01-B1(*)02:01/A1(*)05:01-B1(*)02:01 genotype and an increased BMI. These results support the hypothesis that overweight may contribute to the risk of type 1 diabetes in children positive for HLA-DQ A1(*)05:01-B1(*)02:01.International Journal of Obesity advance online publication, 28 June 2011; doi:10.1038/ijo.2011.122.
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4.
  • Ivarsson, Sten-A., et al. (författare)
  • Glutamate decarboxylase antibodies in non-diabetic pregnancy precedes insulin-dependent diabetes in the mother but not necessarily in the offspring
  • 1997
  • Ingår i: Autoimmunity. - Taylor & Francis. - 0891-6934. ; 26:4, s. 261-269
  • Tidskriftsartikel (refereegranskat)abstract
    • We studied the risk for diabetes of glutamate decarboxylase (GAD65Ab) and islet cell (ICA) autoantibodies in non-diabetic pregnant mothers and their children. Pregnancy and cord blood sera were collected in 1970-87 from about 35,000 mothers who delivered a child in the city of Malmo, Sweden. A total of 42 mothers were identified in 1988 who, 1-18 years after their pregnancies, had developed either insulin-dependent (n = 22) or non-insulin dependent (n = 20) diabetes mellitus. First, in 123 pregnant mothers selected as controls, 0.8% had GAD65Ab and 0.8% ICA. Second, among the mothers with non-insulin dependent diabetes, 7/20 (35%) had GAD65Ab eight months to 13 years, 10 months before clinical diagnosis. Third, in mothers who later developed insulin-dependent diabetes, 12/22 (55%) had GAD65Ab and 10/22 (45%) had ICA in pregnancies preceding the clinical diagnosis by 13 months to 9 years, 4 months. In 1996, none of the children born to the 42 mothers have developed diabetes. GAD65Ab and ICA in non-diabetic pregnancies may predict insulin-dependent diabetes in the mother but not necessarily in the offspring.
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5.
  • Asad, Samina, et al. (författare)
  • HTR1A a Novel Type 1 Diabetes Susceptibility Gene on Chromosome 5p13-q13
  • 2012
  • Ingår i: PLoS ONE. - Public Library of Science. - 1932-6203. ; 7:5
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: We have previously performed a genome-wide linkage study in Scandinavian Type 1 diabetes (T1D) families. In the Swedish families, we detected suggestive linkage (LOD <= 2.2) to the chromosome 5p13-q13 region. The aim of our study was to investigate the linked region in search for possible T1D susceptibility genes. Methodology/Principal Findings: Microsatellites were genotyped in the Scandinavian families to fine-map the previously linked region. Further, SNPs were genotyped in Swedish and Danish families as well as Swedish sporadic cases. In the Swedish families we detected genome-wide significant linkage to the 5-hydroxytryptamine receptor 1A (HTR1A) gene (LOD 3.98, p<9.8x10(-6)). Markers tagging two separate genes; the ring finger protein 180 (RNF180) and HTR1A showed association to T1D in the Swedish and Danish families (p<0.002, p<0.001 respectively). The association was not confirmed in sporadic cases. Conditional analysis indicates that the primary association was to HTR1A. Quantitative PCR show that transcripts of both HTR1A and RNF180 are present in human islets of Langerhans. Moreover, immunohistochemical analysis confirmed the presence of the 5-HTR1A protein in isolated human islets of Langerhans as well as in sections of human pancreas. Conclusions: We have identified and confirmed the association of both HTR1A and RFN180, two genes in high linkage disequilibrium (LD) to T1D in two separate family materials. As both HTR1A and RFN180 were expressed at the mRNA level and HTR1A as protein in human islets of Langerhans, we suggest that HTR1A may affect T1D susceptibility by modulating the initial autoimmune attack or either islet regeneration, insulin release, or both.
6.
