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Case Report

Case Report of Gouty Arthritis Complicated by Septic Arthritis

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DOI:

10.3791/69787

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March 13th, 2026

 ,  ,  ,  ,  ,  , 
1The First School of Clinical Medicine, Zhejiang Chinese Medical University, 2Department of Orthopedic Surgery, the First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), 3Fenghua District Traditional Chinese Medicine Hospital of Ningbo

In This Article

Erratum Notice

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Summary

This protocol describes combined medical and surgical management for diagnosing and treating gouty arthritis complicated by septic arthritis.

Abstract

Gouty knee arthritis shares numerous clinical similarities with septic knee arthritis. Core overlapping manifestations include sudden onset of unilateral knee symptoms such as redness, swelling, heat, and pain, accompanied by significant functional impairment and restricted mobility. Inflammatory markers like erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are often markedly elevated in both conditions. Early imaging studies typically fail to reveal bone destruction. Due to highly overlapping clinical presentations, misdiagnosis between the two conditions is common, often requiring joint aspiration and synovial fluid analysis for definitive diagnosis. This report describes a case of gouty arthritis complicated by suppurative arthritis. The patient presented with a sudden onset of swelling and pain in the right knee lasting 2 days, accompanied by increased skin temperature and limited mobility. The patient had no prior history of gout and was otherwise in good health. Routine synovial fluid analysis showed a white blood cell count of 4+ and a red blood cell count of 1+. Culture identified Staphylococcus aureus (MRSA) in the sample. After vancomycin treatment, symptoms significantly improved, and the patient was discharged 1 week later. However, 2 days post-discharge, the patient returned with recurrent knee swelling and pain. Following a multidisciplinary consultation, arthroscopic debridement was performed. Intraoperative findings revealed extensive chalky crystal deposits within the joint cavity. Postoperative pathology confirmed gouty arthritis. The patient was discharged after symptom resolution following postoperative allopurinol therapy to reduce uric acid levels. This case underscores the importance of early differentiation between gouty arthritis and septic arthritis in clinical practice, as well as the necessity of scientific management.

Introduction

Gouty arthritis (GA) is an inflammatory disease caused by the deposition of monosodium urate (MSU) crystals in the joints, surrounding soft tissues, tendons, and other sites. Clinically, it manifests as acute joint redness, swelling, and pain, initially affecting a single joint, with 50% of cases occurring in the first metatarsophalangeal joint1. Gout predominantly affects the lower extremities, such as the dorsum of the foot, heel, ankle, and knee joints, though the fingers, elbows, wrists, and shoulders may also be involved2,3. Statistics indicate that the prevalence of gout in Western countries ranges from 2.7% to 6.7%, reaching 9.7% in individuals over 80 years old. In China, the prevalence is approximately 1.1%, but with changes in dietary patterns, the incidence of gouty arthritis shows an increasing trend year by year4,5. Even in the United States, the prevalence of gout has nearly doubled over the past few decades6.

Acute gout attacks, also termed acute aseptic inflammation, involve an acidic internal environment and MSU crystal-activated signaling pathways in macrophages and neutrophils. This leads to a massive accumulation of these cells within the joint cavity, making concurrent septic arthritis highly unlikely during gout attacks7. However, the presence of MSU crystals does not preclude infection8,9,10. Studies indicate that among patients with monoarticular gout, the incidence of infectious arthritis complicating crystal-induced arthropathy ranges from 1.5% to 5.2%11,12. Previous reports have described GA complicated by septic arthritis (SA), but these cases all had relevant histories, such as prior gout, long-term steroid use, or surgical history13,14,15. In our case, the patient had no relevant history, and the onset was extremely rapid. Under combined medical and surgical management, the patient's symptoms improved significantly, function was restored, and the patient ultimately recovered and was discharged.

Case presentation
A 46-year-old patient presented with swelling and pain in the right knee joint for 2 days. On examination, the right knee exhibited pain, redness, elevated skin temperature, limited range of motion, low-grade fever, and night sweats. The patient reported that the knee pain began after a cold, with an intensity of 10/10 on the pain scale, worsening with activity. The patient is otherwise healthy with no significant medical history. On admission, the patient's temperature was 100.4 °F (38.0 °C), blood pressure was 149/88 mmHg, and heart rate was normal. Cardiac, pulmonary, abdominal, and neurological examinations were unremarkable. Physical examination revealed swelling of the suprapatellar pouch on the right knee with elevated skin temperature. Both active and passive range of motion were restricted. Muscle strength in both lower extremities was normal. Distal pulses in both limbs were present. Pathological reflexes were absent. Upon admission, an emergency magnetic resonance imaging (MRI) was performed, and blood and joint fluid samples were collected for testing (Table 1, Figure 1).

