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Objectives: Patients with seronegative spondyloarthritis (SpA) - psoriatic arthritis (PsA) and ankylosing spondylitis (AS) - have a higher risk of cardiovascular morbidity and mortality. The aim of the present study was to evaluate the incidence and type of dyslipidemia, a potent atherosclerosis risk factor, in SpA patients., Material and Methods: It was a two-center, case-control study. Patients diagnosed with PsA and AS aged 23-60 years, with disease duration < 10 years, were enrolled. The inflammatory activity, serum levels of C-reactive protein (CRP) and lipid profile were evaluated in each patient. In patients > 40 years old, the 10-year risk of fatal cardiovascular disease (CVD), using Systematic Coronary Risk Evaluation (SCORE), was estimated., Results: In total 79 patients with SpA were included in the study, with PsA diagnosed, n = 39 (mean age 45.1 ±9.6 years; 21, 53.9%, women), and with AS diagnosed, n = 40 (age 40.3 ±9.5; 12.3%, women), control group (CG): n = 88 (age 42.3 ±8.1; 42, 47.7% women). Based on the interview and laboratory tests, dyslipidemia was diagnosed in 19 (47.5%) patients with AS and in 28 (71.8%) patients with PsA. Most patients had hypercholesterolemia or mixed hyperlipidemia. Types of dyslipidemia were similar. In SpA patients (PsA and AS), the level of triglycerides (TG) and atherogenic index (AI) were significantly higher than in the CG, respectively TG in SpA: 116 (83-156) and in the CG: 91.2 (72.6-134.6) mg/dl, p = 0.0182; AI in SpA: 3.77 ±1.26 and in the CG: 2.58 ±1.27, p < 0.0001.The low-density cholesterol (LDL) level was significantly lower in SpA patients than in the CG, SpA: 109.1 ±29.4 vs. CG: 125.2 ±35.9 mg/dl, p = 0.0023. There was a strong negative correlation between CRP levels and HDL cholesterol levels in patients with PsA, rho = 0.42, p = 0.0132. Mean SCORE values were 2.33% in PsA patients and 2.38% in AS patients, which results in moderate 10-year risk of death from CVD., Conclusions: In young patients with spondyloarthropathies, inflammatory factors significantly influence dyslipidemia patterns, which result in higher TG and lower LDL cholesterol levels. In patients with PsA, dyslipidemia was diagnosed more often than in patients with AS., Competing Interests: The authors declare no conflict of interest., (Copyright: © 2021 Narodowy Instytut Geriatrii, Reumatologii i Rehabilitacji w Warszawie.)

Introduction There is substantial evidence that spondyloarthropathies, such as ankylosing spondylitis (AS) and psoriatic arthritis (PsA), may increase cardiovascular risk. Objectives The study aimed to compare development of atherosclerotic lesions in coronary arteries between patients with AS and individuals without rheumatic dise ases. Patients and methods A total of 37 adult patients with AS (mean [SD] age, 40.4 [9.6] years; men, 26 [70.3%]), with disease duration of less than 10 years were enrolled. The control group consisted of 76 participants without rheumatic diseases. Controls were matched for age, sex, history of hypertension, dyslipidemia, and smoking status. Coronary computed tomography angiography was performed in both groups. Results Atherosclerotic lesions in the coronary arteries were present in 18 patients (48.7%) with AS compared with 20 controls (26.3%) (P = 0.02). Univariate analysis performed in the AS group demonstrated an association between the presence of lesions and age (P = 0.02), hypertension (P = 0.003), and dyslipidemia (P = 0.001). The multivariable logistic regression analysis showed a significant association between coronary atherosclerosis and hypertension (P = 0.008) and with dyslipidemia (P = 0.001). The average plaque burden was higher in patients with AS than in controls (mean [SD], 42.2% [4.7%] vs 36.5% [3.1%], P <0.0001). Conclusions Atherosclerotic plaques in the coronary arteries were significantly more prevalent in patients with AS. A strong association was demonstrated between atherosclerotic lesions and age, hypertension, and dyslipidemia. Our results confirm the need for cardiovascular risk assessment in patients with AS and cardiovascular prevention, if indicated.

