| 361. |
- Martinell, Mats, 1971-, et al.
(författare)
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Education immigration and income as risk factors for hemoglobin a1c >70 mmol/mol when diagnosed with type 2 diabetes or latent autoimmune diabetes in adult : A population-based cohort study
- 2017
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Ingår i: BMJ Open Diabetes Research and Care. - : BMJ. - 2052-4897. ; 5:1
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Tidskriftsartikel (refereegranskat)abstract
- Objectives The aim of this research is to study education, income and immigration as risk factors for high hemoglobin A1c (HbA1c >70 mmol/mol (8.6%)) when diagnosed with type 2 diabetes (T2D) or latent autoimmune diabetes in the adult (LADA). Research design and methods Patients were included from the All New Diabetics in Scania study (2008-2013). Level of education, disposable income and immigration year were retrieved from the longitudinal integrated database for labour market research (LISA) register compiled by Statistics Sweden. Logistic regression models were used to estimate ORs for HbA1c >70 mmol/mol (8.6%) at diagnosis. Results A total of 3794 patients with incident T2D (n=3 525) or LADA (n=269) were included. Patients with T2D with a low (≤9 years) or medium (10-12 years) levels of education were more likely to have high HbA1c at diagnosis compared with patients with T2D with a high (>12 years) level of education (OR 1.34, 95% CI 1.08 to1.66, OR 1.26, 95% CI 1.03 to 1.54). Low-income patients with T2D (<60% of median) were more likely to have high HbA1c at diagnosis compared with high-income patients withT2D (>150% of median) (OR 1.35, 95% CI 1.02 to 1.79). Conclusions Patients with lower levels of education or low income and are more likely to have HbA1c is >70 mmol/ mol (8.6%) when diagnosed with T2D. An understanding of how socioeconomic position influences the clinical presentation at diagnosis may facilitate screening programs designed to target populations at risk for delayed diagnosis.
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| 362. |
- Martinell, Mats, 1971-, et al.
(författare)
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Prevalence and risk factors for diabetic retinopathy at diagnosis (DRAD) in patients recently diagnosed with type 2 diabetes (T2D) or latent autoimmune diabetes in the adult (LADA)
- 2016
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Ingår i: Journal of diabetes and its complications. - : Elsevier BV. - 1056-8727 .- 1873-460X. ; 30:8, s. 1456-1461
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: To study prevalence of diabetic retinopathy (DR) at diagnosis (DRAD) and to estimate contributing risk by sociodemographic, cardiovascular and metabolic characteristics present in patients recently diagnosed with type 2 diabetes (T2D) or latent autoimmune diabetes in the adult (LADA).METHODS: Patients (n=2174) recently diagnosed T2D (93%) or LADA (7%) were included upon arrival for their baseline DR screening. Fundus photographs of 4902 eyes were graded by a senior ophthalmologist according to the International Diabetic Retinopathy Disease Severity Scale. Official registers held by Statistics Sweden provided sociodemographic variables. The National Patient Register and Swedish Prescribed Drug Register were used to assess cardiovascular risk. Beta cell function (HOMA2%b) and insulin sensitivity (HOMA2%s) were estimated from fasting (f) C-Peptide using the homeostasis model assessment (HOMA) 2 calculator. Odds ratios (OR) for DRAD were estimated using generalized estimating equation models.RESULTS: The prevalence of DRAD was 12% (7% mild and 5% moderate) and of diabetic macular edema it was 11% (all within vascular arch). The prevalence did not significantly differ between T2D and LADA. Due to sample size, the regression analysis of LADA patients did not yield any significant estimates. In T2D low educational level (≤9years) increased risk for DRAD by 44% (OR 1.44; 95% CI 1.07-1.93) and <50% beta-cell function adjusted for HbA1c and insulin sensitivity at diagnosis increased the risk by 77% (OR 1.77; 95% CI 1.28-2.44). For every unit increase in BMI, risk for DRAD decreased by 3% (OR 0.97; 95% CI 0.95-0.99).CONCLUSIONS: DRAD prevalence in patients recently diagnosed with T2D or is 12%. Low educational level and low beta cell function at diagnosis are risk factors for DRAD. Estimation of beta cell function from (f)C-Peptide and (f)P-Glucose may be a valuable tool in identifying patients at risk for DRAD.
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| 363. |
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| 364. |
- McCarthy, JJ, et al.
