Enhanced arthrocentesis of the effusive knee with pneumatic compression.

AIM: Complete arthrocentesis of the effusive knee ameliorates patient pain, reduces intra-articular and intraosseous pressure, removes inflammatory cytokines, and has been shown to substantially improve the therapeutic outcomes of intra-articular injections. However, conventional arthrocentesis incompletely decompresses the knee, leaving considerable residual synovial fluid in the intra-articular space. The present study determined whether external pneumatic circumferential compression of the effusive knee permitted more successful arthrocentesis and complete joint decompression. METHODS: Using a paired sample design, 50 consecutive effusive knees underwent conventional arthrocentesis and then arthrocentesis with pneumatic compression. Pneumatic compression was applied to the superior knee using a conventional thigh blood pressure cuff inflated to 100 mm Hg which compressed the suprapatellar bursa and patellofemoral joint, forcing fluid from the superior knee to the anterolateral portal where the fluid could be accessed. Arthrocentesis success and fluid yield in mL before and after pneumatic compression were determined. RESULTS: Successful diagnostic arthrocentesis (≥3 mL) of the effusive knee was 82% (41/50) with conventional arthrocentesis and increased to 100% (50/50) with pneumatic compression (P = .001). Synovial fluid yields increased by 144% (19.8 ± 17.1 mL) with pneumatic compression (conventional arthrocentesis; 13.7 ± 16.4 mL, pneumatic compression: 33.4 ± 26.5 mL; 95% CI: 10.9 < 19.7 < 28.9 mL, P < .0001). CONCLUSIONS: Conventional arthrocentesis routinely does not fully decompress the effusive knee. External circumferential pneumatic compression markedly improves arthrocentesis success and fluid yield, and permits complete decompression of the effusive knee. Pneumatic compression of the effusive knee with a thigh blood pressure cuff is an inexpensive and widely available technique to improve arthrocentesis outcomes.

Hypertrophic pulmonary osteoarthropathy: an unusual presentation.

OBJECTIVES: Hypertrophic pulmonary osteoarthropathy (HPOA) is a syndrome characterized by the triad of periostitis, digital clubbing and painful arthropathy of the large joints, especially involving the lower limbs. HPOA without clubbing of the digits is considered an incomplete form of HPOA and has been rarely reported. We are presenting here a case of HPOA without clubbing in a patient with lung cancer. METHODS: A 52-year-old female active smoker presented with a complaint of multiple joint pains with associated morning stiffness, swelling and weight loss for 3 months. On examination, the patient had tenderness to palpation over the anterior shin, but no obvious clubbing was noted. X-rays of the lower extremities revealed periosteal thickening compatible with HPOA. RESULTS: A bone scan showed increased uptake along the periosteum and cortex of the long bones. In view of her smoking history and weight loss, a chest X-ray was done that revealed an upper lung mass. A diagnosis of lung carcinoma was made on biopsy. CONCLUSION: Our case demonstrates that the unusual finding of HPOA in the absence of clubbing is a rare entity and can often be missed. Once diagnosed, a prompt search of other associated conditions should be conducted.

Progression of noncalcified and calcified coronary plaque by CT angiography in SLE.

Premature coronary artery disease remains the major cause of late death in systemic lupus erythematosus (SLE). Coronary artery calcium (CAC) represents an advanced stage of atherosclerosis, whereas noncalcified coronary atherosclerotic plaque (NCP) typically is more prone to trigger acute coronary events. The aim of this study was to assess the stability of NCP over time and identify factors associated with changes in NCP in patients with SLE. CT coronary angiography and calcium scanning were performed at baseline and follow-up in thirty-six SLE patients. Duration between baseline and follow-up NCP assessment ranged from 2 to 8 years. CAC was quantified by the Agatston score and classified as none, low (1-99), moderate (100-299) or high calcium score (300 and above). NCP was quantified based on a previously validated score and classified as none, low (<0.5) or high (0.5+). SLE disease activity was quantified using the SELENA-SLEDAI and physician global assessment indices. To assess the association between quantitative clinical variables and changes in NCP, adjusting for time, we used linear regression models. The group of 36 SLE patients were 75% females, 75% Caucasians, 17% African-Americans, 8% other ethnicities. The mean age of patients was 46.6 years. For NCP, 17/36 (47%) of the patients switched qualitative NCP class (none, low, high) between baseline and follow-up, whereas for CAC only 3/35 (9%) switched qualitative class. Increasing years between assessments were associated with an increase in NCP (P = 0.038). The proportion of time on immunosuppressants was associated with a decrease in NCP (P = 0.06). Calcified coronary plaque levels remained relatively stable over a period of 2-8 years. Noncalcified coronary plaque levels were more variable. Use of immunosuppressive drugs appeared to be protective against noncalcified coronary plaque progression.

