bluuebunny/crossref_metadata_2025_split huggingface dataset:
Renal vascular damage in systemic sclerosis patients without clinical evidence of nephropathy
Authors: Rivolta Roberto , Mascagni Barbara , Berruti Vittorio , di Palo Filippo Quarto , Elli Attilio , Scorza Raffaella , Castagnone Daniela 
Published: February 2007

AbstractObjective. To evaluate the use of color‐flow Doppler ultrasonography, a direct, noninvasive technique, for measurement of kidney blood flow in patients with systemic sclerosis (SSc).Methods. Twenty‐five normal volunteers and 25 SSc patients (median disease duration 8 years, range 2–21 years) were studied. All were free of clinical symptoms of renal damage. The resistance index (RI) was determined on main, interlobar, and cortical vessels.Results. In SSc patients, the RI was significantly increased at every sampling site examined (P < 0.001). RI values were strongly correlated with disease duration (main artery r = 0.56, P < 0.04; interlobar artery r = 0.63, P < 0.02; cortical artery r = 0.75, P < 0.002). Regression analysis showed no relationship between RI and creatinine clearance values.Conclusion. Color‐flow Doppler ultrasonography is a sensitive and noninvasive technique for evaluating vascular damage of the kidney in patients with SSc.
Utility of anti‐Sm, anti‐RNP, anti–Ro/SS‐A, and anti–La/SS‐B (extractable nuclear antigens) detected by enzyme‐linked immunosorbent assay for the diagnosis of systemic lupus erythematosus
Authors: Sánchez‐Guerrero Jorge , Lew Robert A. , Fossel Anne H. , Schur Peter H. 
Published: February 2007

AbstractObjective. To determine the utility of anti‐extractable nuclear antigen (anti‐ENA) antibodies detected by enzyme‐linked immunosorbent assay as a predictor for the diagnosis of systemic lupus erythematosus (SLE).Methods. Among 2,185 serum samples sent for testing for antinuclear antibodies (ANA) by indirect immunofluorescence, 259 consecutive patients with positive ANA were identified. Medical charts of these patients were reviewed to assess the clinical diagnosis, with the reviewer having no knowledge of the anti‐ENA result. Clinical data were abstracted for all patients, and diagnoses established using American College of Rheumatology criteria. The utility of ENA antibodies in the diagnosis of SLE was determined by univariate and multivariate analysis among all patients who were positive for ANA, patients who were positive for ANA and for anti‐double‐stranded DNA (anti‐dsDNA), and patients who were positive for ANA and negative for anti‐dsDNA. Clinical differences between SLE patients with and those without anti‐ENA antibodies were assessed.Results. Anti‐ENA antibodies, especially anti‐Ro/SS‐A, showed strong predictive diagnostic value among ANA+/anti‐dsDNA– patients, but were of no utility among ANA+/anti‐dsDNA+ patients. The only clinical manifestations that were more common among anti‐ENA+ SLE patients were pleuritis and the use of hydroxychloroquine.Conclusion. The presence of anti‐ENA antibodies, especially anti‐Ro/SS‐A, is a useful predictor for the diagnosis of SLE, primarily among patients attending a referral rheumatology center who are positive for ANA and negative for anti‐dsDNA. No major clinical differences were noted among ANA+ SLE patients with versus those without ENA.
Deactivation of vascular endothelium by monoclonal anti–tumor necrosis factor α antibody in rheumatoid arthritis
Authors: Paleolog Ewa M. , Hunt Mary , Elliott Michael J. , Feldmann Marc , Maini Ravinder N. , Woody James N. 
Published: February 2007

