Desempeño diagnóstico del modelo FullPIERS como predictor de complicaciones perinatales en pacientes con preeclampsia / Diagnostic performance of FullPIERS model as predictor of perinatal complications in patients with preeclampsia

Resumen OBJETIVO: Determinar el desempeño diagnóstico del modelo FullPIERS como predictor de complicaciones perinatales en pacientes con preeclampsia atendidas en un hospital público del Noroeste de México. MATERIALES Y MÉTODO: Estudio retrospectivo, para evaluación de una prueba diagnóstica, efectuado en pacientes con diagnóstico de preeclampsia atendidas en un hospital público de segundo nivel entre octubre de 2018 y febrero 2019. Criterios de inclusión: expedientes con datos suficientes para introducirlos en la calculadora FullPIERS (saturación de oxígeno, recuento de plaquetas, creatinina, aspartato, transaminasa y existencia o no de disnea). Criterios de exclusión: pacientes con diagnóstico previo de padecimientos hepáticos agudos, pulmonares o renales. Se comparó el porcentaje de riesgo al ingreso de cada paciente versus la cantidad de pacientes con y sin complicaciones. Se calcularon: sensibilidad, especificidad y valores predictivos del modelo. RESULTADOS: Se estudiaron 100 expedientes de pacientes con preeclampsia: 11 con resultados positivos según la calculadora Full PIERS (más de 5% de riesgo), en 7 de 11 fue verdadero positivo. Para el modelo Full PIERS se obtuvieron: sensibilidad de 58.3% y especificidad de 95.5%, valor predictivo positivo de 59%, y valor predictivo negativo de 95% para la predicción de complicaciones de la preeclampsia, con área bajo la curva de 0.799. CONCLUSIÓN: La calculadora FullPIERS es una herramienta útil para predecir complicaciones a corto plazo y poder indicar el tratamiento adecuado a cada paciente.

Abstract OBJECTIVE: To determine the diagnostic performance of the FullPIERS model as a predictor of perinatal complications in patients with preeclampsia from a public hospital in Northwest Mexico. MATERIALS AND METHODS: Retrospective study, for the evaluation of a proper diagnosis, performed in patients with diagnosis of preeclampsia attended at a second-level public hospital between October 2018 and February 2019. Inclusion criteria: sufficient data to introduce them into the FullPIERS calculator (saturation of oxygen, platelet retreat, creatinine, aspartate, transaminases and the existence of dysnea). Exclusion criteria: patients with previous diagnosis of acute, pulmonary or renal liver diseases. It is compared to the percentage of the ingrowth risk of each patient versus the number of patients with complications. Calculated: sensitivity, specificity and predictive values of the model. RESULTS: If 100 patients were studied with preeclampsia: 11 with positive results according to the Full PIERS calculator (over 5% risk), and 7 out of 11 were true. For the Full PIERS model, it was obtained: 58.3% sensitivity and 95.5% specificity, 59% positive predictive value, and 95% negative predictive value for the prediction of complications of preeclampsia, with a curve area of 0.799. CONCLUSION: The FullPIERS calculator is a useful tool for predicting complications to cut and can indicate the appropriate treatment for each patient.

Suboptimal inhibition of platelet cyclooxygenase 1 by aspirin in systemic lupus erythematosus: association with metabolic syndrome.

