Rheumatoid Arthritis: Rozenbaum M

Slobodin G, Rozenbaum M, Boulman N, Rosner I. · Department of Internal Medicine A, Bnai Zion Medical Center and Ruth and Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel. · Semin Arthritis Rheum. · Pubmed #17350676 No free full text.

Abstract: BACKGROUND: The concept of "enthesis organ" allows a new look at the nature of enthesis involvement in some rheumatic and nonrheumatic systemic disorders. OBJECTIVES: To describe the various presentations of enthesopathy in the course of systemic medical disorders using the available literature data. METHODS: Review of relevant articles from 1996 to 2006 retrieved by a Medline search utilizing the index terms "enthesis," "enthesitis," and "tendonitis." The list of articles reviewed herein is not exhaustive, with preference given, where possible, to studies and surveys over case reports as well as the most recent literature reflecting new developments on the subject. RESULTS: Enthesis is defined as the site of insertion of a tendon, ligament, fascia, or articular capsule into bone. Pain originating in the free nerve endings enriched entheses (enthesalgia) may represent a potential cause of chronic musculoskeletal pain in some individuals. Enthesis involvement in the disease process is well appreciated in spondyloarthropathies and in rheumatoid arthritis, though overshadowed by synovitis in the latter. Calcium deposition diseases may constitute the most significant articular cause of enthesopathies in the general population. New data may shed light on the possible pathophysiologic role of enthesopathy in the development of osteoarthritis. Various metabolic and endocrine conditions may manifest with enthesopathy features. The pathogenic mechanisms of enthesis involvement are not uniform and differ in the diverse disorders. CONCLUSIONS: The concept of enthesopathy as a variety of syndromes in the course of many rheumatic, metabolic, and endocrine disorders should be appreciated. Exercise of a high level of suspicion toward enthesopathic involvement, and greater knowledge of enthesopathy's characteristic patterns and diagnostic possibilities, may allow better management of many patients in rheumatology practice.

Rosner I, Rozenbaum M, Toubi E, Kessel A, Naschitz JE, Zuckerman E. · Department of Rheumatology, Bnai Zion Medical Center, Faculty of Medicine, Technion, Haifa, Israel. · Semin Arthritis Rheum. · Pubmed #15190523 No free full text.

Abstract: OBJECTIVE: To present the data available supporting the existence of an arthropathy associated with hepatitis C infection. METHODS: The MEDLINE database was searched for "arthritis" intersecting with "hepatitis C" in addition to the authors' investigations and experience on this subject. RESULTS: Arthritis, not otherwise explained, has been noted in 2% to 20% of hepatitis C virus (HCV) patients. This arthritis is rheumatoid-like in two thirds of the cases and a waxing/waning oligoarthritis in the rest. Cryoglobulinemia alone does not explain the arthritis, and there is difficulty in differentiating it from rheumatoid arthritis. The arthropathy is nonerosive/nondeforming. Whereas nonsteroidal anti-inflammatory drugs, low-dose corticosteroids, and hydroxychloroquine may be helpful, conventional treatment of arthritis may be problematic in the context of viral hepatitic arthropathy. Antiviral therapy is most effective, even without viral clearance, but rheumatic complications may ensue. CONCLUSIONS: HCV arthropathy should be considered in the differential diagnosis of new-onset arthritis.

Rozenbaum M, Rosner I, Portnoy E. · No affiliation provided · Ann Rheum Dis. · Pubmed #11830448 links to  free full text

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Naschitz JE, Rosner I, Rozenbaum M, Zuckerman E, Yeshurun D. · Department of Internal Medicine A, Bnai Zion Medical Center and Bruce Rappaport, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa. · Semin Arthritis Rheum. · Pubmed #10468414 No free full text.