Coronary calcification in SLE: comparison with the Multi-Ethnic Study of Atherosclerosis.

OBJECTIVE: Accelerated atherosclerosis is a major cause of morbidity and death in SLE. The purpose of this study was to determine whether the prevalence and extent of coronary artery calcium (CAC) is higher in female SLE patients compared with a non-SLE sample from the Multi-Ethnic Study of Atherosclerosis (MESA). METHODS: CAC was measured in 80 female SLE patients and 241 female MESA controls from the Baltimore Field Centre, ages 45-64 years, without evidence of clinical cardiovascular disease. Binary regression was used to estimate the ratio of CAC prevalence in SLE vs MESA controls, controlling for demographic and cardiovascular risk factors. To compare the groups with respect to the quantity of CAC among those with non-zero Agatston scores, we used linear models in which the outcome was a log-transformed Agatston score. RESULTS: The prevalence of CAC was substantially higher in SLE. The differences were most pronounced and statistically significant in those aged 45-54 years (58% vs 20%, P < 0.0001), but were still observed among those aged 55-65 years (57% vs 36%, P = 0.069). After controlling for age, ethnicity, education, income, diabetes mellitus, hypertension, hyperlipidaemia, high-density lipoprotein levels, smoking, education and BMI, SLE patients still had a significantly higher prevalence of CAC than controls. Among those with CAC, the mean log Agatston score did not differ significantly between SLE and MESA participants. CONCLUSION: Women with SLE have a higher prevalence of CAC than comparable women without SLE, even after adjusting for traditional cardiovascular risk factors, especially among those aged 45-54 years.

The Role of MicroRNAs and Human Epidermal Growth Factor Receptor 2 in Proliferative Lupus Nephritis.

OBJECTIVE: To understand the roles of microRNAs (miRNAs) in proliferative lupus nephritis (LN). METHODS: A high-throughput analysis of the miRNA pattern of the kidneys of LN patients and controls was performed by molecular digital detection. Urinary miRNAs were measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Target gene expression in human mesangial cells was evaluated by arrays and qRT-PCR. Human epidermal growth factor receptor 2 (HER-2) was analyzed by immunohistochemistry in kidney samples from LN patients and in a murine model of lupus. Urinary levels of HER-2, monocyte chemotactic protein 1 (MCP-1), and vascular cell adhesion molecule 1 (VCAM-1) were measured by enzyme-linked immunosorbent assay. RESULTS: Levels of the miRNAs miR-26a and miR-30b were decreased in the kidneys and urine of LN patients. In vitro these miRNAs controlled mesangial cell proliferation, and their expression was regulated by HER-2. HER-2 was overexpressed in lupus-prone NZM2410 mice and in the kidneys of patients with LN, but not in other mesangioproliferative glomerulonephritides. HER-2 was found to be up-regulated by interferon-α and interferon regulatory factor 1. Urinary HER-2 was increased in LN and reflected disease activity, and its levels correlated with those of 2 other recognized LN biomarkers, MCP-1 and VCAM-1. CONCLUSION: The kidney miRNA pattern is broadly altered in LN, which contributes to uncontrolled cell proliferation. Levels of the miRNAs miR-26a and miR-30b are decreased in the kidneys and urine of LN patients, and they directly regulate the cell cycle in mesangial cells. The levels of these miRNAs are controlled by HER-2, which is overexpressed in NZM2410 mice and in the kidneys and urine of LN patients. HER-2, miR-26a, and miR-30b are thus potential LN biomarkers, and blocking HER-2 may be a promising new strategy to decrease cell proliferation and damage in this disease.

Myocardial T2 mapping by cardiovascular magnetic resonance reveals subclinical myocardial inflammation in patients with systemic lupus erythematosus.

