Inflammatory bowel diseases (IBDs) and spondyloarthropathies (SpAs) frequently co-occur, yet the subtype-specific genetic architecture and effector tissues that implement this gut-joint coupling remain poorly defined. We integrated European-ancestry GWAS summary statistics for IBD, Crohn's disease, ulcerative colitis, ankylosing spondylitis, psoriatic arthritis, reactive arthritis and enteropathic arthritis, covering 22.21 million variants across 1,263,767 individuals. We quantified genome-wide and local sharing (S-LDSC/LDSC, ρ-HESS), identified pleiotropic loci (MTAG, CPASSOC) in trait pairs with significant genome-wide genetic correlation, and prioritized shared loci by integrating local-correlation evidence with GWAS-PW and GCTA-COJO, mapped signals to tissues/cell types (LDSC-SEG, gsMap), prioritized effector genes (UTMOST, FUSION, SMR, immune-cell scPrediXcan), and assessed directionality using bidirectional Mendelian randomization. IBD showed 16.4% liability-scale SNP heritability (CD 21.5%; UC 15.2%), whereas SpA subtype heritability ranged from 2.4% (ReA) to 62.9% (AS). Genetic correlations were positive but heterogeneous, with the strongest sharing observed for EnA-related pairs. Local genetic analyses indicated structured but uneven regional sharing across subtype pairs, with the most robust local support concentrated in PsA- and EnA-related comparisons. Tissue and cell-type analyses converged mainly on immune- and barrier-related contexts, including blood, synovial fluid, spleen, lung, and lymphoid tissues, as well as T-lineage and myeloid immune compartments. Complementary gsMap projection suggested a developmentally informed gut-immune spatial scaffold rather than a uniform anatomical pattern. Pair-specific transcriptomic integration further prioritized recurrent candidate effectors across the IBD-SpA axis, while bidirectional Mendelian randomization supported a predominantly forward component from intestinal inflammatory liability to selected SpA phenotypes. These results provide a multi-layer genetic and biological framework for gut-joint comorbidity, implicating shared immune and barrier niches and supporting a gut-first component in the IBD-SpA axis.

Reactive arthritis induced by Mycobacterium tuberculosis (M.tb) causes severe cartilage degradation, yet the underlying mechanisms remain elusive. This study investigated the molecular mechanisms and potential therapeutic targets for M.tb-induced cartilage damage. A mouse model of BCG-induced tuberculous arthritis was established. Cartilage matrix degradation, chondrocyte apoptosis, and metabolic balance were evaluated histologically and biochemically. Activation of the NF-κB p65 and STAT3 signaling pathways was assessed, followed by pharmacological inhibition. BCG infection significantly reduced cartilage matrix content and promoted chondrocyte apoptosis, disrupting the metabolic balance between matrix synthesis and degradation. Mechanistically, BCG markedly activated the NF-κB p65 and STAT3 pathways in articular cartilage. Pharmacological inhibition of these pathways effectively prevented cartilage matrix loss and reduced chondrocyte apoptosis at the protein level. BCG induces cartilage damage through activation of NF-κB p65 and STAT3 pathways, leading to chondrocyte apoptosis and matrix catabolism. Targeting these signaling cascades represents a promising therapeutic strategy for preventing cartilage degeneration in tuberculous arthritis.

Reactive arthritis after treatment with immune checkpoint inhibitors: A case report