(författare)
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Polymorphisms of the HDL receptor gene associated with HDL cholesterol levels in diabetic kindred from three populations
- 2003
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Ingår i: Human Heredity. - : S. Karger AG. - 1423-0062 .- 0001-5652. ; 55:4, s. 163-170
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Tidskriftsartikel (refereegranskat)abstract
- Objective: We examined polymorphisms in the HDL receptor, SR-BI, for association with plasma HDL cholesterol levels. Methods: Study subjects, including 847 women and 725 men, were from families originally ascertained for type 2 diabetes from Finland, Sweden and Israel. Four common polymorphisms were examined in linear regression analysis: an exon 1 missense (EX1), exon 8 silent (EX8), intron 5 (IVS5) and intron 10 (IVS10) variants. Results: Genotype combinations for the three polymorphisms in linkage disequilibrium (IVS5, EX8 and IVS10) were found to be associated with HDL-C among women from the Israeli (p = 0.01) and Swedish (p = 0.06) populations. In Finnish women, the association was only apparent after taking into account effect modification by triglyceride levels (p = 0.04). One specific pattern of genotypes, denoted by presence of the IVS5_T and EX8_C alleles, and absence of the IVS10_G allele, was consistently associated with the lowest mean levels of HDL-C in women from all three populations. These same associations were not found in men. Conclusions: Polymorphic variation of the SR-BI gene may influence HDL-C levels and act in a sex-dependent manner. Copyright (C) 2003 S. Karger AG, Basel.
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| 365. |
- McCarthy, Shane, et al.
(författare)
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A reference panel of 64,976 haplotypes for genotype imputation
- 2016
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 48:10, s. 1279-1283
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Tidskriftsartikel (refereegranskat)abstract
- We describe a reference panel of 64,976 human haplotypes at 39,235,157 SNPs constructed using whole-genome sequence data from 20 studies of predominantly European ancestry. Using this resource leads to accurate genotype imputation at minor allele frequencies as low as 0.1% and a large increase in the number of SNPs tested in association studies, and it can help to discover and refine causal loci. We describe remote server resources that allow researchers to carry out imputation and phasing consistently and efficiently.
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| 366. |
- Melander, Olle, et al.
(författare)
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Association between a variant in the 11 beta-hydroxysteroid dehydrogenase type 2 gene and primary hypertension
- 2000
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Ingår i: Journal of Human Hypertension. - 1476-5527. ; 14:12, s. 819-823
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Tidskriftsartikel (refereegranskat)abstract
- The enzyme 11 beta-hydroxysteroid dehydrogenase type 2 (11BHSD2) converts cortisol to cortisone in the kidney, thereby protecting the mineralocorticoid receptor from the mineralocorticoid actions of cortisol. The syndrome of Apparent Mineralocorticoid Excess (AME), a rare monogenic form of early onset hypertension with autosomal recessive inheritance, is caused by homozygous or compound heterozygous loss of function mutations in the 11BHSD2 gene. Association has been reported between a microsatellite marker flanking the 11BHSD2 gene (D16S496) and primary hypertension. The aim of this study was to identify variants in the 11BHSD2 gene and to test if such variants or the D16S496 are associated with primary hypertension, in Swedes. To address this, the coding sequences of the 11BHSD2 gene was screened for mutations in 20 patients with primary hypertension with single strand conformation polymorphism and direct DNA sequencing techniques. A polymorphism was identified in exon 3; G534A (Glu178Glu). This polymorphism and the D16S496 microsatellite were tested for association with primary hypertension in a population consisting of 292 patients with primary hypertension and 263 normotensive control subjects. The frequency of G534G homozygotes was higher in patients with primary hypertension than in normotensive control subjects (92.8% vs 87.8%; P < 0.05). The allele frequencies of the D16S496 microsatellite did not differ between the two groups (chi(2) = 11.0, df = 10; P = 0.36). In conclusion, over-representation of individuals homozygous for the G534 allele in hypertensive patients compared with control subjects suggests that a mutation in linkage disequilibrium with the G534A polymorphism could increase susceptibility to primary hypertension. Journal of Human Hypertension (2000) 14, 819-823
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| 367. |
- Melander, Olle, et al.
(författare)
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Genetic variants of thiazide-sensitive NaCl-cotransporter in Gitelman's syndrome and primary hypertension
- 2000
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Ingår i: Hypertension. - 1524-4563. ; 36:3, s. 389-394
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Tidskriftsartikel (refereegranskat)abstract
- Gitelman's syndrome is an autosomal recessive disorder characterized by electrolyte disturbances and low blood pressure. The disease is caused by homozygous or compound heterozygous inactivating mutations in the thiazide-sensitive NaCl-cotransporter gene leading to reduced renal sodium reabsorption. We report 4 patients with Gitelman's syndrome from southern Sweden, all in whom we identified compound heterozygous mutations in the thiazide-sensitive NaCl-cotransporter gene (Gly439Ser, Gly731Arg, Gly741Arg, Thr304Pro, and 2745insAGCA), of which the latter 2 have not been described before. We hypothesized that such mutations in their heterozygous form protect against primary hypertension in the general population and that the gene may also harbor activating mutations that increase the risk for primary hypertension. Accordingly, the gene was screened for mutations in 20 patients with primary hypertension and in 20 normotensive subjects by single-strand conformation polymorphism and direct DNA sequencing. The Arg904Gln, Gly264Ala, and C1420T variants, found in the mutation screening of subjects without Gitelman's syndrome, were studied further. Population genotype frequencies were determined in 292 unrelated patients with primary hypertension and 264 unrelated normotensive subjects from southern Sweden. Gln904 homozygotes were overrepresented in hypertensive patients compared with normotensive subjects (5 of 292 versus 0 of 264; P:=0.03). In conclusion, we confirm that Gitelman's syndrome is caused by mutations in the thiazide-sensitive NaCl-cotransporter gene. Our results further suggest that subjects homozygous for the Gln904 variant have an increased risk for development of primary hypertension.
