Diagnostic delay in spondyloarthritis (SpA) results in the occurrence and progression of structural damage, which is irreversible and presented by a unique combination of inflammation-induced bone loss (erosions, periarticular and systemic osteoporosis), together with new bone formation and extraosseous ossification (ligaments/entheses). The most significant opponent of diagnostic delay is misdiagnosis, leading to incorrect treatment with its complications, together with the consequences of an untreated but present disease. In the second part of the review, the problems of early diagnosis in axial spondyloarthritis (axSpA) and psoriatic arthritis (PsA) will be considered - related to the available criteria, the accessible diagnostic methods, or arising from other factors (related to the patient or the systems for specialized medical care).
Synovial fluid offers a direct window into the intra-articular environment, but individual biomarkers rarely separate arthritis subtypes reliably. This narrative review compares conventional tests with cytokines, proteomic markers, extracellular vesicles, microRNAs, metabolomics, and machine-learning-assisted multi-omics across rheumatoid arthritis, osteoarthritis, psoriatic arthritis, septic arthritis, periprosthetic joint infection, crystal-induced arthritis, connective tissue disease-associated arthritis, and Lyme arthritis. Relevant publications from 2017–2026 were identified through structured searches of PubMed, Scopus, Web of Science, and Google Scholar, supplemented by manual screening of reference lists; selection prioritized systematic and narrative reviews, translational studies, and clinically relevant biomarker investigations, and reporting followed the SANRA framework for narrative reviews. The most clinically mature applications remain conventional cell count, crystal analysis, microbiological testing, and alpha-defensin assessment for periprosthetic joint infection, whereas extracellular vesicles, microRNAs, and multi-omics remain largely translational.
Psoriatic arthritis (PsA) is associated with increased cardiovascular morbidity and mortality that cannot be fully explained by traditional cardiovascular risk factors. Adhesion molecules, particularly intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), have emerged as important mediators linking chronic inflammation with endothelial dysfunction and atherosclerosis. To review current evidence regarding the role of adhesion molecules in endothelial dysfunction and cardiovascular disease in patients with psoriatic arthritis. A narrative literature review was conducted using PubMed, Scopus, and Web of Science databases. Studies evaluating ICAM-1, VCAM-1, endothelial dysfunction, subclinical atherosclerosis, and cardiovascular risk in PsA were identified and analyzed. Available evidence demonstrates that elevated adhesion molecule levels are associated with endothelial dysfunction, increased carotid intima-media thickness, inflammatory activity, and cardiovascular risk in PsA. Histopathological studies further support their involvement in synovial and vascular inflammation. Recent data suggest that VCAM-1 may be more closely associated with inflammatory burden and endothelial activation than ICAM-1. Emerging evidence also indicates that modern biologic and targeted therapies may influence adhesion molecule expression. Adhesion molecules play an important role in the pathogenesis of endothelial dysfunction and atherosclerosis in PsA. VCAM-1 appears to be a promising candidate biomarker of endothelial activation, although its prognostic value remains to be established.
Background: Hidradenitis suppurativa (HS) is an inflammatory skin disease primarily affecting large folds, which can be associated with spondyloarthritis (SpA). However, the rare coexistence of HS, SpA, and demyelinating lesions presents significant challenges in therapeutic decision-making, especially when resistant to first-line therapies. Case Presentation: We report the case of a 17‐year‐old boy with a three-year history of stage III hidradenitis suppurativa (HS) who presented with chronic inflammatory back pain for three months and a two-month history of a waddling gait. Initial treatments, including topical and oral antibiotics, failed to control his skin lesions. Physical examination revealed lumbar stiffness, positive sacroiliac tests, and brisk lower limb reflexes. Pelvic X-ray revealed bilateral stage III sacroiliitis, and brain MRI showed T2 and FLAIR hyperintensities suggestive of demyelinating lesions. Extensive workup, including cerebrospinal fluid analysis and normal levels of ANA, anti‐DNA, anti‐NMO, anti‐MOG antibodies, syphilitic and HIV serologies, vitamin B12, and folate, concluded to non-specific demyelinating lesions. A diagnosis of radiographic axial SpA and peripheral enthesitis associated with HS was established. Worsening skin condition prompted initiation of anti-TNF-α therapy (adalimumab) after multidisciplinary consultation. His gait disturbances improved with physiotherapy, with neurological evaluation favoring a functional origin. Conclusion: Managing concurrent HS and SpA with demyelinating lesions is challenging. Although anti-TNF-α therapy is effective for HS and SpA, its link to demyelinating diseases demands caution. Further research is needed to refine treatment strategies and improve patient outcomes.
Background: Gastrointestinal (GI) involvement in systemic lupus erythematosus (SLE) is uncommon and often presents with nonspecific symptoms that mimic primary gastrointestinal disorders or postoperative complications, resulting in delayed diagnosis and inappropriate management. Lupus enteritis is a rare but potentially life-threatening manifestation of SLE and may occasionally represent its initial presentation, further complicating the diagnostic process. Case Presentation: A 27-year-old woman presented with a one-year history of persistent nausea, vomiting, and progressive weight loss leading to severe malnutrition. She had previously undergone abdominal surgery for presumed gastrointestinal disease without clinical improvement. During hospitalization, she developed systemic manifestations including alopecia, pancytopenia, hypocomplementemia, and positive antinuclear antibodies, raising suspicion for active SLE. Contrast-enhanced abdominal computed tomography demonstrated small-bowel wall thickening with a target sign and mesenteric vessel engorgement, findings consistent with lupus enteritis. Endoscopic evaluation excluded structural obstruction and malignancy. Based on the integration of clinical, serological, and radiological findings, a diagnosis of lupus enteritis as the initial presentation of SLE was established. Treatment with high-dose corticosteroids followed by cyclophosphamide resulted in rapid clinical, nutritional, and hematologic improvement. Conclusion: Lupus enteritis should be considered in patients with persistent unexplained gastrointestinal symptoms, particularly when accompanied by systemic autoimmune features. Recognition of characteristic radiologic findings together with serologic evidence of disease activity is crucial for timely diagnosis. Early immunosuppressive therapy may prevent unnecessary surgical interventions and reduce the risk of serious complications.
