A 15 year old girl who had pain, oedema of her left hand, and fever of four months' duration is described. Marked demineralisation of her hand was shown by radiography, and increased articular uptake by technetium-99m bone scan. All these changes were indistinguishable from reflex sympathetic dystrophy. After two admissions to hospital and multiple explorations we discovered that she had induced her symptoms herself and a diagnosis of Munchausen's syndrome was made. As far as we know this presentation has not been previously reported and might help to explain the physiopathology of some signs of reflex sympathetic dystrophy.It is unusual to find the term Munchausen's syndrome in rheumatological reports because it is essentially a psychiatric disorder, defined by the Diagnostic and Statistical Manual of Mental Disorders as the presentation of physical symptoms that are apparently under a patient's voluntary control.' This disorder must be distinguished from conversion disorders or malingering. Usually the patient requires multiple admissions to hospital and has the secondary effects of unnecessary explorations and treatments.We present the first case, to our knowledge, of Munchausen's syndrome presenting as reflex sympathetic dystrophy. We have not delved into the psychopathological aspects of the syndrome, more characteristic of psychiatric reports, but this case illustrates the poorly defined limits of the reflex sympathetic dystrophy syndrome and might explain the physiopathology of some of the manifestations ofthis disorder, such as the regional osteoporosis or the bone scan uptake. (fig 1), tenderness, and impaired motion of the left hand and wrist. Elbow, shoulder, and the other articular regions were normal.Laboratory studies showed the following values: erythrocyte sedimentation rate (Westergren) 3 mm/h; packed cell volume 39 5; haemoglobin 127 g/l; platelet count 213x 109/1; white blood cell count 5-01 x 109/1 with a normal differential count. Normal results were obtained for glucose, serum electrolytes, creatinine, calcium, phosphorus, bilirubin, serum glutamic oxaloacetic transaminase, serum glutamic oxalopyruvic transaminase, alkaline phosphatase, creatine kinase, prothrombin time, activated partial thromboplastin time, and urine analysis. Serological tests for hepatitis B antigen and antibody, antinuclear antibodies, rheumatoid factor, brucella, and lues were negative. Purified protein derivative skin test and cultures of blood and urine were also negative. Radiology of the hands showed increased juxtaarticular osteoporosis (fig 2), and a technetium99m (99'Tc) bone scan showed marked uptake of 9'Tc in all joints of the left hand (fig 3).Despite the normality of the laboratory tests and because of the fever, radiological and bone scan changes we performed a synovial biopsy of the wrist suspecting an infection. Examination showed only interstitial oedema without cellular infiltrates. Bacterial, mycobacterial, and fungal cultures were negative. Because of the absence of infection we started tr...

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Background Tocilizumab is a humanized monoclonal antibody that blocks IL-6 mediated pro-inflammatory signalling in rheumatoid arthritis patients. The safety profile of tocilizumab has been extensively evaluated in clinical trials. However, there is little data on markers at the initiation of tocilizumab therapy that may predict the development of adverse effects requiring drug withdrawal. Objectives To identify markers that predict the development of secondary effects that required drug withdrawal the 6 first months after initiating tocilizumab therapy. Methods Forty-six rheumatoid arthritis patients treated with tocilizumab in routine clinical practice were retrospectively evaluated 24 weeks after initiating therapy. Demographic and clinical data, complete blood cell counts, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), titers of rheumatoid factor (RF) and anti-cyclic citrullinated peptide (CCP) antibodies, serum cytokines (IL-6, IL-15 and IL-17) and the frequency of activated CD4+, CD8+ and Treg cells were collected before tocilizumab administration (baseline). Characteristics of patients with and without adverse effects were compared. Results Twelve (26.1%) patients developed adverse effects that required drug withdrawal during the first six months of tocilizumab therapy. Seven patients suffered an allergic or infusional reaction and two patients had neutropenia. All recovered after drug withdrawal. Two further patients suffered an infection requiring hospitalization (salpingitis and periappendiceal abscess) and one patient had a myocardial infarction. Patients with and without adverse effects had comparable ages and disease evolution. Patients with adverse effects had lower neutrophil counts (4.1±2.6 vs 5.6±1.8, p<0.05) and lower DAS28-CRP (5.1±1.2 vs 4.3±1.2, p<0.05) at baseline than those without. No significant differences in IgG, IgM and IgA were observed between the two groups. However, fewer patients with higher CRP, titers of anti-CCP antibodies, or serum concentrations of IL-6 and IL-15 were observed in the group with adverse effects (Table 1). There were no differences in the frequency of T cell subsets and Tregs between patients with and without adverse effects before the treatment. Conclusions Patients with adverse effects presented fewer prognostic markers of severe disease. Higher levels of some markers (CRP, anti-CCP antibodies, IL-6, IL-15 and neutrophil counts) may identify patients less likely to suffer adverse effects due to tocilizumab therapy. Disclosure of Interest None Declared