To evaluate whether T2 mapping techniques can detect myocardial edema in patients with systemic lupus erythematosus (SLE). Twenty-four patients (mean age 54 ± 9 years) with SLE and twelve controls (mean age 50 ± 7 years) underwent cardiac MRI at 1.5 T. Standard cine images were obtained. Single-slice T2 maps and non-contrast T1 maps were acquired in a mid-cavity short-axis plane. Late gadolinium enhancement (LGE) images were obtained 15 min after 0.2 mmol/kg of contrast. SLE patients had low disease activity (mean SLE disease activity index score 0.71 ± 0.8). There were no differences in LV size or function between SLE patients and controls. No subjects had LGE. T2 times were higher in SLE patients (58.2 ± 5.6 vs. 52.8 ± 4.4 ms, p = 0.009). On multivariate analysis including demographic and LV parameters, only the diagnosis of SLE was associated with T2 time (p = 0.01). T1 times trended lower in SLE patients, (981.6 ± 65.5 vs. 963.9 ± 32.5), however, differences were not significant (p = 0.3). Repeated measures were highly correlated by linear regression for both inter- and intraobserver analysis (both R = 0.95, p < 0.001). Inter- and intraobserver bias and limits of agreement were -0.4 ± 3.8 and 1.0 ± 3.3 ms, respectively. T2-mapping identifies increased myocardial T2 times in SLE patients, likely due to subclinical myocardial edema. These findings suggest that even in SLE patients with inactive disease and normal cardiac function, low grade myocardial inflammation can be detected by this novel quantitative and highly reproducible technique.

Apolipoprotein-containing lipoprotein subclasses and subclinical atherosclerosis in systemic lupus erythematosus.

OBJECTIVE: Traditional classification of hyperlipidemia using high-density lipoprotein, low-density lipoprotein (LDL), and very low-density lipoprotein does not provide information on lipoprotein function. Apolipoproteins (Apos), which are protein components of plasma lipoproteins (including A, B, C, D, E) with their different composition, metabolic, and atherogenic properties, provide insight on lipoprotein functioning. In particular, the Apo B/A-I ratio is associated with atherogenic LDL and development of cardiovascular disease. We explored the baseline association between these nontraditional risk factors with subclinical measures of atherosclerosis (coronary artery calcification [CAC] and carotid intima-media thickness [IMT]) in systemic lupus erythematosus (SLE). METHODS: A total of 58 SLE patients (97% women, 58% white, 40% African American, and 2% other, mean ± SD age 44 ± 11 years) had measurement of Apo and lipoproteins by immunoturbidimetric procedures, electroimmunoassays, and immunoprecipitation. CAC was measured by helical computed tomography and carotid IMT by carotid duplex. This study was based on the baseline assessment of subclinical atherosclerosis in the Lupus Atherosclerosis Prevention Study. The measurement of the lipoproteins was made on sera collected at the same time. RESULTS: There was no association between cardioprotective Apos (Apo A-I, LpA-I, LpA-I:A-II) and CAC (P < 0.15, P < 0.41, and P < 0.39, respectively) or carotid IMT (P < 0.97, P < 0.53, and P < 0.76, respectively). CAC and carotid IMT did not associate with atherogenic Apos either, including LpB:E+LpB:C:E, Apo B, LpB, LpB:C, Apo C-III, Apo C-III-HS, Apo C-III-HP, Apo C-III-R, LpA-II:B:C:D:E, and Apo B/Apo A-I. Measures of disease activity, including physician's global assessment and Systemic Lupus Erythematosus Disease Activity Index, were not associated with CAC or carotid IMT. CONCLUSION: Neither cardioprotective nor atherogenic lipoproteins were associated with measures of subclinical atherosclerosis in this series of SLE patients. Further studies with a larger sample size are warranted to confirm our findings.

Vitamin D deficiency does not predict progression of coronary artery calcium, carotid intima-media thickness or high-sensitivity C-reactive protein in systemic lupus erythematosus.