Abstract: OBJECTIVES: Rheumatic disorders associated with cancer include a variety of conditions, most of which have no features distinguishing them from idiopathic rheumatic disorders. It is generally held that an extensive search for occult malignancy in most rheumatic syndromes is not recommended unless accompanied by specific findings suggestive of malignancy. The objective of this review are to identify rheumatic syndromes associated with cancer, to call attention to features that may suggest the presence of a hidden cancer, and to examine the role to additional clinical and laboratory data as clues to the possible neoplastic cause of those syndromes. METHODS: A MEDLINE search of the literature dealing with cancer-associated rheumatic syndromes was conducted. RESULTS: Review of the literature identified significant progress in this area. First, the association of malignancy with certain rheumatic syndromes was convincingly established, such as asymmetric polyarthritis presenting in the elderly with an explosive onset, rheumatoid arthritis with monoclonal gammopathy, Sjögren's syndrome with monoclonality, hypertrophic osteoarthropathy, dermatomyositis, polymyalgia rheumatica with atypical features, Lambert-Eaton myasthenic syndrome, palmar fasciitis and arthritis, eosinophilic fasciitis poorly responsive to corticosteroid therapy, erythema nodosum lasting more than 6 months, and onset of Raynaud's phenomenon or cutaneous leukocytoclastic vasculitis after age 50 years. Second, the list of cancer-associated rheumatic syndromes was extended by including additional entities such as benign edematous polysynovitis, sacroiliitis, adult-onset Still's disease, dermatomyositis sine myositis, systemic sclerosis, Sweet's syndrome, osteomalacia, skeletal hyperostosis, antiphospholipid syndrome, and essential mixed cryoglobulinemia. Third, evidence was provided substantiating that certain long-standing rheumatic syndromes, in particular rheumatoid arthritis, Felty's syndrome, Sjögren's syndrome, dermatomyositis, systemic sclerosis, systemic lupus erythematosus, and temporal arteritis behave like "premalignant conditions." Fourth, it was shown that the recognized tumor markers alpha-fetoprotein, prostate-specific antigen, CA-125, CA 19-9, and CA-3 have low sensitivity and specificity in screening for occult cancer in a population of rheumatic patients, whereas the presence of a monoclonal gammopathy in rheumatoid arthritis and the monoclonal antibody 17-109 in Sjögren's syndrome are reliable signs of malignant transformation. CONCLUSIONS: The presence of specific rheumatic syndromes and certain clinical and laboratory findings may justify a workup for hidden cancer. Studies of the epidemiology of the cancer-associated rheumatic syndromes and evaluation of the validity of aforementioned clues in prospective studies are goals for future investigations.

Silverman MH, Strand V, Markovits D, Nahir M, Reitblat T, Molad Y, Rosner I, Rozenbaum M, Mader R, Adawi M, Caspi D, Tishler M, Langevitz P, Rubinow A, Friedman J, Green L, Tanay A, Ochaion A, Cohen S, Kerns WD, Cohn I, Fishman-Furman S, Farbstein M, Yehuda SB, Fishman P. · Can-Fite BioPharma Ltd, Petach Tikva, Israel. · J Rheumatol. · Pubmed #18050382 No free full text.

Abstract: OBJECTIVE: Adenosine exerts antiinflammatory effects via activation of the A3 adenosine receptor (A3AR), a Gi protein-associated cell-surface receptor, overexpressed in synovial tissue and peripheral blood mononuclear cells (PBMC) in patients with active rheumatoid arthritis (RA). CF101 is a highly specific orally bioavailable A3AR agonist. METHODS: This was a multicenter study, blinded to dose, designed to assess the clinical activity and safety of CF101 in active RA. Seventy-four patients were randomized to receive 0.1, 1.0, or 4.0 mg CF101 bid for 12 weeks. The primary efficacy endpoint was American College of Rheumatology 20% response (ACR20) at Week 12. A3AR expression levels were analyzed in PBMC from 18 patients. RESULTS:. Maximal responses were observed with 1.0 mg bid, lower at 0.1 and 4.0 mg bid. At 12 weeks, 55.6%, 33.3%, and 11.5% of the patients receiving 1.0 mg CF101 achieved ACR20%, 50%, and 70% responses, respectively. CF101 was generally well tolerated, with mild headache (4.1%), nausea (2.7%), and rash (2.7%) being the most common treatment-related adverse events. Statistically significant correlations between A3AR overexpression at baseline and ACR50 and ACR70 responses were observed. CONCLUSION: CF101 administered bid for 12 weeks resulted in improvement in signs and symptoms of RA that did not achieve statistical significance, and was safe and well tolerated. The expression level of A3AR was directly correlated with patient responses to CF101, suggesting its utilization as a biomarker for the pharmacodynamic and therapeutic effects of this novel agent. These findings require confirmation in a double-blind randomized placebo-controlled trial, currently under way.

