Randomised prospective trial to assess the clinical utility of multianalyte assay panel with complement activation products for the diagnosis of SLE.

Objective: We compared the physician-assessed diagnostic likelihood of SLE resulting from standard diagnosis laboratory testing (SDLT) to that resulting from multianalyte assay panel (MAP) with cell-bound complement activation products (MAP/CB-CAPs), which reports a two-tiered index test result having 80% sensitivity and 86% specificity for SLE.

Methods: Patients (n=145) with a history of positive antinuclear antibody status were evaluated clinically by rheumatologists and randomised to SDLT arm (tests ordered at the discretion of the rheumatologists) or to MAP/CB-CAPs testing arm. The primary endpoint was based on the change in the physician likelihood of SLE on a five-point Likert scale collected before and after testing.

Tumor Necrosis Factor dynamically regulates the mRNA stabilome in rheumatoid arthritis fibroblast-like synoviocytes.

During rheumatoid arthritis (RA), Tumor Necrosis Factor (TNF) activates fibroblast-like synoviocytes (FLS) inducing in a temporal order a constellation of genes, which perpetuate synovial inflammation. Although the molecular mechanisms regulating TNF-induced transcription are well characterized, little is known about the impact of mRNA stability on gene expression and the impact of TNF on decay rates of mRNA transcripts in FLS. To address these issues we performed RNA sequencing and genome-wide analysis of the mRNA stabilome in RA FLS.

Micro-RNA analysis of renal biopsies in human lupus nephritis demonstrates up-regulated miR-422a driving reduction of kallikrein-related peptidase 4.

Background: Aberrancies in gene expression in immune effector cells and in end-organs are implicated in lupus pathogenesis. To gain insights into the mechanisms of tissue injury, we profiled the expression of micro-RNAs in inflammatory kidney lesions of human lupus nephritis (LN).

Methods: Kidney specimens were from patients with active proliferative, membranous or mixed LN and unaffected control tissue.

Refractory sarcoid arthritis in World Trade Center-exposed New York City firefighters: a case series.

Objective: The objective of this study was to describe cases of sarcoid arthritis in firefighters from the Fire Department of the City of New York (FDNY) who worked at the World Trade Center (WTC) site.

Methods: All WTC-exposed FDNY firefighters with sarcoidosis and related chronic inflammatory arthritis (n = 11) are followed jointly by the FDNY-WTC Health Program and the Rheumatology Division at the Hospital for Special Surgery. Diagnoses of sarcoidosis were based on clinical, radiographic, and pathological criteria.

Prolonged tumor necrosis factor α primes fibroblast-like synoviocytes in a gene-specific manner by altering chromatin.

Objective: During the course of rheumatoid arthritis (RA), fibroblast-like synoviocytes (FLS) are chronically exposed to an inflammatory milieu. The purpose of this study was to test the hypothesis that prolonged exposure of FLS to tumor necrosis factor α (TNFα) augments inflammatory responses to secondary stimuli (priming effect).

Methods: FLS obtained from RA patients were exposed to TNFα for 3 days and were then stimulated with interferons (IFNs).

Eosinophilic fasciitis in a pediatric patient.

We report the case of a pediatric patient with eosinophilic fasciitis, who was successfully treated with early high dose corticosteroids and subsequent use of mycophenolate mofetil. We believe that the early institution of corticosteroids helped to suppress the early inflammatory part of the disease and the subsequent use of mycophenolate mofetil maintained this and may have also helped prevent fibrotic skin changes.