The objective of this study is to describe the clinical and laboratory features of macrophage activation syndrome (MAS) in systemic onset juvenile idiopathic arthritis (SOJIA) at a tertiary care center in northwest India. Review of medical records of all children with SOJIA admitted during the period January 1995-December 2008 in Pediatric Allergy and Immunology Unit, Advanced Pediatrics Centre, Postgraduate Institute of Medical Education and Research, Chandigarh, was done. Six patients (5 boys and 1 girl) with SOJIA and MAS were identified. Mean age at time of disease onset was 6.5 years. MAS was the presenting manifestation of SOJIA in 4 patients. Clinical manifestations included fever (6/6), clinical shock (6/6), encephalopathy (5/6), generalized lymphadenopathy (4/6), hepatosplenomegaly (3/6), jaundice and abdominal tenderness (3/6), cardiac involvement (3/6), and meningeal irritation (2/6). Laboratory findings at onset of MAS included decreasing total leukocyte and platelet counts, coagulopathy, elevated transaminases, hyponatremia, and lipid abnormalities. Hemophagocytosis was demonstrable in the bone marrow in 4 patients and in the lymph node in 1. For treatment, we used intravenous methylprednisolone (4/6), oral prednisolone (2/6), and intravenous immunoglobulin (2/6). Outcome was favorable in all patients except one who died of rapidly progressive disease. This paper describes the experience of JIA-related macrophage activation syndrome in a tertiary Indian center. We have shown that MAS can be the early presenting manifestation of evolving SOJIA. Early diagnosis and aggressive management can have a significant impact on the mortality associated with this syndrome. We stress on the role of glucocorticoids in the management of this condition and believe that glucocorticoids have a far more important role in the management of this condition than what has been previously reported.
Background: Measles is a significant public health problem in India and many other developing countries. A single dose of measles vaccine is administered at 9 months of age, assuming that infants are protected by transplacental antibodies till this age.Objective: In infants born to unimmunized mothers, to (i)serially measure the level of anti-measles antibodies from birth to 9 months, (ii)study the pattern of decline, and (iii)identify possible factors that could predict lack of protection.Methods & Materials: Institutional ethical clearance was obtained. Written informed consent was taken from women preparing to deliver babies in the hospital. Serum anti-measles IgG was measured by quantitative ELISA in 61 consecutively born infants at birth (cord blood from infant side), 14 weeks (coinciding with visit for EPI vaccination), 24 weeks (coinciding with visit for third dose Hepatitis B vaccine) and 36weeks (just before measles vaccination). Proportion of unprotected infants (antibody titre <200 mIU/ml) was calculated at each time-point. Gestational age (preterm vs term), gestational weight (small-for-age vs appropriate-for-age), initial antibody level at birth, were evaluated as possible predictors.Results: Anti-measles IgG antibody levels (±standard deviation) were 3235±169 IU/ml at birth, 994±127 IU/ml at 14weeks, 208±34 IU/ml at 24 weeks, and 85±8 IU/ml at 36weeks (Figure 1A and 1B). The proportion of unprotected infants was 0%, 11.5%, 72%, and 94% respectively. Lack of protection did not correlate with premature birth (odds ratio; 95% CI for preterm vs term was 0.90; 95%CI 0.26, 3.10 at 14weeks, and 0.40; 95%CI 0.04, 3.56 at 24 weeks). There was also no relationship to birth weight (odds ratio; 95% CI for SGA vs AGA was 1.63; 0.33, 8.11 at 14 weeks and 0.86, 95%CI 0.26,2.78 at 24 weeks).Conclusion: Majority of infants lose transplacental anti-measles antibodies between 14 and 24 weeks of age, and are susceptible to measles. The lack of protection cannot be predicted by gestational age or birth weight.
