| 1. |
- Lindskog, Sven, et al.
(författare)
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Validation of an Algorithm for Chronic Periodontitis Risk Assessment and Prognostication : Analysis of an Inflammatory Reactivity Test and Selected Risk Predictors
- 2010
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Ingår i: Journal of Periodontology. - : American Academy of Periodontology. - 0022-3492 .- 1943-3670. ; 81:6, s. 837-847
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Tidskriftsartikel (refereegranskat)abstract
- Background: Patients with severe forms of chronic periodontitis present with varying degrees of decreased inflammatory reactivity. A previously reported algorithm for chronic periodontitis risk assessment and prognostication is based on the analysis of some 20 risk predictors. One of these predictors is a skin provocation test that assesses the individual patient's reactivity to a lipid A challenge. The aim of this report was to analyze results from validation data for the algorithm with respect to the contribution of results of the skin provocation test as a risk predictor for the progression of chronic periodontitis and to compare these results with the contribution from other predictors, namely smoking, angular bony destruction, furcation involvement, abutment teeth, and endodontic pathology. Methods: Data from a previously reported clinical validation sample were used for the analysis, including the calculation of quality measures and explanatory values using different types of regression analysis and non-parametric testing. Results: Smoking, endodontic pathology, abutment teeth, angular bony destruction, and furcation involvement presented with individual explanatory values for periodontitis progression between 4% and 13% and highly significant parameter estimates. Explanatory values for the results of the skin provocation test ranged between 2.6% and 5.1% depending on the disease severity group, with a positive predictive value of 82% for the identification of high-risk patients. Conclusion: The skin provocation test provided a clinically significant contribution to the quality of analysis with the periodontitis risk and prognostication algorithm, in particular in the selection of high-risk patients for in-depth individual tooth analysis.
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| 2. |
- Lindskog, Sven, et al.
(författare)
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Validation of an Algorithm for Chronic Periodontitis Risk Assessment and Prognostication: Risk Predictors, Explanatory Values, Measures of Quality, and Clinical Use
- 2010
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Ingår i: JOURNAL OF PERIODONTOLOGY. - : American Academy of Periodontology. - 0022-3492 .- 1943-3670. ; 81:4, s. 584-593
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Tidskriftsartikel (refereegranskat)abstract
- Background: The American Academy of Periodontology has recently stated that, "[risk assessment will become] increasingly important in periodontal treatment planning and should be part of every comprehensive dental and periodontal evaluation." (J Periodontol 2006;77:1608). Unaided risk assessment and prognostication show significant variability because chronic periodontitis is a multifactorial disease. This report summarizes the clinical validation of an algorithm for chronic periodontitis risk assessment and prognostication. The algorithm is a Web-based analytic tool that integrates some 20 risk predictors and calculates scores indicating levels of risk for chronic periodontitis for the dentition (Level I) and, if an elevated risk is found, prognosticates disease progression tooth by tooth (Level II). Methods: An independent clinical validation sample was generated in an open, prospective clinical trial and analyzed in a predetermined validation plan. Results: The analyses identified two threshold scores above which significant progression of periodontitis was found. Based on these scores, sufficiently high explanatory values with significant and increasing parameter estimates for increasing risk were established in Level I, justifying detailed analysis tooth by tooth in Level II. Subsequent prognostication of chronic periodontitis in Level II was found to be accompanied by clinically relevant measures of quality in relation to rates of disease progression. Three score intervals representing increasing levels of periodontitis progression were identified corresponding to increasing levels of significant annual marginal bone loss. Conclusions: The predictors included in the algorithm reflect a relevant selection for periodontitis risk assessment. Risk assessment and prognostication with the algorithm provides the clinician with a validated, reliable, consistent, and objective tool supporting treatment planning.
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| 3. |
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| 4. |
- Eriksson, Anna-Lena, 1971, et al.
