Femoral neck stress fractures in young adults are uncommon and usually not considered in the differential diagnosis of low back pain. However, if the patient has groin and anterior thigh pain, it is ...important to thoroughly examine the hips. To illustrate this point, we present a patient with a femoral neck stress fracture who was misdiagnosed as having mechanical back pain.
Celotno besedilo
Dostopno za:
DOBA, FSPLJ, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
Spatiotemporal analysis of real freeway traffic reveals that carpool lanes are not as damaging as previously reported. To the contrary, the analysis unveils a surprising benefit of carpool lanes that ...should be even greater when special lanes are used to segregate very different vehicle classes, such as buses and cars. The paper pursues this finding and shows how reserving lanes on freeways and city streets for bus-use only can favorably affect not just buses, but also cars.
Background/Purpose:
Anti‐TNF therapy for polyarticular forms (extended oligo‐, rheumatoid factor +/− polyarthritis) of JIA (PF‐JIA) results in up to 50% of patients (pts) demonstrating clinically ...inactive disease (CID). This study determined the pattern of serum S100A12 levels at the time of withdrawal of anti‐TNF therapy.
Methods:
In 16 centers, 137 pts with PF‐JIA in CID on anti‐TNF therapy were enrolled and followed for at least 14 months (mos). During the first 6 study mos pts were maintained on anti‐TNF therapy and if CID was maintained, then anti‐TNF therapy was stopped. Background medications were stable. S100A12 levels were obtained at the time of anti‐TNF withdrawal. The primary outcome was disease “flare” defined by worsening of ≥30% in ≥ 3 of the 6 core set variables, with no more than 1 improving by ≥30%. Parameters had to increase by at least the following amounts: MD and parent globals by 2 units, active and limited joints by 2, CHAQ by 0.125 and ESR from normal to abnormal.
Results:
24 pts failed to maintain CID in the first 6 study mos and 7 pts were discontinued from the study for other reasons. 106 pts were available for this analysis of whom 39 (37%) experienced flare. The S100A12 levels at time of anti‐TNF withdrawal did not differ significantly in regards to JIA type, presence of ANA, MTX co‐therapy, or type of anti‐TNF therapy and did not correlate with previous duration of CID. Globally, S100A12 at the time of withdrawal did not differ significantly according to disease flare (flare 73 +/− 117 ng/ml, no flare 80 +/− 220 ng/ml) (median ++/− standard deviation). Receiver‐operating curve (ROC) analysis computing S100A12 at time of anti‐TNF withdrawal against flare for the entire study period demonstrated an area‐under‐the‐curve (AUC) of 0.51, 95% confidence interval (CI) 0.39–0.62, for prediction of flare within 60 days AUC 0.66, 95% CI 0.56–0.75, for prediction of flare within 90 days AUC 0.64, 95% CI 0.54–0.74 and for prediction of flare within 120 days AUC 0.54, 95% CI 0.44–0.64. The S100A12 level at time of withdrawal correlated inversely with the time to flare (Spearman rank correlation = −0.34, p = 0.05). Flares occurred earlier in pts with predefined high (>120 ng/ml) vs. low (≤120 ng/ml). S100A12 levels at time of withdrawal among pts who flared (median time to flare 36 vs. 114 days, p = 0.02). The overall flare rate in patients with high vs. low S100A12 levels at time of withdrawal was 35% vs. 38%, respectively. Kaplan‐Meier analysis of disease flare in pts with high vs. low S100A12 levels at time of withdrawal also demonstrated a trend towards earlier disease flare in pts with high S100A12 levels (log rank test significance 0.07).
Conclusion:
In this prospective study, a substantial proportion of pts with PF‐JIA experienced disease flare after anti‐TNF withdrawal. Serum S100A12 levels at time of anti‐TNF withdrawal did not differ between pts subsequently experiencing disease flare and those not experiencing flare throughout the entire study period. However, pts with high S100A12 levels (>120 ng/ml) experienced earlier disease flare.
