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1.	Forouzanfar, Mohammad H, et al. (författare) Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990-2013 : a systematic analysis for the Global Burden of Disease Study 2013. 2015 Ingår i: The Lancet. - 0140-6736 .- 1474-547X. ; 386:10010, s. 2287-2323 Tidskriftsartikel (refereegranskat)abstract BACKGROUND: The Global Burden of Disease, Injuries, and Risk Factor study 2013 (GBD 2013) is the first of a series of annual updates of the GBD. Risk factor quantification, particularly of modifiable risk factors, can help to identify emerging threats to population health and opportunities for prevention. The GBD 2013 provides a timely opportunity to update the comparative risk assessment with new data for exposure, relative risks, and evidence on the appropriate counterfactual risk distribution.METHODS: Attributable deaths, years of life lost, years lived with disability, and disability-adjusted life-years (DALYs) have been estimated for 79 risks or clusters of risks using the GBD 2010 methods. Risk-outcome pairs meeting explicit evidence criteria were assessed for 188 countries for the period 1990-2013 by age and sex using three inputs: risk exposure, relative risks, and the theoretical minimum risk exposure level (TMREL). Risks are organised into a hierarchy with blocks of behavioural, environmental and occupational, and metabolic risks at the first level of the hierarchy. The next level in the hierarchy includes nine clusters of related risks and two individual risks, with more detail provided at levels 3 and 4 of the hierarchy. Compared with GBD 2010, six new risk factors have been added: handwashing practices, occupational exposure to trichloroethylene, childhood wasting, childhood stunting, unsafe sex, and low glomerular filtration rate. For most risks, data for exposure were synthesised with a Bayesian meta-regression method, DisMod-MR 2.0, or spatial-temporal Gaussian process regression. Relative risks were based on meta-regressions of published cohort and intervention studies. Attributable burden for clusters of risks and all risks combined took into account evidence on the mediation of some risks such as high body-mass index (BMI) through other risks such as high systolic blood pressure and high cholesterol.FINDINGS: All risks combined account for 57·2% (95% uncertainty interval [UI] 55·8-58·5) of deaths and 41·6% (40·1-43·0) of DALYs. Risks quantified account for 87·9% (86·5-89·3) of cardiovascular disease DALYs, ranging to a low of 0% for neonatal disorders and neglected tropical diseases and malaria. In terms of global DALYs in 2013, six risks or clusters of risks each caused more than 5% of DALYs: dietary risks accounting for 11·3 million deaths and 241·4 million DALYs, high systolic blood pressure for 10·4 million deaths and 208·1 million DALYs, child and maternal malnutrition for 1·7 million deaths and 176·9 million DALYs, tobacco smoke for 6·1 million deaths and 143·5 million DALYs, air pollution for 5·5 million deaths and 141·5 million DALYs, and high BMI for 4·4 million deaths and 134·0 million DALYs. Risk factor patterns vary across regions and countries and with time. In sub-Saharan Africa, the leading risk factors are child and maternal malnutrition, unsafe sex, and unsafe water, sanitation, and handwashing. In women, in nearly all countries in the Americas, north Africa, and the Middle East, and in many other high-income countries, high BMI is the leading risk factor, with high systolic blood pressure as the leading risk in most of Central and Eastern Europe and south and east Asia. For men, high systolic blood pressure or tobacco use are the leading risks in nearly all high-income countries, in north Africa and the Middle East, Europe, and Asia. For men and women, unsafe sex is the leading risk in a corridor from Kenya to South Africa.INTERPRETATION: Behavioural, environmental and occupational, and metabolic risks can explain half of global mortality and more than one-third of global DALYs providing many opportunities for prevention. Of the larger risks, the attributable burden of high BMI has increased in the past 23 years. In view of the prominence of behavioural risk factors, behavioural and social science research on interventions for these risks should be strengthened. Many prevention and primary care policy options are available now to act on key risks.FUNDING: Bill & Melinda Gates Foundation.
2.	Kassebaum, Nicholas J., et al. (författare) Global, regional, and national disability-adjusted life-years (DALYs) for 315 diseases and injuries and healthy life expectancy (HALE), 1990-2015 : a systematic analysis for the Global Burden of Disease Study 2015 2016 Ingår i: The Lancet. - 0140-6736 .- 1474-547X. ; 388:10053, s. 1603-1658 Tidskriftsartikel (refereegranskat)abstract Background Healthy life expectancy (HALE) and disability-adjusted life-years (DALYs) provide summary measures of health across geographies and time that can inform assessments of epidemiological patterns and health system performance, help to prioritise investments in research and development, and monitor progress toward the Sustainable Development Goals (SDGs). We aimed to provide updated HALE and DALYs for geographies worldwide and evaluate how disease burden changes with development. Methods We used results from the Global Burden of Diseases, Injuries, and Risk Factors Study 2015 (GBD 2015) for all-cause mortality, cause-specific mortality, and non-fatal disease burden to derive HALE and DALYs by sex for 195 countries and territories from 1990 to 2015. We calculated DALYs by summing years of life lost (YLLs) and years of life lived with disability (YLDs) for each geography, age group, sex, and year. We estimated HALE using the Sullivan method, which draws from age-specific death rates and YLDs per capita. We then assessed how observed levels of DALYs and HALE differed from expected trends calculated with the Socio-demographic Index (SDI), a composite indicator constructed from measures of income per capita, average years of schooling, and total fertility rate. Findings Total global DALYs remained largely unchanged from 1990 to 2015, with decreases in communicable, neonatal, maternal, and nutritional (Group 1) disease DALYs off set by increased DALYs due to non-communicable diseases (NCDs). Much of this epidemiological transition was caused by changes in population growth and ageing, but it was accelerated by widespread improvements in SDI that also correlated strongly with the increasing importance of NCDs. Both total DALYs and age-standardised DALY rates due to most Group 1 causes significantly decreased by 2015, and although total burden climbed for the majority of NCDs, age-standardised DALY rates due to NCDs declined. Nonetheless, age-standardised DALY rates due to several high-burden NCDs (including osteoarthritis, drug use disorders, depression, diabetes, congenital birth defects, and skin, oral, and sense organ diseases) either increased or remained unchanged, leading to increases in their relative ranking in many geographies. From 2005 to 2015, HALE at birth increased by an average of 2.9 years (95% uncertainty interval 2.9-3.0) for men and 3.5 years (3.4-3.7) for women, while HALE at age 65 years improved by 0.85 years (0.78-0.92) and 1.2 years (1.1-1.3), respectively. Rising SDI was associated with consistently higher HALE and a somewhat smaller proportion of life spent with functional health loss; however, rising SDI was related to increases in total disability. Many countries and territories in central America and eastern sub-Saharan Africa had increasingly lower rates of disease burden than expected given their SDI. At the same time, a subset of geographies recorded a growing gap between observed and expected levels of DALYs, a trend driven mainly by rising burden due to war, interpersonal violence, and various NCDs. Interpretation Health is improving globally, but this means more populations are spending more time with functional health loss, an absolute expansion of morbidity. The proportion of life spent in ill health decreases somewhat with increasing SDI, a relative compression of morbidity, which supports continued efforts to elevate personal income, improve education, and limit fertility. Our analysis of DALYs and HALE and their relationship to SDI represents a robust framework on which to benchmark geography-specific health performance and SDG progress. Country-specific drivers of disease burden, particularly for causes with higher-than-expected DALYs, should inform financial and research investments, prevention efforts, health policies, and health system improvement initiatives for all countries along the development continuum.
3.	Abbafati, Cristiana, et al. (författare) 2020 Tidskriftsartikel (refereegranskat)
4.	Agardh, Daniel, et al. (författare) HLA-DQB10201/0302 is associated with severe retinopathy in patients with IDDM 1996 Ingår i:* Diabetologia. - : Springer Science and Business Media LLC. - 1432-0428 .- 0012-186X. ; 39:11, s. 1313-1317 Tidskriftsartikel (refereegranskat)abstract Some insulin-dependent diabetic (IDDM) patients develop severe forms of retinopathy. Putative risk factors such as hypertension, poor metabolic control, nephropathy and growth hormone levels do not fully explain the progress of retinopathy in these patients. It has been discussed whether there is a genetic marker, since some diabetic patients without any known predisposing risk factors develop severe retinopathy and others do not. In the present study, HLA-DR and DQ were compared in two patient groups with IDDM. One group consisted of patients with early-onset diabetes, with severe non-proliferative or proliferative retinopathy; the other group had no or only mild signs of retinopathy. High resolution HLA typing was carried out by polymerase chain reaction (PCR) and hybridization with allele specific probes. Alleles on the DR3-DQ2 haplotype, DRB10301, DQA10501 and DQB10201, were more frequent in patients with severe retinopathy. A difference was seen when combining certain alleles in the genotypes of DQA103/0501 (p > 0.05) and DQB10201/0302 (p < 0.01). The findings of the present study suggest that DQB10201/0302 is the strongest genetic marker for severe retinopathy and DRB10301/0401 only has a secondary influence when combined with this genotype. It seems as if IDDM patients who are positive for the genotype DR3-DQ2/DR4-DQ8 (DRB10301-DQA10501-DQB10201/DRB10401 -DQA103-DQB1*0302) are at greater risk of developing severe retinopathy.
5.	Agardh, Daniel, et al. (författare) Inverse relationship between GAD65 antibody levels and severe retinopathy in younger type 1 diabetic patients 1998 Ingår i: Diabetes Research and Clinical Practice. - 1872-8227. ; 40:1, s. 9-14 Tidskriftsartikel (refereegranskat)abstract Several risk factors for severe non-proliferative and proliferative retinopathy in type 1 diabetes mellitus have been proposed without explaining the rapid progression of retinopathy in some patients. Since GAD65 autoantibodies (GAD65Abs) are detected against glutamic acid decarboxylase (GAD), which is mainly expressed in islets and nervous tissue in type 1 diabetic patients, the aim of the present investigation was to test the hypothesis whether GAD65Abs are associated with rapidly progressing severe retinopathy. Patients with severe non-proliferative or proliferative retinopathy (n = 27) were compared with another group, which in spite of long diabetes duration had no or only mild signs of retinopathy (n = 28). GAD65Abs were analysed in a radioimmunoassay using in vitro translated human GAD65, and the levels were expressed as an index in relation to positive and negative reference samples. Using a cut-off level representing the 99th percentile of normals, 6/27 (22%) with and 9/28 (32%) without severe retinopathy were considered GAD65Ab positive. Although there was no difference in the number of GAD65Ab positive patients, the GAD65Ab levels were lower in patients with (0.30; 0.11-0.64) than without (0.68; 0.34-1.12) severe retinopathy (P = 0.03). The patients were also subjected to HLA-DR and DQ typing by PCR and hybridization with oligospecific probes. DQ2/8 was more common in patients with (56%) than without (29%) severe retinopathy (P = 0.05), but DQ2/8 could not account for the lower GAD65Ab levels in patients with severe retinopathy. It is concluded that GAD65Ab levels are inversely correlated with severe retinopathy in young type 1 diabetic patients.
