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Primary Sjögren’s syndrome (pSS) is an autoimmune disease, with B cell hyperactivation and autoantibody production as its immunological hallmarks. Although the distinction between immunoglobulin G4-related disease (IgG4-RD) and pSS, based on the presence or absence of certain autoantibodies, seems easy to make, possibility of elevated serum IgG4 concentration and often similar organ involvement may lead to a misdiagnosis. The increased serum concentration of IgG4 in IgG4-RD is not clearly linked to the pathogenesis of IgG-RD and it has been suggested that it may constitute just an epiphenomenon. The aim of this article is to discuss the presence of IgG4 in pSS and IgG4-RD and its potential significance for these two diseases.

Primary Sjögren’s syndrome (pSS) is an autoimmune disease with a clinical picture of not only mainly exocrine gland involvement, with dryness symptoms, but also internal organ and systems involvement. The epithelial damage and releasing of antigens, which, in some circumstances, become autoantigens, underlay the pathogenesis of pSS. The activation of autoimmune processes in pSS leads to the hyperactivation of B cells with autoantibody production and other immunological phenomena such as hypergammaglobulinemia, production of cryoglobulins, or formation of extra-nodal lymphoid tissue. Among the risk factors for the development of this disease are viral infections, which themselves can activate autoimmune reactions and influence the host’s immune response. It is known that viruses, through various mechanisms, can influence the immune system and initiate autoimmune reactions. These mechanisms include molecular mimicry, bystander activation, production of superantigens—proteins encoded by viruses—or a programming to produce viral cytokines similar to host cytokines such as, e.g., interleukin-10. Of particular importance for pSS are viruses which not only, as expected, activate the interferon pathway but also play a particular role, directly or indirectly, in B cell activation or present tropism to organs also targeted in the course of pSS. This article is an attempt to present the current knowledge of the influence specific viruses have on the development and course of pSS.

The distinguishing of the IgG4-related disease (IgG4-RD) from among other rheumatic diseases has brought attention to the IgG4 subclass of immunoglobulins. It is the least numerous subclass among immunoglobulins G. In general, IgG4 is considered to be non-inflammatory and tolerance inducing, due to its unique structure. However, in IgG4-RD this antibody plays a pathogenic role in activation of the fibrinogenesis and of the inflammatory process; there are also suggestions that it may be a marker of an abnormal inflammatory response. The importance of IgG4 for the pathogenesis of allergic diseases, with a vital role of its ratio to immunoglobulin E (IgE/IgG4 ratio), has been known for years. The role of IgG4 in the course and pathogenesis of rheumatic diseases is still being researched and is not yet fully understood. Increased IgG4 levels have been revealed in rheumatoid arthritis, although no clear link between this phenomenon and disease activity has been demonstrated. There are articles on the potential importance of IgG4 concentration (of both elevated and decreased serum levels) in Sjogren’s syndrome. Additionally, anti-nuclear IgG4 antibody significant titers have been detected in SLE patients, and it has been suggested that the effect of these antibodies on complement consumption and the production of proinflammatory cytokines may play a role in inhibiting the progression of SLE. IgG4 plays a role in autoimmune diseases other than rheumatic diseases, such as pemphigus, bullous pemphigoid, idiopathic membranous glomerulonephritis, or myasthenia gravis, but also in helmints infections. Research shows the importance of IgG4 in malignancy of neoplasms. Melanoma cells are known to stimulate IgG4 production through a modified Th2-based inflammatory response. The role of this immunoglobulin in cholangiocarcinoma is also considered as possible. The aim of this review article is to discuss the current knowledge of IgG4 not only from the perspective of the IgG4-RD but also from a point of view of other autoimmune diseases with particular emphasis on rheumatic diseases.