Elderly-onset rheumatoid arthritis (EORA), defined as rheumatoid arthritis (RA) with the onset at the age > or =60 differs sligthy at presentation from younger-onset RA (YORA) by a more equal sex distribution, a higher frequency of an acute onset, more frequent involvement of large joints, especially of the shoulder, and higher disease activity. Longitudinal studies have shown greater disease activity, more severe radiographic damage and functional decline in patients with EORA than in those with YORA. These differences were only found in seropositive patients. In seronegative EORA patients a less severe course of the disease and a better outcome have been observed, with the clinical manifestations of polymyalgia rheumatica or remitting seronegative symmetrical synovitis with pitting edema. This article is a review of available data concerning differences between EORA and YORA.

Introduction: The purpose of this study was to analyze the data of patients with T-cell large granular lymphocyte (T-LGL) lymphocytosis associated with inflammatory arthropathy or with no arthritis symptoms., Methods: Clinical, serological as well as histopathological, immunohistochemical, and flow cytometric evaluations of blood/bone marrow of 21 patients with T-LGL lymphocytosis were performed. The bone marrow samples were also investigated for T-cell receptor (TCR) and immunoglobulin (IG) gene rearrangements by polymerase chain reaction with heteroduplex analysis., Results: Neutropenia was observed in 21 patients, splenomegaly in 10, autoimmune diseases such as rheumatoid arthritis (RA) in 9, unclassified arthritis resembling RA in 2, and autoimmune thyroiditis in 5 patients. T-LGL leukemia was recognized in 19 cases. Features of Felty syndrome were observed in all RA patients, representing a spectrum of T-LGL proliferations from reactive polyclonal through transitional between reactive and monoclonal to T-LGL leukemia. Bone marrow trephines from T-LGL leukemia patients showed interstitial clusters and intrasinusoidal linear infiltrations of CD3+/CD8+/CD57+/granzyme B+ lymphocytes, reactive lymphoid nodules, and decreased or normal granulocyte precursor count with left-shifted maturation. In three-color flow cytometry (FCM), T-LGL leukemia cells demonstrated CD2, CD3, and CD8 expression as well as a combination of CD16, CD56, or CD57. Abnormalities of other T-cell antigen expressions (especially CD5, CD7, and CD43) were also detected. In patients with polyclonal T-LGL lymphocytosis, T cells were dispersed in the bone marrow and the expression of pan-T-cell antigens in FCM was normal. Molecular studies revealed TCRB and TCRG gene rearrangements in 13 patients and TCRB, TCRG, and TCRD in 4 patients. The most frequently rearranged regions of variable genes were Vbeta-Jbeta1, Jbeta2 and Vgamma If Vgamma10-Jgamma. Moreover, in 4 patients, additional rearrangements of IG kappa and lambda variable genes of B cells were also observed., Conclusion: RA and neutropenia patients represented a continuous spectrum of T-LGL proliferations, although monoclonal expansions were most frequently observed. The histopathological pattern and immunophenotype of bone marrow infiltration as well as molecular characteristics were similar in T-LGL leukemia patients with and without arthritis.

Published data were reviewed to evaluate the occurrence of antiphospholipid antibodies (aPL) in rheumatoid arthritis (RA) patients and to investigate their clinical relevance in this population. The mean prevalence of aPL in RA patients was calculated at 28%. Few studies have found a relationship between aPL and thrombosis, particularly in combination with other risk factors. Conflicting results have been reported on the association of anticardiolipin antibodies (aCL) positivity and neurologic symptoms, Reynaoud's phenomenon, radiologic erosions, extra-articular RA manifestations, rheumatoid factor, and atherosclerosis. Some studies, however, suggest that there is a correlation present between those antibodies and C-reactive protein levels, rheumatoid factor (RF) and antinuclear antibodies. Tumor necrosis factor blocking agents may cause an induction of aCL, but it seems like they do not cause any clinical features related to the antiphospholipid syndrome.