Campylobacter species, particularly Campylobacter jejuni and Campylobacter coli, are among the leading global causes of bacterial gastroenteritis and are primarily transmitted through contaminated food, water and animal products. Despite their recognised role in enteric infections, the broader clinical and public health significance of Campylobacter remains underappreciated, particularly in developing countries such as India. Beyond gastrointestinal illness, these pathogens are increasingly associated with a range of extraintestinal complications, including bacteremia, neurological disorders and immune-mediated sequelae. Their zoonotic nature, environmental persistence, and evolving antimicrobial resistance further complicate disease management and control. In India, limited surveillance and diagnostic challenges contribute to underestimating the true burden of Campylobacter infections. This review examines the epidemiology of Campylobacter infections in India and highlights the expanding spectrum of extraintestinal manifestations associated with these pathogens. It also seeks to explore the mechanisms underlying immune-mediated complications and assess the growing concern of antimicrobial resistance in Campylobacter species. The review discusses the epidemiological trends and transmission pathways of Campylobacter, emphasizing zoonotic reservoirs, contaminated food and water, occupational exposure, and travel-related risks. It further explores extraintestinal manifestations such as bacteraemia, Guillain-Barré syndrome, and reactive arthritis, with attention to pathogenic mechanisms including molecular mimicry and immune response. Advances and limitations in diagnostic approaches, particularly the detection of Campylobacter from non-stool and systemic samples, are also addressed. Additionally. The review highlights the emerging threat of antimicrobial resistance, particularly linked to antibiotic use in animal husbandry. Finally, it underscores the importance of integrated prevention and control strategies under the One Health framework, along with strengthened surveillance, improved diagnostics and continued research to address the growing public health challenge posed by Campylobacter.

Background and objective Reactive arthritis (ReA), formerly termed Reiter's syndrome, is an autoimmune inflammatory arthritis that develops in response to a gastrointestinal or genitourinary infection. Although nearly two-thirds of patients have a self-limited course, the remaining patients go on to develop chronic symptoms and complications. In the absence of a curative treatment, the treatment goal remains the alleviation of symptoms, for which diverse treatments have been used with variable responses. Apremilast, an oral phosphodiesterase 4 (PDE4) inhibitor typically used for psoriatic arthritis and plaque psoriasis, appears to be a promising therapeutic option for ReA. This study aimed to evaluate the efficacy and safety of oral apremilast as an adjuvant therapy in patients with treatment-refractory ReA. In this study, adjuvant therapy refers to the addition of apremilast to ongoing conventional treatment with the aim of improving disease control and facilitating the reduction or discontinuation of concomitant medications such as corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDs). Material and methods This was a retrospective, observational pilot study conducted at a tertiary care center. Medical records of 12 adult patients with treatment-refractory ReA, defined according to the criteria of the Third International Workshop on Reactive Arthritis (1996), who received oral apremilast as adjuvant therapy for 40 weeks between June 2024 and May 2025, were reviewed. Apremilast was administered at a dose of 30 mg twice daily following one week of dose titration. Treatment efficacy was primarily assessed using the American College of Rheumatology 20% improvement criteria (ACR20) along with secondary outcomes including ACR50/70 responses, changes in swollen and tender joint counts, inflammatory markers, improvement in functionaloutcomes measured by the Health Assessment Questionnaire-Disability Index (HAQ-DI) status, and evaluation of the corticosteroid-sparing effect. Results The mean age of the patients at the time of diagnosis was 26.91 years (range 19-36 years). Of the patients receiving apremilast (n=12), 10 (83.33%) achieved an ACR20 response at week 40. Although observed in a smaller proportion of patients, the higher-efficacy outcome measures, such as ACR50 and ACR70 responses, were sustained over 40 weeks in eight (66.67%) and five (41.67%) patients with continued treatment. The mean swollen joint count (SJC) and tender joint count (TJC) improved by 79.3% and 68.8%, respectively, at week 40. Around two-thirds of the treated patients (n=8, 66.67%) achieved a HAQ-DI minimal clinically important difference of ≥0.35 at 40 weeks. No serious infections or any other severe adverse effects were recorded in any of the patients. Conclusions Apremilast appears to be an efficacious and safe novel therapeutic option for treatment-refractory ReA. In addition to providing direct and substantial improvements in joint-related symptoms and beneficial effects on extra-articular manifestations, its corticosteroid-sparing effect makes it a promising candidate as an adjuvant in the treatment of ReA. The results of this study warrant further validation in larger controlled trials.

