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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to examine the incidence of different renal lesions in rheumatoid arthritis (RA) and to determine their relationships with the type of previous drug therapy and with the specific features of immune disorders. Ninety four patients, 84 (89.9%) females and 10 (10.6%) males) with RA whose mean age was 45.2 +/- 11.9 years and duration of the disease 7.5 +/- 6.5 years were examined. Most of them had degrees 2 and 3 PA (62.7 and 24.4%, respectively). Systemic manifestations were encountered in 60 (63.8%) patients. Eighty one patients took nonsteroidal antiinflammatory drugs (NSAID) continuously: 18 patients for a year, 32 for 5 years, 14 for 6 to 10 years, and 17 for over 10 years. All the patients underwent clinical, laboratory, and instrumental study of partial functions of the kidney. Immunological study involved solid-phase immunoassay of IgA and IgM rheumatoid factor, von Willebrand factor antigens (WF:Ag), C-reactive protein. The serum concentrations were measured by the Mancini method. Changes in urinalysis and/or signs of decreased glomerular and tubular functions were found in 69 (73.%) patients, 25 (26.6%) had arterial hypertension. Tubular dysfunctions were more common [31 (32.9%) patients]. Signs of early renal failure were detected in 20 (21.2%) patients. There were no cases of acute renal failure. Amyloidosis, glomerulonephritis, pyelonephritis were diagnosed in 5 (5.3%), 16 (17%), and 13 (13.8%) patients, respectively. The above renal lesions were concurrent in some patients. Renal lesion correlated with the progression and severity of RA, the presence of systemic manifestations, and age. There was no relationship of both 5- and 10-year use of NSAID to the symptoms of renal disease. The use of these drugs for over 10 years was concurrent with the signs of chronic renal failure and arterial hypertension. Analyzing immunological disorders showed an association of increased erythrocytic sedimentation rates and WF:Ag with amyloidosis, that of higher IgA concentrations with proteinuria and tubular dysfunctions. It is concluded that renal lesion is common in RA, there is a predominance of tubular interstitial changes. In rare cases nephropathy is characterized by a benign course and fails to result in uremia. The symptoms of renal diseases are largely associated with RA progression and severity and the patients' age. Prolonged continuous use of NSAID may contribute to the development of renal failure. Different immune mechanisms are involved in the pathogenesis of glomerular and tubular nephropathy in RA.
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PMID:[Clinico-immunological aspects of renal lesions in rheumatoid arthritis]. 1152 52

Women with diabetes mellitus are at high risk of myocardial infarction (MI), and it is well recognized that smoking, hypertension, hyperlipidaemia and the diabetic state itself do not fully explain this increased risk. During the last decade, growing evidence has accumulated that the immune system, with oxidized low-density lipoprotein (LDL) as a key antigen, plays an important role in the development of atherosclerosis. The aim of the present study was to explore the association between the immune response, as measured by antibody titres to malondialdehyde-treated LDL (MDA-LDL) and levels of C-reactive protein (CRP; a marker of inflammation), and diabetes mellitus and MI in women. Women (35-64 years) with diabetes (n=18) and non-diabetic women (n=46) who had been treated in hospital for MI were compared with diabetic women without MI (n=35) and healthy controls (n=70). Blood samples were collected after an overnight fast. CRP was determined with a highly sensitive immuno-enzymometric assay. IgM and IgG antibodies against MDA-LDL were analysed with a solid-phase ELISA technique. Women with diabetes but without previous MI were more similar to women with previous MI (both with and without diabetes) than to the healthy controls. Compared with healthy women, the women with diabetes and/or MI had higher IgG (P<0.05) and lower IgM (P=0.006) antibody titres against oxidized LDL and higher CRP levels (P<0.001), associations that were independent of other cardiovascular risk factors. These findings might indicate a differentiated immune response against modified LDL, more pronounced inflammation and a more aggressive atherosclerotic process in women with diabetes.
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PMID:Autoantibodies against oxidized low-density lipoprotein and C-reactive protein are associated with diabetes and myocardial infarction in women. 1167 58

Urinary tract infections are common in infants and children. Pyelonephritis may result in serious complications, such as renal scarring, hypertension, and renal failure. Identification of the timing of release of inflammatory cytokines in relation to pyelonephritis and its treatment is essential for designing interventions that would minimize tissue damage. To this end, we measured urinary cytokine concentrations of interleukin-1 beta (IL-1 beta), IL-6, and IL-8 in infants and children with pyelonephritis and in healthy children. Children that presented to our institution with presumed urinary tract infection were given the diagnosis of pyelonephritis if they had a positive urine culture, pyuria, and one or more of the following indicators of systemic involvement: fever, elevated peripheral white blood cell count, or elevated C-reactive protein. Urine samples were obtained at the time of presentation prior to the administration of antibiotics, immediately after completion of the first dose of antibiotics, and at follow up 12 to 24 h after presentation. IL-1 beta, IL-6, and IL-8 concentrations were measured by enzyme-linked immunosorbent assay. Creatinine concentrations were also determined, and cytokine/creatinine ratios were calculated to standardize samples. Differences between pre-antibiotic and follow-up cytokine/creatinine ratios were significant for IL-1 beta, IL-6, and IL-8 (P < 0.01). Differences between pre-antibiotic and control cytokine/creatinine ratios were also significant for IL-1 beta, IL-6, and IL-8 (P < 0.01). Our study revealed that the urinary tract cytokine response to infection is intense but dissipates shortly after the initiation of antibiotic treatment. This suggests that renal damage due to inflammation begins early in infection, underscoring the need for rapid diagnosis and intervention.
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PMID:Cytokine profiles of pediatric patients treated with antibiotics for pyelonephritis: potential therapeutic impact. 1168 40