OBJECTIVE: Low-dose aspirin prevents platelet aggregation by suppressing thromboxane A2 (TXA2 ) synthesis. However, in some individuals TXA2 suppression by aspirin is impaired, indicating suboptimal inhibition of platelet cyclooxygenase 1 (COX-1) by aspirin. Because patients with systemic lupus erythematosus (SLE) have increased risk of thrombotic events, many receive aspirin; however, the efficacy of aspirin in SLE has not been determined. We examined the hypothesis that aspirin response is impaired in SLE. METHODS: We assessed the effect of aspirin by measuring concentrations of the stable metabolite of TXA2 , serum thromboxane B2 (sTXB2 ), before and after treatment with daily aspirin (81 mg) for 7 days in 34 patients with SLE and 36 control subjects. The inability to suppress sTXB2 synthesis to <10 ng/ml represents suboptimal inhibition of platelet COX-1 by aspirin. RESULTS: Aspirin almost completely suppressed sTXB2 in control subjects to median 1.5 ng/ml (interquartile range [IQR] 0.8-2.7) but had less effect in patients with SLE (median 3.1 ng/ml [IQR 2.2-5.3]) (P = 0.002). A suboptimal effect of aspirin was present in 15% (5 of 34) of the patients with SLE but not in control subjects (0 of 36) (P = 0.023). Incomplete responders were more likely to have metabolic syndrome (P = 0.048), obesity (P = 0.048), and higher concentrations of C-reactive protein (CRP) (P = 0.018). CONCLUSION: The pharmacologic effect of aspirin is suboptimal in 15% of patients with SLE but in none of the control subjects, and the suboptimal response was associated with metabolic syndrome, obesity, and higher CRP concentrations.

The role of complement in the antiphospholipid syndrome-associated pathology.

The antiphospholipid syndrome (APS) is characterized by arterial and/or venous thromboses, pregnancy loss, and the presence of anticardiolipin antibodies. The pathogenic mechanisms that lead to these clinical manifestations are incompletely understood. Although a direct pathogenic role of antiphospholipid antibodies has been established, including their role in endothelial cell and platelet activation, there is growing evidence that activation of the complement pathway may contribute to the pathogenesis of APS. Vital information has been obtained from studies exploring the features of pregnancy morbidity and thrombosis using complement deficient murine models. These studies are providing the foundation for the development of new therapeutic options to optimize the management of APS.

Oxidative stress in fibromyalgia and its relationship to symptoms.

Oxidative stress is thought to play a role in the pathogenesis of fibromyalgia. We examined the hypothesis that oxidative stress was increased in patients with fibromyalgia and related to the severity of symptoms. Urinary F(2)-isoprostane excretion was measured in 48 patients with fibromyalgia and compared to those of 96 control subjects. In patients, we examined the association between oxidative stress and symptoms. Patients with fibromyalgia were significantly more symptomatic than control subjects, but urinary F(2)-isoprostane excretion did not differ significantly (2.3+/-1.9 vs. 2.8+/-2.2 ng/mg creatinine, p=0.16). In patients with fibromyalgia, F(2)-isoprostane excretion was associated with fatigue visual analog scale (rho=0.30, p=0.04) but not with pain, quality of life, functional capacity, depression, number of tender points, or overall impact of fibromyalgia. Oxidative stress is not increased in patients with fibromyalgia, but as was previously found in patients with systemic lupus erythematosus, oxidative stress was associated with fatigue.

Amino-terminal fragment of the prohormone brain-type natriuretic peptide in rheumatoid arthritis.

