Risk Factor Identification and Primary Prevention of Stroke in African-American Populations.

1998 ◽  
pp. 118-128
Author(s):  
W.R. Johnson Jr
2020 ◽  
Author(s):  
Stefano Ciardullo ◽  
Tommaso Monti ◽  
Gianluca Perseghin

<b>Objective:</b> Type 2 diabetes mellitus (T2DM) is an important risk factor for the progression of metabolic liver disease to advanced fibrosis. Here, we provide an estimate of the prevalence of steatosis and fibrosis in US adults with T2DM based on transient elastography (TE) and identify factors associated with these conditions. <p><b>Research Design and Methods: </b>This is a cross-sectional study of US adults with T2DM participating in the 2017-2018 cycle of the National Health and Nutrition Examination Survey who were evaluated by TE. Hepatic steatosis and fibrosis were diagnosed by the median value of Controlled Attenuation Parameter (CAP) and Liver Stiffness Measurement (LSM), respectively.</p> <p><b>Results:</b> Among the 825 patients with reliable TE exams, 484 (53.7%) were assessed using the M probe and 341 (46.3%) using the XL probe. Liver steatosis (CAP≥274 dB/m), advanced fibrosis (LSM≥9.7 Kpa) and cirrhosis (LSM≥13.6 Kpa) were present in 73.8% (95% CI 68.5%-78.5%), 15.4% (95% CI 12.2%-19.0%) and 7.7% (95% CI 4.8%-11.9%) of patients, respectively. Mean age of patients with advanced fibrosis and cirrhosis was 63.7 ± 2.2 years and 57.8 ± 1.6 years, respectively. In the multivariable logistic regression model, body mass index (BMI), non-African American ethnicity and alanine aminotransferase levels were independent predictors of steatosis, while BMI, non-African American ethnicity, aspartate aminotransferase and gamma-glutamyltranspeptidase levels were independent predictors of advanced fibrosis.</p> <p><b>Conclusions:</b> Prevalence of both liver steatosis and fibrosis are high in patients with T2DM from the US and obesity is a major risk factor. Our results support the screening of these conditions among diabetic patients.</p>


2019 ◽  
Vol 47 (6) ◽  
pp. 535-547 ◽  
Author(s):  
I. N. Voynovan ◽  
Yu. V. Embutnieks ◽  
D. V. Mareeva ◽  
S. V. Kolbasnikov ◽  
D. S. Bordin

Russia is a country with a high prevalence of Helicobacter pylori (HP) infection, a high incidence of gastric cancer, and its late diagnosis. HР infection has been recognized as the leading manageable risk factor for gastric cancer. Accurate diagnostic tests must be used to identify and control the effectiveness of HP eradication, and effective schemes must be implemented for HP eradication. The aim of this article was to analyze the latest consensus documents, systematic reviews and meta-analyzes that reflected the role of HP as a risk factor for the development of gastric cancer, as well as measures for the risk reduction. We describe in detail the diagnostic methods for HP infection, provide data on their use in the Russian Federation, and analyze the efficacy of eradication regimens. In all HPinfected individuals, HP leads to chronic inflammation in the gastric mucosa and launches a precancerous cascade (Correa's cascade). The risk of gastric cancer increases with severe atrophy, intestinal metaplasia and dysplasia. Primary prevention of gastric cancer is most effective if the eradication is performed before atrophic gastritis develops. The available consensus documents underline the importance of HP infection identification by accurate diagnostics at this stage of chronic gastritis. In Russia, the primary HP diagnosis is based on histology (37.7%), rapid urease test (29.2%), and serology (29.7%). HP stool antigen test (31.3%), 13C-urea breath test (23.4%) and the histological method (23.3%) are most often used to control eradication. Currently, the first line of eradication therapy is recommended as triple therapy with clarithromycin prescribed for 14 days. It is recommended to use double dose of proton pump inhibitors and bismuth to increase the effectiveness of this scheme. A 14-days triple regimen enhanced by bismuth has been recommended as the first-line therapy in the Russian Federation.


2018 ◽  
Vol 29 (7) ◽  
pp. 1939-1947 ◽  
Author(s):  
Adrienne Tin ◽  
Girish Nadkarni ◽  
Anne M. Evans ◽  
Cheryl A. Winkler ◽  
Erwin Bottinger ◽  
...  