We present a rare case of Poncet's disease, a sterile reactive arthritis associated with active tuberculosis (TB), mimicking seronegative spondyloarthritis in a young diabetic male. We aim to highlight the diagnostic challenges and emphasize the importance of considering Poncet's disease in patients with inflammatory arthritis, especially in the context of subclinical TB. We present a detailed case report of a 28-year-old male with poorly controlled diabetes mellitus type 2 [glycated hemoglobin (HbA1c) 13.9%] who presented with a 3-week history of bilateral ankle pain, swelling, and redness. The pain progressed to involve multiple small joints of the hands, wrists, elbows, and knees, significantly impacting his mobility, with no history of trauma, fever, rash, or urinary symptoms. Physical examination revealed tenderness and swelling in the affected joints with limited range of motion. Laboratory investigations showed an elevated erythrocyte sedimentation rate (ESR) of 74 mm/hour and C-reactive protein (CRP) of 104 mg/L. Chest X-ray revealed bilateral hilar lymphadenopathy, and computed tomography (CT) scan confirmed multiple enlarged lymph nodes in the mediastinum and bilateral hilar regions, suggestive of pulmonary TB. Despite the absence of acid-fast bacilli in bronchoalveolar lavage (BAL), the clinical presentation, imaging findings, exclusion of other causes of reactive arthritis, and a dramatic response to anti-TB therapy within days of initiation strongly supported the diagnosis of Poncet's disease. The patient completed 6 months of anti-TB therapy and achieved complete resolution of joint pain and swelling, regaining his full range of motion. The patient's symptoms, including joint pain, swelling, and inflammatory markers, significantly improved within weeks of starting anti-TB therapy. Serial CRP and ESR readings showed a downward trend, confirming the response to treatment. This case report highlights the importance of considering Poncet's disease in the differential diagnosis of seronegative spondyloarthritis, particularly in patients with underlying TB. A high index of suspicion and prompt initiation of anti-TB therapy can lead to rapid improvement in symptoms and prevent unnecessary investigations and potentially harmful immunosuppressive medications.

Reactive arthritis is a form of sterile inflammatory oligoarthritis that occurs days to weeks following a genitourinary or gastrointestinal infection presenting with joint pain and swelling. Extra-articular manifestations include uveitis, oral ulcers, urethritis, and skin rashes. It is commonly due to gram negative bacteria such as Chlamdyia, Campylobacter, Salmonella, Shigella, and Yersinia. Recently, rare pathogens such as Streptococci, Clostridium difficile, Escherichia coli, Mycoplasma pneumoniae have also been implicated. However, Abiotrophia defectiva, a gram-positive bacterium, is not listed among them. We present to the best of our knowledge the only case of Abiotrophia defectiva as a causative agent of reactive arthritis.

Advanced glycation end products (AGEs), and particularly the unique AGE10 epitope, may be a potential biomarker of immunopathology in rheumatic diseases. They may be associated with inflammation, joint damage and ossification processes. AGE10 present in human and animal tissues could be detected with monoclonal antibody against melibiose-derived glycation product MAGE synthesized in anhydrous conditions. This MAGE product was different from the classic synthesis in water solution. The epitope was determined in serum with ELISA using these anti-MAGE monoclonal antibodies. This work aims to determine serum AGE10 levels in patients with reactive arthritis (ReA)-caused with Chlamydia trachomatis (group 2) and ReA with C. trachomatis during the reactivation of EBV infection (group 3). Additionally, ankylosing spondylitis (AS) patients (group 4) were involved in the study, due to the potential evolution of ReA toward AS. The control group maintained physiological AGE10 levels (316µg/ml), while the combined infection group showed elevated AGE10 (850µg/ml) compared to the chlamydial-only group (17µg/ml). Fluorescent fAGE were at the highest level in AS patients. A striking finding was the complete absence of detectable AGE10 antigen in the AS group, coinciding with notably elevated immune complex AGE10-anti-AGE10 levels. A similar pattern was observed in patients with ReA caused by C. trachomatis alone (Group 2), albeit to a lesser extent. In contrast, both the control group and patients with ReA associated with EBV coinfection (group 3) displayed an inverse relationship, characterized by higher antigen levels and lower immune complex concentrations. Thus, diminished level of AGE10 could be caused, besides local accumulation, also by immune complexes formation, a pathogenic factor. Therefore, evaluating disease activity in ReA and AS is crucial to further our understanding of the pathophysiology of AGEs formation and predicting prognosis.