OBJECTIVE: Increased concentrations of N-terminal pro-brain natriuretic peptide (NT-proBNP) are associated with cardiovascular morbidity and mortality, but little is known about their relationship to chronic inflammation. Patients with rheumatoid arthritis (RA) have chronic inflammation, increased arterial stiffness, and accelerated coronary atherosclerosis. This study was undertaken to test the hypothesis that NT-proBNP concentrations are elevated in patients with RA and are associated with coronary artery calcification and markers of inflammation. METHODS: In 159 patients with RA (90 with early RA and 69 with longstanding RA) without heart failure and 88 control subjects, serum concentrations of NT-proBNP, interleukin-6 (IL-6), and tumor necrosis factor alpha (TNFalpha) were measured and coronary calcification was assessed. Associations between NT-proBNP levels and the other parameters were investigated. RESULTS: NT-proBNP concentrations were elevated in patients with longstanding RA (median 142.8 pg/ml [interquartile range 54.8-270.5]) and those with early RA (median 58.1 pg/ml [interquartile range 19.4-157.6]) compared with controls (18.1 [3.2-46.0]) (P < 0.001). In patients with RA, NT-proBNP concentrations were associated with age (rho = 0.35, P < 0.001), levels of IL-6 (rho = 0.33, P < 0.001), TNFalpha (rho = 0.23, P = 0.003), and C-reactive protein (CRP) (rho = 0.21, P = 0.01), coronary calcium score (rho = 0.30, P < 0.001), systolic blood pressure (rho = 0.30, P < 0.001), and disease activity (rho = 0.29, P < 0.001). After adjustment for age, race, and sex, the associations between NT-proBNP concentrations and disease activity, TNFalpha, IL-6, and CRP remained significant, but those with systolic blood pressure and coronary calcium score were attenuated. CONCLUSION: NT-proBNP concentrations are increased in patients with RA without clinical heart failure and may indicate subclinical cardiovascular disease and a chronic inflammatory state.

N-terminal pro-brain natriuretic peptide in systemic lupus erythematosus: relationship with inflammation, augmentation index, and coronary calcification.

OBJECTIVE: Cardiovascular mortality is increased in systemic lupus erythematosus (SLE). Increased plasma concentrations of N-terminal pro-brain natriuretic peptide (NT-proBNP) are associated with cardiovascular morbidity and mortality in the general population. We examined the hypothesis that NT-proBNP concentrations are higher in patients with SLE, and are related to inflammation, augmentation index, coronary atherosclerosis, and cardiovascular risk factors. METHODS: Serum concentrations of NT-proBNP were measured in 113 patients with SLE and in 80 control subjects. Coronary calcification and augmentation index were measured by electron beam computed tomography and noninvasive pulse wave analysis, respectively. RESULTS: Patients with SLE had higher concentrations of NT-proBNP [median 38.6 (interquartile range 2.5-126.9) pg/ml] than controls [11.7 (1.6-47.9) pg/ml] (p = 0.002). Augmentation index was higher in patients with SLE [25.0% (20.5%-31.5%)] than controls [20.5% (12.0%-29.0%)] (p = 0.04). In patients with SLE, NT-proBNP concentrations were associated with disease damage (rho = 0.31, p < 0.001) and duration (rho = 0.21, p = 0.02) but not with disease activity, C-reactive protein, erythrocyte sedimentation rate, tumor necrosis factor-alpha, interleukin 6, coronary calcium score, or augmentation index (all p > or = 0.18). CONCLUSION: Patients with SLE have increased concentrations of NT-proBNP, but this is not explained by atherosclerotic burden, augmentation index, or inflammatory state.

T cells and in situ cryoglobulin deposition in the pathogenesis of lupus nephritis.

We discuss a 53-year-old woman with systemic lupus erythematosus who presented with vasculitis, hypocomplementemia and nephritis. Although her serum complement 4 (C4) levels were zero, she had four copies of C4 gene. Renal biopsy revealed membranoproliferative glomerulonephritis and the presence of cryoglobulins, detected by electron microscopy, and significant numbers of T cells in the interstitium. Cryoglobulins were considered responsible for the complete consumption of C4 in the serum the levels of which improved gradually after treatment. T cells in the kidney were found to express CD44 and phosphorylated ezrin/radixin/moiesin which explain why they homed to the kidney inappropriately. The contribution of cryoglobulins and T cells in the expression of kidney pathology is discussed.

Inflammation-associated insulin resistance: differential effects in rheumatoid arthritis and systemic lupus erythematosus define potential mechanisms.