(författare)
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Association between the low activity genotype of catechol-O-methyltransferase and myocardial infarction in a hypertensive population
- 2004
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Ingår i: Eur Heart J. ; 25:5, s. 386-91
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Tidskriftsartikel (refereegranskat)abstract
- AIM: Estrogens regulate several biological processes involved in the pathogenesis of myocardial infarction. Catechol-O-methyltransferase (COMT) is a key enzyme in the degradation of estrogens. There is a functional polymorphism in the COMT gene (Val158Met), affecting the activity of the enzyme. We investigated if the low activity genotype of COMT is associated with an altered risk of myocardial infarction. METHODS AND RESULTS: In a prospectively followed hypertensive cohort we identified 174 patients who suffered a myocardial infarction during the study and compared them to 348 controls from the same cohort. The COMT polymorphism and serum levels of sex hormones were analysed. Patients homozygous for the low activity COMT genotype had a decreased risk of myocardial infarction compared to those with the high activity genotype, odds ratio 0.65 (95% CI 0.44-0.97, p=0.033 ). The protective effect of the low activity genotype was most evident among older patients (> 58 years of age), odds ratio 0.43 (95% CI 0.23-0.79, p=0.006 ). Serum levels of estradiol were increased ( p=0.006 ) in males with the low activity genotype. CONCLUSIONS: Our findings suggest that the low activity COMT genotype is protective against myocardial infarction. One may speculate that the altered estrogen status could be involved in this effect.
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| 5. |
- Huth, Cornelia, et al.
(författare)
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IL6 gene promoter polymorphisms and type 2 diabetes - Joint analysis of individual participants' data from 21 studies
- 2006
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Ingår i: DIABETES. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 55:10, s. 2915-2921
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Tidskriftsartikel (refereegranskat)abstract
- Several lines of evidence indicate a causal role of the cytokine interleukin (IL)-6 in the development of type 2 diabetes in humans. Two common polymorphisms in the promoter of the IL-6 encoding gene IL6, −174G>C (rs1800795) and −573G>C (rs1800796), have been investigated for association with type 2 diabetes in numerous studies but with results that have been largely equivocal. To clarify the relationship between the two IL6 variants and type 2 diabetes, we analyzed individual data on >20,000 participants from 21 published and unpublished studies. Collected data represent eight different countries, making this the largest association analysis for type 2 diabetes reported to date. The GC and CC genotypes of IL6 −174G>C were associated with a decreased risk of type 2 diabetes (odds ratio 0.91, P = 0.037), corresponding to a risk modification of nearly 9%. No evidence for association was found between IL6 −573G>C and type 2 diabetes. The observed association of the IL6 −174 C-allele with a reduced risk of type 2 diabetes provides further evidence for the hypothesis that immune mediators are causally related to type 2 diabetes; however, because the association is borderline significant, additional data are still needed to confirm this finding.
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| 6. |
- Niklason, Anders, 1960, et al.
(författare)
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Development of diabetes is retarded by ACE inhibition in hypertensive patients--a subanalysis of the Captopril Prevention Project (CAPPP).
- 2004
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Ingår i: Journal of hypertension. - 0263-6352 .- 1473-5598. ; 22:3, s. 645-52
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: The Captopril Prevention Project (CAPPP) was designed as a prospective intervention trial comparing the effect of a treatment based on the angiotensin-converting enzyme (ACE) inhibitor captopril with that of a conventional diuretic and/or beta-blocker-based therapy, in 10,985 hypertensive patients. There was no difference in the primary cardiovascular morbidity and mortality endpoint. A lower incidence of diabetes mellitus during captopril treatment was observed in the whole CAPPP cohort that was non-diabetic at baseline (n = 10,413) as well as in such CAPPP patients that were previously untreated (n = 5033). METHODS AND RESULTS: A multivariate analysis of variables associated with the risk of developing diabetes in CAPPP demonstrated that glucose, body mass index (BMI), haemoglobin (Hb), age, 'SBP x Untreated' (the interaction between systolic blood pressure at baseline and newly diagnosed hypertension), cholesterol and prior antihypertensive treatment came out as risk factors. Based on these factors, a risk score for development of diabetes was calculated for all non-diabetic patients, who were divided into tertiles. For each tertile of risk, captopril therapy was associated with a reduced risk of diabetes development compared with conventional diuretic and/or beta-blocker therapy. When the non-diabetic cohort was divided into two subcohorts; previously treated and previously untreated patients, it turned out that the risk factors for developing diabetes differed between these two subcohorts. Only glucose, BMI and Hb came out as risk factors in all analysed cohorts. CONCLUSION: A captopril-based antihypertensive treatment regimen is associated with a lower risk of diabetes development, compared with conventional therapy based on diuretics and/or beta-blockers.
