Fatigue is a prevalent symptom in various rheumatic diseases, such as rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. It is characterised as a subjective, enduring feeling of generalised tiredness or exhaustion, impacting the patient’s life quality and exacerbating disability. The fatigue nature is multifaceted, encompassing physiological, psychological, and social factors, and although the exact cause of inflammatory joint diseases is not fully understood, several factors are believed to contribute to its development. Despite high prevalence and importance, the symptom is often underestimated in clinical practice. Chronic inflammation, commonly associated with rheumatic diseases, has been proposed as a potential contributor to fatigue development. While current treatments effectively target inflammation and reduce disease activity, fatigue remains a persistent problem. Clinical evaluation of rheumatic diseases primarily relies on objective criteria, whereas fatigue, being a subjective symptom, is solely experienced and reported by the patient. Managing fatigue in inflammatory joint diseases involves a multifaceted approach. Identifying and comprehensively assessing the subjective components of fatigue in individual patients is crucial for effectively managing this symptom in everyday clinical practice.

Systemic connective tissue disorders constitute a heterogenous group of autoimmune diseases with the potential to affect a range of organs. Rheumatoid arthritis (RA) is a chronic, progressive, autoimmune inflammatory disease affecting the joints. Systemic lupus erythematosus (SLE) may manifest with multiple system involvement as a result of inflammatory response to autoantibodies. Spondyloarthropathies (SpAs) such as ankylosing spondylitis (AS) or psoriatic arthritis (PsA) are diseases characterised by the inflammation of spinal joints, paraspinal tissues, peripheral joints and enthesitis as well as inflammatory changes in many other systems and organs. Physiologically, sclerostin helps to maintain balance in bone tissue metabolism through the Wnt/β-catenin pathway, which represents a major intracellular signalling pathway. This review article aims to present the current knowledge on the role of sclerostin in the Wnt/β-catenin pathway and its correlation with clinical data from RA, SLE, AS and PsA patients.

Aseptic abscess syndrome (AAS) is a rare, potentially life-threatening disorder, with numerous features of neutrophilic dermatoses. The main symptoms include aseptic abscess-like collections in internal organs (spleen, liver, lungs), lack of microbes (bacteria, viruses, or parasites) after an exhaustive search, ineffectiveness of antibiotics, and high sensitivity to corticosteroid therapy. AAS is characterized by the development of deep, inflammatory abscesses and systemic symptoms (weight loss, abdominal pain, fever, and leukocytosis). They may be associated with inflammatory bowel disease (IBD) and autoimmune diseases. The patient in this study is a 67-year-old man, suffering from rheumatoid arthritis (RA), with numerous purulent abscesses in the mediastinum, within the subcutaneous tissue above the extension surfaces of the joints, and on the dorsum of the hands. The lesions are accompanied by bone destruction. The patient was treated with prednisone 40 mg and adalimumab, which resulted in a quick reduction of inflammatory markers and clinical improvement, as well as the healing and absorption of abscesses. Despite COVID-19 infection, treatment with remdesivir, prednisone, and adalimumab was continued, with the complete resolution of the lesions. AAS is difficult to recognize, so practitioners have to be aware of this condition, especially in patients with RA.

Macrophage activation syndrome (MAS) is one of the few entities in rheumatology with the potential to quickly cause multiple organ failure and loss of life, and as such, requires urgent clinical intervention. It has a broad symptomatology, depending on the organs it affects. One especially dangerous aspect of MAS’s course of illness is myocarditis leading to acute heart failure and possibly death. Research in recent years has proved that macrophages settled in different organs are not a homogenous group, with particular populations differing in both structure and function. Within the heart, we can determine two major groups, based on the presence of the C-C 2 chemokine receptor (CCR2): CCR2+ and CCR2−. There are a number of studies describing their function and the changes in the population makeup between normal conditions and different illnesses; however, to our knowledge, there has not been one touching on the matter of changes occurring in the populations of heart macrophages during MAS and their possible consequences. This review summarizes the most recent knowledge on heart macrophages, the influence of select cytokines (those particularly significant in the development of MAS) on their activity, and both the immediate and long-term consequences of changes in the makeup of specific macrophage populations—especially the loss of CCR2− cells that are responsible for regenerative processes, as well as the substitution of tissue macrophages by the highly proinflammatory CCR2+ macrophages originating from circulating monocytes. Understanding the significance of these processes may lead to new discoveries that could improve the therapeutic methods in the treatment of MAS.

