Study of the natural course and specific immunity after herpes zoster in patients with rheumatoid arthritis receiving biologic DMARDs.

Herpes zoster is a common infection especially in elderly persons. It is caused by reactivation of varicella zoster virus (VZV) that has remained dormant within dorsal root ganglia after primary infection. Besides patients with immunodeficiency and malignancies, zoster incidence is also higher in patients with rheumatic diseases compared to the general population. Especially in the group of rheumatoid arthritis (RA) patients being treated with biologics, the risk seems to be steady among regimens with different modes of action (1.6-2.4/100 patients-years). RA patients receiving tumor necrosis factor (TNF) inhibitors are at increased risk during the first year of treatment. The aim of the current research protocol is to evaluate the natural course of herpes zoster and the effect of biologic and conventional synthetic disease modifying anti-rheumatic drugs (DMARDs) on the VZV-specific cell mediated immunity in RA patients after herpes zoster infection. We will - prospectively - include RA patients who develop herpes zoster, while being treated with biologics (anti-TNF, tocilizumab, rituximab, abatacept) and a control group comprised of patients with herpes zoster [RA patients under non-biologic therapies (corticosteroids/csDMARDs) and age- and sex-matched healthy controls). Titers of IgG specific antibodies against VZV glycoprotein gp1 and the percentage and absolute number of VZV-specific activated CD4+ T cells (CD4+CD69+IFN-γ+) at the time of rash onset and during follow-up will be measured by ELISA and flow cytometry respectively. This study will contribute to the better understanding of various aspects of immune response to VZV in the modern treatment era with biologic DMARDs

Chest CT findings in patients with inflammatory myopathy and Jo1 antibodies

Thoracic high-resolution computed tomography scans (HRCT) of 17 patients with inflammatory muscle disorders (IMD) and positive Jo1 antibodies were retrospectively reviewed regarding presence, extension, and distribution of pathological findings. Abnormal findings were found in 14 (82.3%) patients. The predominant CT abnormality was ground glass attenuation, which was present in seven patients (41.1%), having a bilateral and diffuse distribution. In general, lesions tended to appear in the lower lobes and more specifically in the lung bases. lnterlobular septal thickening was found in six patients (35.3%); it was seen in the upper and lower lobes with peripheral distribution and bilateral localization in five out of six patients. Bronchiectases, reticular opacities, and honeycombing were found in six patients (35.3%). Air space consolidation was seen in about 17% of the patients. Lung involvement is a frequent feature of IMD patients with positive Jo1 antibodies and its most common radiological pattern is that of nonspecific interstitial pneumonia. (c) 2007 Elsevier Ireland Ltd. All rights reserved

Five-year prospective multi-center cohort study of patients with giant cell arteritis in Greece.

Giant cell arteritis (GCA) is the most common systemic vasculitis in the aged population associated with significant morbidity due to the long term administration of corticosteroids and the presence of various comorbidities. Data regarding its current treatment modalities, comorbidities, morbidity and mortality in Greece are limited. In this multi-center, prospective study that begun at the end of 2015 patients with newly diagnosed GCA according to the modified 1990 ACR criteria, as well as individuals with established or relapsing disease have been included. During the 1(st) phase of the study that is still ongoing, data are being collected concerning demographic and clinical characteristics of the patients, treatment at the onset of the disease and at relapses, relapses, adverse events of therapy, comorbidities, hospitalizations and deaths. During the 2(nd) and 3(rd) phase of the study patients will be reevaluated 2 and 5 years after their 1st evaluation. The study is expected to provide valuable data regarding the current clinical characteristics, comorbidities, therapeutic regimens used, relapse rate, morbidity and mortality of patients with GCA

Leukocyte Immunoglobulin-Like Receptor A3 (LILRA3): A Novel Marker for Lymphoma Development among Patients with Young Onset Sjogren’s Syndrome