OBJECTIVE: Insulin resistance is increased by inflammation, but the mechanisms are unclear. The present study was undertaken to test the hypothesis that decreased insulin sensitivity is differentially associated with mediators of inflammation by studying 2 chronic inflammatory diseases of different pathogenesis, systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). METHODS: We measured fasting insulin, glucose, and lipid levels, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNFalpha), and coronary artery calcification in 103 patients with SLE and in 124 patients with RA. Insulin sensitivity was measured using the homeostasis model assessment (HOMA) index. RESULTS: The HOMA value was higher in RA patients (median 2.05 [interquartile range (IQR) 1.05-3.54]) than in SLE patients (1.40 [0.78-2.59]) (P = 0.007). CRP and ESR did not differ significantly in RA and SLE patients. Body mass index (BMI) was significantly correlated with the HOMA index in both RA (rho = 0.20) and SLE (rho = 0.54), independently of age, sex, race, and current use of corticosteroids. In RA patients, the HOMA index was also significantly positively correlated with IL-6 (rho = 0.63), TNFalpha (rho = 0.50), CRP (rho = 0.29), ESR (rho = 0.26), coronary calcification (rho = 0.26), and Disease Activity Score in 28 joints (rho = 0.21); associations adjusted for age, sex, race, BMI, and current use of corticosteroids remained significant (P < 0.05). In SLE patients, the HOMA index was also significantly correlated with ESR (rho = 0.35) and CRP (rho = 0.25), but not with other variables. The association between the ESR and the HOMA value in patients with SLE remained significant after adjustment for confounding covariates (P = 0.008). In multivariable models, the major contributing factors to the HOMA index were the BMI in SLE patients, and IL-6 and TNFalpha levels in RA patients. CONCLUSION: The pathogenesis of insulin resistance and its contribution to atherogenesis varies in different inflammatory settings.

Lipoprotein subclasses and particle size determined by nuclear magnetic resonance spectroscopy in systemic lupus erythematosus.

Patients with systemic lupus erythematosus (SLE) have accelerated atherosclerosis, but the underlying mechanisms are unclear. The size and number of lipoprotein particles may be better predictors of atherosclerosis than conventional cholesterol measurements. We measured lipoprotein subclasses by nuclear magnetic resonance spectroscopy (NMR), coronary artery calcification by electron beam computed tomography, and insulin resistance by homeostasis model assessment in 105 patients with SLE and 77 control subjects. VLDL particles were larger (50.0+/-8.5 versus 47.7+/-8.5 nm, P=0.01) and concentrations of large high-density lipoprotein (HDL) particles lower (10.1+/-5.3 versus 11.3+/-5.1 nmol/L, P=0.03) in patients with SLE than controls. In patients with SLE, small LDL concentration was associated with body mass index (rho=0.27), insulin resistance (rho=0.34), C-reactive protein (CRP; rho=0.30), and erythrocyte sedimentation rate (ESR; rho=0.20); all P<0.05. Large HDL concentration was inversely associated with insulin resistance (rho=-0.29), disease activity (rho=-0.23), and ESR (rho=-0.39); all P<0.05. VLDL concentrations correlated with CRP (rho=0.22), ESR (rho=0.24), disease damage (rho=0.20), and corticosteroid exposure (rho=0.29); all P<0.05. Neither the concentration of lipoprotein subclasses nor particle size was associated with coronary artery atherosclerosis. There were only minor differences in the NMR lipid profiles of patients with SLE and controls. Lipoprotein subclasses were associated with metabolic variables, inflammatory markers, and corticosteroid use but not with coronary artery atherosclerosis in SLE.

Prevalence of the metabolic syndrome is increased in rheumatoid arthritis and is associated with coronary atherosclerosis.

