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ID PMID Title PublicationDate abstract
19483226 The Anatomical Graduated Component total knee replacement: a long-term evaluation with 20- 2009 Jun The long-term success of total knee replacement is multifactorial, including factors relating to the patient, the operation and the implant. The purpose of this study was to examine the 20-year survival of the cemented Anatomical Graduated Component (AGC) total knee replacement. Between 1983 and 2004, 7760 of these were carried out at our institution. Of these, 6726 knees which received the non-modular metal-backed tibial component with compression-moulded polyethylene and had a minimum two-year follow-up were available for study. In all, 36 knees were followed over 20 years with a survival of the tibial and femoral components together of 97.8% (95% confidence interval (CI) 0.9851 to 0.9677), with no implants being revised for polyethylene wear or osteolysis. Age > 70 was associated with increased survival (99.6%, 95% CI 99.0 to 99.8) (p < 0.0001) but pre-operative valgus alignment reduced survival (95.1%, 95% CI 90.0 to 97.6) (p = 0.0056). Age < 55 (p = 0.129), pre-operative varus alignment (p = 0.707), osteonecrosis (p = 0.06), rheumatoid arthritis (p = 0.247), and gender (p = 0.666) were not statistically associated with failure. We attribute the success of the AGC implant to its relatively unconstrained articular geometry and the durability of a non-modular metal-backed tibial component with compression moulded polyethylene.
18726101 Circulating E-selectin and tumor necrosis factor-alpha in extraarticular involvement and j 2009 Jan In this cross-sectional study, we assessed the relationship between circulating TNF-alpha and E-selectin (sE-selectin) with extraarticular involvement and severity of joint disease in RA. We compared 56 patients who had RA and extraarticular involvement (ExRA) with a group of 84 patients with only articular involvement (non-ExRA). ExRA had higher circulating TNF-alpha than non-ExRA (32 +/- 9 vs. 28 +/- 6 pg/mL, P = 0.002). sE-selectin levels did not differ between both groups. sE-selectin correlated with tender joint count (rho = 0.19, P = 0.03), morning stiffness (rho = 0.19, P = 0.03), severity of pain (rho = 0.21, P = 0.02), disease activity (assessed by the patient) (rho = 0.21, P = 0.02), HAQ-DI (rho = 0.29, P = 0.004), and rheumatoid factor titers (rho = 0.31, P = <0.001). Circulating TNF-alpha had no correlation with sE-selectin or disease activity. We concluded that sE-selectin correlated with severity of joint disease, further follow-up studies should evaluate if sE-selectin is useful as prognosis marker for progression of articular damage.
20936988 Small molecules regulating apoptosis in the synovium in rheumatoid arthritis. 2010 OBJECTIVES: To study the rate of apoptosis and expression of pro- and anti-apoptotic molecules in the synovial membrane in early and late rheumatoid arthritis (RA). METHODS: Samples of the synovium, cartilage, synovial fluid, and blood serum were obtained from patients with seropositive RA. The localization of Bcl-2-, p53- and TUNEL-immunoreactive cells in the synovial membrane was studied. The level of the soluble Fas (sFas) receptor was determined in the blood serum and synovial fluid using an immunoassay. RESULTS: In early RA, p53-immunoreactive synovial cells of type A were found to form rare aggregates in the intima. In late RA, on the contrary, these cells increased in number and occurred predominantly in the synovial stroma. Bcl-2-immunoreactive synovial cells were observed in lymphocytic infiltrates in the intima. They were found mainly in early RA. In late RA, their number decreased. The apoptotic index determined from the proportion of TUNEL-reactive synovial cell nuclei reached a maximum in late RA. The temporal differences in the rate of apoptosis were correlated with the humoral level of sFas, which increased significantly in late RA. On the contrary, in the synovial fluid, the sFas level decreased monotonically from early to late RA. CONCLUSION: In early RA, in the synovial membrane, the rate of apoptosis and p-53-immunostaining intensity were low, and Bcl-2-immunostaining intensity was high. The sFas level in synovial fluid was high. In late RA, the rate of apoptosis and p-53-immunostaining intensity increased, Bcl-2-immunostaining intensity decreased, as did the sFas level.