6.	Wang, Haidong, et al. (författare) Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980-2015 : a systematic analysis for the Global Burden of Disease Study 2015 2016 Ingår i: The Lancet. - 0140-6736 .- 1474-547X. ; 388:10053, s. 1459-1544 Tidskriftsartikel (refereegranskat)abstract BACKGROUND: Improving survival and extending the longevity of life for all populations requires timely, robust evidence on local mortality levels and trends. The Global Burden of Disease 2015 Study (GBD 2015) provides a comprehensive assessment of all-cause and cause-specific mortality for 249 causes in 195 countries and territories from 1980 to 2015. These results informed an in-depth investigation of observed and expected mortality patterns based on sociodemographic measures.METHODS: We estimated all-cause mortality by age, sex, geography, and year using an improved analytical approach originally developed for GBD 2013 and GBD 2010. Improvements included refinements to the estimation of child and adult mortality and corresponding uncertainty, parameter selection for under-5 mortality synthesis by spatiotemporal Gaussian process regression, and sibling history data processing. We also expanded the database of vital registration, survey, and census data to 14 294 geography-year datapoints. For GBD 2015, eight causes, including Ebola virus disease, were added to the previous GBD cause list for mortality. We used six modelling approaches to assess cause-specific mortality, with the Cause of Death Ensemble Model (CODEm) generating estimates for most causes. We used a series of novel analyses to systematically quantify the drivers of trends in mortality across geographies. First, we assessed observed and expected levels and trends of cause-specific mortality as they relate to the Socio-demographic Index (SDI), a summary indicator derived from measures of income per capita, educational attainment, and fertility. Second, we examined factors affecting total mortality patterns through a series of counterfactual scenarios, testing the magnitude by which population growth, population age structures, and epidemiological changes contributed to shifts in mortality. Finally, we attributed changes in life expectancy to changes in cause of death. We documented each step of the GBD 2015 estimation processes, as well as data sources, in accordance with Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER).FINDINGS: Globally, life expectancy from birth increased from 61·7 years (95% uncertainty interval 61·4-61·9) in 1980 to 71·8 years (71·5-72·2) in 2015. Several countries in sub-Saharan Africa had very large gains in life expectancy from 2005 to 2015, rebounding from an era of exceedingly high loss of life due to HIV/AIDS. At the same time, many geographies saw life expectancy stagnate or decline, particularly for men and in countries with rising mortality from war or interpersonal violence. From 2005 to 2015, male life expectancy in Syria dropped by 11·3 years (3·7-17·4), to 62·6 years (56·5-70·2). Total deaths increased by 4·1% (2·6-5·6) from 2005 to 2015, rising to 55·8 million (54·9 million to 56·6 million) in 2015, but age-standardised death rates fell by 17·0% (15·8-18·1) during this time, underscoring changes in population growth and shifts in global age structures. The result was similar for non-communicable diseases (NCDs), with total deaths from these causes increasing by 14·1% (12·6-16·0) to 39·8 million (39·2 million to 40·5 million) in 2015, whereas age-standardised rates decreased by 13·1% (11·9-14·3). Globally, this mortality pattern emerged for several NCDs, including several types of cancer, ischaemic heart disease, cirrhosis, and Alzheimer's disease and other dementias. By contrast, both total deaths and age-standardised death rates due to communicable, maternal, neonatal, and nutritional conditions significantly declined from 2005 to 2015, gains largely attributable to decreases in mortality rates due to HIV/AIDS (42·1%, 39·1-44·6), malaria (43·1%, 34·7-51·8), neonatal preterm birth complications (29·8%, 24·8-34·9), and maternal disorders (29·1%, 19·3-37·1). Progress was slower for several causes, such as lower respiratory infections and nutritional deficiencies, whereas deaths increased for others, including dengue and drug use disorders. Age-standardised death rates due to injuries significantly declined from 2005 to 2015, yet interpersonal violence and war claimed increasingly more lives in some regions, particularly in the Middle East. In 2015, rotaviral enteritis (rotavirus) was the leading cause of under-5 deaths due to diarrhoea (146 000 deaths, 118 000-183 000) and pneumococcal pneumonia was the leading cause of under-5 deaths due to lower respiratory infections (393 000 deaths, 228 000-532 000), although pathogen-specific mortality varied by region. Globally, the effects of population growth, ageing, and changes in age-standardised death rates substantially differed by cause. Our analyses on the expected associations between cause-specific mortality and SDI show the regular shifts in cause of death composition and population age structure with rising SDI. Country patterns of premature mortality (measured as years of life lost [YLLs]) and how they differ from the level expected on the basis of SDI alone revealed distinct but highly heterogeneous patterns by region and country or territory. Ischaemic heart disease, stroke, and diabetes were among the leading causes of YLLs in most regions, but in many cases, intraregional results sharply diverged for ratios of observed and expected YLLs based on SDI. Communicable, maternal, neonatal, and nutritional diseases caused the most YLLs throughout sub-Saharan Africa, with observed YLLs far exceeding expected YLLs for countries in which malaria or HIV/AIDS remained the leading causes of early death.INTERPRETATION: At the global scale, age-specific mortality has steadily improved over the past 35 years; this pattern of general progress continued in the past decade. Progress has been faster in most countries than expected on the basis of development measured by the SDI. Against this background of progress, some countries have seen falls in life expectancy, and age-standardised death rates for some causes are increasing. Despite progress in reducing age-standardised death rates, population growth and ageing mean that the number of deaths from most non-communicable causes are increasing in most countries, putting increased demands on health systems.
7.	Agardh, Daniel, et al. (författare) Coeliac disease-specific tissue transglutaminase autoantibodies are associated with osteoporosis and related fractures in middle-aged women 2009 Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 44:5, s. 571-578 Tidskriftsartikel (refereegranskat)abstract Objective. To investigate whether the serological marker for coeliac disease, tissue transglutaminase autoantibody (tTGAb), is associated with decreased bone mass density (BMD) and increased frequency of fractures in middle-aged women screened for osteoporosis. Material and methods. The study comprised 6480 women (mean age 56 years, range 50-64) who answered a number of questionnaires and who underwent dual X-ray absorptiometry of the wrist bone. Serum samples were analysed for tTGAb using radioligand binding assays. A tTGAb level of 4 U/ml was used to determine a positive value and a level of 17 U/ml was used as an alternative discrimination of high levels. Results. A tTGAb level 4 U/ml was found among 90/6480 (1.4%) women and correlated with lower BMD (multiple linear regression coefficient -382.1; 95% CI = - 673.6-90.7, p=0.011) and with fracture frequency (r=0.18, p=0.023). The 59 women with tTGAb levels 17 U/ml had a lower BMD (0.410.08 g/cm2 versus 0.440.08 g/cm2, p=0.001) and a lower T-score (-1.401.28 versus -0.901.40, p=0.003) as well as a higher prevalence of osteoporosis (13.4% versus 6.5%, p=0.008) compared with the remaining 6421 women with tTGAb levels 17 U/ml. Furthermore, fracture frequency was more pronounced in women with tTGAb levels 17 U/ml, among whom 19/59 (32.2%) had fractures during the study period compared with 1204/6421 (18.8%) among women with tTGAb levels 17 U/ml (p=0.009). Conclusions. High levels of tTGAb indicating coeliac disease are associated with lower BMD and higher fracture frequency in women between 50 and 64 years of age. Osteometry is therefore warranted in middle-aged women detected with tTGAb.
8.	Alshiekh, Shehab, et al. (författare) High-resolution genotyping indicates that children with type 1 diabetes and celiac disease share three HLA class II loci in DRB3, DRB4 and DRB5 genes 2021 Ingår i: HLA: Immune Response Genetics. - : Wiley. - 2059-2302. ; 97:1, s. 44-51 Tidskriftsartikel (refereegranskat)abstract Type 1 diabetes (T1D) and celiac disease (CD) share common genetic loci, mainly within the human leukocyte antigen (HLA) class II complex. Extended genotyping of HLA class II alleles and their potential risk for developing both diseases remains to be studied. The present study compared extended HLA-class II gene polymorphisms in children with T1D, CD, and a subgroup diagnosed with both diseases (T1D w/CD). Next-generation targeted sequencing (NGTS) of HLA-DRB3, DRB4, DRB5, DRB1, DQA1, DQB1, DPA1, and DPB1 alleles from DNA collected from 68 T1D, 219 CD, and seven T1D w/CD patients were compared with 636 HLA-genotyped Swedish children from the general population selected as controls. In comparison to controls, the DRB401:03:01 allele occurred more frequently in T1D w/CD (odds ratio (OR) = 7.84; 95% confidence interval (95% CI) = (2.24, 34.5), P = 0.0002) and T1D (OR = 3.86; 95% CI, (2.69, 5.55), P = 1.07 × 10−14), respectively. The DRB301:01:02 allele occurred more frequently in CD as compared to controls (OR = 7.87; 95% CI, (6.17, 10.03), P = 4.24 × 10−71), but less frequently in T1D (OR = 2.59; 95% CI, (1.76, 3.81), P = 7.29 × 10−07) and T1D w/CD (OR = 0.87; 95% CI, (0.09, 3.96), P ≤ 0.999). The frequency of the DRB401:03:01-DRB104:01:01-DQA103:01:01-DQB103:02:01 (DR4-DQ8) haplotype was higher in T1D w/CD (OR = 12.88; 95% CI (4.35, 38.14) P = 3.75 × 10−9), and moderately higher in T1D (OR = 2.13; 95% CI (1.18, 3.83) P = 0.01) compared with controls, but comparable in CD (OR = 1.45; 95% CI (0.94, 2.21), P = 0.08) and controls. Children with T1D and CD are associated with DRB401:03:01, DRB301:01:02, and DRB302:02:01 of which DRB401:03:01 confers the strongest risk allele for developing T1D w/CD.