AbstractObjective. To assess whether monoclonal antibody to tumor necrosis factor α (TNFα) reduces endothelial activation in rheumatoid arthritis (RA).Methods. Levels of serum E‐selectin, intercellular adhesion molecule 1 (ICAM‐1), and vascular cell adhesion molecule 1 (VCAM‐1), and circulating leukocytes (differential counts) were measured in RA patients before and up to 4 weeks after infusion of either placebo or chimeric anti‐TNFα antibody cA2 (1 or 10 mg/kg).Results. Treatment with anti‐TNFα decreased serum E‐selectin and ICAM‐1 levels, with the earliest detectable changes observed on days 1–3 after anti‐TNFα infusion. No effect on VCAM‐1 levels was detected. In parallel, there was a rapid and sustained increase in circulating lymphocytes. The extent of the decrease in serum E‐selectin and ICAM‐1 levels and the increase in lymphocyte counts was significantly higher (P ≤ 0.05) in patients in whom a clinical benefit of anti‐TNFα was observed (≥20% response, by Paulus criteria, at week 4) compared with that in patients who failed to respond to anti‐TNFα at this time point.Conclusion. We propose that decreased serum levels of adhesion molecules may reflect diminished activation of endothelial cells in the synovial microvasculature, leading to reduced migration of leukocytes into synovial joints, and thus prolonging the therapeutic effect of anti‐TNFα in RA.
Lack of association between augmentation mammoplasty and systemic sclerosis (scleroderma)
Authors: Hochberg Marc C. , Perlmutter Donna L. , Medsger Thomas A. , Nguyen Katherine , Steen Virginia , Weisman Michael H. , White Barbara , Wigley Fredrick M. 
Published: February 2007

AbstractObjective. To examine the possible association between augmentation mammoplasty and systemic sclerosis (SSc; scleroderma).Methods. Eight hundred thirty‐seven women with a clinical diagnosis of SSc, recruited as a volunteer sample from 3 university‐based, tertiary care scleroderma clinical research centers, and 2,507 race‐matched local control women, recruited by the technique of random‐digit‐dialing and frequency‐matched on age, completed a questionnaire providing data on history of augmentation mammoplasty, including possible complications of the procedure. The odds ratio (OR) and 95 percent confidence interval (95% CI) for the association of augmentation mammoplasty with SSc were estimated by multivariate logistic regression analysis with adjustment for age, race and center, and by conditional logistic regression analysis with adjustment for age.Results. Eleven (1.31%) of the 837 cases reported a history of augmentation mammoplasty prior to diagnosis of SSc, compared with 31 (1.24%) of the 2,507 controls. The adjusted OR from the unmatched analysis was 1.07 (95% CI 0.53–2.13), while that from the matched analysis was 1.11 (95% CI 0.55–2.24).Conclusion. These results fail to demonstrate a significant association between augmentation mammoplasty and SSc, and are consistent with those reported from other epidemiologic studies.
Pilot study of antithymocyte globulin in systemic sclerosis
Authors: Matteson Eric L. , Shbeeb Mohammad I. , McCarthy Tim G. , Calamia Kenneth T. , Mertz Lester E. , Goronzy Jörg J. 
Published: February 2007

AbstractObjective. Between June 1, 1992 and August 31, 1994 we conducted an open pilot study of antithymocyte globulin (ATGAM; Upjohn, Kalamazoo, MI) in 10 patients with early systemic sclerosis (SSc) to assess whether this agent might prevent the progression of cutaneous and pulmonary involvement in this disease.Methods. Adult patients with early SSc (<3 years) and evidence of progressive skin and pulmonary disease were enrolled. All patients were hospitalized and received a single course of intravenous ATGAM, at a dosage of 10 mg/kg over 4 hours, on 5 consecutive days. Patients were followed up at weeks 1, 2, 3, and 4, and months 2, 4, 6, and 12. Patients were considered to be improved if the Rodnan skin score decreased ≥25%, to be worse if the skin score increased ≥25%, and to be not improved if the skin score was within 25% of baseline. For pulmonary involvement, patients were considered to be improved if either the diffusing capacity for carbon monoxide or the forced vital capacity was increased ≥10%, worse if decreased by ≥10%, and stable if within 10% of baseline.Results. Most patients tolerated the treatment well, although 1 patient developed an allergic reaction necessitating discontinuation of treatment, 1 developed a serum sickness reaction after completion of therapy, and 1 developed a central venous access–related axillary vein thrombosis. Two patients died of SSc‐related complications during the followup period. At 12 months, only 2 patients showed improvement in both skin and pulmonary function measures, whereas 5 patients were worse and 3 were stable.Conclusion. At the dosage administered in this study, ATGAM appears ineffective in improving the skin and pulmonary features of SSc.
Evidence of free radical–mediated injury (isoprostane overproduction) in scleroderma
Authors: Stein C. Michael , Tanner S. Bobo , Awad Joseph A. , Roberts L. Jackson , Morrow Jason D. 
Published: February 2007