22778377 Nocardiosis in a patient with rheumatoid arthritis treated with rituximab and a summary of 2010 Sep 29 Rituximab is a B-cell-depleting monoclonal anti-CD20 antibody. It is widely used in haematology and rheumatology. However, usage of rituximab in immunosupressed patient has been associated with various opportunistic infections. The authors reported a case of refractory rheumatoid arthritis treated with rituximab, which later presented with non-resolving pneumonia with pulmonary nodule. Percutaneous computer tomogram guided lung biopsy was arranged to confirm the suspicion of tuberculosis, but did not yield conclusive results. Later, she presented left-chest abscess and underwent incision and drainage. The pus culture and sensitivity confirmed pulmonary nocardiosis with chest wall dissemination. She was treated with 2-week course of trimethoprim sulfamethoxazole and responded. The authors also reviewed published cases of nocardiosis post-rituximab.
20110520 Longterm safety of patients receiving rituximab in rheumatoid arthritis clinical trials. 2010 Mar OBJECTIVE: To evaluate the longterm safety of rituximab in clinical trials in patients with rheumatoid arthritis (RA). METHODS: Pooled analysis of safety data, including adverse events (AE) and infections, from patients treated with rituximab in combination with methotrexate in a global clinical trial program. RESULTS: A total of 2578 patients with RA received at least 1 course of rituximab. Safety analyses were based on 5013 patient-years of rituximab exposure. The most frequent AE was infusion-related reactions (25% of patients during the first infusion of Course 1). Less than 1% of infusion-related reactions were considered serious. Rates of AE and serious AE (SAE; 17.85 events/100 patient-yrs, 95% CI 16.72, 19.06) were stable following each course. The overall serious infection rate was 4.31/100 patient-years (95% CI 3.77, 4.92). Infections and serious infections over time remained stable across 5 courses at 4-6 events/100 patient-years. Compared with other patients with RA and with the general US population, there was no increased risk of malignancy. CONCLUSION: In this longterm safety update in RA clinical trial patients, rituximab remained well tolerated over multiple courses. SAE and infections remained stable over time and by treatment course.
20020135 Cementless total hip arthroplasty in patients with rheumatoid arthritis using a tapered de 2011 Mar The results of cementless tapered designed femoral stem were studied at a minimum 10-year follow-up in a non-selected, consecutive group of 27 patients (39 hips) with rheumatoid arthritis. Clinical and radiological analyses were performed in 27 hips, 17 patients (mean age at surgery 45 years) after a mean of 12 years. The postoperative Harris hip score was excellent for 14 hips, 9 hips were rated as good and 4 hips were fair or poor. No stem had to be revised for aseptic loosening. Proximal stress shielding was observed in 26 hips (96%); heterotopic ossification was present in 11 hips (41%). Six hips required revision of the acetabular component. With uncemented tapered femoral fixation excellent 12-year results are achieved in patients with rheumatoid arthritis.
19129980 Importance of full evaluation in patients who complain of neck pain. 2009 Jun INTRODUCTION: Although neck pain is common in patients with chronic rheumatic disorders, any change in the quality or severity of pain should be further investigated. MATERIALS AND METHODS: We report two patients who recently presented with increasing neck pain on a background of chronic inflammatory arthritis. RESULTS: Both patients were found to have suffered fractures of the cervical spine. In each case, the bones appeared osteopenic and reduced bone density is likely to have made the patients susceptible to fracture. CONCLUSION: This report highlights the need to comprehensively evaluate patients with chronic rheumatic disorders who note a significant change in their neck symptoms.