Background/Purpose:
Treatment with anti‐TNF therapies (anti‐TNF) for polyarticular forms (extended oligo, Poly RF +/−) of JIA (PF‐JIA) results in >50% demonstrating clinically inactive disease (CID). ...The aims of this study were to determine the frequency, timing and predictors of flare upon withdrawal of anti‐TNF in PF‐JIA in CID.
Methods:
In 16 centers 137 children with PF‐JIA in CID on anti‐TNF were enrolled and followed for ≥14 mos. If CID was maintained for the first 6 study mos, then anti‐TNF was stopped. The primary outcome variable was a validated definition of disease flare within 8 months after stopping anti‐TNF. Background meds were stable. Blood for S100, DEK, DNA and RNA was drawn for current and future biomarker and genetic studies.
Results:
The study population included 18 (13%) extended oligarticular, 17 (12%) RF+ Poly and 102 (74%) RF‐ Poly JIA patients. At enrollment, age (mean/median/range) was 11.3/11.6/3.4–20.1 yrs; disease duration was 5.0/4.1/0.6–18.6 years; 103 (75%) were females and 64 (47%) were ANA+. Duration of CID at baseline was 1.2/0.5/1 day–12.1 yrs. Anti‐TNF was etanercept in 106 (77%), 25 (18%) adalimumab and 6 (5%) infliximab. 40% were on MTX at baseline (mean/median dose 0.4/0.4 mg/kg/week). Other meds: 1 leflunomide, 2 hydroxychloroquine, and 1 prednisolone.
31 (23%) subjects were discontinued from the study in the first 6 mos: 23 (17%) due to loss of CID, 5 (4%) med noncompliance, 2 (1%) moved/LTF, 1 (1%) ILAR subtype changed (oligo to psoriatic). For the extended oligo, Poly RF− and Poly RF+ categories 94%, 82% and 60%, respectively, maintained CID for the first 6 months (c2 6.7, p 0.03). ANA status, MTX use, and type of anti‐TNF were not associated with the ability to maintain CID (c2 p values 0.48, 0.14, and 0.75, respectively).
106 (77%) subjects maintained CID for the first 6 months and stopped anti‐TNF as per protocol. 67/106 (63%) maintained CID for ≥8 mos off anti‐TNF while 39 (37%) flared. Time without flaring after stopping anti‐TNF therapy was duration from the month 6 visit to the last study visit (mean/median/range for duration of followup was 249/250/126–322 days). The mean/median/range for time to flare was 108/105/7–271 days. Time to flare (days) for etanercept was 105/105/7–271, adalimumab 119/120/28–238 and infliximab 28/28/28. Flare was seen in 47% (8/17) extended oligo, 37% (30/80) poly RF– and 11% (1/9) poly RF+ ((c2 p‐value 0.19). In those on background MTX, 33% (13/40) flared at a mean of 90 days, while those not on background MTX, 39% (26/66) flared at a mean of 113 days ((c2 p‐value 0.48). Using univariate analysis of variance, only weak correlations of MTX dose, disease duration, and CID duration with flare/no flare were seen (Spearman correlations −0.03, −0.17, −0.19, respectively).
Conclusion:
In this prospective multicenter study, 77% of the PF‐JIA patients were able to maintain CID for the first 6 months on anti‐TNF. Discontinuation of anti‐TNF in PR‐JIA (who have demonstrated on average 1.8 years of CID) resulted in a flare rate of 37% within 8 mos. Clinical parameters had only minimal predictive ability. Ongoing work includes biomarker identification and continued follow‐up of the cohort.
Background/Purpose:
The nuclear oncoprotein DEK is a biochemically distinct protein, modulating heterochromatin integrity, chemoattractant of neutrophils and T‐cells and vital for the formation of ...neutrophil extracellular traps (NETs). NETs are important for resolution of inflammation suggesting that DEK contributes to the development of autoimmune diseases. High levels of DEK autoantibodies have been found in several autoimmune diseases including juvenile idiopathic arthritis (JIA) but their role in disease pathogenesis is not clear. Since DEK and DEK autoantibodies can contribute to the development of immune complexes and NET formation we suggest that DEK antibody levels can predict flare with the discontinuation of anti‐TNF therapy.