AbstractObjective. Free radical–induced oxidative stress with consequent lipid peroxidation and resultant tissue damage has been suggested as a potential mechanism of the pathogenesis of scleroderma. However, because reliable measurement of lipid peroxidation in vivo is difficult, it has not been possible to adequately examine this hypothesis. We have previously described a series of bioactive prostaglandin F2–like compounds, termed F2‐isoprostanes, produced in vivo in humans by the noncyclooxygenase, free radical–catalyzed, peroxidation of arachidonic acid and have shown them to be a reliable measure of lipid peroxidation in vivo. In the present study, we determined whether scleroderma is associated with enhanced oxidative stress.Methods. As a measure of oxidative stress, we determined urinary concentrations of a tetranordicarboxylic acid metabolite of F2‐isoprostanes (F2IP‐M) by mass spectrometry in 8 patients with scleroderma (representing a wide spectrum of disease, including limited disease with refractory digital ulceration or pulmonary hypertension, and diffuse disease) and in 10 healthy control subjects.Results. F2IP‐M concentrations were significantly higher in patients with scleroderma (mean ± SEM 3.41 ± 0.64 ng/mg of creatinine) than in healthy controls (1.22 ± 0.14 ng/mg of creatinine) (P = 0.002). These elevations occurred in patients with limited disease and in those with diffuse disease.Conclusion. The increased level of urinary F2IP‐M supports the hypothesis that free radical–induced oxidative injury occurs in scleroderma and provides a biologic marker whose relationship to disease activity and disease therapy may be important. These findings may also provide a rationale for exploring whether antioxidant therapy may influence the natural course of the disease.
Autoantibodies to fibrillarin in systemic sclerosis (scleroderma). An immunogenetic, serologic, and clinical analysis
Authors: Arnett Frank C. , Reveille John D. , Goldstein Rose , Pollard K. Michael , Leaird Kimberly , Smith Edwin A. , Leroy E. Carwile , Fritzler Marvin J. 
Published: February 2007

AbstractObjective. To determine the frequency, clinical associations, and any major histocompatibility complex correlations of antifibrillarin antibodies in patients with systemic sclerosis (SSc).Methods. Antifibrillarin antibodies were determined by indirect immunofluorescence, immunoblotting, and immunoprecipitation, and HLA class II alleles by DNA oligotyping, in a large cohort of SSc patients.Results. Antifibrillarin was found in 8% of 335 SSc sera and was significantly more common in blacks (16%) than whites (5%), in males (33%) than females (14%), and in patients with cardiac, renal, or gut involvement. The HLA class II haplotype DRB1*1302, DQB1*0604 was found significantly more frequently in SSc patients with antifibrillarin compared with racematched normal controls and 260 SSc patients without antifibrillarin. In addition, 1 or more of the HLA–DQB1 alleles *0604, *0301, *0602, and/or *0302 was found in all antifibrillarin‐positive patients, and 62% of the antifibrillarin‐positive patients had 2 of these HLA–DQB1 alleles, a highly significant difference from both race‐matched normal controls and antifibrillarin‐negative SSc patients.Conclusion. Antifibrillarin, although an infrequent nucleolar autoantibody, is a marker for severe SSc, especially in blacks and males, and is strongly associated with a unique HLA haplotype, as well as with combinations of certain HLA–DQB1 alleles.
Sensitivity and specificity of plasma and urine complement split products as indicators of lupus disease activity
Authors: Manzi Susan , Rairie Joan E. , Carpenter A. Betts , Kelly Robert H. , Jagarlapudi Santhi P. , Sereika Susan M. , Medsger Thomas A. , Ramsey‐Goldman Rosalind 
Published: February 2007