Psoriatic arthritis is a chronic inflammatory disease associated with psoriasis, and its diagnosis can be challenging owing to nonspecific symptoms, absence of reliable biomarkers, and occasional delay in skin manifestations. Herein, we report a case of psoriatic arthritis that initially presented as an acute finger inflammation mimicking infection. A 46-year-old woman developed sudden swelling and pain in the left ring finger during chemotherapy for cervical cancer. Based on the results of the physical examination, laboratory tests, and magnetic resonance imaging, pyogenic flexor tenosynovitis was suspected, and synovectomy was performed; however, bacterial and mycobacterial cultures yielded negative results. Despite the administration of antibiotics, the inflammation persisted, and she was referred to the Rheumatology Department, where she was diagnosed with reactive arthritis secondary to Chlamydia infection. Although the inflammation improved after antimicrobial therapy, the finger swelling persisted. Follow-up magnetic resonance imaging and serological testing were performed, and the patient was diagnosed with seronegative rheumatoid arthritis. Four years after onset, erythematous skin lesions appeared, and dermatological evaluation confirmed plaque psoriasis; thus, a definitive diagnosis of psoriatic arthritis was established. Disease-modifying antirheumatic drug adjustments improved symptoms, but residual 'pencil-in-cup' deformity and limited finger motion remained. This case highlights the difficulty in diagnosing psoriatic arthritis when arthritis precedes skin lesions. Clinicians should consider psoriatic arthritis in persistent or refractory arthritis and carefully monitor skin and nail changes to achieve an earlier diagnosis and prevent irreversible joint damage.

Reactive arthritis following E. histolytica infection

A 5-year-old girl presented with 15 days of insidious-onset pain in the lower legs (left > right) and mild forearm pain with gradual worsening. Examination showed normal limb bulk with tenderness along the lateral forearms and legs. Laboratory evaluation revealed leukocytosis (28,760/mm3), elevated erythrocyte sedimentation rate (29 mm/h), and elevated C-reactive protein (24 mg/L). A radiograph of the left leg was normal. Magnetic resonance imaging of both legs demonstrated diffuse hypointense marrow signal on T1- and T2-weighted images (Figure 1a), bilateral symmetrical short-tau inversion recovery hyperintensity around the fibular shafts with postcontrast enhancement consistent with periostitis (Figure 1b), and multiple irregular peripherally enhancing tibial meta-diaphyseal lesions with nonenhancing fibular shafts, consistent with bone infarcts. Bone marrow biopsy confirmed B-cell acute lymphoblastic leukemia (ALL) with BCR::ABL1 [t (9; 22) (q34.1; q11.2)]. Magnetic resonance imaging performed on day 11. (a) Coronal T1-weighted images of both legs show diffuse hypointense marrow signal (white arrows), suggestive of marrow infiltration. (b) Axial post-contrast T1-weighted images show marked perilesional enhancement (green arrows), consistent with periostitis. The patient began induction therapy with weekly vincristine and daunorubicin, intrathecal methotrexate, and daily prednisolone for 4–6 weeks. Pegylated asparaginase and daily dasatinib were added from week 2 of treatment. After 1 month, bone marrow examination was normocellular with 3% blast cells, and immunophenotyping showed only 0.18% residual B-cell lymphoblastic leukemia. Multifocal periostitis as an initial manifestation of ALL is rare. Skeletal involvement occurs in 41%–70% of pediatric ALL and may be associated with better survival, supporting the role of skeletal surveys at diagnosis. In pediatric ALL, leukemic blasts infiltrate the bone marrow, leading to medullary cavity expansion, increased intraosseous pressure, and endosteal disruption. This mechanical stress, along with cytokine-mediated periosteal irritation (e.g., interleukins and tumor necrosis factor-α), stimulates subperiosteal new bone formation, appearing radiologically as periostitis. Thus, periostitis may be the initial radiographic manifestation of ALL, even before hematologic abnormalities. Differential diagnoses for pediatric periostitis include psoriatic or reactive arthritis, hypervitaminosis A, prostaglandin therapy, hypertrophic pulmonary osteoarthropathy, pachydermoperiostosis, scurvy, infections, malignancy, and fractures, including traumatic and nonaccidental injury (e.g., battered child syndrome). Persistent or unexplained bone pain in children, even with subtle radiographic findings, carries a risk of misdiagnosis. In such cases, magnetic resonance imaging can detect marrow infiltration earlier than radiography, and hematologic evaluation is essential to exclude acute leukemia. Early recognition prevents diagnostic delay and improves outcomes. Siddhi Chawla: conceptualization (equal), investigation (equal), methodology (equal), project administration (equal), validation (equal), writing – original draft (equal), writing – review and editing (equal). Gajanand Singh Tanwar: conceptualization (equal), data curation (equal), supervision (equal), validation (equal), writing – original draft (equal), writing – review and editing (equal). The authors have nothing to report. The authors have nothing to report. The authors have nothing to report. Written informed consent was obtained from the patient's parents. The authors declare no conflicts of interest. Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