Primary Sjögren’s syndrome (pSS) is a relatively common disease and one of the most common rheumatic diseases of autoimmune and inflammatory origin. It is primarily associated with symptoms of dryness, mainly in the mouth and eyes, but it can also manifest in the internal organs. Epidemiological studies have highlighted that elderly-onset pSS (EOpSS) is common, and it is known that sicca syndrome is a feature often observed in the elderly and can be induced by several factors. However, the presence of autoantibodies in older patients with sicca syndrome can be age-related and does not mean pSS is present. This review article presents the most important elements for making a correct diagnosis of EOpSS and considers clinical and/or laboratory differences between older and younger pSS patients. According to data from the literature, EOpSS is not a distinct subset of disease when compared with younger-onset pSS.

Background and Objectives: Laboratory liver abnormalities can be observed in patients affected with polymyalgia rheumatica (PMR) and/or giant cell arteritis (GCA), especially with a cholestatic pattern. The first objective of our review article is to discuss the potential link between antimitochondrial antibodies (AMA) and/or primary biliary cholangitis (PBC) and PMR/GCA, according to the evidences of literature. The second objective is to discuss the association of PMR/GCA with the other rheumatic diseases having PBC as a common manifestation. Materials and Methods: A literature search was performed on PubMed and Medline (OVID interface) using these terms: polymyalgia rheumatica, giant cell arteritis, antimitochondrial antibodies, primary biliary cholangitis, primary Sjogren’s syndrome, systemic sclerosis, and systemic lupus erythematosus. The search was restricted to all studies and case reports published in any language. Reviews, conference abstracts, comments, and non-original articles were excluded; however, each review’s reference list was scanned for additional publications meeting this study’s aim. When papers reported data partially presented in previous articles, we referred to the most recent published data. Results and Conclusions: Our literature search highlighted that cases reporting an association between AMA, PBC and PMR/GCA were very uncommon; AMA antigenic specificity had never been detected and biopsy-proven PBC was reported only in one patient with PMR/GCA. Finally, the association of PMR/GCA with autoimmune rheumatic diseases in which PBC is relatively common was anecdotal.

Residual pain is a major unmet medical need observed in patients suffering from rheumatoid arthritis (RA), which decreases their quality of life, even after achieving remission or low disease activity. The article has two aims: 1) to present mechanisms involved in the pathophysiology of residual pain, both inflammatory and non-inflammatory, i.e. neuropathic and nociplastic pain, as well as secondary pain syndromes, i.e. osteoarthritis and fibromyalgia, which can contribute to residual pain; 2) to show the limitations of current disease activity measures recommended by European Alliance of Associations for Rheumatology (EULAR) and American College of Rheumatology (ACR), which raise the need for a separate assessment of pain, and examples of methods that could be used by medical professionals to assess the pain and make a differential diagnosis. In conclusion, establishing a valid method to assess pain is essential to identify the pathomechanism of residual pain and to create treatments tailored specifically to individual RA patients.

As severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) evolves, infection management in vulnerable populations requires formalized guidance. Although low-virulence variants of SARS-CoV-2 remain predominant, they pose an increased risk of severe illness in adults with rheumatic and musculoskeletal diseases (RMDs). Several disease-specific (chronic long-grade inflammation, concomitant immunosuppression) and individual (advanced age, multimorbidity, pregnancy, vaccination status) factors contribute to excess risk in RMD populations. Various post-COVID-19 manifestations are also increasingly reported and appear more commonly than in the general population. At a pathogenetic level, complex interplay involving innate and acquired immune dysregulation, viral persistence, and genetic predisposition shapes a unique susceptibility profile. Moreover, incident cases of SARS-CoV-2 infection as a trigger factor for the development of autoimmune conditions have been reported. Vaccination remains a key preventive strategy, and encouraging active education and awareness will be crucial for rheumatologists in the upcoming years. In patients with RMDs, COVID-19 vaccines’ benefits outweigh the risks. Derivation of specialized diagnostic and therapeutic protocols within a comprehensive COVID-19 care plan represents an ideal scenario for healthcare system organization. Vigilance for symptoms of infection and rapid diagnosis are key for introducing antiviral treatment in patients with RMDs in a timely manner. This review provides updated guidance on optimal immunization, diagnosis, and antiviral treatment strategies.

