INTRODUCTION Anaemia is common in rheumatoid arthritis (RA). Clinicians may focus on rheumatological issues and assume anaemia of chronic disease (ACD). This study challenged this assumption and investigated the causes of anaemia in a large cohort of RA patients to assess its implications. METHODS The hospital where the study was conducted monitors regular full blood count and erythrocyte sedimentation rate (ESR) monthly in all RA patients on disease modifying drugs to assess efficacy and safety. A computerised system identifies and records abnormal results. The database for 2009 was interrogated to find all patients with two consecutive haemoglobin values <11 g/dl. Using a proforma, patients were defined as having iron deficiency anaemia (IDA), ACD, macrocytic anaemia (MCA) or another cause. All results of further tests investigating the anaemia were recorded. RESULTS Among 2000 RA patients on the system, 199 (10%) were identified as having anaemia over a year. Of these, 90 had IDA, 78 had ACD, 25 had MCA, and 6 had postoperative anaemia. Among 90 patients with IDA, investigations were performed in 53, with 23 normal. An explanation for IDA was found in 30: gastrointestinal bleeding in 25, gynaecological blood loss in 3, and urinary bleeding in 2. Among 78 patients with ACD, response to intensification of RA treatment occurred in 45, but erythropoietin therapy was required in 9. Within the 25 patients with MCA, 12 had unrecognised vitamin B(12) deficiency, 4 drug induced changes, 3 myeloid malignancy, 2 hypothyroidism, and 2 alcoholism. CONCLUSIONS Anaemia in RA is common, multifactorial, and potentially both serious and correctable. Established malignancy was present in 10 patients and premalignancy in a further 10 (10% of total). Treatable causes were commonly identified. Clinicians need to investigate the nature and cause of persistent anaemia, and must not assume it to be simply ACD without evidence.

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High levels of interleukin 1 and tumor necrosis factor are found in both cases of malaria and cases of septic shock. Since both interleukin 1 and tumor necrosis factor induce expression of the proinflammatory enzyme phospholipase A2 (PLA2), we examined serum PLA2 levels in 14 adults with malaria. Mean serum PLA2 activity was elevated 40-fold above normal (P less than 0.001). Serum PLA2 activity correlated with PLA2 immunoreactivity (r = 0.987; P less than 0.001) by an enzyme-linked immunosorbent assay specific for human group II PLA2, showing that serum PLA2 in cases of malaria is host derived. This article describes the novel finding of elevated PLA2 levels in cases of malaria, further strengthening the notion that mediators of the host response in cases of malaria are similar to those in cases of septic shock.

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Background Clinically relevant interstitial lung disease (ILD) is present in approximately 5% of patients with rheumatoid arthritis (RA). Traditionally, oral steroids have been used to treat this manifestation of RA, but no evidence base exists to support this. Indeed, concern has been raised that such an approach might be associated with increased mortality in ILD [1]. Objectives We have examined the effect of oral steroid therapy on mortality in a large multi centre group of patients retrospectively to assess the effect of these agents on survival. Methods For the purposes of this study, we collected data from multiple centres across the UK on patients with both RA and ILD (proven on HRCT) identified over a 25 year period from 1987 to 2012 using a standard proforma. We analysed the age, duration of both RA and ILD, outcome and, where appropriate, cause of death. Equivalent data were obtained from a control group of RA patients from one centre without lung disease, matched for age, sex and disease duration. We recorded the number of patients with RA-ILD who had received oral prednisone therapy for 3 months or more. We used Chi squared tests to assess the significance of any differences in disease characteristics between those who had steroids and those who had not. We calculated relative risk (RR) of all cause and respiratory mortality in all patients with RA-ILD, and in those treated with steroids. Results A total of 260 patients were identified from across the UK with proven RA-ILD. Steroids had been used in 154 (59%) RA-ILD patients, but only 36 (14%) controls, p=0.01. There were no differences between RA-ILD patients on steroids and those not on steroids with regard to age, gender, disease duration and extent of ILD, smoking, serology and lung function. However, steroid treated patients were significantly more likely to have usual interstitial pneumonia (UIP), p=0.02. The RR of death from any cause was significantly increased in steroid treated RA-ILD patients [1.65 (1.2-2.3)], p=0.002, but was normal in those who had not received steroids [1.07 (0.7-1.6)]. The RR of respiratory death was more significantly increased in those who had been on steroids [2.75 (1.6-4.7)], p=0.0002, than in those who had not received steroids [2.06 (1.1-3.8)], p=0.02. Conclusions Patients with RA-ILD have increased mortality over controls, and over half have been treated with oral steroids. These patients are at increased relative risk of death, especially from respiratory causes. The excess of UIP in the steroid treated group is likely to account for some of the excess mortality. This large retrospective multi centre study suggests long term oral steroids should be avoided where possible in patients with RA-ILD, and reflects earlier findings in patients with ILD alone. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.1247