Synovial fluid culture was initiated immediately upon admission. The joint fluid appeared pale yellow. Given the patient's elevated inflammatory markers, we promptly administered coverage therapy with linezolid plus levofloxacin. After 3 days, the synovial fluid culture identified methicillin-resistant MRSA, prompting antibiotic adjustment to vancomycin. The patient's symptoms gradually improved. After 1 week, blood tests and synovial fluid culture were repeated (Table 1), with the synovial fluid culture returning negative. The patient was discharged after 1 week of treatment with vancomycin tablets.

After 2 weeks, the patient presented again with swelling and pain in the right knee. On examination, the right knee remained painful, red, and warm to the touch, with marked limitation of movement and severe pain. Upon admission, the patient's temperature was 99.5 °F (37.5 °C), with normal heart rate and blood pressure. Cardiac, pulmonary, abdominal, and neurological examinations were unremarkable. Blood and joint fluid samples were collected for further analysis (Table 2, Figure 2). Intravenous vancomycin therapy was initiated. Concurrently, a multidisciplinary consultation was convened. Tuberculosis antibody testing and Mycobacterium tuberculosis/Rifampin (MTB/RIF) assay were performed, yielding negative results that ruled out knee tuberculosis. Additional tests, including Human Leukocyte Antigen B27 (HLA-B27), Cyclic Citrullinated Peptide (CCP), antinuclear antibody (ANA), RF, and Antistreptolysin O (ASO), were conducted, all of which were negative, excluding rheumatoid arthritis and autoimmune diseases. Following a multidisciplinary discussion, surgical intervention was decided. We performed arthroscopic lavage and synovectomy of the right knee, placing one medicated catheter and one drainage tube. Intraoperatively, we observed diffuse synovial congestion and edema with extensive white, chalky crystals throughout the joint cavity. Three soft tissue samples were obtained for microbiological culture, one of which grew MRSA. Postoperative pathology revealed extensive neutrophilic infiltration and abscess formation with a foreign body giant cell reaction, consistent with gouty arthritis. After 1 week of catheter irrigation with negative synovial fluid cultures, the medication catheter and drainage tube were removed. Follow-up blood tests showed improved blood parameters (Table 2).

Diagnosis, Assessment, and Plan:
During the 1st hospitalization, we diagnosed a knee joint infection caused by MRSA. Initial treatment involved coverage with linezolid plus levofloxacin. After the synovial fluid culture results returned, we switched to vancomycin therapy. The 2nd hospitalization revealed a diagnosis of gouty arthritis complicated by knee joint infection based on postoperative pathology findings. Postoperatively, we irrigated the joint cavity with vancomycin for 1 week while administering intravenous vancomycin for infection control and etoricoxib for pain relief. Once pain subsided, we initiated allopurinol 20 mg orally once daily to lower uric acid levels. Following discharge, vancomycin was continued for 4 weeks to combat infection, with long-term uric acid control maintained at 180-300 µmol/L.

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Protocol

Written informed consent for the use of medical history and clinical images was obtained from patients in accordance with institutional guidelines. Patient identifiers are anonymized in all documentation. This study was reviewed and approved by the Ethics Committee, approval number: 2025-KLS-511-01. This case report and any accompanying images have been published with the patient's written informed consent.

1. Patient preparation

  1. The study included a 46-year-old male patient presenting with acute swelling and pain of the right knee. Upon admission, demographic information, detailed medical history, and prior episodes of joint disease were documented. No history of gout, immunosuppressive medication, or previous joint surgery was identified.

2. Clinical and radiological examination

  1. A standardized physical examination of the right knee was performed by an orthopedic specialist. This included inspection for gross swelling and erythema, palpation for localized warmth and joint effusion (assessed via the patellar tap test and bulge sign), and assessment of active and passive range of motion using a goniometer. Pain intensity was recorded using a numerical rating scale (0 = no pain, 10 = worst possible pain)16.
  2. MRI of the affected right knee was performed using a 1.5-Tesla superconducting MRI scanner with a dedicated extremity coil. The patient lies supine. The affected knee joint was placed in the center of the scanning gantry and fixed with a limb coil to minimize motion artifacts.
  3. The joint was kept in slight external rotation and approximately 10°-15° of flexion for better visualization of the anterior cruciate ligament and meniscus. All images were independently reviewed by two musculoskeletal radiologists with 10 and 15 years of experience, respectively. The evaluation included: the amount and distribution of joint effusion, synovial thickening, bone marrow edema, bone erosion or osteoporosis, the integrity of the cruciate and collateral ligaments, meniscus, and changes in periarticular soft tissues, including abscesses or bursitis. Disagreements in interpretation were resolved through consultation.

