76 research outputs found

    Type 1 diabetes incidence in Scotland between 2006 and 2019

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    Aims: To describe type 1 diabetes incidence in Scotland between 2006 and 2019. Methods: Repeated annual cross‐sectional studies of type 1 diabetes incidence were conducted. Incident cases were identified from the Scottish Care Information—Diabetes Collaboration (SCI‐DC), a population‐based register of people with diagnosed diabetes derived from primary and secondary care data. Mid‐year population estimates for Scotland were used as the denominator to calculate annual incidence with stratification by age and sex. Joinpoint regression was used to investigate whether incidence changed during the study period. Age and sex‐specific type 1 diabetes incidence over the whole time period was estimated by quintile of the Scottish Index of Multiple Deprivation (SIMD), an area‐based measure, in which Q1 and Q5 denote the most and least deprived fifths of the population, respectively, with quasi‐Poisson regression used to compare incidence for Q5 compared to Q1. Results: The median (IQR) age of the study population of 14,564 individuals with incident type 1 diabetes was 24.1 (12.3–42.4) years, 56% were men, 23% were in Q1 and 16% were in Q5. Incidence of T1DM was higher in men than women overall (at around 22 and 17 per 100,000, respectively) and in under 15 year olds (approximately 40 per 100,000 in both sexes) than other age groups and was similar across the study period in all strata. There was an inverse association between socio‐economic status and type 1 diabetes incidence for 15–29, 30–49 and 50+ year olds [incidence rate ratio (IRR) for Q5 compared to Q1; IRR (95% CI) 0.52 (0.47–0.58), 0.68 (0.61–0.76) and 0.53(0.46–0.61), respectively] but not for under 15 year olds [1.02 (0.92–1.12)]. Conclusion: Incidence of type 1 diabetes varies by age, sex and socio‐economic status and has remained approximately stable from 2006 to 2019 in Scotland

    The SINS trial: A randomised controlled trial of excisional surgery versus imiquimod 5% cream for nodular and superficial basal cell carcinoma

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    <p>Abstract</p> <p>Background</p> <p>Basal cell carcinoma is the commonest human cancer. Despite increasing incidence it remains poorly researched. While not life threatening it can cause significant cosmetic disfigurement. Imiquimod, a cream which enhances the body's immune response, may help deal with the number of cases that occur in low-risk sites, especially when good cosmetic results and home use without surgery are needed.</p> <p>This study aims 1. To compare excisional surgery with imiquimod cream for nodular or superficial basal cell carcinoma in low risk sites, with respect to 3 year clinical clearance, cost-effectiveness and cosmetic results. 2. To ascertain if certain phenotypic features and gene polymorphisms predict tumour responsiveness to treatment.</p> <p>Methods/Design</p> <p>Five hundred participants with low risk nodular or superficial basal cell carcinoma will be recruited from hospitals to this multi-centre, randomised, parallel group, controlled phase III trial. Treatment in the imiquimod group is for 6 weeks for superficial basal cell carcinoma and 12 weeks for nodular basal cell carcinoma. Both treatment groups are followed up in clinic for 3 years. Primary outcome variable: the proportion of participants with clinical evidence of success (no recurrence) at 3 years. The primary outcome will be compared between the two treatment groups. Secondary outcomes include: i) clinical success at 1, 2 and 5 years, ii) time to first recurrence, iii) cosmetic appearance of lesion site after treatment, iv) level of pain, and v) cost-effectiveness. Safety and tolerability data will also be reported.</p> <p>Discussion</p> <p>This study protocol describes a pragmatic randomised controlled trial which it is hoped will address the above uncertainties. Three-year results will be available towards the end of 2010.</p> <p>Trial registration</p> <p>Meta-register: NCT00066872, Eudract No. 2004-004506-24, ISRCTN48755084.</p

    Preconception maternal iodine status is associated with IQ but not with measures of executive function in childhood