Rozenbaum M, Boulman N, Slobodin G, Ayubkhanov E, Rosner I. · Department of Rheumatology, Bnai Zion Medical Center, Haifa, Israel. · J Clin Rheumatol. · Pubmed #17149054 No free full text.

Abstract: BACKGROUND: The treatment of rheumatoid arthritis (RA) has changed dramatically over the past decade with the introduction of antitumor necrosis factor (anti-TNF) agents. Although subsets of patients may have only partial or no response, there is no report yet on possible worsening of RA with this therapy. OBJECTIVE: The objective of this study was to determine whether infliximab may paradoxically exacerbate RA. METHODS: One hundred seven patients with RA refractory to 3 disease-modifying antirheumatic drugs were treated with 3 mg/kg infliximab and methotrexate for at least 6 months. RESULTS: In 3 patients, there was an exacerbation of RA associated with the use of infliximab. The flare occurred during the first 6 to 12 months of treatment with polyarthritis, fever, and elevated acute phase reactants. Increase of infliximab dose resulted in further deterioration. CONCLUSION: We describe a paradoxic reaction, an exacerbation of RA, with infliximab. The mechanism of this side effect is unclear but may be related to altered immunity induced by the inhibition of TNF activity in predisposed patients.

Toubi E, Kessel A, Slobodin G, Boulman N, Pavlotzky E, Zisman D, Rozenbaum M, Rosner I. · Division of Clinical Immunology and Allergy, Bnai Zion Medical Center, P O Box 4940, Haifa 31048, Israel. · Ann Rheum Dis. · Pubmed #17148544 No free full text.

Abstract: OBJECTIVE: To assess changes in macrophage phenotype and function after rituximab-induced B cell depletion in patients with rheumatoid arthritis (RA). METHODS: 10 patients with RA were treated with rituximab, achieving significant B cell depletion 4 months later. Clinical improvement, rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP) antibodies, mRNA of B cell activating factor (BAFF), interleukin (IL) 10 and CD86 in human monocyte-derived macrophages (HMDMs) and tumour necrosis factor alpha (TNFalpha) secretion from cultured HMDMs were assessed at baseline and after the depletion. RESULTS: A clinical response of American College of Rheumatology (ACR) 50% improvement was noted in six patients, and another two patients responded with moderate improvement, equivalent to ACR 20-50% improvements. RF and anti-CCP antibodies were positive at baseline in seven of ten patients. RF disappeared or declined in six patients 4 months after treatment, correlating with clinical improvement. By contrast, anti-CCP remained unchanged in six patients. After rituximab treatment, and in association with clinical improvement, BAFF, IL10 and CD86 mRNA expression in HMDM were significantly upregulated compared with values at baseline. A significant decrease in TNFalpha in the supernatant of cultured HMDM was also noted. CONCLUSIONS: In addition to B cell depletion and attenuation in some of the specific autoantibodies, clinical improvement in rituximab-treated patients with RA occurred in association with changes in macrophage function.

Rozin A, Yigla M, Guralnik L, Keidar Z, Vlodavsky E, Rozenbaum M, Nahir AM, Balbir-Gurman A. · The B. Shine Department of Rheumatology, Rambam Medical Center, P.O. Box 9602, Haifa 31096, Israel. · Clin Rheumatol. · Pubmed #16211338 No free full text.