Objectives: In this study, our aim is to summarise the available data on the correlation between sarcopenia and sleep disturbances as a consequence of changes in the myokine concentrations. Methods: Our research was conducted by searching through PubMed, Mendeley and Google Scholar. In our analysis, 63 studies are included from the years 2011 to 2025. Among these studies, there are clinical trials, cross-sectional studies, reviews, systematic reviews and meta-analyses. Discussion: There is vast evidence confirming that sleep disturbances are more common among sarcopenic patients. On the other hand, sarcopenia is frequently observed among people with worse quality of sleep. It is also well documented that sarcopenia leads to changes in the myokine serum concentrations, and similar changes are observed among people suffering from sleep disturbances. Sarcopenic patients have lower levels of irisin, BDNF (brain-derived neurotrophic factor), meteorin and IL-15 (interleukin 15) and higher concentrations of FGF-21 (fibroblast growth factor 21) and interleukins 1β, 6 and 10. Lower levels of irisin, BDNF and meteorin, and higher levels of FGF-21 and interleukins 6 and 10, lead to sleep disturbances, like insomnia, reduction of REM (rapid eye movement) sleep time and lower slow-wave activity during the NREM (non-rapid eye movement) sleep phase. These changes are also observed in obstructive sleep apnea (OSA). More severe OSA is correlated with lower levels of irisin and meteorin and higher levels of FGF-21 and interleukins 6 and 8. Conclusions: Taking into account the similarities in the myokine concentration changes in sarcopenia and in sleep disturbances, it may be concluded that alterations in the myokine levels induced by sarcopenia provoke sleep disturbances. However, it is necessary to further investigate these correlations to understand them better.

Introduction: The autoimmune/inflammatory syndrome induced by adjuvants (ASIA) is a rare condition caused by an immune response associated with over-reactivity of the immune system, triggered by adjuvants. The most common adjuvants are aluminium salts but can also be bioimplants or infectious agents. It may lead to the development of various autoimmunologic diseases. Case Report: In the following article, we present the case of a 26-year-old woman who developed SLE likely induced by ASIA syndrome after the aesthetic medicine procedures. The patient was admitted because of arthralgia and fever. She also presented with a butterfly-shaped erythema on her face and erythematous and infiltrative skin lesions on the posterior surface of the thighs and buttocks. We performed numerous diagnostic tests, including laboratory tests, immunological tests, imaging diagnostics such as chest X-ray and USG of the abdomen and joints, and the biopsy of the skin lesion on the left thigh. The results of the diagnostic process led us to diagnose SLE. The patient fulfilled the ACR/EULAR 2019 classification criteria of the SLE. Laboratory results also led to the diagnosis of autoimmune haemolytic anaemia. Due to exposure to numerous adjuvants like tattoo ink, hyaluronic acid, and piercing and the development of the delayed inflammatory reaction (DIR) to hyaluronic acid (HAF), the patient also fulfilled the criteria of ASIA. In the treatment process we applied antibiotics, non-steroidal anti-inflammatory drugs (NSAIDs), steroids, hydroxychloroquine, and cyclosporine. The treatment resulted in an improvement in the general condition, resolution of swelling and joint pain, and improvement in skin lesions. Conclusions: ASIA syndrome after bioimplantation is still underdiagnosed, probably due to ignorance or diagnostic difficulties, as symptoms are uncharacteristic and there is no immunological marker for this syndrome. In addition, as in the presented case, it can develop several years after the procedure, and it is difficult for both patient and physician to become aware of the connection. Early diagnosis requires a multidisciplinary approach and may require immunosuppressive treatment in specific cases.