OBJECTIVE: Vitamin D deficiency is common in SLE. Cardioprotective effects of vitamin D have been postulated due to modulation of inflammatory cytokines. However, the effects of vitamin D supplementation on inflammatory cytokines in trials have been inconsistent. We determined whether levels of vitamin D at baseline were associated with subclinical measures of atherosclerosis, or with changes in subclinical measures over 2 years. METHODS: Of the 200 patients enrolled in the Lupus Atherosclerosis Prevention Study, complete baseline and follow-up data [including coronary artery calcium (CAC), carotid intima-media thickness (IMT), 25-hydroxy vitamin D [25(OH)D] and high-sensitivity CRP (hsCRP) levels] were available for 154 patients. Assessments were repeated 2 years later. RESULTS: 25(OH)D values ranged from 4 to 79 ng/ml. Among African American patients, 25(OH)D values ranged from 4 to 55 ng/ml. With low 25(OH)D (vitamin D <21 ng/ml), a higher proportion had a CAC score >100 (11%) compared with those with vitamin D insufficiency (21-32 ng/ml) (10%) and normal (≥32 ng/ml) 25(OH)D (3%), which was not statistically significant. 25(OH)D was neither associated with nor did it predict progression of CAC or carotid IMT over 2 years. The mean hsCRP decreased over 2 years. CONCLUSION: 25(OH)D was not associated with any measure of subclinical atherosclerosis. 25(OH)D deficiency was associated with higher hsCRP at baseline, but did not predict a change in hsCRP over 2 years.

Predictors of self-reported health-related quality of life in systemic lupus erythematosus.

OBJECTIVE: The Medical Outcomes Short Form-36 Survey (SF-36) has been widely used as a measure of health-related quality of life (HRQOL) in different populations. SLE patients have consistently reported lower scores compared with the general population. The objective of our study was to identify predictors of HRQOL using SF-36 among patients with SLE enrolled in a 2-year randomized controlled trial (RCT). METHODS: We analysed 200 SLE patients enrolled in the Lupus Atherosclerosis Prevention Study (LAPS), an RCT of atorvastatin vs placebo, who completed SF-36 at qualifying, 12- and 24-month (final) visits. RESULTS: At baseline, mean SF-36 domain scores were lower than those of age- and gender-matched population norms. There was no statistical difference reported between Physical Component Summary (PCS), Mental Component Summary and eight domain scores in the atorvastatin vs placebo group at 2 years. In multiple regression analyses, African American patients reported significantly lower scores in Physical Functioning compared with Caucasians. The presence of FM was significantly associated with lower scores in physical functioning, role physical, bodily pain, general health, vitality, social functioning and lower overall mean PCS scores. The Physician's Global Assessment of disease activity was associated with multiple SF-36 domains in univariate analysis. CONCLUSION: This longitudinal study confirmed lower scores reported across all SF-36 domains. No one explanatory variable was independently associated with all domain scores. FM was independently associated with poorer HRQOL in most domains, underscoring the need for effective treatments for FM in SLE.

Semiquantified noncalcified coronary plaque in systemic lupus erythematosus.

OBJECTIVE: A major cause of morbidity and mortality in systemic lupus erythematosus (SLE) is accelerated coronary atherosclerosis. New technology (computed tomographic angiography) can measure noncalcified coronary plaque (NCP), which is more prone to rupture. We report on a study of semiquantified NCP in SLE. METHODS: Patients with SLE (n = 147) with no history of cardiovascular disease underwent 64-slice coronary multidetector computed tomography (MDCT). The MDCT scans were evaluated quantitatively by a radiologist, using dedicated software. RESULTS: The group of 147 patients with SLE was 86% female, 70% white, 29% African American, and 3% other ethnicity. The mean age was 51 years. In our univariate analysis, the major traditional cardiovascular risk factors associated with noncalcified plaque were age (p = 0.007), obesity (p = 0.03; measured as body mass index), homocysteine (p = 0.05), and hypertension (p = 0.04). Anticardiolipin (p = 0.026; but not lupus anticoagulant) and anti-dsDNA (p = 0.03) were associated with higher noncalcified plaque. Prednisone and hydroxychloroquine therapy had no effect, but methotrexate (MTX) use was associated with higher noncalcified plaque (p = 0.0001). In the best multivariate model, age, current MTX use, and history of anti-dsDNA remained significant. CONCLUSION: Our results suggest that serologic SLE (anti-dsDNA) and traditional cardiovascular risk factors contribute to semiquantified noncalcified plaque in SLE. The association with MTX is not understood, but should be replicated in larger studies and in multiple centers.

Urinary vascular cell adhesion molecule, but not neutrophil gelatinase-associated lipocalin, is associated with lupus nephritis.