19401279 Susceptibility variants for rheumatoid arthritis in the TRAF1-C5 and 6q23 loci: a meta-ana 2010 Mar BACKGROUND: Genome-wide association studies have proposed susceptibility variants for rheumatoid arthritis in the TRAF1-C5 locus and 6q23 region. Furthermore, additional independent studies have investigated the same or highly linked polymorphisms in the same regions. OBJECTIVE: To carry out a meta-analysis of the available evidence for the association of polymorphisms in the TRAF1-C5 locus and 6q23 region with rheumatoid arthritis. METHODS: Data were synthesised for four polymorphisms: rs3761847 (n=13 datasets) and rs2900180 (n=9 datasets) in the TRAF1-C5 locus, and rs10499194 (n=5 datasets) and rs6920220 (n=7 datasets) in the 6q23 region. Meta-analyses for subgroups defined by anti-cyclic citrullinated peptide (anti-CCP) and rheumatoid factor (RF) status were also performed. RESULTS: The polymorphism rs6920220 reached genome-wide statistical significance with p=7.9 x 10(-17) and an allelic odds ratio of 1.24 (95% CI 1.18 to 1.30) and no between-study heterogeneity (I(2)=0%). The risk was significantly stronger in patients with anti-CCP antibodies and in patients with RF. The other three variants showed large between-study heterogeneity across datasets (I(2) range 74-82%); rs10499194 was nominally statistically significant after exclusion of the discovery data. Two variants had genome-wide statistical significance in subgroups defined by the presence of RF (rs3761847 and rs6920220) or anti-CCP (rs6920220). CONCLUSIONS: Genetic markers in the 6q23 region and TRAF1-C5 are associated with rheumatoid arthritis, in particular with positive anti-CCP and RF profile. With the exception of rs6920220, which shows highly consistent results, other proposed markers have high between-study heterogeneity that may reflect unrecognised phenotypic or genetic variability (eg, gene environment interactions) within rheumatoid arthritis. Furthermore, these markers may not be the true causative loci but rather be in linkage disequilibrium with the true ones.
21488354 [Economic assessment of the use of biological medications in military medicine]. 2010 Dec By the example of rheumatoid arthritis was considered the methods of economic assessment of advisability of modern biological medication usage in military medicine. The usage of these medications leads to quick clinical response, decrease of the additional medication intake, decrease of the average duration of treatment, "move aside" time of permanent disablement. Modern active therapy can increase the effectiveness of treatment; improve the quality of life, decrease the average duration of hospital stay, following treatment expense and welfare payment for this category of ill.
21138598 A novel preclinical model for rheumatoid arthritis research. 2010 Based on increasing knowledge on the pathogenesis of rheumatoid arthritis (RA), more and more potential therapeutics have been developed. To evaluate their therapeutic efficacy, safety and toxicity, appropriate animal models are required. Although rodent models of RA have been extensively used for preclinical evaluation, the differences between rodents and humans limit their usability for some species-specific therapeutics. Therefore, autoimmune arthritis developed in a non-human primate with essential hallmarks of RA will be an alternative model for preclinical studies.
21128048 [Viral arthritides]. 2010 Dec Viruses are common etiologic agents of acute polyarthritis worldwide. Rheumatic symptoms are often accompanied by other viral symptoms such as fever, rash, myalgia or nausea, but isolated arthritis may occur resembling or imitating early rheumatoid arthritis. In Europe and North America, the most common arthritogenic viruses include parvovirus B19, rubella, hepatitis B and C, whereas mosquito-borne alpha-viruses are endemic in Africa, Australia, the western Pacific and South America. The latter have attracted the interest of European rheumatologists due to the increasing number of tourists travelling to these regions. Viruses may cause arthritis via various mechanisms, including direct synovial infection leading to cell lysis, immune complex formation or pro-inflammatory cytokine induction. Indirect viral pathogenic effects may induce autoimmune reactions via bystander activation or epitope spreading.
20703487 [Selective co-stimulation blockade. CTLA4-Ig (Abatacept)]. 2010 Sep Abatacept is a soluble fusion protein comprising the extracellular domain of human CTLA4 linked to the modified Fc portion of human IgG(1). It is approved for the treatment of rheumatoid arthritis (RA) in combination with methotrexate and juvenile chronic arthritis by blocking the co-stimulatory signal required for full T-cell activation. Abatacept has added to the growing armamentarium of targeted therapies for RA, including the challenging group of RA patients who are refractory to TNF-alpha blockade. To date, abatacept has its main application in cases failing to respond to TNF-alpha blockade. In several studies, the efficacy and safety of abatacept was not only shown for TNF-IR patients, but also for DMARD-IR patients. Recently, the EU has approved abatacept in combination with methotrexate in DMARD-IR patients. The significant and similar response rates in TNF-alpha blockade failure to those observed in only DMARD failure implies that the pathways targeted with the two treatments remain distinct. In terms of safety profile, incidence rates of malignancy in the abatacept trials were consistent with those in a comparable RA population. The rate of opportunistic infections does not seem to be increased in patients treated with abatacept.