AbstractObjective. To determine if measurement of serum complement split products (C4d, Bb, C5b–9) is better than conventional C3 and C4 measurements in distinguishing patients with varying degrees of lupus disease activity, and to determine if the presence of C3d in urine is helpful in distinguishing lupus patients with from those without early lupus nephritis.Methods. Lupus disease activity was prospectively determined at 3 consecutive visits an average of 4 months apart, using the Systemic Lupus Activity Measure (SLAM), the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI), and physician global assessment (PGA). Blood samples were evaluated for the presence of C4d, Bb, and C5b–9 by quantitative microsassay plate enzyme immunoassay at each patient visit. We characterized urinary excretion of C3 fragments (with attention to C3d) by sodium dodecyl sulfate–polyacrylamide gel electrophoresis with Western blotting.Results. Thirty‐one SLE patients were enrolled in the study. The mean SLAM score and the mean SLEDAI score each correlated well with the PGA at all 3 visits. A SLAM score of 6 and a SLEDAI score of 4 had the best overall sensitivity and specificity for predicting moderate‐to‐severe disease activity by PGA (100% and 73%, respectively, for the SLAM and 86% and 94%, respectively, for the SLEDAI). Serum C4d and Bb were more sensitive indicators of current moderate‐to‐severe lupus disease activity at all 3 visits than were serum C5b–9, C3, and C4. C3 and C4 were more specific indicators of moderate‐to‐severe disease activity. Serum C4d and Bb were more sensitive at predicting moderate‐to‐severe disease activity at subsequent visits than were C5b–9, C3, and C4. Urine C3d was better than C3, plasma C4d, Bb, C5b–9 and anti–double‐stranded DNA antibody in distinguishing patients with from those without acute lupus nephritis (P = 0.02).Conclusion. C4d and Bb are sensitive indicators of moderate‐to‐severe lupus disease activity and may be most helpful in situations where conventional measurements are not, such as in lupus patients whose C3 and C4 levels remain normal despite evidence of clinical disease activity. It appears from this study that detection of urine C3d may be a simple way of measuring complement activation in the setting of lupus renal disease. The availability of instruments for clinical disease activity measurement such as the SLAM and the SLEDAI may enable more consistent definition of lupus disease activity and may thus provide a means for better examining the role of complement activation products in predicting lupus disease activity in larger patient populations.
Inhibition and prevention of monosodium urate monohydrate crystal–induced acute inflammation in vivo by transforming growth factor β1
Authors: Lioté Frédéric , Prudhommeaux Florence , Schiltz Corinne , Champy Romuald , Herbelin André , Ortiz‐Bravo Esteban , Bardin Thomas 
Published: February 2007