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| 368. |
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| 369. |
- Melander, Olle, et al.
(författare)
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Nt-proANP in plasma, a marker of salt sensitivity, is reduced in type 2 diabetes patients.
- 2005
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Ingår i: Journal of Internal Medicine. - : Wiley. - 1365-2796 .- 0954-6820. ; 257:3, s. 281-288
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Tidskriftsartikel (refereegranskat)abstract
- Objective. We recently showed that plasma concentration of N-terminal atrial natriuretic peptide (Nt-proANP) is strongly directly related to salt sensitivity. The aims of the present study were to test (i) whether plasma concentration of N-terminal brain natriuretic peptide (Nt-proBNP) is related to salt sensitivity and (ii) whether Nt-proANP, as a marker of salt sensitivity, differs between type 2 diabetes patients and nondiabetic subjects without a history of coronary heart disease. Methods. Nt-proBNP was determined in 30 Swedish normal subjects with heredity for primary hypertension and salt sensitivity was defined as the difference between mean arterial blood pressure after 1 week on a high-salt diet (240 mmol day-1) and 1 week on a low-salt diet (10 mmol day-1). Nt-proANP was measured in 253 patients with type 2 diabetes and in 230 nondiabetic subjects aged 40–70 years, all without a history of coronary heart disease. Results. Amongst the 30 subjects, in whom salt sensitivity was directly measured, Nt-proBNP was not correlated with salt sensitivity (R = −0.18, P = 0.35). Nt-proANP (median, interquartile range) was lower in patients with type 2 diabetes (505, 387–661 pmol L-1) than in nondiabetic subjects (536, 421–696 pmol L-1) (P = 0.02). In a multiple regression analysis heart rate (P < 0.00001), diastolic blood pressure (P = 0.02) and diabetes status (P = 0.02) were inversely related whereas age (P < 0.00001), cystatin C (P = 0.0006), hypertension treatment (P = 0.002) and female sex (P = 0.006) were directly related to ln(Nt-proANP). Conclusion. In contrast to Nt-proANP, Nt-proBNP is not related to salt sensitivity. Salt sensitivity, as estimated by Nt-proANP, seems to be reduced in type 2 diabetes.
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| 370. |
- Melander, Olle, et al.
(författare)
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Plasma ProANP(1-30) reflects salt sensitivity in subjects with heredity for hypertension
- 2002
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Ingår i: Hypertension. - 1524-4563. ; 39:5, s. 996-999
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Tidskriftsartikel (refereegranskat)abstract
- The aim of the present Study was to investigate whether plasma concentration of proANP(1-30), the N-terminal fragment of the atrial natriuretic peptide prohormone, or 24-hour urinary excretion of urodilatin reflects the degree of Salt sensitivity in hypertension-prone individuals. Plasma concentration of proANP(1-30) and urinary urodilatin excretion were determined at baseline, after I week on a low-salt diet (10 nmol/d) and after another week on a high-salt diet (240 mmol/d) in 30 healthy, subjects with heredity for hypertension. Salt sensitivity was defined as the difference between mean arterial blood pressure after the high-salt diet and the mean arterial blood pressure after the low-salt diet. High- versus low-salt intake increased proANP(1-30) (668+/-330 versus 358+/-150 pmol/L P<0.00001) and urodilatin (18.7+/-5.2 versus 16.0+/-8.3 pmol/24 h P<0.05). ProANP(1-30) correlated with salt sensitivity at baseline (r=0.76, P<0.000001). after the low- (r=0.80. P<0.0000001) and high-salt diets (r=0.85, P<0.00000001). The increase proANP(1-30) induced by changing from the low- to the high-salt diet was also directly related to salt sensitivity (r=0.78, P<0.000001). ProANP(1-30) was not related to urinary sodium excretion. Neither urodilatin nor the sodium-induced change in urodilatin correlated with salt sensitivity. However, urodilatin was related to the urinary sodium excretion at baseline (r=0.58, P<0.01) and after the high-salt diet (r=0.62, P<0.001). In conclusion, the close correlations between proANP(1-30) and salt sensitivity suggest that proANP(1-30) may serve as a marker for salt sensitivity and could be useful in identifying subjects who would benefit from dietary salt restriction to prevent development of hypertension.
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