20858032 N-aryl pyrazoles, indazoles and azaindazoles as antagonists of CC chemokine receptor 1: pa 2010 Nov BACKGROUND: CC chemokine receptor 1 (CCR1) is a GPCR involved in the migration and activation of leukocytes. A number of studies have highlighted a role for CCR1 in preclinical animal models of inflammatory diseases, including MS and rheumatoid arthritis. OBJECTIVE: This review examines three reports on a new series of CCR1 antagonists. METHODS: The compounds of the title inventions are put in the context of earlier work in the area of CCR1 antagonism. The structure-activity relationships disclosed in the inventions are also discussed. CONCLUSIONS: Several of the compounds disclosed in patent cooperation treaty applications WO 2010/036632, WO 2009/134666 and WO 2009/137338 are sub-nanomolar antagonists of MIP-1α-induced calcium flux in CCR1-bearing cells. Further preclinical studies are required with these new CCR1 antagonists in order to understand their potential for ameliorating human inflammatory diseases.
19734175 Do specialized centers and specialists produce better outcomes for patients with chronic d 2009 Dec PURPOSE: Although specialized centers are generally accepted for treatment of relatively uncommon diseases, such as cystic fibrosis, statements regarding the amount of expertise or minimum number of patients treated are increasingly included in guidelines for the treatment of other chronic diseases such as rheumatoid arthritis and diabetes mellitus. DATA SOURCES: Medline and Embase from 1987 through March 2008 were searched. STUDY SELECTION: Studies reporting the effect of treatment in a specialized or high-volume center or by subspecialists on a clinically relevant outcome. Data extraction Two reviewers extracted the data independently and assessed the methodological quality. RESULTS OF DATA SYNTHESIS: We included 22 articles. Two randomized-controlled trials and a quasi-experimental study compared the effect of outpatient team care with traditional outpatient care for patients with rheumatoid arthritis. These studies showed no difference or were inconsistent. Studies on the outcomes of care for diabetic patients (5 prospective or historical cohort studies and 10 retrospective cohort studies) were generally of poor quality. Studies comparing the subspecialist care with the care provided by general internists or primary care providers produced inconsistent results. Similar inconsistency and poor quality were found for three observational studies on cystic fibrosis. CONCLUSION: The available literature suggests that among patients with rheumatoid arthritis, diabetes mellitus or cystic fibrosis, outcomes are not superior in specialized centers or with subspecialists compared with other forms of chronic illness care.
19773288 Tumour necrosis factor alpha blockade impairs dendritic cell survival and function in rheu 2010 Jun OBJECTIVES: Tumour necrosis factor alpha (TNFalpha) blockade is an effective therapy for rheumatoid arthritis (RA). The immunomodulatory effects of TNFalpha antagonists are thought to contribute to their therapeutic action. This study investigated whether anti-TNFalpha therapeutics exerted their immunoregulatory effects through modulation of dendritic cell (DC) function. METHODS: Two complementary approaches were taken: in the first 'in vitro' approach monocyte-derived DC from healthy donors were matured with lipopolysaccharide and treated with TNFalpha antagonists in vitro for 48 h. In the second 'ex vivo' approach monocyte-derived DC were generated from RA patients before and 8-12 weeks into anti-TNFalpha treatment. DC were analysed for survival, phenotype, cytokine production and T-cell stimulatory capacity. RESULTS: TNFalpha blockade during DC maturation in vitro induced approximately 40% of DC to undergo apoptosis. Importantly, the surviving DC displayed a semimature phenotype with reduced levels of HLA-DR, CD80, CD83, CD86 and CCR7, and their production of IL-10 was enhanced compared with DC matured without TNFalpha antagonists. Furthermore, anti-TNFalpha-treated DC were poor stimulators of T-cell proliferation and polarised T-cell development towards a higher IL-10/lower IFNgamma cytokine profile. Similarly, DC derived from RA patients after anti-TNFalpha treatment showed impaired upregulation of CD80 and CD86 upon lipopolysaccharide activation and displayed poor T-cell stimulatory activity. CONCLUSIONS: The data show that TNFalpha blockade has profound effects on DC function with downstream, potentially immunoregulatory, effects on T cells. These data provide an interesting new insight into the potential mechanism by which anti-TNFalpha drugs contribute to the restoration of immunoregulation in RA patients.
