The overall mean length of hospital stay was 6.8 days. Small vessel vasculitis and Sjögren syndrome had the longest and the shortest hospital stays respectively (14.5 vs. 5.3 days). Hospital charges were highest among systemic vasculitis and DM-PM patients. The admission rate for SCNTD in Thailand was 141 per 100 000 admissions among which SLE was the most common. Overall hospital mortality was 4.1%. Although a lower prevalence was found among systemic vasculitis, it had a higher mortality rate, longer length of stay and greater AC220 datasheet therapeutic cost. “
“Some studies have been performed to elucidate the
association between Fc gamma receptor 3B (FCGR3B) copy number (CN) and the risk of systemic lupus erythematosus (SLE) and/or lupus nephritis (LN), yet the results remain conflicting. Therefore,
we have undertaken a systematic review of all the studies published and carried out a meta-analysis to obtain a better understanding of the role of FCGR3B CN in the susceptibility of SLE and LN. A computerized literature search was conducted in databases of PubMed, ISI Web of Knowledge for all studies investigating the association between FCGR3B CN and SLE and/or LN, published up to May 2013. A total of six articles meeting all of the criteria were included in this study. There were five comparisons of SLE between 2490 patients and 4286 controls, and four comparisons of LN between 689 patients and 1924 controls. Our results showed that Verteporfin cell line individuals with FCGR3B CN gain did not suffer an increased risk of SLE or LN as compared to the normal genotype in the total analysis (SLE: OR = 1.07, 95% CI = 0.79–1.45, P = 0.65; LN: OR = 0.83, 95% CI = 0.47–1.46, P = 0.52). However, individuals with FCGR3B CN loss exhibited an increased risk of SLE or LN (SLE: OR = 1.77, 95% CI = 1.51–2.06, P < 0.00001; LN:
OR = 2.02, 95% CI = 1.59–2.57, P < 0.00001). Our meta-analysis indicated that FCGR3B CN loss rather than Linifanib (ABT-869) CN gain was associated with susceptibility to SLE and LN. “
“Juvenile idiopathic arthritis (JIA) is the commonest chronic rheumatic disease of childhood[1] and is an important cause of short- and long-term disability in children. It is not a single disease entity, but rather a group of ‘genetically heterogeneous’ and ‘phenotypically distinct’ disorders.[1, 2] The diagnosis of various subtypes of JIA is essentially clinical and laboratory parameters are only supportive. The International League of Associations for Rheumatology (ILAR) classifies JIA into seven subtypes: oligoarthritis, rheumatoid factor (RF)-positive polyarthritis, RF-negative polyarthritis, systemic onset JIA (SoJIA), enthesitis-related arthritis (ERA), psoriatric arthritis and undifferentiated arthritis. However, the ILAR classification carries several limitations. It is not user-friendly from the clinician’s point of view and one needs to exclude several other diseases before categorizing a given patient into one of the subtypes.
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