Introduction There are no reliable data regarding the prevalence of rheumatoid arthritis (RA) in Poland. Material and methods The first stage was a face-to-face survey on a nationwide representative sample of 3000 people, which identified respondents with a physician-confirmed diagnosis of...

Systemic lupus erythematosus (SLE) is characterized by increased cardiovascular morbidity and mortality. SLE patients have increased prevalence of subclinical atherosclerosis, although the mechanisms of this observation remain unclear. Considering the emerging role of monocytes in atherosclerosis, we aimed to investigate the relationship between subclinical atherosclerosis, endothelial dysfunction and the phenotype of peripheral blood monocytes in SLE patients. We characterized the phenotype of monocyte subsets defined by the expression of CD14 and CD16 in 42 patients with SLE and 42 non-SLE controls. Using ultrasonography, intima-media thickness (IMT) of carotid arteries and brachial artery flow-mediated dilation (FMD) as well as nitroglycerin-induced dilation (NMD) were assessed. Patients with SLE had significantly, but only modestly, increased IMT when compared with non-SLE controls (median (25th/75th percentile) 0.65 (0.60/0.71) mm vs 0.60 (0.56/0.68) mm; p < 0.05). Importantly, in spite of early atherosclerotic complications in the studied SLE group, marked endothelial dysfunction was observed. CD14dimCD16+proinflammatory cell subpopulation was positively correlated with IMT in SLE patients. This phenomenon was not observed in control individuals. Interestingly, endothelial dysfunction assessed by FMD was not correlated with any of the studied monocyte subsets. Our observations suggest that CD14dimCD16+monocytes are associated with subclinical atherosclerosis in SLE, although the mechanism appears to be independent of endothelial dysfunction.

Objective: The objective of this study was to determine the length of delay in diagnosis of inflammatory rheumatic diseases, and to indicate the main factors responsible for such delays. Material and methods: A retrospective multi-centre questionnaire survey carried out among 197 patients with diagnosed inflammatory rheumatic diseases or undergoing the diagnostic process. Results: The most common early symptoms of inflammatory rheumatic disease included joint pain (94%), joint swelling (78%), morning joint stiffness (77%), fatigue (76%), and sleep disturbed by joint pain (74%). When asked about the reasons for seeking medical help, most patients indicated intensification of the symptoms (89%) and the fact that the symptoms made them unable to perform daily activities or work (86%). Limited access to specialists (70%) and the conviction that the symptoms will resolve spontaneously (57%) had the biggest impact on delaying a visit to a doctor. Before visiting a rheumatologist, the patients consulted their symptoms with their general practitioners (GPs, 95%), orthopaedicians (43%), and neurologists (29%). Almost half of the patients (48%) consulted their symptoms with at least 2 non-rheumatologists, whereas as many as 21% of patients visited 4 or more specialists. After the onset of symptoms of rheumatic disease, 28% of patients delayed seeing any doctor for 4 months or longer. 36% of patients waited 4 months or longer for a referral to a rheumatologist. The great majority of the patients (85%) made an appointment with a rheumatologist within a month of receiving a referral. 25% of patients waited 4 months or longer to see a rheumatologist. Conclusions: Diagnostic delays result from both the level of patients’ awareness (ignoring early symptoms) and improper functioning of the health care system. In the case of the health care system, the source of delays is not only “queues to rheumatologists”, but also referring patients to non-rheumatologists.

Evidence from over 10 years of clinical experience demonstrates that biosimilar medicines approved in the European Union can be used for all their registered indications as safely as their originators and with no negative impact on therapeutic efficacy. The debate on the use of biosimilars in rheumatology focuses specifically on the safety of switching between biosimilars and reference products. Studies conducted to date, including randomised double-blind and open-label extension trials, have not demonstrated any significant differences in therapeutic efficacy or safety between patients switched from one medicine to another and those who were continued on a single medicine. According to the latest recommendations for the use of biosimilars in rheumatic diseases, developed by an international task force in 2017, there is no clinical evidence that a single switch from an originator to a biosimilar medicine is associated with any significant risk for patient safety or reduction in therapeutic efficacy.

Tofacitinib is a newly approved small-molecule targeted synthetic disease-modifying antirheumatic drug. The drug was designed as a selective and specific inhibitor of pro-inflammatory receptor signalling. Tofacitinib inhibits the process of intracellular signalling from the receptor to the cellular nucleus and inhibits the inflammation process via a new pathway (inhibition of the Janus kinases), which is unavailable to biological medicines. Tofacitinib has been approved for use in the treatment of patients with moderate to severe active RA. The drug may be used in combination with methotrexate or another conventional synthetic disease-modifying antirheumatic drug or in monotherapy. The efficacy of tofacitinib has been confirmed in several clinical trials. The drug inhibits radiographic progression of the disease. The innovative mechanism of action of tofacitinib is a noteworthy feature because it offers hope of effective treatment for patients who fail to respond to other drugs. The presented article discusses the mechanism of action and the clinical application of tofacitinib. Tofacitinib represents a new group of disease-modifying antirheumatic drugs that can be placed on an equal footing with biological drugs already available.