AbstractObjective. We investigated the effects of transforming growth factor β1 (TGFβ1) on monosodium urate monohydrate (MSU) crystal‐induced acute inflammation in vivo.Methods. One hour after MSU crystal–induced acute inflammation was produced in the rat subcutaneous air pouch model, the effects of recombinant human TGFβ1 (rHuTGFβ1; 10–100 pg/animal) and ultrapure TGFβ1 (UPTGFβ1; 100 and 500 pg/animal) were assessed, based on absolute and differential white blood cell counts in the exudate. The effects of 10 pg of rHuTGFβ1 preincubated with a specific anti‐TGFβ antibody, and the effects of coinjection of crystals and rHuTGFβ1, were also studied.Results. UPTGFβ1 and rHuTGFβ1 markedly reduced MSU crystal–induced inflammation. Recombinant human TGFβ1 also reduced inflammation when administered concomitantly with MSU crystals. Moreover, rHuTGFβ1 and UPTGFβ1, injected 1 hour after MSU crystal injection, reduced the inflammatory response in a dose‐dependent manner. Injection of rHuTGFβ1 (100 pg/animal) resulted in a >90% reduction in the maximal white blood cell count, achieved 6 hours after crystal injection. Preincubation of rHuTGFβ1 with a specific anti‐TGFβ1 antibody significantly (P < 0.01) reversed the inhibitory effect of rHuTGFβ1 on the inflammatory response. Consistent with the regulation of inflammatory cell recruitment into the joint, the percentage of monocytes markedly decreased (P < 0.01) following local injection with rHuTGFβ1 6 hours after MSU crystal injection.Conclusion. Exogenous TGFβ1 prevents and inhibits MSU crystal–induced acute inflammation in vivo. Its role in the self‐limitation of gouty attacks deserves consideration, among the various other factors involved.
Colchicine in breast milk of patients with familial mediterranean fever
Authors: Ben‐Chetrit Eldad , Scherrmann Jean‐Michel , Levy Micha 
Published: February 2007

AbstractObjective. To clarify whether colchicine is excreted in breast milk, and to compare its concentrations in the serum and breast milk of lactating women who have familial Mediterranean fever (FMF).Methods. Using a specific radioimmunoassay, we determined colchicine concentrations in the serum and breast milk of 4 patients at various time points, following oral administration of the drug. The study evaluated 4 patients with FMF who had been taking colchicine on a long‐term basis.Results. Colchicine was found to be excreted in breast milk. Its levels ranged between 1.9 and 8.6 ng/ml, which were similar to those found in the serum (parallel concentration time curves). However, there appeared to be a considerable variation in colchicine milk concentration among the different patients, which might be related to individual breast milk composition and, possibly, to other nutritional or metabolic factors.Conclusion. The extensive peripheral tissue binding and relatively low concentration of colchicine in breast milk suggests that the amount ingested by the infant is small. Furthermore, based on our clinical experience, nursing appears to be safe for lactating women with FMF who continue to take colchicine.
Pediatric rheumatology in adult rheumatology practices in Washington state
Authors: Sherry David D. , Wallace Carol A. , Kahn Stuart J. 
Published: February 2007

AbstractObjective. To determine both the extent to which adult rheumatologists treat children and their level of comfort in doing so.Methods. A questionnaire was sent to all 77 physicians in the state of Washington who were listed as adult rheumatologists in the American College of Rheumatology (ACR) directory.Results. Sixty‐six questionnaires (86%) were returned; 50 were identified as being from privatepracticing adult rheumatologists and were the focus of this study. Sixty‐two percent of the respondents reported that they care for children; predictors included increased exposure to pediatric rheumatology during fellowship (P = 0.003), increased distance from Seattle (P = 0.001), and listing oneself in the ACR directory as treating children (P = 0.03). Most respondents reported feeling discomfort in treating children younger than 6 years of age, treating Kawasaki disease, and treating polyarteritis nodosa, but most reported feeling comfortable treating children with chronic arthritides. Impediments to referring to a pediatric rheumatologist included distance (median distance 35 miles), convenience for the family, personal preference, and experience in caring for children. Twenty‐nine percent reported difficulties referring to a pediatric rheumatologist outside of one's managed care plan. Adult rheumatologists expressed interest in continuing medical education dealing with pediatric rheumatology, preferably with a lecture format in their home communities.Conclusion. A significant number of adult rheumatologists care for children. Pediatric rheumatologists should provide both educational and consultative support for these adult rheumatologist colleagues.
A matrix metalloproteinase–generated aggrecan neoepitope as a marker of skeletal maturation and aging in cartilage
Authors: Olszewski Julie , McDonnell Joseph , Stevens Karla , Visco Denise , Moore Vernon 
Published: February 2007

