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- Frisk, G, et al.
(author)
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A unifying hypothesis on the development of type 1 diabetes and celiac disease : Gluten consumption may be a shared causative factor
- 2008
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In: Medical Hypotheses. - : Elsevier BV. - 0306-9877 .- 1532-2777. ; 70:6, s. 1207-1209
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Journal article (peer-reviewed)abstract
- This paper presents a hypothesis of the aetiology of the increasing incidence of type 1 diabetes (T1D). This together with the global increased incidence of celiac disease (CID) and that these increases cannot be explained by genetic factors suggest a common environmental factor for these two diseases. Even though enterovirus (EV) infections are believed to trigger T1D and gluten is the trigger of CD, the increasing intake of gluten containing products all over the world could be the trigger for both diseases directly and indirectly. It has been shown that the duration of exposure to gluten is related to the prevalence of T1D. It has also been shown that T1D patients at onset have an inflammatory reaction in the gut. Hence, early diagnose of CD followed by elimination of dietary gluten will lead to a decreased incidence of T1D.
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- Gyllenberg, A, et al.
(author)
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Variability in the CIITA gene interacts with HLA in multiple sclerosis.
- 2014
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In: Genes and immunity. - Stockholm : Springer Science and Business Media LLC. - 1476-5470 .- 1466-4879. ; 15, s. 162-167
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Journal article (peer-reviewed)abstract
- The human leukocyte antigen (HLA) is the main genetic determinant of multiple sclerosis (MS) risk. Within the HLA, the class II HLA-DRB1*15:01 allele exerts a disease-promoting effect, whereas the class I HLA-A*02 allele is protective. The CIITA gene is crucial for expression of class II HLA molecules and has previously been found to associate with several autoimmune diseases, including MS and type 1 diabetes. We here performed association analyses with CIITA in 2000 MS cases and up to 6900 controls as well as interaction analysis with HLA. We find that the previously investigated single-nucleotide polymorphism rs4774 is associated with MS risk in cases carrying the HLA-DRB1*15 allele (P=0.01, odds ratio (OR): 1.21, 95% confidence interval (CI): 1.04-1.40) or the HLA-A*02 allele (P=0.01, OR: 1.33, 95% CI: 1.07-1.64) and that these associations are independent of the adjacent confirmed MS susceptibility gene CLEC16A. We also confirm interaction between rs4774 and HLA-DRB1*15:01 such that individuals carrying the risk allele for rs4774 and HLA-DRB1*15:01 have a higher than expected risk for MS. In conclusion, our findings support previous data that variability in the CIITA gene affects MS risk, but also that the effect is modulated by MS-associated HLA haplotypes. These findings further underscore the biological importance of HLA for MS risk.Genes and Immunity advance online publication, 16 January 2014; doi:10.1038/gene.2013.71.
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- Landin-Olsson, Mona, et al.
(author)
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Immunoreactive trypsin(Ogen) in the sera of children with recent-onset insulin-dependent diabetes and matched controls
- 1990
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In: Pancreas. - : Ovid Technologies (Wolters Kluwer Health). - 0885-3177. ; 5:3, s. 241-247
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Journal article (peer-reviewed)abstract
- To evaluate the exocrine pancreatic function at the time of diagnosis of insulin-dependent diabetes mellitus, we determined immunoreactive an-odal and cathodal trypsin(ogen) levels in sera from almost all children (n = 375) 0-14 years of age in Sweden in whom diabetes developed during 1 year, and in sex-, age-, and geographically matched control subjects (n = 312). The median level of anodal trypsin(ogen) was 5 (quartile range, 3-7) µg/L in children with newly diagnosed diabetes, compared with a median level of 7 (quartile range, 4-8) µg/L in control subjects (p < 0.0001). Similarly, the median level of cathodal trypsin(ogen) was 8 (quartile range, 4-10) µg/L in children with diabetes, compared with a median level of 11 (quartile range, 7-15) µg/L in control subjects (p < 0.0001). The median of the individual ratios between cathodal and anodal trypsin(ogen) was 1.4 in the diabetic patients and 1.7 in the control children (p < 0.001). In a multivariate test, however, only the decrease in cathodal trypsin(ogen) concentration was associated with diabetes. The levels of trypsin(ogen)s did not correlate with levels of islet cell antibodies, present in 81% of the diabetic children. Several mechanisms may explain our findings, for example, similar pathogenetic factors may affect both the endocrine and exocrine pancreas simultaneously, a failing local trophic stimulation by insulin on the exocrine cells may decrease the trypsinogen production, and there may be an increased elimination of trypsin(ogen) because of higher filtration through the kidneys in the hyperglycemic state.
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- Neveus, T, et al.
(author)
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Enuresis - Background and treatment
- 2000
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In: SCANDINAVIAN JOURNAL OF UROLOGY AND NEPHROLOGY. - 0036-5599. ; 34, s. 1-44
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Research review (other academic/artistic)
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- Nevéus, T, et al.
(author)
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Enuresis--background and treatment
- 2000
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In: Scandinavian journal of urology and nephrology. Supplementum. - 0300-8886. ; :206, s. 1-44
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Journal article (peer-reviewed)
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- Barrenäs, Marie-Louise, 1952, et al.
(author)
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High risk of sensorineural hearing loss in men born small for gestational age with and without obesity or height catch-up growth: a prospective longitudinal register study on birth size in 245,000 Swedish conscripts
- 2005
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In: J Clin Endocrinol Metab. ; 90:8, s. 4452-6
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Journal article (peer-reviewed)abstract
- BACKGROUND: Several components of the metabolic syndrome coincide with those risk factors linked to sensorineural hearing loss (SNHL). According to the thrifty phenotype hypothesis, the metabolic syndrome can be caused by events during the fetal period. This study tests the thrifty phenotype hypothesis on hearing, using body size at birth and conscription as indirect markers for fetal programming and body mass index as an indicator for the metabolic syndrome. METHODS: Odds ratios were used to analyze birth data regarding body size from birth to conscription as risk factors for hearing loss in 245,092 conscripted Swedish men. FINDINGS: Compared with conscripts born short for gestational age with catch-up growth, those born short with absence of catch-up growth exhibited 134% higher risk of SNHL. Adult short stature was associated with a 50% increased risk. Compared with conscripts with average body mass index, overweight was associated with 30%, obesity with 99%, and overweight if born light for gestational age with 118% higher risk of SNHL. Conscripts born light for gestational age had a 41% increased risk, independent of the later growth pattern. CONCLUSION: The thrifty phenotype hypothesis also seems to be valid for SNHL, meaning that SNHL in adulthood may originate from events during fetal life. SNHL might be a new clinical feature of the metabolic syndrome.
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- Carlsson, A., et al.
(author)
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Prevalence of coeliac disease in Turner syndrome
- 1999
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In: Acta Pædiatrica. - 1651-2227 .- 0803-5253. ; 88, s. 933-
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Journal article (peer-reviewed)abstract
- This study was undertaken to investigate the prevalence of coeliac disease in children and adolescents with Turner syndrome. Eighty-seven children and adolescents with Turner syndrome were screened for IgA- antiendomysium antibodies (EMA) and IgA-antigliadin antibodies (AGA), 5% (4/87) being found to be EMA-positive, and 15% (13/87) to have AGA levels above normal. Of the 10 patients who were either AGA- or EMA-positive and further investigated with intestinal biopsy, four manifested villous atrophy (i.e. all three of the EMA-positive patients, but only one of the seven AGA- positive patients). The results suggest EMA-positivity to be a good immunological marker for use in screening for coeliac disease, and such screening to be justified in patients with Turner syndrome.
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