9.	Alshiekh, Shehab, et al. (författare) High-resolution genotyping of HLA class I loci in children with type 1 diabetes and celiac disease 2021 Ingår i: HLA: Immune Response Genetics. - : Wiley. - 2059-2302. ; 97:6, s. 505-511 Tidskriftsartikel (refereegranskat)abstract Objectives: HLA-DQ2 and DQ8 contribute to the strongest risk haplotypes for type 1 diabetes (T1D) and celiac disease (CD). The variation in genetic risk association is likely linked to different HLA class II loci susceptibility, but association studies of HLA class I alleles are scarce. The aim was to investigate HLA class I A, B, and C alleles polymorphisms in children with only T1D, CD, and a subgroup with both T1D and CD (T1D w/CD). Materials and methods: HLA class I A, B, and C genes were genotyped using next-generation targeted sequencing. A conditional analysis was performed on 68 children with T1D, 219 children with CD and seven children with T1D w/CD enrolled from a birth cohort study at high genetic risk children from the South of Sweden. Results: Among 1764 HLA class I allele variants, A29:02:01 in T1D w/CD was associated with both T1D (OR = 21.42 [1.05, 1322.4], p = 0.0231) and CD (OR = 35 [2.36, 529.12], p = 0.0051) along with C05:01:01 with both T1D (OR = 5.54 [1.06, 24.8], p = 0.02) and CD (OR = 6.84 [1.46, 26.01], p = 0.0077). No independent effects of HLA-B allele associations were observed in T1D w/CD. Conclusion: Although the distribution of HLA class I alleles differs between children with T1D and CD, the A29:02:01 and C05:01:01 alleles showed shared risk association of both diseases.
10.	Auchtung, Thomas A, et al. (författare) Temporal changes in gastrointestinal fungi and the risk of autoimmunity during early childhood : the TEDDY study 2022 Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 13 Tidskriftsartikel (refereegranskat)abstract Fungal infections are a major health problem that often begin in the gastrointestinal tract. Gut microbe interactions in early childhood are critical for proper immune responses, yet there is little known about the development of the fungal population from infancy into childhood. Here, as part of the TEDDY (The Environmental Determinants of Diabetes in the Young) study, we examine stool samples of 888 children from 3 to 48 months and find considerable differences between fungi and bacteria. The metagenomic relative abundance of fungi was extremely low but increased while weaning from milk and formula. Overall fungal diversity remained constant over time, in contrast with the increase in bacterial diversity. Fungal profiles had high temporal variation, but there was less variation from month-to-month in an individual than among different children of the same age. Fungal composition varied with geography, diet, and the use of probiotics. Multiple Candida spp. were at higher relative abundance in children than adults, while Malassezia and certain food-associated fungi were lower in children. There were only subtle fungal differences associated with the subset of children that developed islet autoimmunity or type 1 diabetes. Having proper fungal exposures may be crucial for children to establish appropriate responses to fungi and limit the risk of infection: the data here suggests those gastrointestinal exposures are limited and variable.
11.	Griswold, Max G., et al. (författare) Alcohol use and burden for 195 countries and territories, 1990-2016 : a systematic analysis for the Global Burden of Disease Study 2016 2018 Ingår i: The Lancet. - : Elsevier. - 0140-6736 .- 1474-547X. ; 392:10152, s. 1015-1035 Tidskriftsartikel (refereegranskat)abstract Background: Alcohol use is a leading risk factor for death and disability, but its overall association with health remains complex given the possible protective effects of moderate alcohol consumption on some conditions. With our comprehensive approach to health accounting within the Global Burden of Diseases, Injuries, and Risk Factors Study 2016, we generated improved estimates of alcohol use and alcohol-attributable deaths and disability-adjusted life-years (DALYs) for 195 locations from 1990 to 2016, for both sexes and for 5-year age groups between the ages of 15 years and 95 years and older.Methods: Using 694 data sources of individual and population-level alcohol consumption, along with 592 prospective and retrospective studies on the risk of alcohol use, we produced estimates of the prevalence of current drinking, abstention, the distribution of alcohol consumption among current drinkers in standard drinks daily (defined as 10 g of pure ethyl alcohol), and alcohol-attributable deaths and DALYs. We made several methodological improvements compared with previous estimates: first, we adjusted alcohol sales estimates to take into account tourist and unrecorded consumption; second, we did a new meta-analysis of relative risks for 23 health outcomes associated with alcohol use; and third, we developed a new method to quantify the level of alcohol consumption that minimises the overall risk to individual health.Findings: Globally, alcohol use was the seventh leading risk factor for both deaths and DALYs in 2016, accounting for 2.2% (95% uncertainty interval [UI] 1.5-3.0) of age-standardised female deaths and 6.8% (5.8-8.0) of age-standardised male deaths. Among the population aged 15-49 years, alcohol use was the leading risk factor globally in 2016, with 3.8% (95% UI 3.2-4-3) of female deaths and 12.2% (10.8-13-6) of male deaths attributable to alcohol use. For the population aged 15-49 years, female attributable DALYs were 2.3% (95% UI 2.0-2.6) and male attributable DALYs were 8.9% (7.8-9.9). The three leading causes of attributable deaths in this age group were tuberculosis (1.4% [95% UI 1. 0-1. 7] of total deaths), road injuries (1.2% [0.7-1.9]), and self-harm (1.1% [0.6-1.5]). For populations aged 50 years and older, cancers accounted for a large proportion of total alcohol-attributable deaths in 2016, constituting 27.1% (95% UI 21.2-33.3) of total alcohol-attributable female deaths and 18.9% (15.3-22.6) of male deaths. The level of alcohol consumption that minimised harm across health outcomes was zero (95% UI 0.0-0.8) standard drinks per week.Interpretation: Alcohol use is a leading risk factor for global disease burden and causes substantial health loss. We found that the risk of all-cause mortality, and of cancers specifically, rises with increasing levels of consumption, and the level of consumption that minimises health loss is zero. These results suggest that alcohol control policies might need to be revised worldwide, refocusing on efforts to lower overall population-level consumption.
12.	Landegren, Nils, et al. (författare) A gene-centric approach to biomarker discovery identifies transglutaminase 1 as an epidermal autoantigen 2021 Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 118:51 Tidskriftsartikel (refereegranskat)abstract Autoantigen discovery is a critical challenge for the understanding and diagnosis of autoimmune diseases. While autoantibody markers in current clinical use have been identified through studies focused on individual disorders, we postulated that a reverse approach starting with a putative autoantigen to explore multiple disorders might hold promise. We here targeted the epidermal protein transglutaminase 1 (TGM1) as a member of a protein family prone to autoimmune attack. By screening sera from patients with various acquired skin disorders, we identified seropositive subjects with the blistering mucocutaneous disease paraneoplastic pemphigus. Validation in further subjects confirmed TGM1 autoantibodies as a 55% sensitive and 100% specific marker for paraneoplastic pemphigus. This gene-centric approach leverages the wealth of data available for human genes and may prove generally applicable for biomarker discovery in autoimmune diseases.
13.	Lundgren, Markus, et al. (författare) Analgesic antipyretic use among young children in the TEDDY study : No association with islet autoimmunity 2017 Ingår i: BMC Pediatrics. - : Springer Science and Business Media LLC. - 1471-2431. ; 17:1 Tidskriftsartikel (refereegranskat)abstract Background: The use of analgesic antipyretics (ANAP) in children have long been a matter of controversy. Data on their practical use on an individual level has, however, been scarce. There are indications of possible effects on glucose homeostasis and immune function related to the use of ANAP. The aim of this study was to analyze patterns of analgesic antipyretic use across the clinical centers of The Environmental Determinants of Diabetes in the Young (TEDDY) prospective cohort study and test if ANAP use was a risk factor for islet autoimmunity. Methods: Data were collected for 8542 children in the first 2.5 years of life. Incidence was analyzed using logistic regression with country and first child status as independent variables. Holm's procedure was used to adjust for multiplicity of intercountry comparisons. Time to autoantibody seroconversion was analyzed using a Cox proportional hazards model with cumulative analgesic use as primary time dependent covariate of interest. For each categorization, a generalized estimating equation (GEE) approach was used. Results: Higher prevalence of ANAP use was found in the U.S. (95.7%) and Sweden (94.8%) compared to Finland (78.1%) and Germany (80.2%). First-born children were more commonly given acetaminophen (OR 1.26; 95% CI 1.07, 1.49; p = 0.007) but less commonly Non-Steroidal Anti-inflammatory Drugs (NSAID) (OR 0.86; 95% CI 0.78, 0.95; p = 0.002). Acetaminophen and NSAID use in the absence of fever and infection was more prevalent in the U.S. (40.4%; 26.3% of doses) compared to Sweden, Finland and Germany (p < 0.001). Acetaminophen or NSAID use before age 2.5 years did not predict development of islet autoimmunity by age 6 years (HR 1.02, 95% CI 0.99-1.09; p = 0.27). In a sub-analysis, acetaminophen use in children with fever weakly predicted development of islet autoimmunity by age 3 years (HR 1.05; 95% CI 1.01-1.09; p = 0.024). Conclusions: ANAP use in young children is not a risk factor for seroconversion by age 6 years. Use of ANAP is widespread in young children, and significantly higher in the U.S. compared to other study sites, where use is common also in absence of fever and infection.