Abstract: BACKGROUND: Leflunomide (LEF) is indicated in adults for the treatment of active rheumatoid arthritis (RA). LEF inhibits dehydroorotate dehydrogenase, a key enzyme of the pyrimidine synthesis in activated lymphocytes. Among rare adverse effects, fatal interstitial lung disease has been recently reported during treatment of RA with LEF in Japan. Clinical trials outside Japan do not suggest that LEF causes an excess of pulmonary adverse effects. Development and increase of peripheral rheumatoid nodules in typical sites of RA patients following LEF therapy has been recently reported. OBJECTIVES: Two cases with new and accelerated development of rheumatoid lung nodulosis during LEF therapy were described in this study. METHODS: LEF treatment was administered to two male patients (77 and 66 years old) with long-standing active seropositive nodular RA with failure of multiple second line drugs and without lung involvement. Clinical and laboratory assessment using the American College of Rheumatology response criteria, chest computed tomography (CT), quantification of serum rheumatoid factor (RF), and monocyte count of peripheral blood along with routine laboratory follow up were performed on both patients before and during therapy. In case 1, a bone scan was performed due to sustained limbs pain. Open lung biopsy was performed in case 1 and core lung biopsy in case 2. RESULTS: Both patients achieved full clinical remission during 2 months of LEF therapy. In case 1, the first complaints were limbs pain after 10 months of treatment associated with intensive bone uptake on a bone scan consistent with hypertrophic pulmonary osteopathy. Productive cough developed after 3 months of the therapy in case 2. Initially, these complaints were not attributed to therapy. New lung disease was present on CT with cherry-like progressive cavitary nodules, predominantly involving the basal segments of the right lung. The first lung lesions were found by CT 13 months (case 1) and 7 months (case 2) after the beginning of therapy and were erroneously related to bronchiectasia in case 2. In both cases, the lung biopsy showed necrosis surrounded by epithelioid mononuclear inflammation with giant cells, consistent with rheumatoid lung node. The time that elapsed between the beginning of the first symptoms to LEF discontinuation was very long: 13 months in case 1 and 24 months in case 2. Discontinuation of LEF therapy was followed by an arrest in growth of lung nodules, resolution of limb pain, and gradual improvement of bone scan. A significant decrease of monocyte count and RF level in peripheral blood was observed during LEF therapy in both cases. CONCLUSION: For the first time, we described rheumatoid lung nodulosis as complication of successful LEF therapy for RA. Hypertrophic pulmonary osteopathy with severe limbs pain and dry cough were the first manifestations of the lung nodulosis. Monocytopenia during LEF therapy is proposed to be involved in pathogenesis of this rare complication of LEF therapy.

Toubi E, Kessel A, Mahmudov Z, Hallas K, Rozenbaum M, Rosner I. · Division of Allergy and Clinical Immunology, Bnai-Zion Medical Center, Golomb Str. 47, P. O. Box 4, Haifa, Israel. · Ann N Y Acad Sci. · Pubmed #16126991 No free full text.

Abstract: Increased secretion of tumor necrosis factor-alpha (TNF-alpha), along with interleukin-1 (IL-1) and interleukin-6 (IL-6), is important in the pathogenesis of rheumatoid arthritis (RA). T regulatory CD4(+)CD25(+) cells play a role in maintaining self-tolerance by downregulating Th1-induced proinflammation. This function has been found to be altered in active RA, whereas anti-TNF-alpha therapy has been found to improve the suppressive abilities of these cells. Our objectives were to investigate whether T regulatory cells in patients with active RA display a higher sensitivity to spontaneous apoptosis than in normals, and to look into the potential of infliximab (anti-TNF-alpha therapy) to reduce the sensitivity of these cells to spontaneous apoptosis. Seventeen patients suffering from active RA, having failed multiple disease-modifying antirheumatic drug (DMARD) therapies, were treated with infliximab. Spontaneous apoptosis (as detected by annexin V binding) was determined in all patients and compared with a group of normal individuals at baseline and after three months on infliximab treatment. Peripheral blood mononuclear cells were incubated in 24-well plates at 1 x 10(6) cells/mL for 48 hours. Annexin V binding on CD4(+)CD25(+) was assessed using three-color assay by flow cytometry. Prior to infliximab initiation, spontaneous apoptosis of T regulatory cells from active RA patients was found to be increased in comparison with controls (26 +/- 4.2% vs. 19.8 +/- 4.8%, respectively; P = 0.01). Three months later (while still on infliximab) spontaneous apoptosis was comparable in the two groups (20.7 +/- 5.2% vs. 20.9 +/- 3.4%; P 5 0.8). The absolute number of CD4(+)CD25(+) cells/mL in the peripheral blood at baseline was reduced in 11 out of 17 active RA patients when compared with that of the control group (24 +/- 7 vs. 32 +/- 11, respectively; P = 0.02). Following anti-TNF-alpha therapy, CD4(+)CD25(+) cell counts of patients were equivalent to those of normals. The alteration and reversal in both spontaneous apoptosis and cell count of T regulatory cells was found to correlate with RA disease activity. CD4(+)CD25(+) T regulatory cells display increased proclivity to undergo spontaneous apoptosis in active RA. Alterations in CD4(+)CD25(+) cell apoptosis and cell count were found to correlate with RA disease activity. Reversal of these deviations from normal was documented in association with the beneficial outcome of infliximab therapy.