Background Metabolite levels reflect physiologic homeostasis and may serve as biomarkers of disease progression. Identifying metabolites associated with APOL1 risk alleles—genetic variants associated with CKD risk commonly present in persons of African descent—may reveal novel markers of CKD progression relevant to other populations.Methods We evaluated associations between the number of APOL1 risk alleles and 760 serum metabolites identified via untargeted profiling in participants of the African American Study of Kidney Disease and Hypertension (AASK) (n=588; Bonferroni significance threshold P<6.5×10−5) and replicated findings in 678 black participants with CKD in BioMe, an electronic medical record–linked biobank. We tested the metabolite association with CKD progression in AASK, BioMe, and the Modification of Diet in Renal Disease (MDRD) Study.Results One metabolite, 6-bromotryptophan, was significant in AASK (P=4.7×10−5) and replicated in BioMe (P=5.7×10−3) participants, with lower levels associated with more APOL1 risk alleles. Lower levels of 6-bromotryptophan were associated with CKD progression in AASK and BioMe participants and in white participants in the MDRD Study, independent of demographics and clinical characteristics, including baseline GFR (adjusted hazard ratio per two-fold higher 6-bromotryptophan level, AASK, 0.76; 95% confidence interval [95% CI], 0.64 to 0.91; BioMe, 0.61; 95% CI, 0.43 to 0.85; MDRD, 0.52; 95% CI, 0.34 to 0.79). The interaction between the APOL1 risk alleles and 6-bromotryptophan was not significant. The identity of 6-bromotryptophan was confirmed in experiments comparing its molecular signature with that of authentic standards of other bromotryptophan isomers.Conclusions Serum 6-bromotryptophan is a consistent and novel risk factor for CKD progression.


2022 ◽  
Author(s):  
Theresa A. Hastert ◽  
Julie J Ruterbusch ◽  
Jean A. McDougall ◽  
Jamaica R.M. Robinson ◽  
Shaila M. Strayhorn ◽  
...  

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Amalie C Thavikulwat ◽  
Todd T Tomson ◽  
Bradley P Knight ◽  
Robert O Bonow ◽  
Lubna Choudhury

Introduction: Hypertrophic cardiomyopathy (HCM) is a leading cause of sudden cardiac death (SCD) in young adults. Implantable cardioverter defibrillators (ICD) effectively terminate ventricular tachycardia (VT) and fibrillation (VF) that cause SCD, but the reported prevalence of and patient characteristics leading to appropriate ICD therapy in HCM have been variable. Hypothesis: We hypothesized that some risk factors may be more prevalent than others in patients with HCM who receive appropriate ICD therapy and that the overall incidence of appropriate therapy may be lower than that reported previously. Methods: We retrospectively studied all patients with HCM who were treated with ICDs at our referral center from 2000-2013 to determine the rates of appropriate and inappropriate ICD therapies. Results: Of 1136 patients with HCM, we identified 135 who underwent ICD implantation (125 for primary and 10 for secondary prevention), aged 18-81 years (mean 48±17) at the time of implantation. The mean follow-up time was 5.2±4.5 years. Appropriate ICD intervention occurred in 20 of 135 patients (2.8%/year) by providing a shock or antitachycardia pacing in response to VT or VF. The annual rate of appropriate ICD therapy was 2.4%/year for primary and 7.2%/year for secondary prevention devices. Commonly used risk factors were equally prevalent among patients who received appropriate therapy and those who did not; furthermore, the likelihood of receiving appropriate therapy in the presence of each risk factor was similar (Figure). Inappropriate ICD therapy occurred in 27 patients (3.8%/year). Conclusions: ICDs provide clear benefit to patients who experience life-threatening arrhythmias, particularly those being treated for secondary prevention. However, the appropriate therapy rate for primary prevention was lower than previously reported, and no single risk factor appeared to have stronger association with appropriate ICD therapy than others.


Author(s):  
Deniz Yeter ◽  
Ellen C. Banks ◽  
Michael Aschner

There is no safe detectable level of lead (Pb) in the blood of young children. In the United States, predominantly African-American Black children are exposed to more Pb and present with the highest mean blood lead levels (BLLs). However, racial disparity has not been fully examined within risk factors for early childhood Pb exposure. Therefore, we conducted secondary analysis of blood Pb determinations for 2841 US children at ages 1–5 years with citizenship examined by the cross-sectional 1999 to 2010 National Health and Nutrition Examination Survey (NHANES). The primary measures were racial disparities for continuous BLLs or an elevated BLL (EBLL) ≥5 µg/dL in selected risk factors between non-Hispanic Black children (n = 608) and both non-Hispanic White (n = 1208) or Hispanic (n = 1025) children. Selected risk factors included indoor household smoking, low income or poverty, older housing built before 1978 or 1950, low primary guardian education <12th grade/general education diploma (GED), or younger age between 1 and 3 years. Data were analyzed using a regression model corrected for risk factors and other confounding variables. Overall, Black children had an adjusted +0.83 µg/dL blood Pb (95% CI 0.65 to 1.00, p < 0.001) and a 2.8 times higher odds of having an EBLL ≥5 µg/dL (95% CI 1.9 to 3.9, p < 0.001). When stratified by risk factor group, Black children had an adjusted 0.73 to 1.41 µg/dL more blood Pb (p < 0.001 respectively) and a 1.8 to 5.6 times higher odds of having an EBLL ≥5 µg/dL (p ≤ 0.05 respectively) for every selected risk factor that was tested. For Black children nationwide, one in four residing in pre-1950 housing and one in six living in poverty presented with an EBLL ≥5 µg/dL. In conclusion, significant nationwide racial disparity in blood Pb outcomes persist for predominantly African-American Black children even after correcting for risk factors and other variables. This racial disparity further persists within housing, socio-economic, and age-related risk factors of blood Pb outcomes that are much more severe for Black children.


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