Coronary artery disease (CAD) is the leading cause of death in patients with end-stage renal disease (ESRD). Recent evidence suggests that the expression of Fas, a molecule implicated in the initiation of apoptosis in various cell types, is increased at sites of atherosclerotic plaques. However, the significance of plasma levels of the soluble form of Fas (sFas) and its ligand (sFas-L) as markers of atherosclerosis has yet to be defined. The present report is a cross-sectional analysis of baseline data from an ongoing prospective study designed to evaluate the role of sFas and sFas-L as markers of CAD in ESRD. We evaluated the association between plasma levels of sFas and sFas-L and evidence of CAD in a cohort of 107 chronic hemodialysis patients. Plasma levels of sFas were significantly greater (P = 0.04) among subjects with (n = 64) than without evidence of CAD (n = 43). Plasma levels of sFas-L were similar in both groups. Using multivariate analysis, sFas level was found to be independently associated with CAD (P = 0.01) after adjustment for classic risk factors for CAD (hyperlipidemia, diabetes, hypertension, and smoking), markers of inflammation (C-reactive protein [CRP], intercellular adhesion molecule 1), and other confounders. An increase of one quintile in plasma concentration of sFas was associated with an odds ratio for CAD of 1.64 (95% confidence interval, 1.11 to 2.41). Models that incorporated sFas were significantly better at identifying patients with CAD than models limited to classic risk factors for atherosclerosis, alone (P = 0.008) or in combination with CRP levels (P = 0.006). In summary, increased plasma levels of sFas are associated with CAD in stable patients with ESRD. These results suggest that sFas may represent a novel and independent marker of CAD.
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PMID:Soluble Fas is a marker of coronary artery disease in patients with end-stage renal disease. 1172 60

Inflammation plays a key role in the physiopathology of atherosclerosis. C-reactive protein (CRP) has been found to predict cardiac events in healthy subjects and in patients with coronary heart disease. However, the relationship between CRP and subclinical atherosclerosis is not well established. We examined the potential relationship between CRP and common carotid artery intima-media thickness and carotid plaques in dyslipidemic subjects. Dyslipidemic patients (n=1051) were recruited for the study. All patients had a complete clinical examination and systematically underwent ultrasonographic evaluation of the extracranial carotid arteries on a duplex system. The serum concentration of CRP was measured by using a sensitive immunoradiometric assay. In a univariate model, a strong positive relationship was found between CRP and the severity of carotid stenosis (P<0.0001). In multivariate analysis, the association between CRP and the degree of carotid atherosclerosis remained significant for advanced plaques (P=0.0007) in male subjects only. Significant correlations were found between CRP and body mass index (P<0.0001) and between CRP and other markers associated with the metabolic syndrome. In this large dyslipidemic population, elevated CRP is an independent predictor of advanced carotid plaques in male subjects. Body mass index and other markers of the metabolic syndrome (HDL cholesterol, triglycerides, diabetes, and high blood pressure) are significant determinants of CRP levels in this population.
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PMID:Elevated C-reactive protein constitutes an independent predictor of advanced carotid plaques in dyslipidemic subjects. 1174 71

Risk stratification is a key element of clinical management not only in the primary and secondary prevention, but also during the acute stages of cardiovascular disease. The current risk assessment algorithms in primary prevention are based on established risk factors: gender and age, cigarette smoking, the presence of hypertension and diabetes mellitus, and serum concentrations of total cholesterol, low-density lipoprotein (LDL)-cholesterol and high-density lipoprotein-cholesterol. However, many individuals who are assessed as "low risk" on the basis of traditional risk factors, still develop cardiac events. This article addresses current issues relevant to the assessment of cardiovascular risk. It emphasizes the potential importance of disturbed energy supply for atherogenesis, by introducing the concept of fuel transport (chylomicron, VLDL, and remnants) and overflow (LDL) pathways of lipid metabolism. It highlights the present lack of routine methods to monitor the fuel transport pathway. It considers the measurements of serum C-reactive protein and plasma fibrinogen as new additions to the cardiovascular risk factor profiles. Finally, risk stratification based on the traditional and the new risk factors is linked to that based on the markers of acute myocardial damage such as cardiac troponin I or troponin T. It is concluded that the combined use of the markers of myocardial damage and the "new" cardiovascular risk factors is the way ahead for the assessment of cardiovascular risk.
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PMID:Risk factors for coronary disease: the time for a paradigm shift? 1175 3