A case of reactive arthritis in a patient with advanced untreated human immunodeficiency virus due to enteroinvasive colitis

The development of inflammatory arthritis after bariatric surgery has been sporadically reported, but systematic clinical and imaging descriptions remain limited. Understanding these postoperative inflammatory patterns is crucial, and this study examines the emergence and characteristics of spondyloarthritis following bariatric procedures. We conducted a retrospective case series of patients who developed new-onset inflammatory arthritis after bariatric surgery and were evaluated at a tertiary rheumatology center between 2010 and 2025. Demographic data, pre- and postoperative Body Mass Index (BMI), and the interval between surgery and symptom onset were extracted from hospital records. Laboratory evaluations included measurement of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), as well as serological testing for antinuclear antibody (ANA), rheumatoid factor (RF), anti–cyclic citrullinated peptide antibody (anti-CCP), and human leukocyte antigen B27 (HLA-B27). Clinical features such as inflammatory back pain, enthesitis, dactylitis, psoriasis, uveitis, peripheral arthritis, and gastrointestinal symptoms were recorded. Sacroiliac radiographs and MRI scans were reviewed for sacroiliitis, bone marrow edema, structural lesions, and peripheral inflammatory findings. Treatments after symptom onset were documented. Patients were classified as axial or peripheral spondyloarthritis according to ASAS criteria, and seronegative patients with imaging-negative arthritis were categorized as undifferentiated arthritis. We describe the clinical, laboratory, and MRI features of 14 patients who developed inflammatory arthritis following bariatric surgery, highlighting patterns of axial and peripheral involvement. Six patients (42.9%) had axial spondyloarthritis with MRI-confirmed sacroiliitis, and seven (50%) had peripheral spondyloarthritis—four with MRI-confirmed peripheral inflammation, one with HLA-B27–associated arthritis, and two with reactive arthritis following infection. One patient (7.1%) had undifferentiated arthritis despite negative serologic, microbiologic, and imaging evaluations. The mean age was 48.1 ± 12.3 years, and the mean latency from surgery to symptom onset was 56.7 ± 31.6 months. Enthesitis (35.7%), dactylitis (42.9%), and inflammatory low back pain (78.6%) were common. All patients had prior NSAID exposure, and 6 required biologic or targeted therapy. This case series provides a descriptive overview of inflammatory arthritis phenotypes observed after bariatric surgery and should be regarded as hypothesis-generating, warranting confirmation in larger, controlled studies. Despite substantial postoperative weight loss, a subset developed clinically significant inflammatory disease requiring advanced therapies.

