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Childhood T1D increased dramatically and shifted to a younger age at onset the first 22 years of the study period. We report a reversed trend, starting in 2000, indicating a change in nongenetic risk factors affecting specifically young children.

Aims: To estimate the prevalence of undiagnosed type-2 diabetes in overweight Swedish school children 11-13 years old.

Methods: BMI was measured in 5 528 school-children (11-13 years of age) attending the 6th grade, in five different regions in Sweden. Overweight was defined by international age-sex specific BMI cut-offs, corresponding to adult BMI cut-offs of 25 kg/m² at 18 years of age (ISO-BMI ≥25, n=1 275). Haemoglobin A1c (HbA1c) was measured in 1 126 children with ISO-BMI ≥25. Children with a DCCT-aligned HbA1c ≥ 6.1% on two occasions underwent an oral glucose-tolerance test (OGTT) to establish diabetes diagnosis.

Results: Twenty four children (2.1%) had at least one HbA1c-value ≥6.1%. Three of them had HbA1c ≥6.1% on two occasions and all of them had a normal OGTT.

Conclusion: In this cross-sectional population-based screening study of a high risk group of 11-13 years old Swedish school children we found no indication of undiagnosed diabetes or impaired glucose tolerance.Key

OBJECTIVE—This study aimed to estimate the current cumulativerisk of end-stage renal disease (ESRD) due to diabeticnephropathy in a large, nationwide, population-based prospectivetype 1 diabetes cohort and specifically study the effects ofsex and age at onset.RESEARCH DESIGN AND METHODS—In Sweden, all incidentcases of type 1 diabetes aged 0–14 years and 15–34 years arerecorded in validated research registers since 1977 and 1983,respectively. These registers were linked to the Swedish RenalRegistry, which, since 1991, collects data on patients who receiveactive uremia treatment. Patients with 13 years duration of type1 diabetes were included (n 11,681).RESULTS—During a median time of follow-up of 20 years, 127patients had developed ESRD due to diabetic nephropathy. Thecumulative incidence at 30 years of type 1 diabetes duration waslow, with a male predominance (4.1% [95% CI 3.1–5.3] vs. 2.5%[1.7–3.5]). In both male and female subjects, onset of type 1diabetes before 10 years of age was associated with the lowestrisk of developing ESRD. The highest risk of ESRD was found inmale subjects diagnosed at age 20–34 years (hazard ratio 3.0 [95%CI 1.5–5.7]). In female subjects with onset at age 20–34 years, therisk was similar to patients’ diagnosed before age 10 years.CONCLUSIONS—The cumulative incidence of ESRD is exceptionallylow in young type 1 diabetic patients in Sweden. There isa striking difference in risk for male compared with femalepatients. The different patterns of risk by age at onset and sexsuggest a role for puberty and sex hormones.

Aims/Hypothesis: The aim of this study was to analyze the possible impact of parental and individual socioeconomic status (SES) on all cause mortality in a population based cohort of childhood onset T1D.

Methods: Subjects recorded in the Swedish Childhood Diabetes Registry (SCDR) January 1 1978 to December 31 2008 were included (n=14 409). The SCDR was linked to the Swedish Cause of Death Register (CDR) and the Longitudinal Integration Database for Health Insurance and Labour Market Studies (LISA). SES measures (education and income support) wtypeere retrieved from the LISA for the years 1990-2010. Mortality data were retrieved from the CDR as of December 31, 2010.

Results: At a mean follow-up of 24.4 years (maximum 47.5), 238 deaths occurred in a total of 357 048 person-years at risk. In crude analyses, low maternal education predicted mortality for male cases only (p=0.046), while parental income support predicted mortality in both sexes (p<0.001 for both). In Cox models stratified by age at death groups and adjusted for age at onset and sex, parental income support predicted mortality among young adults ( ≥18 years of age) but not for children. Including the adult patient´s own SES in a Cox model showed that individual income support to the patient predicted mortality occurring at ≥ 24 years of age when adjusting for age at onset, sex and parental SES.

Conclusions/Interpretation: Low parental SES, mirrored by the need of income support, increases mortality risk in childhood onset type-1 diabetics who died after the age of 18 years.