14.	Naghavi, Mohsen, et al. (författare) Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013 2015 Ingår i: The Lancet. - 1474-547X .- 0140-6736. ; 385:9963, s. 117-171 Tidskriftsartikel (refereegranskat)abstract Background Up-to-date evidence on levels and trends for age-sex-specifi c all-cause and cause-specifi c mortality is essential for the formation of global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013) we estimated yearly deaths for 188 countries between 1990, and 2013. We used the results to assess whether there is epidemiological convergence across countries. Methods We estimated age-sex-specifi c all-cause mortality using the GBD 2010 methods with some refinements to improve accuracy applied to an updated database of vital registration, survey, and census data. We generally estimated cause of death as in the GBD 2010. Key improvements included the addition of more recent vital registration data for 72 countries, an updated verbal autopsy literature review, two new and detailed data systems for China, and more detail for Mexico, UK, Turkey, and Russia. We improved statistical models for garbage code redistribution. We used six different modelling strategies across the 240 causes; cause of death ensemble modelling (CODEm) was the dominant strategy for causes with sufficient information. Trends for Alzheimer's disease and other dementias were informed by meta-regression of prevalence studies. For pathogen-specifi c causes of diarrhoea and lower respiratory infections we used a counterfactual approach. We computed two measures of convergence (inequality) across countries: the average relative difference across all pairs of countries (Gini coefficient) and the average absolute difference across countries. To summarise broad findings, we used multiple decrement life-tables to decompose probabilities of death from birth to exact age 15 years, from exact age 15 years to exact age 50 years, and from exact age 50 years to exact age 75 years, and life expectancy at birth into major causes. For all quantities reported, we computed 95% uncertainty intervals (UIs). We constrained cause-specific fractions within each age-sex-country-year group to sum to all-cause mortality based on draws from the uncertainty distributions. Findings Global life expectancy for both sexes increased from 65.3 years (UI 65.0-65.6) in 1990, to 71.5 years (UI 71.0-71.9) in 2013, while the number of deaths increased from 47.5 million (UI 46.8-48.2) to 54.9 million (UI 53.6-56.3) over the same interval. Global progress masked variation by age and sex: for children, average absolute diff erences between countries decreased but relative diff erences increased. For women aged 25-39 years and older than 75 years and for men aged 20-49 years and 65 years and older, both absolute and relative diff erences increased. Decomposition of global and regional life expectancy showed the prominent role of reductions in age-standardised death rates for cardiovascular diseases and cancers in high-income regions, and reductions in child deaths from diarrhoea, lower respiratory infections, and neonatal causes in low-income regions. HIV/AIDS reduced life expectancy in southern sub-Saharan Africa. For most communicable causes of death both numbers of deaths and age-standardised death rates fell whereas for most non-communicable causes, demographic shifts have increased numbers of deaths but decreased age-standardised death rates. Global deaths from injury increased by 10.7%, from 4.3 million deaths in 1990 to 4.8 million in 2013; but age-standardised rates declined over the same period by 21%. For some causes of more than 100 000 deaths per year in 2013, age-standardised death rates increased between 1990 and 2013, including HIV/AIDS, pancreatic cancer, atrial fibrillation and flutter, drug use disorders, diabetes, chronic kidney disease, and sickle-cell anaemias. Diarrhoeal diseases, lower respiratory infections, neonatal causes, and malaria are still in the top five causes of death in children younger than 5 years. The most important pathogens are rotavirus for diarrhoea and pneumococcus for lower respiratory infections. Country-specific probabilities of death over three phases of life were substantially varied between and within regions. Interpretation For most countries, the general pattern of reductions in age-sex specifi c mortality has been associated with a progressive shift towards a larger share of the remaining deaths caused by non-communicable disease and injuries. Assessing epidemiological convergence across countries depends on whether an absolute or relative measure of inequality is used. Nevertheless, age-standardised death rates for seven substantial causes are increasing, suggesting the potential for reversals in some countries. Important gaps exist in the empirical data for cause of death estimates for some countries; for example, no national data for India are available for the past decade.
15.	Vos, Theo, et al. (författare) Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013 2015 Ingår i: The Lancet. - 1474-547X .- 0140-6736. ; 386:9995, s. 743-800 Tidskriftsartikel (refereegranskat)abstract Background Up-to-date evidence about levels and trends in disease and injury incidence, prevalence, and years lived with disability (YLDs) is an essential input into global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013), we estimated these quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013. Methods Estimates were calculated for disease and injury incidence, prevalence, and YLDs using GBD 2010 methods with some important refinements. Results for incidence of acute disorders and prevalence of chronic disorders are new additions to the analysis. Key improvements include expansion to the cause and sequelae list, updated systematic reviews, use of detailed injury codes, improvements to the Bayesian meta-regression method (DisMod-MR), and use of severity splits for various causes. An index of data representativeness, showing data availability, was calculated for each cause and impairment during three periods globally and at the country level for 2013. In total, 35 620 distinct sources of data were used and documented to calculated estimates for 301 diseases and injuries and 2337 sequelae. The comorbidity simulation provides estimates for the number of sequelae, concurrently, by individuals by country, year, age, and sex. Disability weights were updated with the addition of new population-based survey data from four countries. Findings Disease and injury were highly prevalent; only a small fraction of individuals had no sequelae. Comorbidity rose substantially with age and in absolute terms from 1990 to 2013. Incidence of acute sequelae were predominantly infectious diseases and short-term injuries, with over 2 billion cases of upper respiratory infections and diarrhoeal disease episodes in 2013, with the notable exception of tooth pain due to permanent caries with more than 200 million incident cases in 2013. Conversely, leading chronic sequelae were largely attributable to non-communicable diseases, with prevalence estimates for asymptomatic permanent caries and tension-type headache of 2.4 billion and 1.6 billion, respectively. The distribution of the number of sequelae in populations varied widely across regions, with an expected relation between age and disease prevalence. YLDs for both sexes increased from 537.6 million in 1990 to 764.8 million in 2013 due to population growth and ageing, whereas the age-standardised rate decreased little from 114.87 per 1000 people to 110.31 per 1000 people between 1990 and 2013. Leading causes of YLDs included low back pain and major depressive disorder among the top ten causes of YLDs in every country. YLD rates per person, by major cause groups, indicated the main drivers of increases were due to musculoskeletal, mental, and substance use disorders, neurological disorders, and chronic respiratory diseases; however HIV/AIDS was a notable driver of increasing YLDs in sub-Saharan Africa. Also, the proportion of disability-adjusted life years due to YLDs increased globally from 21.1% in 1990 to 31.2% in 2013. Interpretation Ageing of the world's population is leading to a substantial increase in the numbers of individuals with sequelae of diseases and injuries. Rates of YLDs are declining much more slowly than mortality rates. The non-fatal dimensions of disease and injury will require more and more attention from health systems. The transition to non-fatal outcomes as the dominant source of burden of disease is occurring rapidly outside of sub-Saharan Africa. Our results can guide future health initiatives through examination of epidemiological trends and a better understanding of variation across countries.
16.	Adlercreutz, Emma, et al. (författare) A gluten free diet lowers NKG2D and ligand expression in BALB/c and NOD mice. 2014 Ingår i: Clinical and Experimental Immunology. - : Oxford University Press (OUP). - 0009-9104 .- 1365-2249. ; 177:2, s. 391-403 Tidskriftsartikel (refereegranskat)abstract The interplay between diet and immune-parameters which could affect type 1 diabetes (T1D) pathogenesis is not sufficiently clarified. Intestinal upregulation of the activating receptor NKG2D(CD314) and its ligands is a hallmark of celiac disease (CD). However, the direct effect of gluten on NKG2D expression is not known. We studied, by FACS (lymphoid tissues) and RT-qPCR (intestine and pancreatic islets), if a gluten-free diet from 4 weeks (GF diet) or a gluten-free diet introduced in breeding pairs (SGF diet), induces changes in NKG2D expression on NK-cells DX5(+) (CD49b) and CD8(+) T-cells, as well as in intestinal and islet levels of NKG2D and ligands in BALB/c and NOD mice. Gluten-free NOD mice had lower insulitis (p<0.0001). Gluten-free NOD mice had reduced expression of NKG2D on DX5(+) NK-cells in spleen and auricular lymph nodes (p<0.05) and on CD8(+) T-cells in pancreas associated lymph nodes (p=0.04). Moreover, the level of CD71 on DX5(+) NK-cells and CD8(+) T-cells (p<0.005) was markedly reduced. GF and SGF mice had reduced expression of NKG2D and DX5 mRNA in intestine (p<0.05). Differences in intestinal mRNA expression were found in mice of 8, 13 and 20 weeks. Intestinal expression of NKG2D ligands was reduced in SGF mice with lower expression of all ligands. In isolated islets, a SGF diet induced a higher expression of specific NKG2D ligands. Our data shows that a gluten-free diet reduces the level of NKG2D and the expression of NKG2D ligands. These immunological changes may contribute to the lower T1D incidence associated with a gluten-free diet.
17.	Adlercreutz, Emma, et al. (författare) Perinatal risk factors increase the risk of being affected by both type 1 diabetes and celiac disease. 2015 Ingår i: Acta Pædiatrica. - : Wiley. - 1651-2227 .- 0803-5253. ; 104:2, s. 178-184 Tidskriftsartikel (refereegranskat)abstract This study investigated whether perinatal factors influenced the risk of a double diagnosis of type 1 diabetes and celiac disease.
18.	Adlercreutz, Emma, et al. (författare) Prevalence of celiac disease autoimmunity in children with type 1 diabetes: regional variations across the Øresund strait between Denmark and southernmost Sweden. 2015 Ingår i: Pediatric Diabetes. - : Hindawi Limited. - 1399-543X. ; 16:7, s. 504-509 Tidskriftsartikel (refereegranskat)abstract The aim was to determine the prevalence of celiac disease autoimmunity in children with type 1 diabetes (T1D) diagnosed in Denmark and Sweden.
19.	Agardh, Daniel (författare) Antibodies Against Synthetic Deamidated Gliadin Peptides and Tissue Transglutaminase for the Identification of Childhood Celiac Disease. 2007 Ingår i: Clinical Gastroenterology and Hepatology. - : Elsevier BV. - 1542-7714 .- 1542-3565. ; 5, s. 1276-1281 Tidskriftsartikel (refereegranskat)abstract Abstract is not available
20.	Agardh, Daniel, et al. (författare) Autoantibodies Against Soluble and Immobilized Human Recombinant Tissue Transglutaminase in Children with Celiac Disease. 2005 Ingår i: Journal of Pediatric Gastroenterology and Nutrition - Jpgn. - : Ovid Technologies (Wolters Kluwer Health). - 1536-4801 .- 0277-2116. ; 41:3, s. 322-327 Tidskriftsartikel (refereegranskat)abstract Objectives: The conformation of tissue transglutaminase might influence the performance of immunoassays to detect autoantibodies from patients with celiac disease. The present study investigated how the exposure of tissue transglutaminase kept in a liquid phase and fixed to a solid support affected the binding of immunoglobulin (Ig)A and IgG autoantibodies in children with untreated and treated celiac disease. Methods: Included were 73 untreated celiac disease children, 50 controls and 80 children with treated celiac disease. IgA and IgG antitissue transglutaminase were measured with solid phase enzyme-linked immunoassay (ELISA) and liquid phase radioligand binding assays. For IgG antitissue transglutaminase detection with radioligand binding assays antihuman IgG and protein A were used. IgA endomysial autoantibodies were measured by indirect immunofluorescence. Results: Both ELISA and radioligand binding assays detected IgA antitissue transglutaminase in 65 of 73 untreated celiac disease children and in 2 of 50 controls. One additional control child was detected with radioligand binding assays. Endomysial autoantibodies were present in 62 of 73 celiac disease children and in 2 of 50 controls. IgG antitissue transglutaminase was detected with both ELISA and radioligand binding assays in 40 of 73 untreated celiac disease children and in 2 of 50 controls. Radioligand binding assays using protein A detected 20 of 73 additional untreated celiac disease children and one control child with increased IgG antitissue transglutaminase. In treated celiac disease children, 21 of 80 were IgA antitissue transglutaminase positive with radioligand binding assays, 3 of 80 with ELISA, whereas none had endomysial autoantibodies. Conclusions: No qualitative differences between radioligand binding assays and ELISA in IgA or IgG antitissue transglutaminase binding from untreated celiac disease children was demonstrated. However, discrepancies in the binding of IgA antitissue transglutaminase from a subgroup of treated celiac disease children indicated that alterations of tissue transglutaminase might occur on fixation of the antigen. Protein A used for radioligand binding assays seemed not to assess IgG autoantibodies exclusively. IgA antitissue transglutaminase detection in screening of childhood celiac disease can be performed either by ELISA or radioligand binding assays because the two assays are interchangeable.