OBJECTIVE: Vascular cell adhesion molecule-1 (VCAM-1), an adhesion molecule, is involved in the progression of glomerular and tubulointerstitial injury. Neutrophil gelatinase-associated lipocalin (NGAL), a member of the lipocalin superfamily, has been shown to rise in both acute and chronic kidney damage. Both VCAM-1 and NGAL have been found at high levels in the urine of patients with active lupus nephritis. We investigated both as potential biomarkers for lupus nephritis. METHODS: VCAM-1 and NGAL were measured by ELISA during 1 to 8 clinic visits in 107 patients with systemic lupus erythematosus (SLE; 91% women, 51% black, 36% white, 4% Asian, 4% Hispanic, and 5% others) for a total of 190 visits. Patients' mean age was 41 years. We analyzed the relationship between these potential urine biomarkers and the urine protein/creatinine ratio (urine Pr/Cr), the Systemic Lupus International Collaborating Clinics (SLICC) renal activity score, SLE Disease Activity Index renal descriptors, and other clinical variables. RESULTS: VCAM-1 levels were strongly associated with the physician's global estimate of disease activity (p = 0.0002), the renal visual analog scale (p < 0.0001), the urine Pr/Cr (p < 0.0001), and SLICC renal activity score (p < 0.0001). VCAM-1 levels were also associated with a urine Pr/Cr ≥ 0.5 (p < 0.0001). NGAL was not associated with any measure of disease activity or with lupus serologies. CONCLUSION: Urine VCAM-1 had a strong association with measures of disease activity, including multiple renal activity descriptors. In contrast to previous SLE studies, NGAL failed to show any association with lupus nephritis.

Association of noninvasively measured renal protein biomarkers with histologic features of lupus nephritis.

OBJECTIVE: To investigate the relationship of urinary biomarkers and established measures of renal function to histologic findings in lupus nephritis (LN), and to test whether certain combinations of the above-mentioned laboratory measures are diagnostic for specific histologic features of LN. METHODS: Urine samples from 76 patients were collected within 2 months of kidney biopsy and assayed for the urinary biomarkers lipocalin-like prostaglandin D synthase (L-PGDS), α(1) -acid glycoprotein (AAG), transferrin (TF), ceruloplasmin (CP), neutrophil gelatinase-associated lipocalin (NGAL), and monocyte chemotactic protein 1 (MCP-1). Using nonparametric analyses, levels of urinary biomarkers and established markers of renal function were compared with histologic features seen in LN, i.e., mesangial expansion, capillary proliferation, crescent formation, necrosis, wire loops, fibrosis, tubular atrophy, and epimembranous deposits. The area under the receiver operating characteristic curve (AUC) was calculated to predict LN activity, chronicity, or membranous LN. RESULTS: There was a differential increase in levels of urinary biomarkers that formed a pattern reflective of specific histologic features seen in active LN. The combination of MCP-1, AAG, and CP levels plus protein:creatinine ratio was excellent in predicting LN activity (AUC 0.85). NGAL together with creatinine clearance plus MCP-1 was an excellent diagnostic test for LN chronicity (AUC 0.83), and the combination of MCP-1, AAG, TF, and creatinine clearance plus C4 was a good diagnostic test for membranous LN (AUC 0.75). CONCLUSION: Specific urinary biomarkers are associated with specific tissue changes observed in conjunction with LN activity and chronicity. Especially in combination with select established markers of renal function, urinary biomarkers are well-suited for use in noninvasive measurement of LN activity, LN chronicity, and the presence of membranous LN.

Mycophenolate mofetil (MMF) does not slow the progression of subclinical atherosclerosis in SLE over 2 years.

Accelerated atherosclerosis is a major cause of mortality in SLE. Mycophenolate mofetil (MMF) has been shown to suppress growth factor-induced proliferation of vascular smooth muscle and endothelial cells in animal models. We hypothesized that MMF might modify the inflammatory component of atherosclerosis in SLE. We examined the effect of MMF on atherosclerosis as measured by changes in carotid intima-media thickness (IMT) or coronary artery calcium (CAC) over 2 years. CAC and carotid IMT were measured at baseline and 2 years later in a cohort of 187 patients with SLE. The cohort was 91% women, 59% Caucasian, and 35% African-American, with a mean age of 45 ± 11 years. Of these, 12.5% (n = 25) received MMF during follow-up. The daily dose ranged from 500 to 3,000 mg/day, and duration ranged from 84 days to the entire 2 years. We divided MMF users into three groups: low exposure (<1,500 mg average daily dose), high exposure (≥1,500 average daily dose), and any exposure of MMF (<1,500 or ≥1,500 average daily dose) for 2 years. The mean CAC increased in all four groups: no MMF: 1.17-1.28, low MMF: 1.02-1.13, high MMF: 1.44-1.61, and any MMF: 1.21-1.34 log-Agatston units. Compared to no MMF, there was no statistically different change between the three groups (p = 0.99, 0.87, and 0.91). Similarly, mean carotid IMT increased in all four groups: no MMF: 0.58-0.66, low MMF: 0.55-0.60, high MMF: 0.56-0.71, and any MMF: 0.56-0.66. We then adjusted for statin use, lupus nephritis, body mass index, systolic blood pressure, cholesterol, and age during the 2-year follow-up. The association between MMF exposure and change in CAC or carotid IMT was not statistically significant (p = 0.63 for CAC, and p = 0.085 for carotid IMT). There was no evidence that MMF slowed or decreased the progression of atherosclerosis as measured by carotid IMT or CAC. Because the number of patients taking MMF was only twenty-five, larger studies for longer time periods are needed to explore any effect of MMF on subclinical atherosclerosis in SLE.

