Objective Interstitial lung disease (ILD) is a frequent complication of rheumatoid arthritis (RA), occurring in up to 40% of patients during the course of their disease. Early diagnosis is critical, particularly given the shared clinicoepidemiologic features between advanced rheumatoid arthritis–associated ILD (RA‐ILD) and idiopathic pulmonary fibrosis (IPF). This study was undertaken to define the molecular basis of this overlap through comparative profiling of serum proteins in RA‐ILD and IPF. Methods Multiplex enzyme‐linked immunosorbent assays (ELISAs) were used to profile 45 protein biomarkers encompassing cytokines/chemokines, growth factors, and matrix metalloproteinases (MMPs) in sera obtained from RA patients with ILD and those without, individuals with IPF, and healthy controls. Levels of selected serum proteins were compared between patient subgroups using adjusted linear regression, principal component analysis (PCA), and least absolute shrinkage and selection operator (LASSO) modeling. Results Multiplex ELISA‐based assessment of sera from 2 independent cohorts (Veterans Affairs [VA] and Non‐VA) revealed a number of non‐overlapping biomarkers distinguishing RA‐ILD from RA without ILD (RA–no ILD) in adjusted regression models. Parallel analysis of sera from IPF patients also yielded a discriminatory panel of protein markers in models adjusted for age/sex/smoking, which showed differential overlap with profiles linked to RA‐ILD in the VA cohort versus the Non‐VA cohort. PCA revealed several distinct functional groups of RA‐ILD–associated markers that, in the VA cohort, encompassed proinflammatory cytokines/chemokines as well as 2 different subsets of MMPs. Finally, LASSO regression modeling in the Non‐VA and VA cohorts revealed distinct biomarker combinations capable of discriminating RA‐ILD from RA–no ILD. Conclusion Comparative serum protein biomarker profiling represents a viable method for distinguishing RA‐ILD from RA–no ILD and identifying population‐specific mediators shared with IPF.
Antisynthetase (AS) syndrome is a major subgroup of inflammatory myopathies seen in a minority of patients with dermatomyositis and polymyositis. Although it is usually associated with elevated creatine phosphokinase level, some patients may have amyopathic dermatomyositis (ADM) like presentation with predominant skin involvement. Interstitial lung disease (ILD) is the main pulmonary manifestation and may be severe thereby determining the prognosis. It may rarely present with a very aggressive course resulting in acute respiratory distress syndrome (ARDS). We report a case of a 43-year-old male who presented with nonresolving pneumonia who was eventually diagnosed to have ADM through a skin biopsy without any muscle weakness. ADM may be associated with rapidly progressive course of interstitial lung disease (ADM-ILD) which is associated with high mortality. Differentiation between ADM-ILD and AS syndrome may be difficult in the absence of positive serology and clinical presentation may help in clinching the diagnosis.
Cryopyrin associated periodic syndrome (CAPS) is a dominantly-inherited autoinflammatory disease, which is included in the group of periodic fever syndromes. It is caused by a defect in the regulation of inflammatory cytokines, particularly interleukin-1β. CAPS encompasses a spectrum of three phenotypes of increasing severity: familial cold autoinflammatory syndrome, Muckle-Wells syndrome (MWS) and neonatal onset multisystem inflammatory disease. We report the case of a 58-year-old male, who had migratory joint pains, daily urticaria, chills, and episodic conjunctivitis since childhood and hearing loss in his 20s with a family history of similar symptoms. He was diagnosed with MWS after being found to have a <em>R262W</em> gene mutation in <em>NLRP3</em> gene and successfully treated with canakinumab. After his discovery, other 1<sup>st</sup> and 2<sup>nd</sup> degree family members with similar complaints were found to have the same genetic mutation and were also successfully treated with canakinumab.
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