Psoriasis is a chronic, inflammatory, often relapsing disease that is frequently associated with other diseases of similar pathogenesis. The multi-morbidity in the psoriasis population significantly impedes both diagnosis and implementation of appropriate preventive measures. However, the common denominator for this group of diseases is the inflammatory process that initiates the appearance of subsequent symptoms and health consequences, most of which can be avoided or alleviated by modifying the patient’s lifestyle and incorporating appropriate treatment. Health consequences associated with systemic inflammation include cardiovascular incidents and other cardiometabolic diseases. This article was based on available publications on the onset, incidence, and prevention of cardiovascular disease in the psoriasis patient population.

BackgroundAntiphospholipid syndrome (APS) is a multisystemic autoimmune disorder characterized by thrombotic events and/or gestational morbidity in patients with antiphospholipid antibodies (aPL). In a previous single center study, APS-related clinical manifestations that were not included in the classification criteria (livedo reticularis, thrombocytopenia, leukopenia) were associated with the presence of circulating immune-complexes (CIC) formed by beta-2-glycoprotein-I (B2GP1) and anti-B2GP1 antibodies (B2-CIC). We have performed a multicenter study on APS features associated with the presence of B2-CIC.MethodsA multicenter, cross-sectional and observational study was conducted on 303 patients recruited from six European hospitals who fulfilled APS classification criteria: 165 patients had primary APS and 138 APS associated with other systemic autoimmune diseases (mainly systemic lupus erythematosus, N=112). Prevalence of B2-CIC (IgG/IgM isotypes) and its association with clinical manifestations and biomarkers related to the disease activity were evaluated.ResultsB2-CIC prevalence in APS patients was 39.3%. B2-CIC-positive patients with thrombotic APS presented a higher incidence of thrombocytopenia (OR: 2.32, p=0.007), heart valve thickening and dysfunction (OR: 9.06, p=0.015) and triple aPL positivity (OR: 1.83, p=0.027), as well as lower levels of C3, C4 and platelets (p-values:

The primary cause of chronic autoimmune diseases is elusive both in somatic medicine and psychiatry. Examples of such conditions are rheumatoid arthritis and schizophrenic disorders. Immune disturbances occur in both diseases, but it is difficult to combine them into a meaningful pathogenetic model. The immunological hypothesis of schizophrenia is based on non-specific changes in the cytokine system and exponents of chronic inflammation in some patients. In rheumatoid arthritis the cytokine network is much better known than in schizophrenia, and interleukin-6, tumor necrosis factor or Janus kinases became a target of treatment. Microbiome dysbiosis and disturbances of the blood–gut barrier may be a new hypothesis of the pathogenesis of somatic and psychiatric diseases. The purpose of this narrative review was to show, using the example of two chronic diseases – rheumatoid arthritis and schizophrenic disorders – that disturbances in the blood barrier of the intestine can be a common mechanism of somatic and mental disorders. The paper presents the current state of knowledge on the hypothetical relationship between microbiome dysbiosis and the pathogenesis of schizophrenia and rheumatoid arthritis. In conclusion, in the light of discoveries regarding the microbiome–gut–brain axis the immunological model of rheumatoid arthritis and schizophrenia formation may gain importance and contribute to the creation of new strategies for causal treatment of these still incurable diseases.

After battling – for more than a year – the SARS-CoV-2 pandemic and its successive waves affecting different regions of the world, the medical community, regardless of the specialization its members represent, has achieved a basic understanding of the main problems this virus poses. The knowledge gained throughout the pandemic concerns a wide range of issues – from the course of the disease, which is often unpredictable, through the methods of therapeutic treatment, to the emergence of the post-COVID phenomena. Since the emergence of the pandemic one of the fundamental problems encountered by the medical community has been the identification of factors that negatively influence the outcome of the infection and those that seem beneficial for the patients.

Eating habits have been analysed for years as a factor influencing the development of autoimmune diseases and susceptibility to infections. On the basis of research, observational studies and meta-analyses, special attention was paid to omega-3 and omega-6 acids. The purpose of the review is to show the importance of omega-3 and omega-6 acids as important ingredients in the healthy diet and as factors protecting against the development of the most common inflammatory rheumatic diseases. The influence of these omega-3 and -6 acids on the course of rheumatic diseases and arguments for their use as complementary therapy are also presented.