Identification of urinary metabolites that distinguish membranous lupus nephritis from proliferative lupus nephritis and focal segmental glomerulosclerosis.

INTRODUCTION: Systemic lupus erythematosus (SLE or lupus) is a chronic autoimmune disease, and kidney involvement with SLE, a.k.a. lupus nephritis (LN), is a frequent and severe complication of SLE that increases patient morbidity and mortality. About 50% of patients with SLE encounter renal abnormalities which, if left untreated, can lead to end-stage renal disease. Kidney biopsy is considered the criterion standard for diagnosis and staging of LN using the International Society of Nephrology/Renal Pathology Society (ISN/RPS) classification, which was developed to help predict renal outcomes and assist with medical decision-making. However, kidney biopsy-based classification of LN is highly invasive and impractical for real-time monitoring of LN status. Here, nuclear magnetic resonance (NMR) spectroscopy-based metabolic profiling was used to identify urinary metabolites that discriminated between proliferative and pure membranous LN as defined by the ISN/RPS classification, and between LN and primary focal segmental glomerulosclerosis (FSGS). METHODS: Metabolic profiling was conducted using urine samples of patients with proliferative LN without membranous features (Class III/IV; n = 7) or pure membranous LN (Class V; n = 7). Patients with primary FSGS and proteinuria (n = 10) served as disease controls. For each patient, demographic information and clinical data was obtained and a random urine sample collected to measure NMR spectra. Data and sample collection for patients with LN occurred around the time of kidney biopsy. Metabolic profiling analysis was done by visual inspection and principal component analysis. RESULTS: Urinary citrate levels were 8-fold lower in Class V LN compared to Class III/IV patients, who had normal levels of urinary citrate (P < 0.05). Class III/IV LN patients had > 10-fold lower levels of urinary taurine compared to Class V patients, who had mostly normal levels (P < 0.01). Class V LN patients had normal urinary hippurate levels compared to FSGS patients, who completely lacked urinary hippurate (P < 0.001). CONCLUSIONS: This pilot study indicated differences in urinary metabolites between proliferative LN and pure membranous LN patients, and between LN and FSGS patients. If confirmed in larger studies, these urine metabolites may serve as biomarkers to help discriminate between different classes of LN, and between LN and FSGS.

Predictors of progression in atherosclerosis over 2 years in systemic lupus erythematosus.

OBJECTIVES: Cardiovascular disease remains the major cause of death in SLE. We assessed the degree to which cardiovascular risk factors (CVRFs) and disease activity were associated with 2-year changes in measures of subclinical atherosclerosis. METHODS: One hundred and eighty-seven SLE patients participating in a placebo-controlled trial of atorvastatin underwent multi-detector CT [for coronary artery calcium (CAC)] and carotid duplex [for carotid intima-media thickness (IMT) and carotid plaque] twice, 2 years apart. During the 2 years, patients were assessed every 3 months for CVRF. Both groups were combined for analysis, as atorvastatin did not differ from placebo in preventing progression of coronary calcium. We examined the correlation between these clinical measures and progression of CAC, IMT and plaque during the follow-up period. RESULTS: In an analysis adjusting for age, gender and ethnicity, CAC progression was positively associated with total serum cholesterol measured over the 2-year period (P = 0.04) and smoking (P = 0.003). Carotid IMT progression was associated with systolic BP (P = 0.003), high-sensitivity CRP (hsCRP) (P = 0.013) and white blood cell (WBC) count (P = 0.029). Carotid plaque progression, defined as patients without carotid plaque at baseline with subsequent development of plaque at follow-up, was associated with systolic BP (P = 0.003), WBC count (P = 0.02), physician's global assessment (P = 0.05), blood lymphocyte count (P = 0.048), urine protein (P = 0.017) and duration of SLE (P = 0.019). CONCLUSION: Our data did not provide evidence of an association between measures of SLE disease activity (SLEDAI, anti-dsDNA, anti-phospholipid and treatment) and progression of subclinical atherosclerosis. Age and hypertension were associated with the progression of carotid IMT and plaque. Age, smoking and cholesterol were associated with progression of CAC.

