Juan Salvatierra

Successful use of Tocilizumab in a patient with nephrotic syndrome due to a rapidly progressing AA amyloidosis secondary to latent tuberculosis

AA (secondary) amyloidosis is one of the most severe and uncommon complications of several rheumatic disorders and chronic infections such as tuberculosis (TB). Successful treatment depends on the control of the underlying inflammatory process, what can lead to an improvement or a regression in organ dysfunction. If the disorder persists, it has been reported in some cases of AA amyloidosis secondary to rheumatic diseases, that the use of biologic therapy is so far the only opportunity to reduce the development of AA amyloidosis and to reverse established deposits. We report herein a case of a latent TB infection complicated by a life-threatening AA amyloidosis presented as nephrotic syndrome. After an adequate antituberculostatic treatment, AA amyloidosis remained active and Tocilizumab (TCZ) was started with a dramatic resolution of the proteinuria, stabilization of the amyloid deposits and improvement in general condition.

Septic Arthritis Due to Cellulosimicrobium cellulans

ABSTRACT Cellulosimicrobium cellulans has been reported as a rare cause of human pathogenesis. Infections mainly occur in immunocompromised patients and very often are associated with a foreign body. We report the first case of septic arthritis caused by C. cellulans in an immunocompetent patient. Our patient suffered a penetrating palm tree thorn injury to his left knee 8 weeks before admission. Although no foreign objects were found, they were suspected because previous reports suggest a frequent association with this microorganism, and open debridament was performed. Removal of foreign bodies related to this organism must be considered a high-priority treatment in these patients to achieve a complete recovery.

An Examination of the Mechanisms Involved in Secondary Clinical Failure to Adalimumab or Etanercept in Inflammatory Arthropathies

BackgroundBiological therapies against tumor necrosis factor &agr; have revolutionized the treatment of several inflammatory rheumatic diseases. However, 30% of responders will present a clinical failure after having controlled the disease for at least 6 months (secondary clinical failure). Biological therapies may induce an unwanted immune response, which may alter the bioavailability of the drug causing a loss of clinical response. ObjectiveThe objective of this study was to assess the correlation between secondary clinical failure (based on Disease Activity Score in 28 Joints or Bath Ankylosing Spondylitis Disease Activity Index) and the type of mechanism involved in failure (based on drug levels) in patients with inflammatory arthropathies treated with anti–tumor necrosis factor &agr;. MethodsDrug and antidrug antibodies (ADAs) serum levels were determined by enzyme-linked immunosorbent assay immediately before drug administration in patients with rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis who presented secondary clinical failure after at least 6 months of treatment with adalimumab (ADL) or etanercept (ETN). ResultsThirty-six patients with secondary clinical failure were recruited: 63.88% had rheumatoid arthritis, 22.22% had psoriatic arthritis, and 13.88% had ankylosing spondylitis; 58.33% did not respond to ADL, whereas 41.66% did not to ETN. None of the patients treated with ETN showed either subtherapeutic drugs levels or ADAs (failure due to a primary mechanism) whereas it was found that 23.80% of the patients treated with ADL had subtherapeutic drug levels for reasons attributable to immunogenicity (failure due to a secondary mechanism; P = 0.000048). ConclusionsWe suggest the utility of measuring drug and ADA levels in patients with secondary clinical failure to ADL for a better optimization and rational use, but not in patients who fail to ETN.

Acute sarcoidosis as parotid fever in rheumatoid arthritis under anti-tumor necrosis factor-α therapy

Masashi Narazaki, Keisuke Hagihara, Yoshihito Shima, Atsushi Ogata, Tadamitsu Kishimoto and Toshio Tanaka Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, Osaka and Laboratory of Immune Regulation, Osaka University Graduate School of Frontier Biosciences, Osaka, Japan. Accepted 17 March 2011 Correspondence to: Toshio Tanaka, Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita City, Osaka 565-0871, Japan. E-mail: ttanak@imed3.med.osaka-u.ac.jp

SAT0279 Use of a Calibrated Score Chart for Cardiovascular Risk Assessment in Patients with Psoriatic Arthritis, Psoriasis Alone and Controls: Related Variables and Correlation with Carotid Ultrasound

Background A higher prevalence of cardiovascular (CV) risk factors has been described in patients (pts) with psoriatic arthritis (PsA) and with moderate to severe chronic plaque psoriasis (PS). Stratifying cardiovascular risk using calibrated risk charts is central to decision-making on treatment to prevent CV disease Objectives To assess and compare the CV risk in pts with PsA, pts with PS alone and controls without clinically evident CV disease using a calibrated SCORE. Compare these results with the presence of subclinical atherosclerosis assessed by carotid ultrasound (CCA US) Methods We included 80 consecutive PsA patients who fulfilled the CASPAR criteria, 80 patients with PS and 80 age and sex matched controls. Patients with a previous CV event and diabetics were excluded. CV risk was calculated using the cSCORE (high CV risk has been defined by a SCORE ≥ 5%), and the presence of plaques was evaluated by B-doppler US. A one-way ANOVA was performed to analyze the statistical difference between groups and the concordance (Kappa Index) was calculated. Furthermore, multivariate regression analysis was used to adjust for gender, age, body mass index, classic CV risk factors, clinical and laboratory patterns, treatment, activity of disease, and inflammatory markers (p<0,05 was considered significant) Results Based on the classic CV risk factors, the cSCORE in the PsA patients was 1,70 ± 3,22% (mean ± standard deviation) and 7 pts (8,75%) were above the threshold of high or very high CV risk (≥5%). In the groups of PS and controls after applying the cSCORE the values were 1,45 ± 2,41 and 1,17 ± 1,75. Therefore, 5 pts (6,25%) were classified above the threshold in both groups. The CCA US revealed the presence of atherosclerotic plaques in 8 pts (10%) with PsA, 9 pts (11,25%) with PS and 2 (2,5%) in the group of healthy controls. Statistical difference intergroups was not significant for the cSCORE or the presence of plaques. Furthermore the cSCORE showed a bad concordance (Kappa Index 0,51, 0,34 and 0,2, in the PsA, PS and controls group respectively) with the presence of plaques. Multivariate regression analysis showed that the only prognostic factors for predicting the cSCORE in the three groups was the age (p< 0,05) and the variables associated with subclinical atherosclerosis in the PsA pts were the age and the CRP (p< 0,05), in PS, the age, gender and total cholesterol level (< 0,05) and in the group of healthy controls the age. Clinical patterns of the PsA and PS, treatment and activity of the disease were not associated with cSCORE. Conclusions In our study most of the patients with PsA and PS have low and intermediate CV risk using the cSCORE. The correlation between cSCORE and CCA US was poor. cSCORE may understimate the CV risk assessment in patients with PsA and PS. Besides classic CV risk factors, some disease characteristics might contribute to the expression of higher global CV risk in these patients. References Gonzalez-Juanatey C et al. High prevalence of subclinical atherosclerosis in psoriatic arthritis patients without clinically evident cardiovascular disease or classic atherosclerosis risk factors. Arthritis Rheum. 2007;57:1074-80. Disclosure of Interest None Declared

Back pain and headaches in a patient with rheumatoid arthritis and Marfan’s syndrome

Joint Bone Spine - In Press.Proof corrected by the author Available online since samedi 30 juin 2012