Primary Sjögren’s syndrome (pSS) is a systemic autoimmune disease that affects exocrine glands, especially salivary and lacrimal glands, leading to their progressive destruction. With highly differentiated clinical course the approach to the definition of pSS is constantly evolving and the pSS classification criteria have been modified over the past years. In the past sialography and scintigraphy were frequently used in pSS diagnostics. Recently no imaging method has been included in the pSS classification criteria. That raises the question about the benefits of using novel imaging techniques such as ultrasonography, elastography and magnetic resonance imaging to diagnose and monitor pSS patients. The purpose of this review is to evaluate the advantages and limitations of widely used imaging methods in pSS and their possible future development.

Systemic sclerosis is a chronic autoimmune disease of still not fully understood pathogenesis. Fibrosis, vascular wall damage, and disturbances of innate and acquired immune responses with autoantibody production are prominent features. Systemic sclerosis has specific subsets with different autoantibodies, and differences in the affected skin areas. The suspicion of systemic sclerosis and establishing the diagnosis will be facilitated by the criteria created by EULAR/ACR experts. The treatment of this autoimmune disease remains a challenge for clinicians and new therapeutic options are constantly sought. The occurrence of various symptoms and the involvement of many organs and systems make systemic sclerosis a multidisciplinary disease and require a holistic approach. The present article summarizes different clinical features of systemic sclerosis and the profile of autoantibodies and discusses recent rules and future perspectives in disease management.

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.

Objectives : Our study analyses the prevalence of ANA, anti-SS-A, anti-SS-B, and ACA and ACPA antibodies in patients with pSS and with dryness symptoms without pSS confirmation, and the association of ACPA and ACA antibodies with specific clinical symptoms. Materials and methods : 113 patients were divided into two groups: I – with diagnosed pSS (N = 75); and II – with dryness without pSS evidence (N = 38). Diagnostics: indirect immunofluorescence (IF; Hep-2 cell line) of antinuclear antibodies (ANA), anti-SS-A anti-SS-B antibodies determined with semi-quantitative method, autoantibody profile (14 antigens, ANA Profil 3 EUROLINE); basic laboratory, ophthalmic examination tests, minor salivary gland biopsy with focus score (FS), joint and lung evaluation, and ESSDAI questionnaire (pSS activity). Results : 88% of group I had ANA antibodies (1 : 320 titre), 5.3% at 1 : 160. Anti-SS-A antibodies were present in 88% of group I, including all ANA 1 : 160. Anti-SS-A antibodies positively correlated with greater and moderate activity of ESSDAI 5 (p = 0.046) and FS. The presence of SS-B antibodies significantly affected disease activity. ACPA present: group I – 13% (associated with higher arthritis incidence; p = 0.003); group II – 8%. ACA antibodies present in 4% of group I, but not in group II. No ACA association with interstitial lung changes (small ACA + group excludes full conclusions). Conclusions : ANA antibodies should also be considered in a titre of less than 1 : 320, but the presence of anti-SS-A antibodies is still the most important immunological marker for pSS. Anti-SS-A antibodies correlate with higher disease activity (ESSDAI ≥ 5) and higher FS. The presence of the anti-SS-B antibody was significantly affected by higher activity of the disease. The incidence of arthritis was higher in patients with ACPA+ pSS compared to ACPA– (p = 0.003). There was no relationship between ACPA and arthritis in patients with dry-type syndrome without diagnosis of pSS.