21.	Agardh, Daniel, et al. (författare) Calcium activation of tissue transglutaminase in radioligand binding and enzyme-linked autoantibody immunoassays in childhood celiac disease. 2005 Ingår i: Clinica Chimica Acta. - : Elsevier BV. - 0009-8981. ; 358:1-2, s. 95-103 Tidskriftsartikel (refereegranskat)abstract Background Conflicting data have been published concerning the effect of calcium on binding of autoantibodies to tissue transglutaminase (tTG) in celiac disease (CD). Methods IgA-tTG and IgG-tTG were measured with radioligand binding assays (RBA) using human recombinant (hr) 35S-tTG produced in lysate of rabbit reticulocytes and with guinea pig (gp) tTG ELISA in 51 CD children (median: 5.7 years) and 35 controls (median: 2.2 years). Assays were performed with and without calcium. Results In hr-tTG RBA, IgA-tTG levels remained unchanged after calcium detecting 50/51 CD children and 1/35 controls (p < 0.0001). IgG-tTG levels decreased with calcium (p < 0.0001) in CD children and detected 48/51 with and 49/51 without calcium as compared to 1/35 controls (p < 0.0001). In gp-tTG ELISA, levels increased with calcium (p < 0.0001) making it possible to detect an additional three to a total of 50/51 with IgA-tTG and 13 to 39/51 CD children with IgG-tTG compared to 4/35 and 8/35 controls (respectively, p < 0.0001). Rabbit reticulocytes displayed calcium-dependent tTG activity. Conclusions Calcium increased binding of IgA-tTG and IgG-tTG in the ELISA test. The reverse effect observed in RBA may be explained by competitive binding between calcium activated native rabbit reticulocyte tTG and hr 35S-tTG. tTG autoantibody assays may need taking calcium into account for accurate diagnostic sensitivity and specificity for CD.
22.	Agardh, Daniel, et al. (författare) Clinical Features of Celiac Disease: A Prospective Birth Cohort. 2015 Ingår i: Pediatrics. - : American Academy of Pediatrics (AAP). - 1098-4275 .- 0031-4005. ; 135:4, s. 627-634 Tidskriftsartikel (refereegranskat)abstract To investigate clinical features of celiac disease (CD) and their association with risk factors for CD in a genetic risk birth cohort.
23.	Agardh, Daniel, et al. (författare) In reply : Efficiency of Deamidated Gliadin Peptides for Screening Celiac Disease Autoimmunity 2018 Ingår i: JAMA Pediatrics. - : American Medical Association (AMA). - 2168-6203. ; 172:5 Tidskriftsartikel (refereegranskat)
24.	Agardh, Daniel, et al. (författare) Prediction of silent celiac disease at diagnosis of childhood type 1 diabetes by tissue transglutaminase autoantibodies and HLA 2001 Ingår i: Pediatric Diabetes. - : Hindawi Limited. - 1399-543X. ; 2:2, s. 58-65 Tidskriftsartikel (refereegranskat)abstract Aims: The aims were to estimate the diagnostic sensitivity and specificity of autoantibodies to tissue transglutaminase (IgA- and IgG-tTG), gliadin (AGA) and endomysium (EMA) in relation to human leukocyte antigen (HLA)-DQB1 alleles to identify silent celiac disease at diagnosis of type 1 diabetes. Methods: IgA- and IgG-tTG were measured in radioligand binding assays in 165 type 1 diabetic patients. Data on HLA-DQB1 were available for 148 patients and on both AGA and EMA for 164 patients. For patients considered positive for AGA or EMA, or both, an intestinal biopsy was suggested. HLA-DQB1 typing was carried out by polymerase chain reaction and hybridization with allele specific probes. Results: Three patients, left out from further study of antibodies, but not from HLA-DQB1 analysis, had treated celiac disease at diagnosis. Out of the other 162 type 1 diabetic patients tested, nine had IgA-tTG, six IgG-tTG, eight EMA, and 11 AGA. Biopsy was suggested for nine patients, of whom six showed villous atrophy, one did not and two refused to participate. Thus, silent celiac disease was probable in 8/162 and biopsy-verified in 6/162, where five patients were AGA-positive and six either EMA-, IgA-tTG- or IgG-tTG-positive. Of the 11 patients with celiac disease (three with treated and eight with silent celiac disease), 10 were HLA-DQB1-typed, of whom 65% (13/20) had the DQB102 allele, compared with 36% (100/276; p = 0.011) of those without celiac disease. IgA-tTG levels were higher in patients having either 02 or 0302 (0.6; −1.3–112.4 RU) compared with those not having these alleles (0.4; −0.7–3.4 RU; p = 0.023). Conclusion: IgA-tTG are HLA-DQB102-associated autoantibodies with high sensitivity and specificity for silent celiac disease at diagnosis of type 1 diabetes.
25.	Agardh, Daniel, et al. (författare) Reduction of tissue transglutaminase autoantibody levels by gluten-free diet is associated with changes in subsets of peripheral blood lymphocytes in children with newly diagnosed coeliac disease. 2006 Ingår i: Clinical and Experimental Immunology. - : Oxford University Press (OUP). - 0009-9104 .- 1365-2249. ; 144:1, s. 67-75 Tidskriftsartikel (refereegranskat)abstract Tissue transglutaminase (tTG) autoantibodies decline after gluten-free diet in patients with coeliac disease. We tested the hypothesis that gluten-free diet-induced change in tTG autoantibody levels affects subsets of peripheral blood lymphocytes. Peripheral blood was obtained from 20 children with biopsy-proven active coeliac disease. Gluten-free diet was initiated and the children examined again after three and six months. tTG autoantibodies were measured in radioligand binding assays and lymphocyte subsets by flow cytometry. IgA-tTG levels at diagnosis, 2204 U/ml (median, range 113–24990), were reduced over six months to 76 U/ml (median, range 1–1261) (P < 0·001). At six months, 12/20 (60%) children had reduced their IgA-tTG levels to < 100 U/ml and these children showed a decrease in B cells (mean change −3·8%, P = 0·014), CD4+ T cells (mean −4·32%, P = 0·011) and CD4+ T cells expressing CD25high (mean change −0·62%, P = 0·036). In contrast, the CD4+CD25highCCR4+ T cell population increased during the same period (mean change 11·5%, P = 0·0036). The decline in IgA-tTG levels correlated to the decrease in B cells (r = 0·56, P = 0·01), CD4+ T cells (r = 0·66, P = 0·004) as well as CD4+CD25high T cells (r = 0·59, P = 0·01). A negative correlation was found between the decline in IgA-tTG and CD4+CD25high T cells expressing CD45RO (r = –0·49, P = 0·03) and CCR4 (r = –0·54, P = 0·01). This is the first observational study on the effect of gluten-free diet on concurrent changes of tTG autoantibodies and specific peripheral blood lymphocyte subsets. Our data suggest that flow cytometry may be a useful complement to tTG autoantibodies when studying the effects of gluten-free diet in children with coeliac disease.
26.	Agardh, Daniel, et al. (författare) Tissue transglutaminase autoantibodies and human leucocyte antigen in Down's syndrome patients with coeliac disease. 2002 Ingår i: Acta Pædiatrica. - 1651-2227. ; 91:1, s. 34-38 Tidskriftsartikel (refereegranskat)
27.	Agardh, Daniel (författare) Tissue transglutaminase autoantibodies in childhood celiac disease 2006 Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract Celiac disease is a prevalent small bowel disease in children caused by permanent intolerance against gliadin, which is the alcohol-soluble fraction of the cereal protein gluten in wheat, rye and barley. Celiac disease is characterized by an inflammatory infiltrate of CD4+ T lymphocytes in the intestinal mucosa leading to damage of villous structure and loss of absorptive surface. As a consequence, gastrointestinal symptoms and signs of malnutrition often occur in children. The exclusion of gluten from the diet results in healing of the intestinal mucosa. Celiac disease is also strongly associated with tissue transglutaminase (tTG) autoantibodies that are considered to be markers for the disease. Moreover, levels of tTG autoantibodies decline after gluten withdrawal, which enables objective evaluation of how patients respond to treatment with gluten-free diet. The use of serological markers for diagnostic purposes in celiac disease will most likely increase as screenings of large populations are performed. It is therefore important to test the current methods for autoantibody detection. The aim of the present thesis was to evaluate radioimmunoassays for the assessment of tTG autoantibodies in children with celiac disease. In Study I, the diagnostic sensitivity and specificity were determined for autoantibodies against human recombinant tTG with liquid phase radioligand binding immunoassays. It was shown that the diagnostic sensitivities for IgA-tTG and IgG-tTG were 85% and 84%, respectively, and the specificity for both isotypes was 94%. The sensitivities were lower compared with previous studies based on similar radioimmunoassays and mainly explained by the inclusion of children diagnosed at two years of age or younger. In Study II, it was examined how human recombinant tTG affected the binding of tTG autoantibodies in liquid phase compared with solid phase immunoassays. We hypothesized that epitopes may be hidden for autoantibodies in the solid phase, but results showed high concordance for IgA-tTG in children with untreated celiac disease. However, the specific binding of IgG-tTG was significantly reduced compared with the two IgA-assays. In contrast, using protein A for binding IgG-tTG in the radioligand binding assays nearly displayed as high diagnostic accuracy as IgA-tTG. In Study III, the effect of gluten-free diet on tTG autoantibody levels and subsets of peripheral blood lymphocytes by flow cytometry were investigated in children with newly diagnosed celiac disease. It was observed that the decline in tTG autoantibody levels subsequent to gluten-free diet was associated with concomitant changes in B cells and a subset of CD4+ regulatory T cells expressing the markers CD25 and CCR4, indicating that flow cytometry might be a useful complement to tTG autoantibodies in monitoring of the disease activity in celiac disease. In Study IV, tTG autoantibodies and endomysial autoantibodies were measured in a screening for celiac disease performed on normal 3-year old children. The outcome of the study diagnosed 0.5% of children with previously unrecognized celiac disease. Although the study revealed a high number of children with transient autoantibodies, the combination of IgA-tTG and IgG-tTG seemed to better predict persistent autoantibodies and a pathological biopsy than any of the autoantibodies alone. In conlusion, this thesis adds new aspects in terms of how tTG autoantibodies can be used as serological markers in children investigated for celiac disease. It is proposed that both IgA-tTG and IgG-tTG are analyzed with radioligand binding assays in children screened for celiac disease with the primary goal to develop a standardized immunoassay in near future.