Background Abatacept is a biologic therapy which suppresses T-cell activation via co-stimulation blockade in rheumatoid arthritis (RA) patients. It became part of our biologic algorithm shortly after initial limited NICE approval in August 2010. In April 2013, NICE widened its recommendation of abatacept in RA patients who have failed to respond adequately to 2 disease-modifying anti-rheumatic drugs (DMARDs) including methotrexate [2]. Objectives In this study we share our experience of abatacept in patients with rheumatoid arthritis (RA) in routine clinical practice from a subregional centre in UK covering a population of 500,000. Methods This was a retrospective analysis of 84 patients who received abatacept therapy from November 2010 to January 2014. Data collected included baseline demographics, number of previous synthetic and biologic DMARDs, change in DAS28 at 3 and 6 months. Response was defined as DAS28 reduction of greater than 1.2. Results 84 patients with RA were commenced on abatacept therapy over 39 months since Nov 2010. The mean age of the patients was 62 years and 74% of them were female. The average number of prior synthetic DMARDs was 2.8 and biologic DMARDs 2.1. Only 2 patients were biologic- naïve before abatacept. 75 patients had received anti-TNF therapy (adalimumab, certolizumab pegol, etanercept, golimumab, infliximab), 40 had received rituximab and 7 tocilizumab. The baseline DAS28 was 5.8 and mean DAS reduction at 3 and 6 months was 1.6 (n=41) and 2.0 (n=37) respectively. 25 out of 41 (61%) patients responded at 3 months and this increased to 76% at 6 months (28/37). 14% (5/37) achieved remission at 6 months. 11 patients stopped abatacept therapy, 5 were intolerant of which 3 had infusion reactions, 1 patient had lack of efficacy and 2 loss of efficacy (between 3 and 6 months), 1 patient refused further infusions and 2 patients moved out of area. In a subgroup, the mean DAS reduction at 6 months in seropositive (Rheumatoid Factor or Anti-CCP antibody positive n=14) and seronegative patients (n=16) were 2.54 and 1.88 respectively. Conclusions Our experience shows that abatacept is safe, well tolerated and effective in RA patients with inadequate response to previous synthetic and biologic DMARDs in routine clinical practice. The improvement in DAS28 at 3 months was sustained at 6 months. The numbers are small to draw any conclusion about better response in seropositive RA patients. References NICE recommends wider use of abatacept for treating rheumatoid arthritis (Guidance TA195) August 2010 NICE technology appraisal guidance: Abatacept for treating rheumatoid arthritis after the failure of conventional disease-modifying anti-rheumatic drugs (Guidance TA280 rapid review of TA234) April 2013 Acknowledgements We would like to thank all members of the Rheumatology team at Cannock Hospital and the patients who participated. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.3037
Abstracts labour ≤37°C, gestational age ≥37 weeks and birthweight centile ≥10%. Analysis was performed on plasma EDTA, using ELISA Quantikine® (R&D Systems, Europe). Results The study consisted of samples from 48 infants with two different modes of delivery; unassisted vaginal delivery (n=12 male, n=12 female) and pre-labour elective caesarean section (n=12 male, n=12 female). The range of all samples was normally distributed between 87.0 and 114.6 pg/ml. Mean (SD) for IL-16 was 103.1 (± 21.9) pg/ml. Levels were not affected by gender or mode of delivery. Conclusion For the first time we have described the expected range of cord plasma IL-16 levels in healthy term infants. Background and Aims Production of C-reactive protein (CRP), an acute phase reactant of hepatic origin, may be affected by perinatal asphyxia. This study tested hypotheses that circulatory CRP concentrations correlate with clinical severity of hypoxic-ischaemic encephalopathy (HIE) and that total body hypothermia modulates CRP response. Methods Clinical records in three centres were reviewed for neonates ≥36 weeks' gestation admitted between 01/07/06 and 30/06/11 with HIE of any severity (grades 1-3 Sarnat-Sarnat). Participating centres adopted routine cooling at different dates. Data extracted included CRP concentrations in the first postnatal week measured during routine clinical practice, clinical HIE grading, and reception of therapeutic hypothermia. Proportions with raised CRP (>10 mg/L), and maximum CRP concentrations were assessed according to HIE grade and whether cooled. Conclusion A raised CRP is a common finding in the first postnatal week in neonates admitted with HIE and is found in most infants with moderate-severe HIE. Peak CRP concentrations did not differ with clinical HIE grade and whole body hypothermia did not significantly affect peak CRP concentrations. C-REACTIVE PROTEIN CONCENTRATIONS IN NEONATES
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