3. Synovial fluid aspiration and laboratory tests

  1. The procedure was performed with the patient supine, right knee flexed at approximately 30° with a pillow under the knee to relax the quadriceps and open the joint space. After strict skin disinfection using a three-step method with 70% alcohol and 10% povidone-iodine, the area was covered with a sterile drape, and subcutaneous and local infiltration anesthesia of the joint capsule was administered using 3 mL of 1% lidocaine.
  2. A high-frequency linear array probe was used, covered with a sterile probe sheath, to locate the area of ​​maximum effusion in the suprapatellar bursa under real-time ultrasound guidance, avoiding adjacent blood vessels using color Doppler. Using a manual technique, a 20G lumbar puncture needle connected to a 20 mL sterile syringe was inserted into the joint cavity under continuous ultrasound guidance.
  3. After gently aspirating to obtain joint fluid, aspiration continued until 30 mL of joint fluid was obtained, which was immediately aliquoted into multiple sterile containers and sent to the laboratory. After needle removal, firm pressure was applied to the aspiration site for 2-3 min to achieve hemostasis. A sterile adhesive bandage was applied. The patient was observed for 30 min for any immediate complications such as bleeding or vasovagal reactions. The knee was rested for 24 h post-procedure.
  4. The aspirated synovial fluid was immediately subjected to comprehensive analysis. Gross appearance was assessed by visual inspection, noting color, clarity, and viscosity. For cell counting, a small aliquot of non-centrifuged synovial fluid was loaded into a Neubauer hemocytometer, and white blood cell counts were performed manually under light microscopy.
  5. Differential count was performed on Wright-stained smears to determine the percentage of polymorphonuclear neutrophils. For crystal analysis, a drop of synovial fluid was placed on a clean glass slide, coverslipped, and examined under compensated polarized light microscopy to identify monosodium urate crystals or calcium pyrophosphate dihydrate crystals.
  6. Gram staining was performed by heat-fixing a smear of synovial fluid, applying crystal violet, iodine, alcohol decolorizer, and safranin counterstain sequentially, then examining under oil immersion for bacterial morphology and Gram reaction. For bacterial culture, synovial fluid was inoculated onto blood agar plates and chocolate agar plates using sterile loops and incubated at 36 °C in 5% CO2 for 48 h. Bacterial identification was performed using standard biochemical tests or automated systems when growth was observed.
  7. Simultaneously, peripheral venous blood was collected for comprehensive laboratory evaluation. Complete blood count was performed using an automated hematology analyzer with differential counting to assess leukocytosis and left shift. Erythrocyte sedimentation rate was determined by the Westergren method, measuring the distance erythrocytes fall in 1 h in a standardized pipette.
  8. C-reactive protein was quantified by immunoturbidimetric assay on a Cobas analyzer, with results >10 mg/L indicating significant inflammation. Procalcitonin was measured using electrochemiluminescence immunoassay, with levels >0.5 ng/mL suggesting bacterial infection and >2.0 ng/mL strongly indicating sepsis.
  9. To exclude other potential etiologies, a panel of immunological and infectious disease tests was performed. HLA-B27 testing was conducted by flow cytometry using specific monoclonal antibodies. Cyclic Citrullinated Peptide antibodies were detected by ELISA. Antinuclear antibody testing was performed by indirect immunofluorescence on HEp-2 cells. Rheumatoid factor was measured by immunoturbidimetric assay. Antistreptolysin O titers were determined by latex agglutination. For tuberculosis evaluation, the MTB/RIF assay was performed on synovial fluid to detect Mycobacterium tuberculosis DNA and rifampin resistance.

4. Medical management

  1. Initial empiric antibiotic therapy with linezolid 600 mg was administered intravenously every 12 h, combined with levofloxacin 500 mg administered intravenously 1x daily. At 2 days after synovial fluid culture, MRSA was cultured. Antimicrobial susceptibility testing was performed using a VITEK 2 AST-GP67 card.
  2. The systematic report showed that the strain was sensitive to vancomycin, with a MIC of 1 µg/mL (according to CLSI criteria: sensitive ≤2 µg/mL, intermediate 4-8 µg/mL, resistant ≥16 µg/mL). Based on this result, the antibiotic regimen was adjusted to vancomycin, with an initial intravenous dose of 2000 mg over 2 h, followed by a maintenance dose of 1000 mg every 12 h. Renal function was monitored daily, and the dose was adjusted according to creatinine clearance.