Prevalence of arthritis in India and Pakistan: a review.

Recent studies of rheumatoid arthritis worldwide suggest that prevalence of arthritis is higher in Europe and North America than in developing countries. Prevalence data for major arthritis disorders have been compiled in West for several decades, but figures from the third world are just emerging. A coordinated effort by WHO and ILAR (International League Against Rheumatism) has resulted in collecting data for countries like Philippines, China, Malaysia, Indonesia, and rural South Africa but the information about prevalence of arthritis in India and Pakistan is scarce. Since both countries, i.e., India and Pakistan, share some ethnic identity, we reviewed published literature to examine the prevalence of arthritis in these countries. Medline and Pubmed were searched for suitable articles about arthritis from 1980 and onwards. Findings from these articles were reviewed and summarized. The prevalence, clinical features, and laboratory findings of rheumatoid arthritis are compiled for both India and Pakistan. Data collected from these two countries were compared with each other, and some of the characteristics of the disease were compared with Europe and North America. It is found to be quite similar to developed countries. Additionally, juvenile rheumatoid arthritis is of different variety than reported in West. It is more of polyarticular onset type while in West pauciarticular predominates. Additionally, in systemic onset, JRA uveitis and ANA are common finding in developed countries; on the other hand, they are hardly seen in this region. Although the prevalence of arthritis in Pakistan and India is similar to Western countries, there are inherent differences (clinical features, laboratory findings) in the presentation of disease. The major strength of the study is that it is the first to pool reports to provide an estimate of the disease in the Indian subcontinent. Scarcity of data is one of the major limitations. This study helps to understand the pattern of disease in this part of country that can be stepping-stone for policy makers to draft policies that can affect target population more appropriately.

Quality-of-life measurements versus disease activity in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic disease affecting the physical, social, and psychological well-being of patients. Different instruments have been developed to measure health-related quality of life, some of which are SLE-specific. Contributors to poor quality of life in patients with SLE include fatigue, fibromyalgia, depression, and cognitive dysfunction. Health-related quality of life is not strongly associated with disease activity or organ damage. The Medical Outcomes Survey Short Form 36 is the most common instrument used to measure quality of life in SLE.

Noncalcified coronary plaque in systemic lupus erythematosus.

OBJECTIVE: To study noncalcified coronary plaque (NCP) in systemic lupus erythematosus (SLE). METHODS: Sixty-four-slice coronary multidetector computed tomography (MDCT) was performed in 39 consecutive patients with SLE. MDCT scans were evaluated semiquantitatively by a radiologist using dedicated software. The presence or absence of NCP in each coronary artery was assessed. Patients with mixed plaque (calcified and noncalcified portions) were included in the NCP group. RESULTS: The patient group was 90% women, 64% Caucasian, 31% African American, 5% other; mean age 50.5 +/- 9.6 years. Fifty-four percent (21/39) had NCP. Seventy-six percent (16/21) of those with NCP also had coronary calcium (range 0.7 to 1264.1 Agatston units). In univariate analysis, NCP was associated with age (p = 0.01), current nonsteroidal antiinflammatory drug (NSAID) use (p = 0.04), hormone replacement therapy (p = 0.02), current use of immunosuppressive drugs (p = 0.02), current low serum C3 level (p = 0.07), current physician's global assessment of activity (PGA; p = 0.05), and low-density lipoprotein cholesterol (p = 0.04). NCP was not associated with other risk factors for atherosclerosis, including total serum cholesterol, high sensitivity C-reactive protein, and lipoprotein(a). CONCLUSION: Unlike coronary calcium, which is not associated with SLE activity measures or with active serologies, NCP is more common in patients with SLE with current, 3-, and 6-month activity by PGA. NCP was also associated with the need for current NSAID or immunosuppressive therapy. NCP is an important part of the total atherosclerotic burden in SLE.