Large increases in mortality related to premature atherosclerosis with coronary artery disease and stroke have been reported in patients with systemic lupus erythematosus (SLE), antiphospholipid syndrome (APLS), or rheumatoid arthritis (RA). Studies found relative risks of 5 for myocardial infarction, 6 to 10 for stroke in SLE patients, and 3.6 for cardiovascular deaths in RA patients. The main risk factors for atherosclerosis included not only the classic factors identified in epidemiological studies such as the Framingham study (advanced age, high cholesterol levels, hypertension, diabetes mellitus, and obesity), but also prolonged glucocorticoid therapy, long duration of SLE, postmenopausal status, and heart failure. SLE per se is an independent risk factor. The current pathogenic hypothesis for atherosclerosis involves an inflammatory response (erythrocyte sedimentation rate, C-reactive protein, and fibrin), autoantibodies, immune complexes (containing antibodies to phospholipids, to oxidized LDLs, and to endothelial cells), cytokine-producing activated T cells, and bacterial or viral infections responsible for an immune response against heat shock proteins (endogenous HSP60 and its equivalent, bacterial HSP65). Early risk factor intervention and effective control of inflammation should be incorporated into the management of connective tissue disease with the goal of protecting patients against atherosclerosis.
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PMID:Atherosclerosis and connective tissue diseases. 1295 20

The pathophysiology of coronary atherosclerosis is complex and multifactorial. The probability of the development of symptomatic coronary heart disease may be predicted by standard risk factor stratification involving hypertension, dyslipidemia, age, positive family history, and diabetes. However, risk factor stratification has been demonstrated to have significant limitations in the individual patient, which has generated a search for more specific and sensitive markers. Evidence is increasing that atherosclerosis is a disease characterized by inflammation, beginning with the earliest identifiable lesion (fatty streak) to the advanced vulnerable plaque. Clinical markers of inflammation, including C-reactive protein, modified low-density lipoprotein, homocysteine, tumor necrosis factor, and thermogenicity, have been identified as emerging risk factors that may add prognostic information in patient management. This review centers on inflammation as a potential pathogenetic factor in atherosclerosis and the role that clinical markers may play in the identification of patients at risk.
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PMID:Atherosclerosis and inflammation. 1182 71

Individuals with diabetes are at high risk of cardiovascular (CV) disease, a risk that is significantly greater in the presence of traditional CV risk factors (hyperlipidaemia, hypertension, prothrombotic state). Glucose control and management of these risk factors decreases but does not eliminate CV events, reflecting the complexity of atherosclerosis. Novel risk factors (C-reactive protein, lipoprotein a, homocysteine, and endothelial dysfunction) have been proposed and are potentially modifiable. However, clinical trials data are not yet available to guide therapy. At this time, no single agent can achieve adequate risk reduction in patients with diabetes. Even with the use of multiple agents and classes of agents to manage CV risk, 75% of patients with diabetes are expected to die from CV causes. Despite the recent advances in primary and secondary prevention of CV events, new approaches are needed. Data from the Heart Outcomes Prevention Evaluation (HOPE) trial demonstrated that CV risk can be further reduced by the addition of the ACE inhibitor ramipril to the existing treatment regimen of high-risk patients with diabetes.
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PMID:Attenuating CV risk factors in patients with diabetes: clinical evidence to clinical practice. 1184 49

Elevated pulse pressure has been associated with an increased risk of cardiovascular disease, which is increasingly being seen as an inflammatory disease. Thus, the mechanism underlying the link between elevated pulse pressure and cardiovascular disease risk may be inflammation. However, investigators have not examined the relationship between pulse pressure and C-reactive protein, an inflammation marker that has been closely linked to cardiovascular risk. We examined the cross-sectional relationship between pulse pressure and C-reactive protein among 9867 healthy persons 17 years of age or older who participated in the Third National Health and Nutrition Examination Survey. The association between pulse pressure and the odds of having an elevated C-reactive protein level (> or = 0.66 mg/dL) was assessed by logistic regression. In a model that adjusted for systolic blood pressure, demographic factors, cholesterol, measures of obesity, smoking, alcohol consumption, physical activity, and antihypertensive medication use, a 10 mm Hg increase in pulse pressure was associated with a 15% increase in the odds of having an elevated C-reactive protein level (odds ratio, 1.15; 95% confidence interval, 1.01 to 1.31; P=0.04). When the same model was re-run adjusting for diastolic blood pressure instead of systolic blood pressure, a 10 mm Hg rise in pulse pressure was associated with a significant 12% increase in the odds of having an elevated C-reactive protein level. Systolic and diastolic blood pressure were unrelated to C-reactive protein once pulse pressure had been accounted for. Our results suggest that increases in pulse pressure are associated with elevated C-reactive protein levels among apparently healthy US adults, independent of systolic and diastolic blood pressure.
Hypertension 2002 Feb
PMID:Association between pulse pressure and C-reactive protein among apparently healthy US adults. 1184 83


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