Methods:
In16 pediatric rheumatology centers, sera samples were collected from 137 children with polyarticular JIA with clinically inactive disease (CID) on anti‐TNF therapy. The therapy was stopped and disease activity was monitored for at least 8 months or until disease flare. DEK antibody levels were measured in sera collected at time of enrollment and 6 months (when anti‐TNF therapy was stopped) by ELISA. DEK antibody levels relative to healthy controls were calculated by area under the curve (AUC), expressed as unit‐free ratios.
Results:
103 females and 34 males patients were enrolled. Mean age 11.3 years and disease duration 5.0 years. JIA included: 13% extended oligoarthritis, 74% polyarthritis rheumatoid factor (RF) negative and 12 % polyarthritis RF positive and 46% positive ANA. 77% were taking etanercept, 18% adalimumab, 5% infliximab and 40% methotrexate. 31 patients (23%) discontinued the study prior stopping the therapy for various reasons, including loss of CID. Of 106 subjects who stopped the therapy, 39 (37%) flared within 8 months (mean of 104.8 days). 67 subjects (63%) had no flares within 8 months after stopping the therapy. 71 out of 106 patients samples were analyzed thus far for DEK antibody levels. DEK antibody level ratios compared to healthy controls was −0.36 (some patients had lower antibody levels than did healthy controls) to 1.41, median ratio of 0.11 (Q1–Q3 of 0.09–0.24) and 0.13 (SD, 0.3). High levels of DEK antibodies, mean and SD of 0.209 ± 0.36 were detected in the 21 patients that flared within 8 months compared to lower levels of DEK antibodies (0.09 ± 0.27) in 50 patients with CID for at least 8 months (ANOVA P= 0.1832). Negative correlation was observed between the days to flare and DEK antibody levels (spearman rho = −0.31, P = 0.07), suggesting that when therapy stopped, patients with higher levels of DEK antibodies will flare sooner with estimated odds ratio of 3.3 (95% CI, 0.61, 18.0), suggesting that each unit increase in DEK antibodies is associated (P = 0.17) with more than a 2‐fold increased risk of flare within 8 months.
Conclusion:
In children with JIA extended oligoarthritis and polyarthritis on anti‐TNF therapy that maintain CID for at least 6 months while on therapy, high DEK antibody levels may be correlated with flare within the first 8 months after stopping the therapy. This study suggests that DEK antibody levels can predict the outcome of discontinuation of anti‐TNF therapy, although more patient samples need to be analyzed from this study and future studies.
Background/Purpose:
Treatment with anti‐TNF therapies for polyarticular forms (extended oligoarthritis, rheumatoid factor RF +/− polyarthritis) of JIA (PF‐JIA) results in up to 50% of patients (pts) ...demonstrating clinically inactive disease (CID). Serum S100A12 protein levels have been demonstrated to predict failure to maintain CID after withdrawal of methotrexate (MTX). This study determined the pattern of baseline serum S100A12 levels during CID on anti‐TNF therapy.
Methods:
In 16 centers, 137 pts with PF‐JIA in CID on anti‐TNF therapy were enrolled. During the first 6 study months patients were maintained on anti‐TNF therapy and monitored. If CID was maintained for first 6 study months, then anti‐TNF therapy was stopped. Pts were followed for up to 14 mos total or until loss of CID on anti‐TNF therapy or until flare off anti‐TNF therapy, whichever came first. Background medications were stable throughout the study. Blood for serum S100A12 measurement was drawn at study enrollment. S100A12 measurements were obtained via a validated ELISA. The secondary outcome of this part of the analysis was failure to maintain CID during the first 6 study months.