Patients with rheumatoid arthritis (RA) have accelerated atherosclerosis. The metabolic syndrome, a cluster of cardiovascular risk factors, identifies cardiovascular risk. We tested the hypotheses that patients with RA have a higher prevalence of the metabolic syndrome, particularly the WHO-defined syndrome that requires insulin resistance, and that this is associated with coronary atherosclerosis. The prevalence of the metabolic syndrome was determined using the modified WHO and NCEP III criteria in 154 patients with RA (88 with early RA and 66 with long-standing RA) and 85 control subjects. Coronary-artery atherosclerosis was detected by electron beam computed tomography. The WHO-defined metabolic syndrome was present in 42% of patients with long-standing RA, 31% with early RA and 11% of controls (P<0.001); the NCEP-defined metabolic syndrome was present in 42% of patients with long-standing RA, 30% with early RA and 22% of controls (P=0.03). Patients with the WHO-defined metabolic syndrome had an increased risk of having higher coronary-artery calcification scores, independent of age and sex (OR=2.02, 95% CI: 1.03-3.97, P=0.04). In conclusion, patients with RA have a higher prevalence of the metabolic syndrome than control subjects. Inflammation-associated metabolic syndrome is a mechanism that may contribute to increased coronary-artery atherosclerosis in RA.

Increased augmentation index in rheumatoid arthritis and its relationship to coronary artery atherosclerosis.

OBJECTIVE: Arterial stiffness, assessed by the augmentation index and pulse wave velocity, is an independent risk factor for cardiovascular disease. Rheumatoid arthritis (RA) is associated with accelerated atherosclerosis and increased cardiovascular mortality. We examined the hypothesis that augmentation index and pulse wave velocity are increased in RA, and are related to coronary artery atherosclerosis. METHODS: We measured augmentation index and brachial pulse wave velocity in 117 patients with RA [57 with early (< 6 yrs) and 60 with late disease (> 10 yrs)] and 65 healthy controls. Coronary artery calcification was measured by electron beam computed tomography. Augmentation index and pulse wave velocity were compared in patients with early RA, late RA, and controls, and the association with coronary atherosclerosis was examined. RESULTS: Patients with late RA had a higher augmentation index (median 33.8%, interquartile range 27.5% 37.0%) than those with early disease (median 27.5%, IQR 21.0% 34.0%) (p = 0.008) and controls (median 27.0%, IQR 20.4% 33.0%) (p < 0.001). After adjusting for height and cardiovascular risk factors, the association between late disease and augmentation index remained significant (p = 0.02). Augmentation index was associated with coronary calcification score (rs = 0.19, p = 0.046), and the association was marginal after adjustment for cardiovascular risk factors, disease status, and disease activity (p = 0.09). There was no significant difference in brachial pulse wave velocity among patients with late (9.2 +/- 1.7 m/s) and early RA (9.1 +/- 1.6 m/s) and controls (8.9 +/- 1.5 m/s) (p = 0.78). CONCLUSION: Patients with RA have increased augmentation index independent of cardiovascular risk factors. Augmentation index was associated with coronary artery calcification in patients with RA; this was attenuated after adjusting for cardiovascular risk factors.

Aspirin therapy and thromboxane biosynthesis in systemic lupus erythematosus.

Incomplete suppression of thromboxane biosynthesis during aspirin therapy is associated with increased cardiovascular risk. Since systemic lupus erythematosus (SLE) is associated with platelet activation and increased cardiovascular mortality, we compared thromboxane and prostacyclin biosynthesis in patients with SLE and control subjects, and measured inhibition of thromboxane excretion in aspirin-treated subjects. We measured the urinary excretion of 11-dehydro thromboxane B( 2) (TXB(2)) and 2,3-dinor 6-ketoPGF(1alpha) (PGI-M), the stable metabolites of thromboxane A(2) and prostacyclin, respectively, in 74 patients with SLE and 70 controls. In subjects who were not receiving aspirin, TXB(2) excretion was higher in patients with SLE [0.40 ng/mg creatinine (0.26-0.64), median (interquartile range)] than controls [0.31 ng/mg creatinine (0.23-0.44)] (P = 0.04), and in these patients, TXB(2) excretion correlated with disease activity (rho = 0.28, P = 0.03) and tumor necrosis factor alpha (rho = 0.48, P < 0.001). Aspirin therapy resulted in significantly lower TXB(2) excretion in controls (P = 0.01), but not in patients with SLE (P = 0.10), compared with subjects not receiving aspirin. Prostacyclin biosynthesis did not differ among patients and controls, and was not affected by aspirin (P all >0.35). Thromboxane biosynthesis is increased in SLE and is associated with disease activity. Additionally, response to aspirin may be attenuated in some patients with SLE.