28.	Agardh, Daniel, et al. (författare) Tissue transglutaminase immunoglobulin isotypes in children with untreated and treated celiac disease 2003 Ingår i: Journal of Pediatric Gastroenterology and Nutrition - Jpgn. - 1536-4801. ; 36:1, s. 77-82 Tidskriftsartikel (refereegranskat)abstract Objectives: Tissue transglutaminase (tTG) autoantibodies are serologic markers for celiac disease (CD). The aim was to determine the diagnostic sensitivity and specificity of different immunoglobulin isotypes against tTG. Methods: Immunoglobulin A (IgA)-tTG, IgG-tTG, and IgGl-tTG were measured in radioligand binding assays in 67 children with untreated and 89 children with treated CD and compared with 48 biopsy controls. IgM-tTG was measured in children with untreated CD and in biopsy controls. IgA endomysial autoantibodies (EMA) were analyzed in all children using an immunofluorescence method. Results: The sensitivity of IgA-tTG and IgG-tTG was 85.1% (57 of 67) and 83.6% (56 of 67), respectively, which both increased to 93.8% (45 of 48) in children diagnosed at age 2 years or older. Both had a specificity of 93.8% (45 of 48). IgA-EMA had a sensitivity of 80.6% (54 of 67) and a specificity of 91.7% (44 of 48). In treated CD, IgA-tTG and IgG-tTG were detected in 21.3% (19 of 89) and in 14.6% (13 of 89), respectively, despite negative EMA titers. IgGl-tTG was correlated to age (r = -0.47, P = 0.0005) and detected in 50.7% (34 of 67) with untreated CD compared with 11.2% (10 of 89) with treated CD and with 4.2% (2 of 48) of biopsy controls (P < 0.0001, respectively). IgM-tTG was detected in 1.5% (1 of 67) with untreated CD and in none of biopsy controls. Conclusion: IgA-tTG and IgG-tTG analyzed in radioligand binding assays are equivalent to IgA-EMA as screening tests for CD during childhood, but an intestinal biopsy is still the method of choice to establish the diagnosis. Although IgGl-tTG was more common at young age of diagnosis, both IgGl-tTG and IgM-tTG had low specificity and sensitivity and may not be useful as screening tests for CD.
29.	Agardh, Daniel, et al. (författare) Using radioligand-binding assays to measure tissue transglutaminase autoantibodies in young children. 2004 Ingår i: Acta Pædiatrica. - 1651-2227. ; 93:8, s. 1046-1051 Tidskriftsartikel (refereegranskat)
30.	Alexander, Lind, et al. (författare) Antibody detection by agglutination-PCR (ADAP) assays for the analysis of tissue transglutaminase autoantibodies in celiac disease 2023 Ingår i: Journal of Immunological Methods. - 0022-1759. ; 518 Tidskriftsartikel (refereegranskat)abstract Background & aims: Tissue transglutaminase autoantibodies (tTGA) are used as diagnostic markers of celiac disease. Different methods have been developed for the detection of tTGA of which enzyme-linked immunosorbent assays (ELISA), radiobinding assays (RBA) and electrochemiluminescence (ECL) assays are the most commonly used. Here we aimed to evaluate a novel antibody detection by agglutination-PCR (ADAP) assay for the detection of tTGA. Methods: Included were 126 children with untreated celiac disease (UCD), 64 disease controls (DC), 21 children with potential celiac disease (PCD), and 1501 children from the general population. Tissue TGA were determined using an automated ADAP assay platform and compared with two RBAs for the detection of IgA-tTG and IgG-tTG, respectively. Results: ADAP detected tTGA in 123/126 (97.6%) UCD children compared with 122/126 (96.8%) using RBA-IgA-tTG and RBA-IgG-tTG (p > 0.9999), respectively. Among DC, ADAP detected 5/64 (7.8%) children with tTGA compared with 4/64 (6.3%) with RBA-IgA-tTG (p > 0.9999) and 8/64 (12.5%) with RBA-IgG-tTG (p = 0.5600), respectively. Tissue TGAs were equally detected in children with PCD in both assays. In the general population, 4/1501 (0.3%) were tTGA positive using ADAP compared with 3/1501 (0.2%) for RBA-IgA-tTG and RBA-IgG-tTG (p > 0.9999), respectively. The area under the curves (AUCs) were 0.998 for ADAP, 0.994 for RBA-IgA-tTG, and 0.999 for RBA-IgG-tTG, respectively. Conclusions: No difference in specificity and sensitivity of tTGA for the diagnosis of celiac disease was reported between ADAP and RBA. ADAP could be recommended as the first-line screening method of larger populations for celiac disease.
31.	Andrén Aronsson, Carin, et al. (författare) 25(OH)D Levels in Infancy Is Associated With Celiac Disease Autoimmunity in At-Risk Children : A Case–Control Study 2021 Ingår i: Frontiers in Nutrition. - : Frontiers Media SA. - 2296-861X. ; 8 Tidskriftsartikel (refereegranskat)abstract Objectives: An observed variation in the risk of celiac disease, according to the season of birth, suggests that vitamin D may affect the development of the disease. The aim of this study was to investigate if vitamin D concentration is associated with the risk of celiac disease autoimmunity (CDA) in genetically at-risk children. Study Design: Children prospectively followed in the multinational The Environmental Determinants of Diabetes in the Young study, conducted at six centers in Europe and the US, were selected for a 1-to-3 nested case–control study. In total, 281 case–control sets were identified. CDA was defined as positivity for tissue transglutaminase autoantibodies (tTGA) on two or more consecutive visits. Vitamin D was measured as 25-hydroxyvitamin D [25(OH)D] concentrations in all plasma samples prior to, and including, the first tTGA positive visit. Conditional logistic regression was used to examine the association between 25(OH)D and risk of CDA. Results: No significant association was seen between 25(OH)D concentrations (per 5 nmol/L increase) and risk for CDA development during early infancy (odds ratio [OR] 0.99, 95% confidence interval [CI] 0.95–1.04) or childhood (OR 1.02, 95% CI 0.97–1.07). When categorizing 25(OH)D concentrations, there was an increased risk of CDA with 25(OH)D concentrations <30 nmol/L (OR 2.23, 95% CI 1.29, 3.84) and >75 nmol/L (OR 2.10, 95% CI 1.28–3.44) in early infancy, as compared with 50–75 nmol/L. Conclusion: This study indicates that 25(OH)D concentrations <30 nmol/L and >75 nmol/L during early infancy were associated with an increased risk of developing CDA in genetically at-risk children. The non-linear relationship raises the need for more studies on the possible role of 25(OH)D in the relation to celiac disease onset.
32.	Andrén Aronsson, Carin, et al. (författare) Age at Gluten Introduction and Risk of Celiac Disease. 2015 Ingår i: Pediatrics. - : American Academy of Pediatrics (AAP). - 1098-4275 .- 0031-4005. ; 135:2, s. 239-245 Tidskriftsartikel (refereegranskat)abstract The goal of this study was to determine whether age at introduction to gluten was associated with risk for celiac disease (CD) in genetically predisposed children.
33.	Andrén Aronsson, Carin, et al. (författare) Association of gluten intake during the first 5 years of life with incidence of celiac disease autoimmunity and celiac disease among children at increased risk 2019 Ingår i: JAMA - Journal of the American Medical Association. - : American Medical Association (AMA). - 0098-7484. ; 322:6, s. 514-523 Tidskriftsartikel (refereegranskat)abstract Importance: High gluten intake during childhood may confer risk of celiac disease. Objectives: To investigate if the amount of gluten intake is associated with celiac disease autoimmunity and celiac disease in genetically at-risk children. Design, Setting, and Participants: The participants in The Environmental Determinants of Diabetes in the Young (TEDDY), a prospective observational birth cohort study designed to identify environmental triggers of type 1 diabetes and celiac disease, were followed up at 6 clinical centers in Finland, Germany, Sweden, and the United States. Between 2004 and 2010, 8676 newborns carrying HLA antigen genotypes associated with type 1 diabetes and celiac disease were enrolled. Screening for celiac disease with tissue transglutaminase autoantibodies was performed annually in 6757 children from the age of 2 years. Data on gluten intake were available in 6605 children (98%) by September 30, 2017. Exposures: Gluten intake was estimated from 3-day food records collected at ages 6, 9, and 12 months and biannually thereafter until the age of 5 years. Main Outcomes and Measures: The primary outcome was celiac disease autoimmunity, defined as positive tissue transglutaminase autoantibodies found in 2 consecutive serum samples. The secondary outcome was celiac disease confirmed by intestinal biopsy or persistently high tissue transglutaminase autoantibody levels. Results: Of the 6605 children (49% females; median follow-up: 9.0 years [interquartile range, 8.0-10.0 years]), 1216 (18%) developed celiac disease autoimmunity and 447 (7%) developed celiac disease. The incidence for both outcomes peaked at the age of 2 to 3 years. Daily gluten intake was associated with higher risk of celiac disease autoimmunity for every 1-g/d increase in gluten consumption (hazard ratio [HR], 1.30 [95% CI, 1.22-1.38]; absolute risk by the age of 3 years if the reference amount of gluten was consumed, 28.1%; absolute risk if gluten intake was 1-g/d higher than the reference amount, 34.2%; absolute risk difference, 6.1% [95% CI, 4.5%-7.7%]). Daily gluten intake was associated with higher risk of celiac disease for every 1-g/d increase in gluten consumption (HR, 1.50 [95% CI, 1.35-1.66]; absolute risk by age of 3 years if the reference amount of gluten was consumed, 20.7%; absolute risk if gluten intake was 1-g/d higher than the reference amount, 27.9%; absolute risk difference, 7.2% [95% CI, 6.1%-8.3%]). Conclusions and Relevance: Higher gluten intake during the first 5 years of life was associated with increased risk of celiac disease autoimmunity and celiac disease among genetically predisposed children.