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    Background: adverse effects of severe maternal iodine deficiency in pregnancy on fetal brain development are wellestablished, but the effects of milder deficiency are uncertain. Most studies examine iodine status in pregnancy; less is known about iodine nutrition before conception. Objective: we examined relations between maternal preconception iodine status and offspring cognitive function, within a prospective mother-offspring cohort. Methods: maternal iodine status was assessed through the use of the ratio of iodine:creatinine concentrations (I/Cr) in spot urine samples [median (IQR) period before conception 3.3 y (2.2-4.7 y)]. Childhood cognitive function was assessed at age 6-7 y. Full-scale IQ was assessed via the Wechsler Abbreviated Scale of Intelligence, and executive function through the use of tests from the Cambridge Neuropsychological Test Automated Battery (CANTAB). Analyses (n = 654 mother-child dyads) were adjusted for potential confounders including maternal intelligence, education, and breastfeeding duration. Results: the median (IQR) urinary iodine concentration was 108.4 ÎŒg/L (62.2-167.8 ÎŒg/L) and the I/Cr ratio 114 ÎŒg/g (76- 164 ÎŒg/g). The preconception I/Cr ratio was positively associated with child IQ, before and after adjustment for potential confounding influences [ÎČ = 0.13 (95% CI: 0.04, 0.21)/SD, P = 0.003]. 8.9% of women had a preconception urinary I/Cr ratio &lt; 50 ÎŒg/g; compared with those with an I/Cr ratio ≄150 ÎŒg/g, the IQ of their offspring was 0.49 (95% CI: 0.79, 0.18) SD lower. There were no associations with the executive function outcomes assessed via CANTAB, before or after adjustment for confounders. Conclusions: the positive association between iodine status before conception and child IQ provides some support for demonstrated links between low maternal iodine status in pregnancy and poorer cognitive function reported in other studies. However, given the negative effects on school performance previously observed in children born to iodine-deficient mothers, the lack of associations with measures of executive function in the present study was unexpected. Further data are needed to establish the public health importance of low preconception iodine status.</p

    Maternal Iodine Status During Pregnancy Is Not Consistently Associated with Attention-Deficit Hyperactivity Disorder or Autistic Traits in Children

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    BACKGROUND: Severe iodine deficiency during pregnancy can cause intellectual disability, presumably through inadequate placental transfer of maternal thyroid hormone to the fetus. The association between mild-to-moderate iodine deficiency and child neurodevelopmental problems is not well understood. OBJECTIVES: We investigated the association of maternal iodine status during pregnancy with child attention-deficit hyperactivity disorder (ADHD) and autistic traits. METHODS: This was a collaborative study of 3 population-based birth cohorts: Generation R (n = 1634), INfancia y Medio Ambiente (n = 1293), and the Avon Longitudinal Study of Parents and Children (n = 2619). Exclusion criteria were multiple fetuses, fertility treatment, thyroid-interfering medication use, and pre-existing thyroid disease. The mean age of assessment in the cohorts was between 4.4 and 7.7 y for ADHD symptoms and 4.5 and 7.6 y for autistic traits. We studied the association of the urinary iodine-to-creatinine ratio (UI/Creat) <150 Όg/g-in all mother-child pairs, and in those with a urinary-iodine measurement at ≀18 weeks and ≀14 weeks of gestation-with the risk of ADHD or a high autistic-trait score (≄93rd percentile cutoff), using logistic regression. The cohort-specific effect estimates were combined by random-effects meta-analyses. We also investigated whether UI/Creat modified the associations of maternal free thyroxine (FT4) or thyroid-stimulating hormone concentrations with ADHD or autistic traits. RESULTS: UI/Creat <150 Όg/g was not associated with ADHD (OR: 1.2; 95% CI: 0.7, 2.2; P = 0.56) or with a high autistic-trait score (OR: 0.8; 95% CI: 0.6, 1.1; P = 0.22). UI/Creat <150 Όg/g in early pregnancy (i.e., ≀18 weeks or ≀14 weeks of gestation) was not associated with a higher risk of behavioral problems. The association between a higher FT4 and a greater risk of ADHD (OR: 1.3; 95% CI: 1.0, 1.6; P = 0.017) was not modified by iodine status. CONCLUSIONS: There is no consistent evidence to support an association of mild-to-moderate iodine deficiency during pregnancy with child ADHD or autistic traits

    Surgery versus 5% imiquimod for nodular and superficial basal-cell carcinoma: five year results of the SINS randomised controlled trial

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    Background: We previously reported modest clinical 3-year benefit for topical imiquimod compared with surgery for superficial or nodular basal cell carcinoma (sBCC, nBCC) at low risk sites in our non-inferiority randomised controlled SINS trial. Here we report 5-year data. Methods: Participants were randomised to imiquimod 5% cream once daily (sBCC, 6 weeks; nBCC, 12 weeks) or excisional surgery (4 mm margin). Primary outcome was clinical absence of initial failure or signs of recurrence at 3 year dermatology review. Five year success was defined as 3 year success plus absence of recurrences identified through hospital, histopathology and general practitioner records. Results: Of 501 participants randomised, 401 contributed to the modified intention-to-treat analyses at year 3 (primary outcome), 383 (96%) of whom had data at year 5. Five year success rates for imiquimod were 82·5% (170/206) compared to 97·7% (173/177) for surgery (relative risk of imiquimod success 0·84, 95% CI 0·77 to 0·91, p<0.001). These were comparable to year 3 success rates of 83·6% (178/213) and 98.4% (185/188), for imiquimod and surgery, respectively. Most imiquimod treatment failures occurred in year one. Interpretation: Although surgery is clearly superior to imiquimod, this study shows sustained benefit for lesions that respond early to topical imiquimod
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