Inflammatory mechanisms affecting the lipid profile in patients with systemic lupus erythematosus.

OBJECTIVE: Increased low density lipoprotein (LDL) cholesterol and triglycerides, and decreased high density lipoprotein (HDL) cholesterol concentrations are associated with adverse cardiovascular risk in the general population. Patients with systemic lupus erythematosus (SLE) have an altered lipid profile characterized by increased triglycerides and decreased HDL cholesterol concentrations. We examined the relationships between lipid concentrations, cytokines, and inflammatory markers in patients with SLE. METHODS: Fasting lipid concentrations, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were measured in 110 patients with SLE. Disease activity was quantified by the SLE Disease Activity Index (SLEDAI), and disease damage by the Systemic Lupus International Collaborating Clinics (SLICC) score. Concentrations of circulating tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and insulin were measured and insulin sensitivity calculated. RESULTS: Lower concentrations of HDL cholesterol were independently associated with higher ESR (p < 0.001), IL-6 (p = 0.02), SLEDAI (p = 0.04), and TNF-alpha (p = 0.04) after adjustment for age, sex, race, body mass index, insulin sensitivity, and current use of corticosteroids or hydroxychloroquine. Triglyceride concentrations were associated with higher CRP concentrations (p = 0.02) and SLICC score (p = 0.04). CONCLUSION: Deleterious changes in lipid profile are independently associated with higher concentrations of markers and mediators of inflammation and disease activity and damage in patients with SLE.

Serum osteoprotegerin is increased and independently associated with coronary-artery atherosclerosis in patients with rheumatoid arthritis.

Osteoprotegerin (OPG), a soluble decoy receptor for receptor activator of nuclear factor kappaB ligand, is implicated in the pathogenesis of atherosclerosis. Patients with rheumatoid arthritis (RA) have inflammation and increased atherosclerosis. We examined the hypothesis that OPG concentrations are increased in patients with RA and are associated with coronary-artery atherosclerosis. Serum OPG concentrations were measured by ELISA and coronary-artery calcification by electron-beam computer tomography in 157 patients with RA and 87 control subjects. OPG concentrations were higher in patients with long-standing RA (n=67) [median (interquartile range)]: [1895 (1337-2847) pg/mL, and early RA (n=90): [1340 (1021-1652) pg/mL, than controls 1068 (692-1434) pg/mL; (p<0.001)]. In patients with RA, OPG concentrations were associated with erythrocyte sedimentation rate (p<0.001), homocysteine (p=0.001), disease duration (p=0.02), coronary calcium score (p=0.03), and cumulative dose of corticosteroids (p=0.04) after adjustment for age and sex. In patients with long-standing RA, OPG was associated with coronary-artery calcification independently of cardiovascular risk factors and disease activity [OR for every increase in 500 pg/mL of OPG=2.22 (1.43-3.34), p<0.001]. In conclusion, OPG concentrations are increased in patients with RA and are associated with inflammation. In patients with long-standing disease, OPG is independently associated with coronary-artery calcification.

Atherosclerosis and inflammation: insights from rheumatoid arthritis.

