ISSN:0002-9629    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Cardiovascular disease (CVD) is the No. 1 cause of mortality in the United States and it disproportionately affects African Americans. However, there are earlier reports that African Americans had significantly less CVD than whites. This racial discrepancy in CVD rates was noticed primarily for coronary heart disease (CHD). This issue was examined in the Evans County (Georgia) Cardiovascular Disease Study conducted in the 1960s. It showed that African American men had significantly lower rates of CHD than white men. Over the last couple of decades, the rates of CVD have been declining. However, the rate of decline of CVD in African Americans has not been equal to that seen in whites, such that African Americans now have a disproportionate share of CVD in the United States. In the 1990s, the Jackson Heart Study was designed to explore the reasons for the current racial discrepancy. This articles reviews the findings of the Evans County Study and explores various hypotheses for why CVD in African Americans has evolved from a disease from which African Americans may have been “protected” to one in which they shoulder a disproportionate burden.

ISSN:0002-9629    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

This article provides an overview of the evidence on the ways racism can affect the disproportionate rates of cardiovascular disease (CVD) in African Americans. It describes the significant health disparities in CVD for blacks and whites and suggests that racial disparities should be understood within the context of persistent inequities in societal institutions and relations. Evidence and potential pathways for exploring effects of 3 levels of racism on cardiovascular health risk factors and outcomes are reviewed. First,institutional racismcan lead to limited opportunities for socioeconomic mobility, differential access to goods and resources, and poor living conditions that can adversely affect cardiovascular health. Second,perceived/personally mediated racismacts as a stressor and can induce psychophysiological reactions that negatively affect cardiovascular health. Third, in race-conscious societies, such as the United States, the negative self-evaluations of accepting negative cultural stereotypes as true (internalized racism) can have deleterious effects on cardiovascular health. Few population-based studies have examined the relationship between racism and CVD. The findings, though suggestive of a positive association, are neither consistent nor clear. The research agenda of the Jackson Heart Study in addressing the role of racism in CVD is presented.

ISSN:0002-9629    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Diabetes mellitus (DM) is an important risk factor for the development of cardiovascular disease. Extensive clinical, epidemiologic, and basic studies suggest that excessive tissue iron stores may contribute to the occurrence and complications of DM. Secondary diabetes occurs in inherited pathologic iron overload syndromes of European- and African-derived populations and is an established complication of transfusional iron overload. Epidemiologic studies have repeatedly shown positive correlation between levels of serum ferritin and those of fasting glucose, insulin, and glycosylated hemoglobin. Iron reduction therapy in hereditary hemochromatosis and transfusional iron overload is associated with improved glucose tolerance and reduced incidence of secondary diabetes. Trials of iron reduction therapy in diabetes mellitus, although limited and inconclusive, have shown clinical improvement in some patients. The current article reviews evidence suggesting that tissue iron contributes to DM and its complications and presents preliminary data that emphasize the potential importance of iron overload in DM of African Americans.

ISSN:0002-9629    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Dyslipidemia is a cardiovascular disease (CVD) risk factor that is associated with enhanced atherosclerosis and plaque instability. Renal insufficiency is associated with abnormalities in lipoprotein metabolism in both the early and the advanced stages of chronic renal failure. These include alterations in apolipoprotein A (apo A)- and B- containing lipoproteins, high-density lipoproteins, and triglycerides. In animal models, these alterations in lipid metabolism and action lead to macrophage activation and infiltration in the kidney with resultant tubulointerstitial and endothelial cell injury. Limited data in humans suggest that, in addition to contributing to CVD, dyslipidemia may be a risk factor for the progression of renal disease. The effects of dyslipidemia on the kidney are mainly observed in those with other risk factors for renal disease progression such as hypertension, diabetes, and proteinuria. Renal disease is a strong risk factor for CVD and African Americans have high rates of renal disease. Therefore, examining the effects of dyslipidemia on the development or progression or renal disease will be an important question for the Jackson Heart Study and is the topic of this review.

ISSN:0002-9629    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Medications cause renal failure through a variety of mechanisms. Hemodynamic renal failure may result from drugs that reduce renal prostaglandins and hence renal blood flow and glomerular filtration rate. A relatively new group of drugs with this potential is the cyclooxygenase-2 selective inhibitors. Direct renal tubular toxicity has also been described with a number of new medications with unique effects on the epithelial cells of the kidney. These include the antiviral agents cidofovir, adefovir, and tenofovir as well as the bisphosphonate pamidronate. Additionally, crystal deposition in the kidney may promote the development of renal failure. Several different drugs have been described to induce crystal nephropathy, including the antiparasitic drug sulfadiazine, the antiviral agent acyclovir, and the protease inhibitor indinavir. Finally, an unusual form of renal failure characterized by swollen, vacuolated proximal tubular cells can develop from hyperosmolar substances. Agents recently described to induce an “osmotic nephrosis” include intravenous immunoglobulin and the plasma expander hydroxyethyl starch.

ISSN:0002-9629    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

We report a rare case of a patient with long-standing familial Mediterranean fever who presented with sudden onset of dyspnea, abdominal pain, and cutaneous manifestations. Chest CT and histologic preparations disclosed pulmonary hemorrhage and signs of systemic vasculitis. Cyclophosphamide and steroid therapy were initiated, with marked improvement. Based on this and 1 other case, we propose that systemic vasculitis should be included as a clinical manifestation of FMF.

ISSN:0002-9629    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Infections withBacteroidesspecies have been noted to occur in association with cases of thrombophlebitis. This association has led to the speculation that the microorganisms themselves may contribute to the pathogenesis of thrombus formation through elaborated enzymes, including heparinases, or by interactions between the clotting cascade and the unique structure of theBacteroideslipopolysaccharide. Anti-phospholipid antibodies have been linked with hypercoagulable states and thrombus formation. Although a number of infections have been associated with the transient production of anti-cardiolipin antibodies, the effect the antibodies may have in contributing to thrombus formation is not well understood. The occurrence ofBacteroidesspecies infection with transient anti-cardiolipin antibody has not been previously reported.

ISSN:0002-9629    

出版商:OVID    

年代:2003

数据来源: OVID