Objectives: The aim of this study was to find markers related to activation of B cells, which show a correlation with the systemic inflammation markers – erythrocyte sedimentation rate and C-reactive protein and with the intensity of in situ inflammation. Material and methods: Forty-one primary Sjögren’s syndrome (pSS) patients (33 female, 8 male) of the mean age 52.9 ±15 years were included. A group of 20 healthy volunteers was applied as a control. Erythrocyte sedimentation rate (ESR), concentration of gamma-globulins, C-reactive protein (CRP) and rheumatoid factor (RF) were measured by routine laboratory tests. Titres of antinuclear antibodies (ANAs) were determined by the indirect immunofluorescence method, while anti-SS-A/SS-B antibodies were detected by both the dot-blot method and an enzyme immunoassay. The concentrations of BAFF in sera were measured by sandwich ELISA. Biopsies of minor salivary glands were taken and the focus score (FS) was calculated. Correlations between quantitative variables were assessed using the Spearman correlation coefficient (r). Results: Serum concentrations of BAFF was significantly higher in the pSS patients than in the control group. The study revealed a statistically significant correlation between ANAs titre and the FS (r = 0.421). Anti-SS-A/Ro and anti-SS-B/La antibodies positively correlated with ESR. There was also a positive correlation between the gamma globulin level and the titres of all tested autoantibodies. Conclusions : The positive correlation between ANAs and FS confirms the importance of these autoantibodies in the local inflammatory process. The positive correlation between anti-SS-A/SS-B antibodies and ESR suggests involvement of these antibodies in generalization of the inflammatory response. In the pSS group serum concentrations of BAFF were statistically significantly higher than healthy volunteers. All presented results confirm the role of activity of B cells in the course of pSS.

Objectives: The aim of this study was to determine how often patients and undiagnosed people who complain of musculoskeletal system and rheumatic diseases look for knowledge contained on an Internet forum. Content analysis was used to identify the level of Internet users’ activity in the rheumatology section, compared to other areas of medicine. Material and methods : Material included information posted on the Internet forum established at http://medyczka.pl/. The method employed was a quantitative and qualitative analysis of the content. The method was based on qualitative assessment of the first post in each thread presented on the rheumatologic subforum, by assigning keywords, subjectively determined by the researcher, to such a post. For each keyword a specific definition was established, determining a situation in which a given keyword was used. Results: The quantitative analysis qualified rheumatology in the last place in terms of Internet users’ activity compared to other branches of medicine. The qualitative assessment of the rheumatologic forum indicated that the three most common keywords were joint pain (32), joints swelling (13), and schoolage (13). The three most common intentional keywords (arranged in order of their decreasing number) were diagnosis based on symptoms (29), interpretation of the laboratory test results (9), and how to deal with symptoms (8). Conclusions : The analysis leads to the conclusion that the rheumatologic subforum, along with other subforums listed above, presents a critically low level of discussion. There is a large disproportion between the number of active and passive forum users, suggesting that numerous individuals search the forum for presented information. Based on the qualitative analysis of the information stocks of the rheumatologic subforum, it was established that most of the questions posted concerned young individuals, who complained of joint pain and swelling, and asked for a possible diagnosis based on the presented symptomatology, interpretation of the laboratory test results and alleviation of disease symptoms.

Polymyositis (PM) is an idiopathic inflammatory myopathy that affects striated muscles. Dermatomyositis (DM) is an idiopathic inflammatory myopathy with presence of skin symptoms. Both are characterized by acute or subacute onset, symmetrical proximal muscle weakness, the presence of mononuclear cell infiltrates of the muscles and increased activity of muscle enzymes. The treatment still remains glucocorticoids and disease-modifying drugs. Symptoms of PM/DM can be a signal of developing cancer. Known risk factors for cancer in patients with PM/DM are older age, male gender, dysphagia, skin necrosis, cutaneous vasculitis, rapid onset of the disease, elevated creatinine kinase (CK) and C reactive protein (CRP), and an increase in the erythrocyte sedimentation rate (ESR). Recently three new myositis-specific autoantibodies (MSA) predicting the risk of cancer have been discovered: melanoma differentiation-associated protein 5 (anti-MDA-5), transcription intermediary factor 1γ (TIF-1γ), and nuclear matrix protein NXP-2.