Cardiovascular disease is a major health care problem and the most common cause of death among individuals from developed nations. Our understanding of atherosclerosis has evolved from a passive process resulting in narrowing of the lumen and consequent myocardial ischemia to a dynamic process that involves inflammation. The study of atherosclerosis in patients with chronic inflammation, such as rheumatoid arthritis (RA), will provide insights into the relationship between inflammation and atherosclerosis. We review the relationship between atherosclerosis and inflammation within the context of RA, providing evidence that patients with RA have increased cardiovascular morbidity and mortality and accelerated coronary and extra-coronary atherosclerosis. In addition, traditional and novel cardiovascular risk factors are discussed. Finally, actions that a rheumatologist can take to better control this cardiovascular morbidity are suggested. These can be summarized as follows: (1) careful assessment and treatment of cardiovascular risk, (2) better control of inflammation, and (3) individual risk-benefit evaluation of need for cyclo-oxygenase-2 inhibitors, nonsteroidal anti-inflammatory drugs, and high doses of corticosteroids.

High prevalence of the metabolic syndrome in patients with systemic lupus erythematosus: association with disease characteristics and cardiovascular risk factors.

BACKGROUND: The metabolic syndrome is an independent risk factor for ischaemic heart disease. Patients with systemic lupus erythematosus (SLE) have accelerated atherosclerosis; however, there are no controlled studies of the metabolic syndrome in patients with SLE. OBJECTIVE: To compare the prevalence of the metabolic syndrome in patients with SLE and controls and to evaluate its relationship to other cardiovascular risk factors and inflammation. METHODS: 102 patients with SLE and 101 controls were studied. The prevalence of the metabolic syndrome was compared in patients and controls using the National Cholesterol Education Program Adult Treatment Panel III (NCEP) and the World Health Organization (WHO) definitions, and associations with cardiovascular risk factors and lupus characteristics were examined. RESULTS: The metabolic syndrome was present in 32.4% of patients and in 10.9% of controls subjects (p<0.001) using the WHO definition that requires direct determination of insulin resistance, and in 29.4% of patients with SLE and in 19.8% of controls (p = 0.14) using the NCEP definition. Among patients with SLE, both definitions were significantly associated with higher concentrations of C reactive protein (p = 0.001) and the NCEP definition was significantly associated with higher concentrations of homocysteine (p<0.001), lipoprotein (a) (p = 0.02) and cholesterol (p = 0.04). Neither lupus disease activity nor damage scores were associated with the metabolic syndrome. CONCLUSIONS: Patients with SLE have a higher prevalence of insulin resistance and consequently of the WHO-defined metabolic syndrome than controls. In patients with SLE, the metabolic syndrome was associated with higher levels of inflammation and may provide a link between inflammation and increased cardiovascular risk.

Utility of the Framingham risk score to predict the presence of coronary atherosclerosis in patients with rheumatoid arthritis.

The prevalence of ischemic heart disease and atherosclerosis is increased in patients with rheumatoid arthritis (RA). In the general population, but not in patients with systemic lupus erythematosus, the Framingham risk score identifies patients at increased cardiovascular risk and helps determine the need for preventive interventions. We examined the hypothesis that the Framingham score is increased and associated with coronary-artery atherosclerosis in patients with RA. The Framingham score and the 10-year cardiovascular risk were compared among 155 patients with RA (89 with early disease, 66 with long-standing disease) and 85 control subjects. The presence of coronary-artery calcification was determined by electron-beam computed tomography. The Framingham score was compared in patients with RA and control subjects, and the association between the risk score and coronary-artery calcification was examined in patients. Patients with long-standing RA had a higher Framingham score (14 [11 to 18]) (median [interquartile range]) compared to patients with early RA (11 [8 to 14]) or control subjects (12 [7 to 14], P < 0.001). This remained significant after adjustment for age and gender (P = 0.015). Seventy-six patients with RA had coronary calcification; their Framingham risk score was higher (14 [12 to 17]) than that of 79 patients without calcification (10 [5 to 14]) (P < 0.001). Furthermore, a higher Framingham score was associated with a higher calcium score (odds ratio [OR] = 1.20, 95% confidence interval [CI] 1.12 to 1.29, P < 0.001), and the association remained significant after adjustment for age and gender (OR = 1.15, 95% CI 1.02 to 1.29, P = 0.03). In conclusion, a higher Framingham risk score is independently associated with the presence of coronary calcification in patients with RA.