Background. Chlamydia-induced urogenic reactive arthritis (x/iUREA) is a complex interdisciplinary problem, as its clinical manifestations are characterized by a combined lesion of the urogenital tract, joints, skin, mucous membranes and other organs. Despite belonging to the group of spondylarthritides, the leading role in the primary diagnosis and management of patients belongs to the dermatovenereologist. Polymorphism and non-simultaneous manifestation of symptoms, along with the frequent subclinical course of urogenital inflammation, cause significant difficulties in timely diagnosis and often lead to the chronicization of the process. Objective. To study and systematize the clinical features of x/uUREA in male patients living in the Moscow region, as well as to assess the diagnostic significance of immunomorphological examination of intact skin using direct immunofluorescence (DIF) in this disease. Materials and methods. A prospective study was conducted on 65 men with a verified diagnosis of x/uUREA who were hospitalized in the Department of Dermatovenereology at the Moscow Regional Research Institute of Dermatology and Venereology. All patients underwent a comprehensive clinical and laboratory examination, which included detection of chlamydia infection, assessment of joint syndrome, urethroscopy, examination of prostate secretion, dermatological examination, and immunomorphological examination of intact skin biopsies. Results. The average age of the patients was 30 [24; 39] years. The average duration of the disease before hospitalization was 12 [6; 24] months, and only 6.2% of patients were hospitalized in the first 3 months of the disease. All patients (100%) were diagnosed with a combination of arthritis and chronic urethroprostatitis of chlamydial etiology, and in 30.8% of cases, the urogenital inflammation was asymptomatic. Eye lesions were detected in 44 (67.7%) patients, and dermatological lesions (skin and/or mucous membranes) were detected in 60% of patients, with circinous/xerotic balanitis (46.2%) and psoriiform rashes (27.7%) being the most common. The classic triad of symptoms (urethritis-arthritis-eye damage) was diagnosed in 30.8% of patients, the tetrad (with inclusion of dermatological pathology) – in 36.9%. Axial lesions (mainly sacroiliitis) were found in 69.2% of patients. In an immunofluorescence study, diffuse deposits of IgG were detected in the reticular layer of the dermis of apparently healthy skin in 95.3% of cases. Conclusion. Chronic urogenital reactive arthritis is characterized by pronounced clinical polymorphism. Its obligate, although often asymptomatic, manifestations include damage to the urogenital tract, as well as joint syndrome, which necessitates mandatory testing for chlamydia infection in all men with asymmetric arthritis. Although not pathognomonic, dermatological symptoms are observed in more than half of patients and have several distinctive features. The inclusion of an immunomorphological study (direct immunofluorescence method) in the diagnostic algorithm, aimed at detecting IgG deposits in the reticular layer of the dermis, can serve as an additional laboratory marker of the disease, reflecting the systemic immune-mediated nature of inflammation in this pathology.

Background and Objective: Clavicular pain and swelling in children can have multiple causes and often require a multidisciplinary approach. We aimed to describe the characteristics and final diagnoses of children with clavicular involvement and to review the literature on this topic. Methods: We retrospectively reviewed patients younger than 18 years who were evaluated for clavicular symptoms at two pediatric rheumatology centers and one pediatric oncohematology center. These data were then descriptively compared with findings from 63 patients reported across 7 published articles. Results: Twelve patients (9 females, median age 10 years [IQR 9.4–10.5]) were included. Final diagnoses were chronic nonbacterial osteomyelitis (CNO; 8), Langerhans cell histiocytosis (LCH; 2), reactive arthritis (1), and Tietze syndrome (1). Clavicular involvement was mostly unilateral and localized to the medial clavicle in CNO. The most frequent presenting symptom was local swelling (11/12), followed by pain (9/12). Diagnostic delay was a median of 4 months (IQR 1–10.5). Whole-body MRI revealed multifocal lesions in 6/8 CNO patients. Biopsy was often required for diagnosis primarily to exclude malignancy and to clarify atypical or unifocal presentations. The literature review confirmed CNO as the most frequent cause, followed by rare tumors. Conclusions: CNO predominates among pediatric non-traumatic clavicular lesions, but LCH and rare conditions are not uncommon, underscoring the need for careful differential diagnosis and targeted imaging.