Kessel A, Toubi E, Rozenbaum M, Zisman D, Sabo E, Rosner I. · Division of Allergy and Clinical Immunology, Bnai Zion Medical Center, 47 Golomb Street, P.O. Box 4940, Haifa, 31048, Israel. · Rheumatol Int. · Pubmed #15703951 No free full text.

Abstract: BACKGROUND: It is relatively difficult in a community setting to perform salivary gland biopsy or reliable diagnostic tests for salivary gland involvement in a patient suspected to suffer from Sjögren's syndrome (SS). OBJECTIVE: To investigate whether anti-Ro/La antibodies are a good substitute for salivary gland biopsy in community patients suspected to suffer from SS. METHODS: Forty-one patients suspected as having SS due to dry eyes and mouth, articular complaints, and/or serological findings were examined for the presence of anti-Ro/La, and underwent minor salivary gland biopsy. RESULTS: Sixteen patients (39%) were classified as primary SS by the American-European Consensus Group criteria. Twelve subjects had anti-Ro/La antibodies and 11 subjects in this group had positive biopsy findings. Of 29 patients without anti-Ro/La antibodies, only four manifested positive biopsy findings. A significant association was found between the presence of anti-Ro/La antibodies and positive salivary gland findings characteristic for SS (p<0.0001, Fisher's exact test). CONCLUSION: These findings tend to support the suggestion that a patient suspected to suffer from SS in a community setting may be first tested for the presence of anti-Ro/La antibodies to confirm the diagnosis. Only those with a negative result for the presence of anti-Ro/La antibodies need to be referred for salivary gland biopsy.

Rozenbaum M, Rosner I. · Department of Rheumatology, Bnai Zion Medical Center, Haifa, Israel. · Clin Exp Rheumatol. · Pubmed #15515792 No free full text.

Abstract: Juvenile Idiopathic Arthritis (JIA) and Familial Mediterranean Fever (FMF) may involve the same population of children and be confused at times. In a cohort of 350 consecutive FMF patients followed by us, 98 had onset before 10 years of age and, of those, JIA was present in 3. All three had the M694 V mutation of the MEFV gene and were of North African ancestry. The prognosis of these 3 was extremely poor: one developed bilateral knee osteonecrosis with total joint replacement, repeated ileal obstruction with small bowel resection, renal failure and sterility due to amyloidosis and osteoporotic fractures and died at 42 years of age; a second developed deforming erosive arthropathy and underwent bilateral total hip replacement; the third developed severe erosive polyarthritis and also underwent bilateral hip replacements. Aggressive treatment is indicated when JIA and FMF coexist.

Toubi E, Zuckerman E, Kessel A, Rozenbaum M, Rosner I. · No affiliation provided · Clin Exp Rheumatol. · Pubmed #12942711 No free full text.

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Toubi E, Kessel A, Grushko G, Sabo E, Rozenbaum M, Rosner I. · Division of Clinical Immunology, Bnai Zion Medical Center, Faculty of Medicine, Technion-Haifa, Israel. · Clin Exp Rheumatol. · Pubmed #12051403 No free full text.