Obesity is an independent contributor to functional capacity and inflammation in systemic lupus erythematosus.

OBJECTIVE: Obesity induces a proinflammatory state and is a major cause of morbidity in the general population. However, little is known about the effects of obesity in patients with chronic inflammatory illnesses such as systemic lupus erythematosus (SLE). METHODS: One hundred consecutive patients with SLE were studied to determine the relationship between body mass index (BMI) and functional capacity, measures of fatigue, quality of life, and the inflammation markers C-reactive protein (CRP), the erythrocyte sedimentation rate, and interleukin-6 (IL-6). The association between BMI and patient characteristics was determined, and multiple logistic regression models were used to adjust for age, sex, disease activity, and disease-related damage. RESULTS: Thirty-three patients had a normal BMI (< 25 kg/m(2)), 28 were overweight (25-29.9 kg/m(2)), and 39 were obese (> or =30 kg/m(2)). Obese patients had worse functional capacity, more fatigue, and higher concentrations of inflammation markers. The mean +/- SD modified Health Assessment Questionnaire (M-HAQ) score was 0.6 +/- 0.4 in obese patients compared with 0.3 +/- 0.4 and 0.2 +/- 0.3 in overweight patients and those with a normal BMI, respectively (P = 0.001). The mean +/- SD concentrations of CRP in obese patients (10.0 +/- 8.6 mg/liter) were higher than those in patients who were overweight (4.7 +/- 5.4 mg/liter) or had a normal BMI (6.2 +/- 9.9 mg/liter) (P < 0.001). Similarly, concentrations of IL-6 were higher in obese patients (P = 0.003). After adjusting for age, sex, disease activity, and damage indices, the associations between BMI and CRP (P < 0.001), M-HAQ scores (P = 0.005), and IL-6 concentrations (P = 0.01) remained significant. CONCLUSION: Obesity is independently associated with impaired functional capacity and inflammation markers in patients with lupus. Thus, weight loss may improve functional capacity and decrease cardiovascular risk factors.

Increased coronary-artery atherosclerosis in rheumatoid arthritis: relationship to disease duration and cardiovascular risk factors.

OBJECTIVE: To compare the prevalence and severity of coronary-artery atherosclerosis in patients with early and established rheumatoid arthritis (RA) and controls. METHODS: Electron-beam computed tomography was used to measure the extent of coronary-artery calcification in 227 subjects, of whom 70 had early RA, 71 had established RA, and 86 were controls. Coronary-artery calcification calculated according to the Agatston calcium score was compared in patients and controls, and its relationship to clinical characteristics was examined. Adjusted odds ratios (ORs) were obtained with the use of proportional odds logistic regression models to determine independent associations of early and established RA and coronary-artery calcification. RESULTS: Calcium scores were higher in patients with established RA (median 40.2, interquartile range [IQR] 0-358.8) compared with those with early disease (median 0, IQR 0-42.6) and controls (median 0, IQR 0-19.2) (P = 0.001). Coronary-artery calcification occurred more frequently in patients with established RA (60.6%) than in patients with early RA (42.9%) and control subjects (38.4%) (P = 0.016) The OR for the likelihood of having more severe coronary-artery calcification (defined as an Agatston score >109) in patients with established disease was 3.42 (P = 0.002) after adjusting for cardiovascular risk factors. Among patients with RA, smoking (OR 1.02, P = 0.04) and an elevated erythrocyte sedimentation rate (OR 1.02, P = 0.05) were associated with more severe coronary-artery calcification after adjustment for age and sex. CONCLUSION: The prevalence and severity of coronary calcification is increased in patients with established RA and is related, in part, to smoking and an increased erythrocyte sedimentation rate.