34.	Andrén Aronsson, Carin, et al. (författare) Effects of Gluten Intake on Risk of Celiac Disease: a case-control study on a Swedish birth cohort. 2016 Ingår i: Clinical Gastroenterology and Hepatology. - : Elsevier BV. - 1542-7714 .- 1542-3565. ; 14:3, s. 403-409 Tidskriftsartikel (refereegranskat)abstract It is not clear how intake of gluten during infancy affects subsequent risk of celiac disease. We investigated whether gluten intake before 2 years of age increases risk for celiac disease in genetically susceptible children.
35.	Andrén Aronsson, Carin, et al. (författare) Gluten in infants and celiac disease risk 2016 Ingår i: Expert Review of Gastroenterology and Hepatology. - : Informa UK Limited. - 1747-4124 .- 1747-4132. ; 10:6 Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
36.	Andrén Aronsson, Carin, et al. (författare) Intervention strategies in early childhood to prevent celiac disease—a mini-review 2023 Ingår i: Frontiers in Immunology. - : Frontiers Media SA. - 1664-3224. ; 14 Tidskriftsartikel (refereegranskat)abstract A higher intake of gluten during childhood is associated with increased risk of celiac disease, and the incidence of celiac disease peaks shortly after the time point when associations with higher gluten intake during the second and third year of life occur. Additional environmental factors are most likely necessary for celiac disease to develop. It is hypothesized that gastrointestinal infections increase gut permeability and exposure to gluten. Alternatively, infections may lead to gut dysbiosis and chronic inflammation, with leakage of self-antigens that mimic gluten peptides that leads to an autoimmune-like response. Different gluten interventions to prevent celiac disease have been proposed. Early clinical studies suggested an optimal time point introducing gluten between 4 and 6 months of age while the infant is being breastfed. However, later clinical trials on reduced gluten intake given to infants have shown no protection from celiac disease if gluten introduction was delayed or if gluten was introduced in small amounts during the child’s first year of life. Still, more randomized clinical trials (RCTs) are warranted to answer the question if a reduced amount of gluten, not only at the time of introduction during infancy but also in a longer time frame, will prevent children at genetic risk from having lifelong celiac disease. It needs to be clarified whether dietary interventions are effective strategies to be proposed as future prevention of celiac disease in the general population. The present mini-review provides an overview of ongoing or completed RCTs that have focused on interventions during early childhood with the aim of preventing celiac disease.
37.	Aydemir, Özkan, et al. (författare) Polymorphisms in Intron 1 of HLA-DRA Differentially Associate with Type 1 Diabetes and Celiac Disease and Implicate Involvement of Complement System Genes C4A and C4B Ingår i: eLife. - 2050-084X. Tidskriftsartikel (refereegranskat)abstract Polymorphisms in genes in the human leukocyte antigen (HLA) class II region comprise the most important inherited risk factors for many autoimmune diseases including type 1 diabetes (T1D) and celiac disease (CD): both diseases are positively associated with the HLA- DR3 haplotype (DRB103:01-DQA105:01-DQB1*02:01). Studies of two different populations have recently documented that T1D susceptibility in HLA-DR3 homozygous individuals isstratified by a haplotype consisting of three single nucleotide polymorphisms (“tri-SNP”) in intron 1 of the HLA-DRA gene. In this study, we use a large cohort from the longitudinal “The Environmental Determinants of Diabetes in the Young” (TEDDY) study to further refine the tri-SNP association with T1D and with autoantibody-defined T1D endotypes. We found that the tri-SNP association is primarily in subjects whose first-appearing T1D autoantibody is to insulin. In addition, we discovered that the tri-SNP is also associated with celiac disease (CD), and that the particular tri-SNP haplotype (“101”) that is negatively associated with T1D risk is positively associated with risk for CD. The opposite effect of the tri-SNP haplotype on two DR3-associated diseases can enhance and refine current models of disease prediction based on genetic risk. Finally, we investigated possible functional differences between the individuals carrying high and low-risk tri-SNP haplotypes, and found that differences in complement system genes C4A and C4B may underlie the observed divergence in disease risk.
38.	Björck, Sara, et al. (författare) Reduced Bone Mineral Density in Children with Screening-detected Celiac Disease 2017 Ingår i: Journal of Pediatric Gastroenterology and Nutrition. - 0277-2116. ; 65:5, s. 526-532 Tidskriftsartikel (refereegranskat)abstract Objectives: The aim of the study was to assess whether bone mass and metabolism are impaired in genetically at-risk children with screening-detected celiac disease. Methods: Included were 71 children with screening-detected celiac disease diagnosed at 10.0 ± 0.7 (mean ± standard deviation) years and 142 matched controls and 30 children with screening-detected celiac disease diagnosed at 3.3 ± 0.4 years of age presently on a gluten-free diet for 6.9 ± 1.1 years and 60 matched controls. All participants were assessed for bone mineral density (BMD) of total body and spine by dual X-ray absorptiometry, serum 25(OH) vitamin D3, parathyroid hormone (PTH), interleukin (IL)-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70, IL-13, IL-15, interferon gamma, and tumor necrosis factor alpha. Results: At diagnosis, screening-detected celiac disease children as compared to controls had a mean-0.03 g/cm 2 reduced BMD of both total body and spine (P = 0.009 and P = 0.005, respectively), a mean-11.4 nmol/L lower level of 25(OH) vitamin D3 (P < 0.001), and a mean +1.0 pmol/L higher PTH level (P < 0.001). Systemic levels of the cytokines IL-1β, IL-6, IL-8, IL-10, IL-12p70, IL-13, and tumor necrosis factor alpha were all increased in screening-detected celiac disease as compared to controls (P < 0.001). No difference in BMD, 25(OH) vitamin D3, PTH, and cytokine levels were detected in children on a gluten-free diet compared with controls. Conclusions: Children with screening-detected celiac disease have reduced BMD, lower levels of vitamin D3, higher levels of PTH, and signs of systemic inflammation compared with controls. These differences were not found in celiac disease children on a gluten-free diet, indicating that children with screening-detected celiac disease benefit from an early diagnosis and treatment.
39.	Björck, Sara, et al. (författare) Repeated Screening is Necessary for Detection of Celiac Disease But Can be Restricted to at Genetic Risk Birth Cohorts. 2016 Ingår i: Journal of Pediatric Gastroenterology and Nutrition - Jpgn. - 1536-4801. ; 62:2, s. 271-275 Tidskriftsartikel (refereegranskat)abstract Celiac disease is associated with tissue transglutaminase autoantibodies (tTGA) in individuals carrying the HLA risk-haplotypes DQA105:01-DQB102:01 (DQ2) and/or DQA103:01-DQB103:02 (DQ8). The aim was to identify celiac disease in a HLA genotyped birth-cohort prospectively screened for celiac disease.
40.	Björck, Sara, et al. (författare) Response to Letter: Early Screening in Children at Genetic Risk of Coeliac Disease. 2016 Ingår i: Journal of Pediatric Gastroenterology and Nutrition - Jpgn. - 1536-4801. ; 62:2, s. 22-22 Tidskriftsartikel (refereegranskat)
41.	Björck, Sara, et al. (författare) Screening Detects a High Proportion of Celiac Disease in Young HLA-genotyped Children. 2010 Ingår i: Journal of Pediatric Gastroenterology and Nutrition - Jpgn. - 1536-4801. ; 50, s. 49-53 Tidskriftsartikel (refereegranskat)abstract BACKGROUND AND AIMS:: Celiac disease is associated with tissue transglutaminase autoantibodies (tTGAb) and the human leukocyte antigen (HLA)-risk alleles DQB102 and DQB10302. The aim was to estimate the proportion of undiagnosed celiac disease in children with HLA risk at 3 years of age. PATIENTS AND METHODS:: From a population-based HLA-DQ screening study of newborns born between June 2001 and August 2004 in the southern part of Sweden, 6206 children with HLA-risk alleles were identified and asked to participate at a mean 3.3 +/- 0.4 years of age. As controls, 7654 children with HLA-nonrisk alleles were asked to participate. In all, 1620 (26.1%) children with HLA risk and 1815 (23.7%) controls were screened for tTGAb using radioligand-binding assays. Celiac disease was established by intestinal biopsy in children with a confirmed positive tTGAb test. RESULTS:: Twenty-three children reported already having clinically diagnosed celiac disease and did not participate further. In children with HLA-risk genotypes, 73 of 1620 (4.5%, 95% CI 3.5%-5.5%) were tTGAb-positive compared with none of 1815 from the controls (P < 0.0001). Seventy-one children underwent biopsy (1 refused biopsy and 1 biopsy failed), of whom 56 of 1618 (3.5%, 95% CI 2.6%-4.4%) had damaged intestinal mucosa classified as celiac disease. The ratio between clinically and screening detected celiac disease in this study was 1:2.4 (23:56). CONCLUSIONS:: The proportion of clinically undetected celiac disease may be particularly high among 3-year-old children with HLA-DQB102 and DQB10302 in Sweden, where these 2 HLA-risk alleles frequently occur.
42.	Björck, Sara, et al. (författare) Serum cytokine pattern in young children with screening detected celiac disease. 2015 Ingår i: Clinical and Experimental Immunology. - : Oxford University Press (OUP). - 0009-9104 .- 1365-2249. ; 179:2, s. 230-235 Tidskriftsartikel (refereegranskat)abstract Celiac disease is an autoimmune disease characterized by inflammation localized to the small bowel, but less is known about systemic signs of inflammation. The aim was to measure cytokines of the T helper 1 (Th1) and T helper 2 (Th2) cell patterns in children with screening detected celiac disease before and after treatment with a gluten free diet.
43.	Browaldh, Lars, et al. (författare) Celiaki är en vanlig sjukdom som är lätt att missa 2014 Ingår i: Läkartidningen. - : Swedish Medical Association. - 0023-7205 .- 1652-7518. ; 111:11, s. 484-488 Tidskriftsartikel (refereegranskat)abstract Celiaki ansågs länge som en ovanlig barnsjukdom, men är en vanlig sjukdom som drabbar alla åldrar. Genomförda screeningar av normalbefolkningen visar att merparten inte fått diagnos eller behandling. Den kliniska bilden varierar: alltifrån diffusa besvär eller inga symtom alls till allvarliga gastrointestinala symtom med grav avmagring och tillväxtrubbning till följd av malabsorption. Klinisk misstanke om eller hereditet för celiaki bör föranleda analys av specifika serologiska markörer. Gastroskopi med tunntarmsbiopsi bör övervägas för att bekräfta eller utesluta diagnosen.