  • Jensen, Rikke Beck, et al. (författare)
  • Genetic Markers of Insulin Sensitivity and Insulin Secretion Are Associated With Spontaneous Postnatal Growth and Response to Growth Hormone Treatment in Short SGA Children: the North European SGA Study (NESGAS)
  • 2015
  • Ingår i: Journal of Clinical Endocrinology and Metabolism. - Oxford University Press. - 1945-7197. ; 100:3, s. 503-507
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose: The wide heterogeneity in the early growth and metabolism of children born small for gestational age (SGA), both before and during GH therapy, may reflect common genetic variations related to insulin secretion or sensitivity. Method: Combined multiallele single nucleotide polymorphism scores with known associations with insulin sensitivity or insulin secretion were analyzed for their relationships with spontaneous postnatal growth and first-year responses to GH therapy in 96 short SGA children. Results: The insulin sensitivity allele score (GS-InSens) was positively associated with spontaneous postnatal weight gain (regression coefficient [B]: 0.12 SD scores per allele; 95% confidence interval [CI], 0.01-0.23; P = .03) and also in response to GH therapy with first-year height velocity (B: 0.18 cm/y per allele; 95% CI, 0.02-0.35; P = .03) and change in IGF-1 (B: 0.17 SD scores per allele; 95% CI, 0.00-0.32; P = .03). The association with first-year height velocity was independent of reported predictors of response to GH therapy (adjusted P = .04). The insulin secretion allele score (GS-InSec) was positively associated with spontaneous postnatal height gain (B: 0.15; 95% CI, 0.01-0.30; P = .03) and disposition index both before (B: 0.02; 95% CI, 0.00-0.04; P = .04) and after 1 year of GH therapy (B: 0.03; 95% CI, 0.01-0.05; P = .002), but not with growth and IGF-1 responses to GH therapy. Neither of the allele scores was associated with size at birth. Conclusion: Genetic allele scores indicative of insulin sensitivity and insulin secretion were associated with spontaneous postnatal growth and responses to GH therapy in short SGA children. Further pharmacogenetic studies may support the rationale for adjuvant therapies by informing the mechanisms of treatment response.
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7.
  • Ludvigsson, Johnny, et al. (författare)
  • Decline of C-peptide during the first year after diagnosis of Type 1 diabetes in children and adolescents
  • 2013
  • Ingår i: Diabetes Research and Clinical Practice. - Elsevier. - 1872-8227. ; 100:2, s. 203-209
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims/hypothesis: We studied the decline of C-peptide during the first year after diagnosis of Type 1 diabetes (T1D), and its relation to various factors. Methods: 3824/4017 newly diagnosed patients (95%) were classified as T1D in a national study. In a non-selected subgroup of 1669 T1D patients we determined non-fasting C-peptide both at diagnosis and after 1 year, and analyzed decline in relation to clinical symptoms and signs, initial C-peptide and occurrence of auto-antibodies. Results: Younger children lost more C-peptide (p < 0.001) and the higher the C-peptide at diagnosis the larger the decline during the first year (p < 0.0000). Patients with higher BMI had higher C-peptide at diagnosis but lost more (p < 0.01), and those with lower HbA1c, without symptoms and signs at diagnosis, and with higher BMI, had higher C-peptide at diagnosis, but lost more during the first year (p < 0.001). Finally, patients diagnosed during autumn had higher C-peptide at diagnosis, but lost more during the coming year (p < 0.001). Occurrence of auto-antibodies did not correlate with C-peptide decline, except possibly for a more rapid loss in IAA-positive patients. Conclusions/interpretation: Even in a restricted geographical area and narrow age range (< 18 years), the natural course of Type 1 diabetes is heterogeneous. This should be considered in clinical trials. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
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8.
  • Resic-Lindehammar, Sabina, et al. (författare)
  • Temporal trends of HLA genotype frequencies of type 1 diabetes patients in Sweden from 1986 to 2005 suggest altered risk
  • 2008
  • Ingår i: Acta Diabetologica. - Springer Milan. - 0940-5429 .- 1432-5233. ; 45:4, s. 231-235
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>The aim of this study was to compare the frequency of human leukocyte antigen (HLA) genotypes in 1–18-year-old patients with type 1 diabetes newly diagnosed in 1986–1987 (<em>n</em> = 430), 1996–2000 (<em>n</em> = 342) and in 2003–2005 (<em>n</em> = 171). We tested the hypothesis that the <em>HLA DQ</em> genotype distribution changes over time. Swedish type 1 diabetes patients and controls were typed for HLA using polymerase chain reaction amplification and allele specific probes for <em>DQ A1</em>* and <em>B1</em>* alleles. The most common type 1 diabetes HLA <em>DQA1*-B1*</em>genotype <em>0501-0201/0301-0302</em> was 36% (153/430) in 1986–1987 and 37% (127/342) in 1996–2000, but decreased to 19% (33/171) in 2003–2005 (<em>P</em> &lt; 0.0001). The <em>0501-0201/0501-0201</em> genotype increased from 1% in 1986–1987 to 7% in 1996–2000 (<em>P</em> = 0.0047) and to 5% in 2003–2005 (<em>P</em> &gt; 0.05). This study in 1–18-year-old Swedish type 1 diabetes patients supports the notion that there is a temporal change in HLA risk.</p>
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9.