Abstract Background Spondyloarthritis (SpA) represents the most common extraintestinal manifestation observed in patients with Inflammatory Bowel Disease (IBD), with an estimated prevalence of approximately 15%. SpA, encompasses a group of disorders —including radiographic ankylosing spondylitis, psoriatic arthritis, reactive arthritis, non-radiographic axial SpA, undifferentiated SpA, and IBD-associated SpA—characterized by similar clinical, radiological and genetic features. The similarities between SpA and other non-SpA spondyloarthropaties often complicates differential diagnosis. In this context, multidisciplinary collaboration can facilitate accurate classification and early diagnosis, enabling timely intervention and preventing long-term structural damage. This cross-sectional study evalutes the impact of a collaborative multidisciplinary approach between gastroenterologist and rheumatologist on the early diagnosis of IBD-related spondylarthritis (IBD-SpA) and its differentiation from other musculoskeletal manifestations. Methods This is cross-sectional study in which IBD out-patients were evaluated simultaneously by a gastroenterologist and a rheumatologist. Patients underwent a comprehensive rheumatologic assessment, the DETAIL questionnaire and laboratory and imaging investigations if indicated. The suspected cases were classified as newly diagnosed IBD-SpA, alternative diagnoses, or nonspecific arthralgias. Results A total of 605 IBD patients were screened for IBD-spA (Table 1). Among them, 81 (13%) had a known diagnosis of SpA, and 117 (19.3%) were suspected of having IBD-SpA. Upon further assessment, SpA was confirmed in 18 (15%) suspected cases, yielding a 22% relative increase in SpA prevalence. mostly identified within the first year of symptom onset (44% of cases). A longer diagnostic delay was observed in patients with axial vs peripheral involvement (mean ±SD 12.4 ± 10.2 vs 2.9 ± 2.9, p = 0.035). SpA was excluded in 85% of suspected cases, which were ultimately diagnoses as other arthropaties (60%) or non-specific arthralgias (25%). Figure 1. Swollen joint count was the only predictor of SpA diagnosis (adjOR 5.70, 95%CI 2.18-1.61, p < 0.001). Finally, while 67% of patients with suspected SpA reported back pain, only 18% met ASAS criteria for inflammatory back pain. Magnetic Risonance Imaging was performed in all patients with IBP, showing evidence of sacroiliitis and/or spondylitis in 24% of cases. Conclusion A multidisciplinary approach significantly enhances the early and accurate identification of IBD-SpA. This strategy improves diagnostic accuracy, facilitating timely intervention and tailored management for affected patients.

ObjectiveTo investigate the correlation and association between dynamic contrast–enhanced magnetic resonance imaging (DCE‐MRI) quantification (DEMRIQ) parameters with local and systematic markers of inflammation in patients with various etiologies of acute knee arthritis.MethodsIn a cross‐sectional setting, patients with symptoms of acute knee arthritis underwent DCE‐MRI, and DEMRIQ parameters were acquired. Markers of inflammation were obtained from the blood and synovial fluid through ultrasound‐guided arthrocentesis of the affected joint. Spearman correlation and linear regression were performed to assess the correlation and association between DEMRIQ parameters and markers of inflammation, respectively.ResultsForty‐one patients, including 12 with rheumatoid factor–positive rheumatoid arthritis (RF+RA), 6 with rheumatoid factor–negative RA (RF−RA), 6 with psoriatic arthritis, 3 with reactive arthritis, and 14 with osteoarthritis (OA), were imaged. In the RF+RA group, all DEMRIQ variables correlated significantly with joint fluid interleukin‐6 level (r ≥ 0.6) and number of neutrophils and polymorphonuclear (PMN) cells (r ≥ 0.8), whereas MExNvoxel and IRExNvoxel correlated with synovial inflammatory cells and blood C‐reactive protein (CRP) levels (r ≥ 0.6). In patients with RF−RA, MExNvoxel correlated with blood CRP level (r = 0.8), joint fluid white blood cells, and neutrophils and PMN cells (r = 1). In the seronegative arthritis group, IRExNvoxel correlated with blood CRP, joint fluid PMN cells, and neutrophils (r ≥ 0.7). No significant correlation was seen in the OA group. There was a significant regression correlation between MExNvoxel and inflammatory infiltrates from joint fluid in RF+RA group (P < 0.05).ConclusionDEMRIQ parameters exhibit varying relationships with local synovial and systemic inflammatory blood biomarkers across different etiologies of knee arthritis, which could provide insight into the level of inflammation in the affected joint.