AbstractObjective. To quantify the matrix metalloproteinase–induced neoepitope F(M/V)DIPEN (Phe–[Met/Vall]‐Asp–Jle–Pro–Glu–Asn341) in guinea pig and rabbit cartilage during aging.Methods. Cartilage was taken from the stifle joint, nasal septum, and xiphoid process in guinea pigs and rabbits at selected ages. The cartilage was then extracted and evaluated for F(M/V)DIPEN levels by radioimmunoassay.Results. In the 3 tissues studied, there were major increases in F(M/V)DIPEN levels during skeletal maturation and aging in both the guinea pig and rabbit cartilage. Except for spontaneous osteoarthritis that develops in guinea pigs with aging, increases in the neoepitope were not correlated with arthritis pathology.Conclusion. Increases in the level of F(M/V)‐DIPEN in cartilage occur as a result of skeletal maturation and aging. This physiologic accumulation of F(M/V)DIPEN in cartilage should be considered when using the neoepitope as a disease marker in arthritis.
Focal myositis presenting as pseudothrombophlebitis of the neck in a patient with mixed connective tissue disease
Authors: Rivest Charles , Miller Frederick W. , Love Lori A. , Turgeon Pierre‐Paul , Blier Claude , Senécal Jean‐Luc 
Published: February 2007

AbstractThis report describes a case of focal myositis in a patient with mixed connective tissue disease. The patient presented with diffuse neck swelling and pseudothrombophlebitis of the left internal jugular vein. Other clinical features included a high fever, elevated erythrocyte sedimentation rate, and prompt improvement after administration of high‐dose intravenous corticosteroid therapy. Criteria for polymyositis were absent, serum levels of creatine kinase remained normal, and there was no sign of recurrence during 3 years of followup. Results of immunoprecipitation for anti–Jo‐1 and other myositis‐specific autoantibodies remained negative in serial serum samples obtained before, during, and after the episode.
The CD69 activation pathway in rheumatoid arthritis synovial fluid t cells
Authors: Hernández‐García César , Fernández‐Gutiérrez Benjamín , Morado Inmaculada C. , Bañares Antonio A. , Jover Juan A. 
Published: February 2007

AbstractObjective. To study the CD69 activation pathway in synovial fluid (SF) T lymphocytes from patients with rheumatoid arthritis (RA).Methods. Peripheral blood mononuclear cells (PBMC) or SF mononuclear cells (SFMC) were used in proliferation assays with anti‐CD69, anti‐CD28, anti‐CD3, phorbol myristate acetate (PMA), and/or recombinant interleukin‐2 (IL‐2). CD69+, CD69—, and resting SF T cells were also proliferated. CD25 expression and production of IL‐2 after CD69 activation were assessed by flow cytometry and in a bioassay with the IL‐2‐dependent cell line CTLL‐2.Results. RA SFMC did not proliferate either in the presence of anti‐CD69 monoclonal antibodies alone or with concomitant PMA activation, when compared with paired or control PBMC. Similar low proliferative responses via the CD3 or CD28 pathway with PMA were observed. This defective proliferation of RA SFMC after stimulation through the CD69 molecule was explained in part by a failure to express CD25 and to produce IL‐2. SF CD69‐ T cells and resting SF T cells had higher rates of proliferation through the alternative costimulatory pathway CD28 than did SF CD69+ T cells or freshly isolated SF T cells.Conclusion. Freshly isolated SF T cells present a profound state of hyporesponsiveness through the CD69 and CD28 costimulatory pathways. This state appears to be dependent on the activation status of SF T cells, since CD69— and resting SF T cells showed recovery of the ability to proliferate through the CD28 activation pathway.