Abstract: OBJECTIVE: Matrix metalloproteinase 3 (MMP-3) is reported to play an important role in the pathogenesis of systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Studies have also investigated the association of different tissue inhibitors of MMPs (TIMPs) with fibrosis in scleroderma (SSc). The aim of this study was to evaluate the correlation of serum MMP-1, 3 and TIMP-1 with severity and disease specific markers of SSc and RA. METHODS: Serum MMP-1,3 and TIMP-1 were measured in 42 SSc patients (age range 28-68 yr mean 47 yr) and compared to 29 RA and 30 healthy age- and sex-matched individuals. Elevated values of MMPs and TIMP-1 were defined as those greater than 2 SD above the normal mean. All SSc and RA patients were scored for disease severity. RESULTS: Serum MMP-1 was significantly elevated in 8/42 (19%) SSc patients (p = 0.01) but only in 2/29 (7%) RA patients (p = 0.2). Whereas MMP-3 levels were elevated in 10/29 (34%) RA patients (p = 0.002), it was elevated in only 5/42 (12%) SSc patients (p = 0.03). TIMP-1 was found elevated in 17/42 (40%) SSc patients (p = 0.001) and in only 4/29 RA patients (with a strong trend towards significance, p = 0.052). We found a significant association between the elevation of both MMPs and TIMP-1 levels, with the severity of SSc. Those who had an increase of more than one MMP and/or TIMP, demonstrated life-threatening major organ involvement such as end stage lung fibrosis, GI aperislasis, and severe cardiacfailure. Contrary to that in SSc, the severity of RA showed some trend of association with MMP-3 only. CONCLUSION: We confirm previous observations that MMPs and TIMPs may play an important role in various rheumatic diseases. Whereas serum increase of MMP-3 correlated with RA severity, SSc severity was more characterized by the increase of both MMP-1 and TIMP-1. This suggests that the MMPs and TIMPs involved in SSc are different than those playing a role in RA, which may indicate that in SSc they are produced in different locations than in RA.

Zuckerman E, Keren D, Rozenbaum M, Toubi E, Slobodin G, Tamir A, Naschitz JE, Yeshurun D, Rosner I. · Department of Internal Medicine A, B'nai Zion Medical Center, Bruce Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel. · Clin Exp Rheumatol. · Pubmed #11072597 No free full text.

Abstract: OBJECTIVE: To characterize hepatitis C virus (HCV)-related arthropathy and to evaluate the response to treatment with interferon-alpha (INF-alpha). METHODS: We studied 28 HCV-infected patients with arthritis. All patients underwent complete clinical, laboratory and radiological evaluation, including assessment and follow-up by a rheumatologist. Twenty-five patients were treated with INF-alpha for a median period of 12 months. RESULTS: All patients were HCV-RNA positive (genotype 1b in 65%). The mean duration of arthropathy-related symptoms prior to the diagnosis of HCV infection was 12 months. 19 patients (68%) had symmetric polyarthritis and 19 (68%) had morning stiffness > or = 60 min. None of the patients had erosive disease or subcutaneous nodules. 12 (43%) had detectable cryoglobulin (mean cryocrit: 3.6 +/- 3.5%), 17 (61%) had rheumatoid factor (RF) (median titer: 1:80), and only 15 (54%) had elevated ESR. 14 patients (50%) had > or = 4 ACR (American College of Rheumatology) criteria for the diagnosis of rheumatoid arthritis (RA), 9 of whom were mistakenly diagnosed and previously treated as RA patients. Only 3 patients had a satisfactory response to previous treatment with anti-inflammatory or disease modifying drugs. Complete or partial response of arthritis-related symptoms in INF-alpha treated patients was observed in 44% and 32%, respectively. Cryoglobulin became undetectable in 9 of 12 patients. However, a complete biochemical and virological end-of-treatment response was achieved in only 8 (36%) and 5 patients (20%), respectively. CONCLUSION: HCV arthropathy should be considered in the differential diagnosis of any patient with arthritis, even in the absence of liver disease. Treatment with interferon-alpha may lead to substantial clinical improvement of HCV-related arthritis even without a complete biochemical or virological response.

Abraham Z, Rozenbaum M, Rosner I. · Department of Dermatology, Reish Policlinic, Haifa, Israel. · J Dermatol. · Pubmed #10554438 No free full text.

Abstract: Accelerated nodulosis developed on the fingers of a woman successfully treated with low dose methotrexate for rheumatoid arthritis. Colchicine therapy resulted in regression of these nodules for twelve months. To our knowledge, this is the first report in the dermatological literature on this relatively new entity in which the skin is also involved.

Rosner I, Haddad A, Boulman N, Feld J, Avshovich N, Slobodin G, Rozenbaum M. · No affiliation provided · Rheumatology (Oxford). · Pubmed #17684027 No free full text.

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Boulman N, Rozenbaum M, Slobodin G, Rosner I. · No affiliation provided · Clin Exp Rheumatol. · Pubmed #17207395 No free full text.

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Rimar D, Rozenbaum M, Zisman D, Boulman N, Slobodin G, Eder L, Feld J, Rosner I. · No affiliation provided · J Rheumatol. · Pubmed #16862661 No free full text.

This publication has no abstract.