19627609 DAS-28-based EULAR response and HAQ improvement in rheumatoid arthritis patients switching 2009 Jul 23 INTRODUCTION: No definitive data are available regarding the value of switching to an alternative TNF antagonist in rheumatoid arthritis patients who fail to respond to the first one. The aim of this study was to evaluate treatment response in a clinical setting based on HAQ improvement and EULAR response criteria in RA patients who were switched to a second or a third TNF antagonist due to failure with the first one. METHODS: This was an observational, prospective study of a cohort of 417 RA patients treated with TNF antagonists in three university hospitals in Spain between January 1999 and December 2005. A database was created at the participating centres, with well-defined operational instructions. The main outcome variables were analyzed using parametric or non-parametric tests depending on the level of measurement and distribution of each variable. RESULTS: Mean (+/- SD) DAS-28 on starting the first, second and third TNF antagonist was 5.9 (+/- 2.0), 5.1 (+/- 1.5) and 6.1 (+/- 1.1). At the end of follow-up, it decreased to 3.3 (+/- 1.6; Delta = -2.6; p > 0.0001), 4.2 (+/- 1.5; Delta = -1.1; p = 0.0001) and 5.4 (+/- 1.7; Delta = -0.7; p = 0.06). For the first TNF antagonist, DAS-28-based EULAR response level was good in 42% and moderate in 33% of patients. The second TNF antagonist yielded a good response in 20% and no response in 53% of patients, while the third one yielded a good response in 28% and no response in 72%. Mean baseline HAQ on starting the first, second and third TNF antagonist was 1.61, 1.52 and 1.87, respectively. At the end of follow-up, it decreased to 1.12 (Delta = -0.49; p < 0.0001), 1.31 (Delta = -0.21, p = 0.004) and 1.75 (Delta = -0.12; p = 0.1), respectively. Sixty four percent of patients had a clinically important improvement in HAQ (defined as > or = -0.22) with the first TNF antagonist and 46% with the second. CONCLUSION: A clinically significant effect size was seen in less than half of RA patients cycling to a second TNF antagonist.
20097226 Targeting B cells in immune-mediated inflammatory disease: a comprehensive review of mecha 2010 Mar B cell-depletion therapy, particularly using anti-CD20 treatment, has provided proof of concept that targeting B cells and the humoral response may result in clinical improvements in immune-mediated inflammatory disease. In this review, the mechanisms of action of B cell-targeting drugs are investigated, and potential biomarkers associated with response to treatment in patients with autoimmune diseases are identified. Most available data relate to B cell depletion using anti-CD20 therapy (rituximab) in patients with rheumatoid arthritis (RA). Treatment leads to significant clinical benefit, but apparently fails to deplete long-lived plasma cells, and discontinuation is associated with relapse. Biomarkers commonly used in studies of B cell-targeted therapies include rheumatoid factor, anti-citrullinated peptide antibodies, and immunoglobulin (Ig) levels. More recently, there has been interest in markers such as B cell phenotype analysis, and B lymphocyte stimulator (BLyS)/a proliferation-inducing ligand (APRIL), the latter particularly in studies of the IgG Fc-transmembrane activator and CAML interactor (TACI) fusion protein (atacicept) and anti-BLyS therapy (belimumab). Data from clinical trials of B cell-depleting agents in RA suggest that specific autoantibodies, BLyS, APRIL, and circulating and synovial B lineage cell levels may have potential as biomarkers predictive of response to treatment. Further trials validating these markers against clinical outcomes in RA are required. In patients with systemic lupus erythematosus, Fc receptors and levels of circulating immune cells (including B cells and natural killer cells) may be relevant markers.