Musculoskeletal pain is a very common complaint, affecting 30–40% of the European population. It is estimated that approximately 400,000 Poles suffer from inflammatory rheumatic diseases, such as rheumatoid arthritis, ankylosing spondylitis and psoriatic arthritis, and a vast majority of those affected are working-age individuals. Patients with suspected arthritis require prompt diagnosis and treatment, as any delays may result in irreversible joint destruction and disability. Currently in Poland, the lag time between the onset of symptoms and diagnosis is, on average, as much as 35 weeks. In this paper, we review the current state of specialist rheumatology care in Poland and propose a reorganised care model that includes early diagnosis of inflammatory arthritis. The main goal we wish to achieve with our reorganised model is to enhance access to outpatient specialist rheumatology care for patients with suspected arthritis. We believe that our model should make it possible to considerably reduce the lag time between GP referral and the diagnosis and treatment by a rheumatologist to as little as 3 to 4 weeks. This article provides a proposal of changes that would achieve this goal and is a summary of the report published by the Institute of Rheumatology in September 2014.

Sjögren’s syndrome is an autoimmune exocrinopathy which manifests itself with dryness of the eyes and the oral cavity. These symptoms comprise a so-called sicca syndrome (xerostomia and xerophthalmia). Two forms of this disease may be distinguished: primary Sjögren’s syndrome which affects salivary glands and secondary Sjögren’s syndrome with other autoimmune diseases present such as rheumatoid arthritis, systemic lupus erythematosus or systemic scleroderma. The diagnosis is based on the classification criteria established in 2002 by a group of American and European scientists (American-European Consensus Group), which involve the interview and physical examination as well as serological, histopathological and radiological tests. Most of these examinations show some limitations such as invasiveness, expensiveness or limited accessibility. The latest research suggests that ultrasound examination may appear promising in the diagnostics of the main salivary glands: submandibular and parotid glands. It is an accessible and relatively cheap examination with high sensitivity and specificity values which are comparable to those obtained via conventional means used in the diagnostics of this disease, i.e. biopsy of the minor salivary glands, sialography and scintigraphy, as well as superior to those obtained in sialometry and Schirmer’s test. Additionally, ultrasonography correlates with the results of magnetic resonance imaging. Therefore, a number of authors claim that US examination should be included in the classification criteria of Sjögren’s syndrome. The aim of this article is to present the diagnostic capacity of the US examination in Sjögren’s syndrome using the current ultrasound classification systems based on the grey-scale, Doppler and contrast-enhanced examinations. The latest research confirms that the most valuable diagnostic criterion in Sjögren’s syndrome is the heterogeneity of the glandular parenchyma. The outcome of the examination greatly depends on the examiner’s experience.

Ludzi kształtują czasy i okoliczności. Niekiedypodczas lektury czyjejś biografii wydajesię nam, że zawartych w niej wątków starczyłobydla kilku osób. Tak jest właśnie, gdypoznajemy szczegóły z życia prof. EleonoryReicher.

Reaktywne zapalenie stawów (reactive arthritis – ReA) należy doseronegatywnych spondyloartropatii. Jest to autoimmunologicznezapalenie stawów, poprzedzone najczęściej infekcją bakteryjnąukładu pokarmowego lub moczowo-płciowego. U 65–85% pacjentówchorujących na ReA stwierdza się obecność antygenu HLA--B27. Reaktywne zapalenie stawów jest chorobą o różnorodnejmanifestacji klinicznej dotyczącej stawów obwodowych, kręgosłupa,skóry, narządu wzroku, układu pokarmowego i innych.Różnorodność objawów powoduje, że pacjenci, zwłaszczaw początkowym okresie choroby, są leczeni przez lekarzy różnychspecjalności.Obraz kliniczny ReA jest podobny bez względu na rodzajpoprzedzającego go zakażenia, natomiast postępowanie terapeutycznemoże być uzależnione od rodzaju bakterii będącej przyczynąwcześniejszej infekcji. Zakażenie Chlamydia może byćzakażeniem przetrwałym i leczenie ReA indukowanego tymi bakteriamiopiera się na antybiotykoterapii. W innych przypadkachzastosowanie antybiotyków budzi kontrowersje. Przebieg ReAmoże być ostry i często samoograniczający. U części pacjentówdochodzi do rozwoju przewlekłego zapalenia stawów. Wczesnerozpoznanie reaktywnego zapalenia stawów i zastosowanieskutecznego leczenia może zapobiec rozwojowi przewlekłejpostaci choroby i doprowadzić do całkowitego wyleczenia.