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| 7. |
- Skrtic, Stanko, 1970, et al.
(författare)
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Risk factor identification and assessment in hypertension and diabetes (RIAHD) study.
- 2006
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Ingår i: Blood pressure. - : Informa UK Limited. - 0803-7051 .- 1651-1999. ; 15:6, s. 367-74
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Tidskriftsartikel (refereegranskat)abstract
- The RIAHD (Risk factor Identification and Assessment in Hypertension and Diabetes) study was conducted as a non-interventional study in 699 patients with hypertension without additional risk factors (low-risk) or with additional risk factors (high-risk), primarily diabetes and/or micro/macroalbuminuria (MA/A). The RIAHD study aimed to assess novel cardiovascular risk factors (RFs) such as blood viscosity, inflammatory markers and selected genetic polymorphisms. In addition, the RIAHD study also aimed to examine home versus office blood pressures (BPs), objective cardiovascular risk according to ESH/ESC Systematic Coronary Risk Evaluation systems (SCORE) and subjectively expressed risk (clinical judgment) by physicians and patients. The health economic impact of other RFs, associated clinical conditions and target organ damage was also studied by evaluating healthcare utilization and sick leave in high-risk patients. In terms of circulating RFs, measured and calculated whole blood viscosity did not differ between the high and low-risk patient groups. Fibrinogen was significantly increased in the high-risk group, while hsCRP did not differ between the two groups. Self-measured BPs at home differed from BPs measured in the office. The average systolic home BPs was 11.8 mmHg lower in the low-risk group and 6.7 mmHg lower in the high-risk group. The diastolic home BPs averages differed 7.1 mm Hg and 4.1 mmHg from office BPs in the low-risk and high-risk groups, respectively. A higher home BP compared with the office BP, i.e. masked high BP values, was found in 21% of patients in the low-risk group and 32% of patients in the high-risk group. Global CV risk assessment (high-risk or low-risk) by the physicians corresponded well to objective risk evaluation (ESH/ESC) in the high-risk hypertensive patients, while physicians tended to underestimate the patients CV risk in the low-risk group (without diabetes and/or MA/A). Proper global risk assessment by judgement is often difficult in cardiovascular patients. The RIAHD study emphasizes the importance of performing a more extended RF assessment in hypertensive patients with as well as without diabetes and/or micro/macroalbuminuria in order to expose the full RF profile.
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| 8. |
- Wallerstedt, Susanna Maria, 1970, et al.
(författare)
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Serum leptin and myocardial infarction in hypertension.
- 2004
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Ingår i: Blood pressure. - : Informa UK Limited. - 0803-7051 .- 1651-1999. ; 13:4, s. 243-6
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Tidskriftsartikel (refereegranskat)abstract
- The adipose tissue-derived hormone leptin is among the physiologic processes involved in cardiovascular regulation. The aim of the present study was to elucidate if serum leptin may predict cardiovascular risk, particularly myocardial infarction (MI), in hypertensive men and women. In a prospective study cohort of hypertensive men and women, serum leptin was compared in 171 patients with MI and in 342 matched controls. The mean serum concentration of leptin was 25.1 +/- 20.0 ng/ml in the MI patients and 20.0 +/- 16.6 ng/ml in the controls (p = 0.007). The association between serum leptin and MI was independent of traditional risk factors. Leptin concentrations were higher in women than in men. In women, serum leptin was the most important predictor of MI. The present study indicates that serum leptin is associated with MI in a hypertensive population. Leptin concentrations may be of practical importance when estimating the risk of MI, especially in women, where leptin was found to be the most important predictor for MI.
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