  • Svensson, Matilda1, et al. (författare)
  • Antibodies to influenza virus A/H1N1 hemagglutinin in type 1 diabetes children diagnosed before, during and after the Swedish A(H1N1)pdm09 vaccination campaign 2009-2010.
  • 2014
  • Ingår i: Scandinavian Journal of Immunology. - Wiley-Blackwell. - 1365-3083. ; 79:2, s. 137-148
  • Tidskriftsartikel (refereegranskat)abstract
    • We determined A/H1N1-HA antibodies in relation to HLA-DQ genotypes and islet autoantibodies at clinical diagnosis in 1141 incident 0.7-18 years old type 1 diabetes patients diagnosed April 2009 - December 2010. Antibodies to (35) S-methionine-labeled A/H1N1 hemagglutinin were determined in a radiobinding assay in patients diagnosed before (n=325), during (n=355) and after (n=461) the October 2009 - March 2010 Swedish A(H1N1)pdm09 vaccination campaign, along with HLA-DQ genotypes and autoantibodies against GAD, insulin, IA-2 and ZnT8 transporter. Before vaccination, 0.6% patients had A/H1N1-HA antibodies compared to 40% during and 27% after vaccination (p<0.0001). In children <3 years of age, A/H1N1-HA antibodies were found only during vaccination. The frequency of A/H1N1-HA antibodies during vaccination decreased after vaccination among the 3<6 (p=0.006) and 13<18 (p=0.001) but not among the 6<13 year olds. HLA-DQ2/8 positive children <3 years decreased from 54% (15/28) before and 68% (19/28) during, to 30% (9/30) after vaccination (p=0.014). Regardless of age, DQ2/2; 2/X (n=177) patients had lower frequency (p=0.020) and levels (p=0.042) of A/H1N1-HA antibodies compared to non-DQ2/2; 2/X (n=964) patients. GADA frequency was 50% before, 60% during and 51% after vaccination (p=0.009). ZnT8QA frequency increased from 30% before to 34% during and 41% after vaccination (p=0.002). Our findings suggest that young (<3 years) along with DQ2/2; 2/X patients were low responders to Pandemrix(®) . As the proportion of DQ2/8 patients <3 years of age decreased after vaccination and the frequencies of GADA and ZnT8QA were enhanced, it cannot be excluded that the vaccine affected clinical onset of type 1 diabetes. This article is protected by copyright. All rights reserved.
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10.
  • Wegmann, Mathilde Gersel, et al. (författare)
  • The exon3-deleted growth hormone receptor gene polymorphism (d3-GHR) is associated with insulin and spontaneous growth in short SGA children (NESGAS)
  • 2017
  • Ingår i: Growth Hormone and IGF Research. - Elsevier. - 1096-6374. ; 35, s. 45-51
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective The effect of a common polymorphism in the Growth Hormone (GH) receptor (d3-GHR) gene on growth, metabolism and body composition was examined in short children born small for gestational age (SGA) on GH treatment. Design In 96 prepubertal, short SGA children treated with high-dose GH (67 μg/kg/day) in the NESGAS study, insulin sensitivity (IS), insulin secretion and disposition index (DI) were determined during the first year of treatment. Body composition was analysed by DXA. The d3-GHR locus was determined by simple multiplex PCR. Results At baseline, children in the d3-GHR group (d3/fl (n = 37), d3/d3 (n = 7)) had significantly lower IS (median (25–75 percentile)) (223.3% (154.4–304.8)) vs. (269.7% (185.1–356.7)) (p = 0.03) and higher concentrations of glucose (mean (SD)) (4.4 mmol/L (0.6) vs. 4.2 mmol/L (0.7)) (p = 0.03), C-peptide (232.1 pmol/L (168.8–304.1) vs. 185.1 pmol/L (137.7–253.9)) (p = 0.04) and insulin (19.2 pmol/L (11.8–32.2)) vs. (13.7 pmol/L (9.3–20.8)) (p = 0.04) compared to children homozygous for the full length allele (fl/fl-GHR (n = 52)). There were no differences in DI or insulin secretion. Postnatal, spontaneous growth was significantly greater in the d3-GHR group compared to the fl/fl-GHR group (p = 0.02). There were no significant differences in growth response, body composition or metabolism after one year of GH therapy. Conclusion Short SGA children carrying the d3-GHR polymorphism had increased spontaneous growth, lower IS and a compensatory increase in glucose, C-peptide and insulin before GH therapy compared to children homozygous for the full-length allele.
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