Objawy infekcyjnego zapalenia krążka międzykręgowego mogąimitować objawy spondyloartropatii seronegatywnych i wymagaćróżnicowania wśród tych jednostek chorobowych (tab. I). Spondyloartropatieseronegatywne to grupa zapalnych chorób przebiegającychz zajęciem stawów kręgosłupa i stawów obwodowych.Wśród zapaleń kości i szpiku infekcyjne zapalenie krążka międzykręgowegostanowi ok. 2–4% wszystkich przypadków. Poniżejprzedstawiono opis przypadku 18-letniego mężczyzny diagnozowanegoz powodu podejrzenia spondyloartropatii. U pacjentawystępowały: ból kręgosłupa o charakterze zapalnym, bóle stawówobwodowych oraz epizody stanów gorączkowych. Po wykluczeniuspondyloartropatii ostatecznie rozpoznano u pacjentainfekcyjne zapalenie krążka międzykręgowego. Dzięki diagnostycemetodą rezonansu magnetycznego możliwe było postawienie diag -nozy (ryc. 1, 2) oraz ocena skuteczności leczenia (ryc. 3, 4). Niew każdym przypadku infekcyjnego zapalenia krążka międzykręgowegomożliwe jest ustalenie czynnika etiologicznego, wówczasw leczeniu należy uwzględnić potencjalne czynniki ryzyka zakażeniaoraz najczęstsze patogeny, będące przyczyną spondylodiscitis,takie jak Staphylococcus aureus (w 50% przypadków) i Escherichiacoli (23%). Brak klinicznej poprawy po 2 tygodniach optymalniecelowanej antybiotykoterapii drogą dożylną byłby wskazaniem doleczenia chirurgicznego.Womawianym przypadku rozpoznanie kliniczne potwierdził dobryefekt terapeutyczny prowadzonej antybiotykoterapii, wobec czegonie było wskazań do leczenia operacyjnego. Opisany przypadekwskazuje również na konieczność szybkiej oceny kręgosłupa pierwmetodąrezonansu magnetycznego u pacjentów z bólem zapalnymkręgosłupa i objawami ogólnymi wobec wątpliwości co do ich etiologiii braku wyjaśnienia ich przyczyny klasycznym zdjęciem radiologicznym.Ponieważ bardziej narażeni na infekcyjne zapaleniekrążka międzykręgowego są chorzy z obniżoną odpornością i chorobamiprzewlekłymi oraz leczeni glikokortykosteroidami, problemten może również wystąpić u chorych z chorobami reumatologicznymi.Zarówno diagnostyka, jak i zasady postępowania leczniczegow zapaleniu krążka międzykręgowego są istotne w praktycereumatologicznej.

Macrolides are a group of antibiotics with a distinctive macrocyclic lactone ring combined with sugars (cladinose, desosamine). The action of macrolides is to block protein synthesis by binding to the subunit of 50S ribosome of bacteria. Prototype macrolide was erythromycin, which came into clinical practice in the 50s of the 20th century. Its antimicrobial spectrum covers the scope of the penicillins but is extended to the impact of atypical bacteria. In the 90s more drugs of this group were synthesized—they have less severe side effects than erythromycin, extended spectrum of Gram-negative bacteria. Macrolides are effective in treating mycobacterial infections especially in patients infected with HIV. It is now known that in addition to antibacterial abilities, macrolides have immunomodulatory effects—they inhibit the production of proinflammatory cytokines (TNF, IL1, 6, and 8) affect transcription factors (NF-κB) as well as costimulaton (CD 80) and adhesion molecules (ICAM). This review article focused not only on the their antimicrobial abilities but also on efficacy in the treatment of several inflammatory disorders independent of the infectious agent. Their wider use as immunomodulators requires further study, which can lead to an extension of indications for their administration.