44.	Carlsson, Annelie, et al. (författare) Prevalence of celiac disease : Before and after a national change in feeding recommendations 2006 Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 41:5, s. 553-558 Tidskriftsartikel (refereegranskat)abstract Objective. A national change in infant feeding recommendations was proposed in 1996 in Sweden: a slow introduction to gluten during weaning was stressed, the recommendation being introduction at 4 instead of 6 months of age. The aim of the present study was to compare the prevalence of celiac disease in healthy young children born before and after the new feeding recommendations in 1996. Material and methods. Sera from 679 children at a median age of 2.9 years (range 2.5-4.2 years) born between January 1996 and November 1997 were investigated with IgA-antigliadin antibodies (AGA) and IgA-endomysial autoantibodies (EMA) and compared with 690 age-matched children born between July 1992 and June 1993. Children with a positive test for EMA and AGA or EMA only were re-tested, and if positive at follow up, investigated with intestinal biopsy. Results. At baseline, 2.2% (15/679) children were positive for EMA and another 0.6% (4/679) for both EMA and AGA. One child refused to be re-tested and eight children were still EMA positive at follow-up. Intestinal biopsy was performed in seven children (one declined biopsy), of whom three showed total villous atrophy. Two children with EMA titers 1:640, respectively, refused further participation in the study, but were strongly suspected to have celiac disease. In total, 0.7% (5/679) (95% confidence interval (CI) = 0.1-1.4%) were considered to have celiac disease compared with 1.3% (9/690) (95% CI = 0.4-2.2%) in the control group (p = 0.4217). In addition, 0.3% of the children were diagnosed with symptomatic celiac disease compared with 0.7% in controls (p = 0.0134). Conclusions. The prevalence of symptomatic celiac disease declined after the infant dietary recommendations were introduced in 1996, but we could not find any difference in undiagnosed celiac disease between the screened children born before and those born after 1996. © 2006 Taylor & Francis.
45.	Dahlbom, Ingrid, et al. (författare) Protein A and protein G ELISA for the detection of IgG autoantibodies against tissue transglutaminase in childhood celiac disease 2008 Ingår i: Clinica Chimica Acta. - : Elsevier BV. - 0009-8981 .- 1873-3492. ; 395:1-2, s. 72-6 Tidskriftsartikel (refereegranskat)abstract Objectives: To investigate if the detection of celiac disease (CD) in children was improved by using alternative conjugates for assessment of tissue transglutaminase (tTG) autoantibodies. Methods: Serum samples from 108 biopsy confirmed CD children and 42 control subjects were investigated for the presence of autoantibodies with tTG coated microplates using protein A (PA), protein G (PG), anti-IgG, or anti-IgA as conjugates. Results: Of the 108 CD children, 86 (80%) were IgG-tTG positive, 91 (84%) were positive with the PA-conjugate, 94 (87%) were positive with the PG-conjugate, and 103 (95%) were IgA-tTG positive. Among the 42 controls. 4 (10%) were IgG-tTG positive, 5 (12%) were positive with both the PA- and PG conjugates. whereas 3 (7%) were IgA-tTG positive. Compared with IgG-tTG the concordance was 93% for PA and 95% for PG, with a positive correlation between antibody levels (r=0.967 and r=0.975. p< ;0.0001). All but one CD child were found positive by combining IgG-tTG and IgA-tTG detection. Conclusions: The sensitivity of IgG-tTG detection with ELISA increased by protein A or protein G conjugates, whereas the specificity was reduced as compared with anti-IgG conjugate. The combined measurement of IgA-tTG and IgG-tTG still seems to be the optimal procedure when screening children for CD.
46.	Danielsson, Anna-Karin, et al. (författare) Cannabis use among Swedish men in adolescence and the risk of adverse life course outcomes : results from a 20 year-follow-up study 2015 Ingår i: Addiction. - : Wiley. - 0965-2140 .- 1360-0443. ; 110:11, s. 1794-1802 Tidskriftsartikel (refereegranskat)abstract AimsTo examine associations between cannabis use in adolescence (at age 18) and unemployment and social welfare assistance in adulthood (at age 40) among Swedish men. DesignLongitudinal cohort study. Setting and ParticipantsA total of 49321 Swedish men born in 1949-51, who were conscripted to compulsory military service at 18-20 years of age. MeasurementsAll men answered two detailed questionnaires at conscription and were subject to examinations of physical aptitude psychological functioning and medical status. By follow-up in national databases, information on unemployment and social welfare assistance was obtained. FindingsIndividuals who used cannabis at high levels in adolescence had increased risk of future unemployment and of receiving social welfare assistance. Adjusted for all confounders (social background, psychological functioning, health behaviours, educational level, psychiatric diagnoses), an increased relative risk (RR) of unemployment remained in the group reporting cannabis use >50 times [RR=1.26, 95% confidence interval (CI)=1.04-1.53] only. For social welfare assistance, RR in the group reporting cannabis use 1-10 times was 1.15 (95% CI=1.06-1.26), RR for 11-50 times was 1.21 (95% CI=1.04-1.42) and RR for >50 times was 1.38 (95% CI=1.19-1.62). ConclusionsHeavy cannabis use among Swedish men in late adolescence appears to be associated with unemployment and being in need of social welfare assistance in adulthood. These associations are not explained fully by other health-related, social or behavioural problems.
47.	Danielsson, Anna-Karin, et al. (författare) Cannabis use in adolescence and risk of future disability pension : A 39-year longitudinal cohort study 2014 Ingår i: Drug And Alcohol Dependence. - : Elsevier BV. - 0376-8716 .- 1879-0046. ; 143, s. 239-243 Tidskriftsartikel (refereegranskat)abstract Aims: This study aimed at examining a possible association between cannabis use in adolescence and future disability pension (DP). DP can be granted to any person in Sweden aged 16-65 years if working capacity is judged to be permanently reduced due to long-standing illness or injury. Methods: Data were obtained from a longitudinal cohort study comprising 49,321 Swedish men born in 1949-1951 who were conscripted to compulsory military service aged 18-20 years. Data on DP was collected from national registers. Results: Results showed that individuals who used cannabis in adolescence had considerably higher rates of disability pension throughout the follow-up until 59 years of age. In Cox proportional-hazards regression analyses, adjustment for covariates (social background, mental health, physical fitness, risky alcohol use, tobacco smoking and illicit drug use) attenuated the associations. However, when all covariates where entered simultaneously, about a 30% increased hazard ratio of DP from 40 to 59 years of age still remained in the group reporting cannabis use more than 50 times. Conclusions: This study shows that heavy cannabis use in late adolescence was associated with an increased relative risk of labor market exclusion through disability pension.
48.	Fex, Malin, et al. (författare) First trimester cytokine levels in mothers to children diagnosed with islet autoimmunity or type 1 diabetes before eight years of age 2010 Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 1432-0428 .- 0012-186X. ; 53:Suppl. 1, s. 344-344 Konferensbidrag (refereegranskat)
49.	Gudeta, Adugna Negussie, et al. (författare) Complementary Feeding Habits in Children Under the Age of 2 Years Living in the City of Adama in the Oromia Region in Central Ethiopia : Traditional Ethiopian Food Study 2021 Ingår i: Frontiers in Nutrition. - : Frontiers Media SA. - 2296-861X. ; 8 Tidskriftsartikel (refereegranskat)abstract Updated information on child feeding practices, nutritional status, and trends related to parental sociodemographic variables is required in developing countries. The objective of this study was to describe infant feeding practices and associated sociodemographic factors among Ethiopian children with an emphasis on complementary feeding (CF). Information on infant feeding and anthropometric measures was obtained from 1,054 mother-child pairs participating in a birth cohort study of children born between 2017 and 2020 prospectively followed in the city of Adama located in the Oromia region of central Ethiopia. Logistic regression models were used to identify sociodemographic and food groups associated with the initiation of CF. The introduction of complementary foods at 6 months of age was 84.7% (95% CI, 82.5, 86.8). Vegetables, cereals (teff, wheat, barley), and fruits were most often the earliest types of foods introduced. Wasting, stunting, underweight, and low body mass index (BMI) by age were found in 6.0, 16.9, 2.5, and 6.3%, respectively. Maternal age and occupation were the factors associated with timely initiation of CF [OR = 2.25, (95% CI, 1.14, 4.41)] and [OR = 0.68, (95% CI, 0.48, 0.97)], respectively. This study demonstrates that the majority of Ethiopian children in the Oromia region follow the recommendations of WHO on CF.
50.	Gudeta, Adugna N., et al. (författare) Distribution of HLA-DQ risk genotypes for celiac disease in Ethiopian children 2020 Ingår i: HLA: Immune Response Genetics. - : Wiley. - 2059-2302. ; 96:6, s. 681-687 Tidskriftsartikel (refereegranskat)abstract Most patients with celiac disease are positive for either HLA-DQA105:01-DQB102 (DQ2.5) or DQA103:01-DQB103:02 (DQ8). Remaining few patients are usually DQA102:01-DQB102 (DQ2.2) carriers. Screenings of populations with high frequencies of these HLA-DQA1-DQB1 haplotypes report a 1% to 3% celiac disease prevalence. The aim was to determine the prevalence of HLA-DQ risk haplotypes for celiac disease in Ethiopian children. Dried blood spots collected from 1193 children from the Oromia regional state of Ethiopia were genotyped for HLA-DQA1 and DQB1 genotyping using an asymmetric polymerase chain reaction (PCR) and a subsequent hybridization of allele-specific probes. As references, 2000 previously HLA-genotyped children randomly selected from the general population in Sweden were included. DQ2.2 was the most common haplotype and found in 15.3% of Ethiopian children, which was higher compared with 6.7% of Swedish references (P <.0001). Opposed to this finding, DQ2.5 and DQ8 occurred in 9.7% and 6.8% of Ethiopian children, which were less frequent compared with 12.8% and 13.1% of Swedish references, respectively (P <.0001). The DQ2.5-trans genotype encoded by DQA105-DQB103:01 in combination with DQ2.2 occurred in 3.6% of Ethiopian children, which was higher compared with 1.3% of Swedish references (P <.0001). However, when children with moderate high to very high-risk HLA genotypes were grouped together, there was no difference between Ethiopian children and Swedish references (27.4% vs 29.0%) (P =.3504). The frequency of HLA risk haplotypes for celiac disease is very similar in Ethiopian and Swedish children. This finding of importance will be useful in future screening of children for celiac disease in Ethiopia.

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