Results:
7 pts were discontinued from the study for reasons other than inability to maintain CID and 130 patients were available for analysis. 24 pts failed to maintain CID during the first 6 study months. Demographic and clinical details are reported elsewhere during this conference. Baseline S100A12 levels did not differ significantly according to sex (female 96 +/− 229 ng/ml, male 66 +/− 144 ng/ml), JIA subtype (extended oligo 91 +/− 199 ng/ml, poly RF‐ 93 +/− 219 ng/ml, poly RF+ 114 +/− 157 ng/ml) presence of ANA (positive 83 +/− 174 ng/ml, negative 96 +/− 240 ng/ml), MTX co‐therapy (yes 84 +/− 259 ng/ml, no 95 +/− 167 ng/ml) or type of anti‐TNF therapy (adalimumab 114 +/− 140 ng/ml, etanercept 90 +/− 214 ng/ml, infliximab 120 +/− 330 ng/ml) (values given as median +/− standard deviation) and did not correlate with duration of previous duration of inactive disease (r = −0,06). Globally, S100A12 did not differ significantly according to failure to maintain CID (failure to maintain CID 100 +/− 188 ng/ml, maintaining CID 93 +/− 216 ng/ml). Based on a predefined normal level of S100A12 of <120 ng/ml, 87 (66%) of patients demonstrated normal S100A12 levels and 43 (33%) of patients demonstrated elevated S100A12 levels. However, receiveroperating curve analysis computing baseline S100A12 against failure to maintain CID demonstrated an areaunder‐the‐curve of 0,47 (95% confidence interval 0.33–0.62).
Conclusion:
In this prospective multicenter study, baseline S100A12 levels in pts with PF‐JIA were elevated in a substantial proportion of pts but did not differ among groups according to multiple parameters. Serum S100A12 did not predict failure to maintain CID.
May 31, 1995--REDDI BRAKE SUPPLY CORPORATION (Nasdaq NM Symbol: REDI) today announced that William M. Leider has been appointed as Chief Executive Officer of the company, effective immediately. ...Leider, 57, has served as a member of the Board of Directors since July 1994, and as a member of Reddi Brake's Executive Committee since February 1995. As Reddi Brake's new CEO, Leider joins Bruce Douglass, who will remain as President and Chief Operating Officer. Leider graduated from UCLA and began his career as a Certified Public Accountant. He has extensive experience as a Chief Executive Officer and Chief Operating Officer at distribution companies in both the public and private sectors, and is also a principal of Leider, Murphy & Associates, a management consulting firm which he co-founded in 1982. (excerpt)
March 8, 1995--REDDI BRAKE SUPPLY CORPORATION (Nasdaq Symbol: REDI) today announced that in a meeting held by the Board of Directors, Gordon Werner was elected to the position of Chairman of the ...Board. Prior to his election to Chairman of Reddi Brake Supply Corporation, Mr. Werner held the position of Vice Chairman since 1993. He has been a director of Reddi Brake since 1991. Prior to his involvement with Reddi Brake, Mr. Werner was a Managing Director of DNC Capital Corporation, a merchant banking firm. From 1977 to 1987 he was a partner in Werner & Dudley Associates, a law and merchant banking firm. Mr. Werner received a B.A. from Haverford College and a J.D. from Harvard Law School. (excerpt)
Real data show that reserving a lane for carpools on congested freeways induces a smoothing effect that is characterized by significantly higher bottleneck discharge flows (capacities) in adjacent ...lanes. The effect arises because disruptive vehicle lane changing diminishes in the presence of a carpool lane. The effect is reproducible across days and freeway sites: it was observed, without exception, in all cases tested. Queueing analysis shows that the effect greatly reduces the times spent by people and vehicles in queues. By ignoring the smoothing effect at one of the sites we analyzed, for example, one would predict that its carpool lane increased both the people-hours and the vehicle-hours traveled by well over 300%; when in reality the carpool lane and its attendant smoothing reduced both measures. The effect is so significant, in fact, that even a severely underused carpool lane can in some instances increase a freeway bottleneckâeuro(TM)s total discharge flow. This happens for the site we analyzed when carpool demand is as low as 1200 vph. It follows that strategies designed to induce smoothing by other means also hold promise for managing congestion, both for freeways that have carpool lanes and those that do not. Possible strategies of this kind are discussed.
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