A woman in her 50s contracted Coronavirus disease 2019 (COVID-19), initially presenting with mild symptoms, and managed conservatively. However, she developed a persistent low-grade fever and insidious joint pain for 1 month, prompting further evaluation. Chest computed tomography revealed bilateral pulmonary infiltrates, leading to hospitalization for COVID-19-associated pneumonia. Despite a 2-week course of ceftriaxone and azithromycin, her condition remained unchanged. Postadmission testing revealed elevated rheumatoid factor, anti-cyclic citrullinated peptide (CCP) antibodies, and matrix metalloproteinase-3, suggesting an inflammatory or autoimmune process. Given concerns for immune-mediated inflammation, she was treated with high-dose methylprednisolone. With pneumonia improvement, she was discharged on oral prednisolone (PSL) (20 mg/day) with a planned taper. Her joint symptoms resolved, and anti-CCP antibody levels normalized during steroid therapy. However, upon PSL tapering and discontinuation, her joint pain recurred, and anti-CCP antibodies became positive again. A rheumatology consultation confirmed rheumatoid arthritis (RA). This case provides rare longitudinal documentation of dynamic anti-CCP antibody changes that paralleled clinical disease activity, illustrating the progression from postviral reactive arthritis to classifiable RA. It underscores COVID-19's potential to trigger autoimmune dysregulation and highlights the need for long-term follow-up with serial autoantibody monitoring in patients with persistent musculoskeletal symptoms after infection.

Arthritis associated with sexually transmitted infections (STI) is a significant clinical problem, encompassing reactive arthritis (ReA) and septic arthritis. ReA is an immune-mediated inflammatory response to a distant infection, often caused by Chlamydia trachomatis, whereas septic arthritis, such as gonococcal arthritis (Neisseria gonorrhoeae), results from direct entry of the pathogen into the joint. Syphilitic arthritis (Treponema pallidum) is a rarer but potentially devastating late manifestation. This review summarizes the current knowledge on the pathogenesis, clinical manifestations, diagnosis, treatment, and prevention of these conditions. Particular attention is paid to key differences between them, diagnostic approaches, including nucleic acid amplification tests and serology, and therapeutic strategies, such as antibiotic therapy and immunomodulatory drugs, including Janus kinase inhibitors. The importance of an interdisciplinary approach and preventive measures in management of patients with STI-related arthritis is emphasized.

Acute rheumatic fever (ARF) and post-streptococcal reactive arthritis (PSRA) are complications of infection caused by group A β-hemolytic streptococcus. These conditions share similar clinical manifestations but differ substantially in prognosis and treatment strategies. In clinical practice, differential diagnosis remains challenging, particularly in the absence of cardiac involvement or other major Jones criteria for ARF. Aim - to demonstrate the diagnostic difficulties in distinguishing ARF from PSRA using a clinical case of an adolescent with acute polyarthritis and a pronounced inflammatory response following streptococcal infection. Clinical case. We analyzed clinical data from a 14-year-old patient, including medical history, physical examination, laboratory parameters, instrumental investigations (еlectrocardiogram, echocardiography, and ultrasound evaluation of joints), and treatment strategy. The patient presented with fever, polyarthritis, a pronounced systemic inflammatory response (high C-reactive protein, elevated erythrocyte sedimentation rate, leukocytosis), and a markedly elevated antistreptolysin-O titer (3200 IU/mL), findings compatible with the Jones criteria for ARF. However, the characteristics of arthritis - non-migratory and prolonged, with a poor response to non-steroidal anti-inflammatory drugs (NSAIDs) and absence of carditis - favored the diagnosis of PSRA. Glucocorticoid therapy was required due to insufficient response to NSAIDs. Conclusions. This case illustrates the complexity of differentiating PSRA from ARF in the presence of overlapping clinical features and a pronounced inflammatory response. In such situations, dynamic clinical monitoring, assessment of treatment response, and surveillance for potential development of carditis over the following months are essential. Timely diagnosis and appropriate management of streptococcal infections remain the cornerstone of preventing post-streptococcal complications. The study was conducted in accordance with the principles of the Declaration of Helsinki. Informed consent was obtained from the patient and his parents prior to study participation. The authors declare no conflict of interest.