19956574 Immature blood vessels in rheumatoid synovium are selectively depleted in response to anti 2009 Dec 2 BACKGROUND: Angiogenesis is considered an important factor in the pathogenesis of Rheumatoid Arthritis (RA) where it has been proposed as a therapeutic target. In other settings, active angiogenesis is characterized by pathologic, immature vessels that lack periendothelial cells. We searched for the presence of immature vessels in RA synovium and analyzed the dynamics of synovial vasculature along the course of the disease, particularly after therapeutic response to TNF antagonists. METHODOLOGY/PRINCIPAL FINDINGS: Synovial arthroscopic biopsies from RA, osteoarthritis (OA) and normal controls were analyzed by double labeling of endothelium and pericytes/smooth muscle mural cells to identify and quantify mature/immature blood vessels. To analyze clinicopathological correlations, a cross-sectional study on 82 synovial biopsies from RA patients with variable disease duration and severity was performed. A longitudinal analysis was performed in 25 patients with active disease rebiopsied after anti-TNF-alpha therapy. We found that most RA synovial tissues contained a significant fraction of immature blood vessels lacking periendothelial coverage, whereas they were rare in OA, and inexistent in normal synovial tissues. Immature vessels were observed from the earliest phases of the disease but their presence or density was significantly increased in patients with longer disease duration, higher activity and severity, and stronger inflammatory cell infiltration. In patients that responded to anti-TNF-alpha therapy, immature vessels were selectively depleted. The mature vasculature was similarly expanded in early or late disease and unchanged by therapy. CONCLUSION/SIGNIFICANCE: RA synovium contains a significant fraction of neoangiogenic, immature blood vessels. Progression of the disease increases the presence and density of immature but not mature vessels and only immature vessels are depleted in response to anti-TNFalpha therapy. The different dynamics of the mature and immature vascular fractions has important implications for the development of anti-angiogenic interventions in RA.
20495390 Intracranial hemorrhage and spinal cord injury from a fractured C1-C2 sublaminar cable: ca 2010 Jun OBJECTIVE: This is a unique case report of a fractured atlantoaxial interspinous multistranded cable leading to intracranial hemorrhage and spinal cord injury. CLINICAL PRESENTATION: A 61-year-old woman, with a history of rheumatoid arthritis and C1-C2 interspinous wiring with allograft for atlantoaxial instability, presented with neck pain and progressive decline in mental status. Prior to transfer to our institution from a referral hospital, imaging studies revealed progressive hydrocephalus with interval development of subarachnoid and fourth ventricular hemorrhage. Initial and repeat angiographic work-up was negative for vascular lesions. Magnetic resonance imaging revealed a subdural hematoma and signal changes at the cervicomedullary junction. Computed tomography of the cervical spine revealed a fractured interspinous cable, intradural penetration, and atlantoaxial instability. INTERVENTION: After ventriculostomy, both the patient's mental status and quadriparesis improved to a C on the American Spinal Injury Association (ASIA) scale. During surgery, the fractured cable and subdural hematoma were removed revealing an area of spinal cord impalement. She underwent C1-C3 lateral mass fixation with iliac crest autograft for fusion and was discharged to rehabilitation after a ventriculoperitoneal shunt was placed. At her 6-month follow-up, she was independent and had improved to ASIA E. Computed tomography confirmed fusion. CONCLUSION: Spinal instrumentation eventually fails from pseudarthrosis and can cause neurological injury. In patients with atlantoaxial instability, direct C1-C2 screw fixation with posterior interspinous wiring using autograft offers the best chance for fusion. Cervical spine pathology can cause intracranial hemorrhage, and unconventional causes of injury must be considered when routine workup is negative.
19609487 Efficacy of tocilizumab and evaluation of clinical remission as determined by CDAI and MMP 2009 Tocilizumab, a biological agent developed in Japan, is a human anti-interleukin-6 (anti-IL-6) receptor antibody. Rheumatoid arthritis improves with its use. A remission rate of 59% is attainable, as measured by disease activity score 28 (DAS28) in the SAMURAI study. However, in tocilizumab treatment, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) levels drop to negative values; therefore we sought to utilize a different index for measuring its efficacy. In order to evaluate the effects of tocilizumab we carried out this study using clinical disease activity index (CDAI), as it is not reliant on blood data and would also allow us to determine which markers are present in remission. Twenty-two patients under treatment with tocilizumab participated in this study. Effects of treatment as well as the remission rate were measured by CDAI and DAS28 3 months after initiation of treatment. IL-6 and matrix metalloproteinase-3 (MMP-3) levels were measured at the same time. We studied the clinical efficacy of tocilizumab using DAS28 after treatment; remission as measured by DAS28 was 57.1% at 1 year. However, the remission rate as measured by CDAI was only 19.1% at 1 year. CDAI was not only correlated with DAS28, but also other clinical variables, MMP-3, and IL-6. We conclude that CDAI is effective in measuring clinical response to tocilizumab treatment, and that MMP-3 level is as useful as IL-6 level as an indicator.