Background: Primary Sjogren’s syndrome (SS) is an autoimmune disease with a strong predilection for lymphoma development, with earlier disease onset being postulated as an independent risk factor for this complication. Variations of the Leukocyte immunoglobulin-like receptor A3(LILRA3) gene have been previously shown to increase susceptibility for both SS and non-Hodgkin B-cell lymphoma (B-NHL) in the general population. We aimed to investigate whether variations of the LILRA3 gene could predispose for lymphoma development in the context of SS. Methods: Study population, all of Greek origin, included 101 SS cases with a current or previous diagnosis of lymphoma (SS-lymphoma, SS-L) and 301 primary SS patients not complicated by lymphoma (SS-non-lymphoma, SS-nL). All SS patients fulfilled the 2016 SS American College of Rheumatology/European league against Rheumatism (ACR/EULAR) classification criteria. A total of 381 healthy controls (HC) of similar age/sex/race distribution were also included. On the basis of the age of SS onset and the presence or absence of adverse predictors for lymphoma development, SS patients were further stratified into younger (≤40 years) and older (>40 years) age of disease onset, as well as into high/medium and low risk groups. Polymerase chain reaction (PCR) was implemented for the detection of the following LILRA3 gene variants: homozygous non-deleted or functional wild type (+/+) heterozygous (+/−) and homozygous deleted (−/−). LILRA3 serum protein levels were quantitated by enzyme-linked immunosorbent assay (ELISA) in 85 individuals (29 SS-L, 35 SS-nL patients and 21 HC). Results: While no statistically significant differences were detected in the overall frequency of LILRA3 gene variants between SS-L, SS-nL and HC groups, LILRA3 serum protein levels were increased in the SS-L group compared to HC (1.27 ± 1.34 vs. 0.38 ± 0.34 ng/mL, p-value: 0.004). After stratification according to the age of SS onset and history of lymphoma, as well as the presence or absence of adverse predictors for lymphoma development, the prevalence of the functional LILRA3 gene variant was found to be significantly increased in the young onset SS-L group compared to the HC of similar age and sex distribution (100% vs. 82.9%, p = 0.03), as well as in the high/medium risk SS compared to the low risk SS (91.3 vs. 78.3%, p = 0.0012). Of note, young onset SS-L and SS-nL groups displayed higher LILRA3 serum levels compared to their older counterparts (p-values: 0.007 and 0.0005, respectively). Conclusion: The functional LILRA3 gene variant increases susceptibility to SS-related lymphoma development in patients with a disease onset of <40 years old, implying that genetically determined deranged immune responses in younger SS individuals could underly their pronounced risk for lymphoma development

Combined Brain/Heart Magnetic Resonance Imaging in Systemic Lupus Erythematosus

Cardiovascular Disease (CVD) in Systemic Lupus Erythematosus (SLE) and Neuropsychiatric SLE (NPSLE) has an estimated prevalence of 50% and 40%, respectively and both constitute major causes of death among SLE patients. In this review, we proposea combined brain/heart Magnetic Resonance Imaging (MRI) for SLE risk stratification has been proposed. The pathophysiologic background of NPSLE includes microangiopathy, macroscopic infarcts and accelerated atherosclerosis. Classic brain MRI findings demonstrate lesions suggestive of NPSLE in 50% of the NPSLE cases, while advanced MRI indices can detect pre-clinical lesions in the majority of them, but their clinical impact still remains unknown. Cardiac involvement in SLE includes myo-pericarditis, valvular disease/endocarditis, Heart Failure (HF), coronary macro-microvascular disease, vasculitis and pulmonary hypertension. Classic and advanced Cardiovascular Magnetic Resonance (CMR) indices allow function and tissue characterization for early diagnosis and treatment follow-up of CVD in SLE. Although currently, there are no clinical data supporting the combined use of brain/heart MRI in asymptomatic SLE, it may have a place in cases with clinical suspicion of brain/heart involvement, especially in patients at high risk for CVD/stroke such as SLE with antiphospholipid syndrome (SLE/APS), in whom concurrent cardiac and brain lesions have been identified. Furthermore, it may be of value in SLE with multi-organ involvement, NPSLE with concurrent cardiac involvement, and recent onset of arrhythmia and/or heart failure