5. Surgical intervention

  1. Timing of surgery and indications for reoperation: The patient was readmitted 2 weeks after the initial discharge (approximately 21 days after the initial visit). After readmission, despite the resumption of intravenous vancomycin therapy, the patient continued to experience swelling, severe pain, redness, increased skin temperature, and limited mobility in the right knee, accompanied by low-grade fever.
  2. Follow-up blood tests showed persistently elevated ESR and CRP, and joint fluid analysis showed a white blood cell count of 150,000/mm3 and neutrophils of 95%. Given that standard antibiotic treatment failed to control symptoms 48 h after readmission, and that a large joint effusion and severe pain recurred rapidly, a multidisciplinary consultation was organized involving orthopedics, infectious diseases, respiratory medicine, critical care medicine, and rheumatology.
  3. The consensus was that surgical intervention was clearly indicated for the following reasons: (1) persistent infection was suspected despite the use of targeted antibiotics; (2) there may be undiagnosed comorbidities (such as gout, rheumatoid arthritis, tuberculosis); and (3) if the infection remained uncontrolled, there was a risk of rapid joint destruction. After ruling out tuberculosis and autoimmune diseases, arthroscopic surgery was scheduled on the 3rd day of the second hospitalization.
  4. Preoperative preparation: Complete blood count, coagulation function tests, and electrocardiogram were performed to assess anesthesia tolerance. The right knee joint was marked as the surgical site, and vancomycin 1000 mg was administered intravenously prophylactically 30 min before the incision, continuing the established treatment regimen.
  5. The patient was placed in a supine position. A pneumatic tourniquet was applied to the right groin. First, a standard medial-lateral approach was established at the joint line level, along the medial and lateral borders of the patellar tendon. A systematic diagnostic arthroscopy was then performed to assess all compartments of the knee joint.
  6. Extensive synovial hyperplasia, hyperemia, and edema were observed in the suprapatellar bursa, with multiple rice-grain-sized loose bodies and numerous white chalk-like crystalline deposits on the synovium and cartilage surface. Synovial inflammation was observed in the intercondylar fossa, but the cruciate ligaments remained intact. No significant cartilage erosion was observed in the medial and lateral compartments.
  7. A joint shaver was introduced through the anteromedial approach and used in swing mode at 2000 rpm for a thorough synovectomy, systematically removing the inflammatory hyperplastic synovial tissue of the suprapatellar bursa, medial and lateral grooves, and intercondylar region. Multiple loose bodies and crystalline deposits were removed using grasping forceps and shavers.
  8. Following synovectomy, the joint cavity was thoroughly irrigated with approximately 12 mL of normal saline to remove any remaining crystals, debris, and inflammatory material. Three different sites of synovial membrane and soft tissue specimens were obtained using sterile biopsy forceps.
  9. Postoperatively, two catheters were percutaneously inserted into the joint cavity. One multi-port catheter was placed in the suprapatellar bursa for postoperative local antibiotic infusion. The other silicone drainage tube was placed at the lowest point on the posteromedial aspect of the joint to drain fluid. Both catheters were secured to the skin with 2-0 nylon sutures and connected to their respective closed collection systems. The incision was closed with 3-0 nylon sutures, and the knee joint was pressure-bandaged from distal to proximal using sterile dry gauze, cotton pads, and an elastic bandage.
  10. A closed continuous irrigation and drainage system was established postoperatively. Vancomycin solution (500 mg vancomycin dissolved in 500 mL of normal saline, final concentration 1 mg/mL) was continuously infused via an infusion pump at a rate of 50 mL/h through the administration tube. The drainage tube was connected to a low-pressure continuous suction system.
  11. The system was maintained for 7 days, with daily monitoring of fluid balance and checks for blockages or leaks. Intravenous infusion of vancomycin continued at 1000 mg every 12 h. The continuous irrigation and drainage system was maintained until: (1) clinical symptoms significantly improved; (2) joint fluid cultures were negative for three consecutive days; and (3) the drainage fluid was clear.
  12. On postoperative day 7, when all indicators were within the target range, both catheters were removed. The knee joint was immobilized and rested in an extended position for 1 week postoperatively. After catheter removal on postoperative day 7, assisted active joint range of motion training was initiated.

6. Discharge and follow-up

  1. Discharge criteria: (1) No fever for at least 48 h, vital signs returned to normal. Acute symptoms subsided, including a significant reduction in knee swelling, VAS score ≤3, and the ability to perform gentle assisted active joint movements without severe discomfort. (2) Inflammatory markers showed a decreasing trend, ESR <40 mm/h and CRP <20 mg/L. White blood cell count returned to normal range (4.0-10.0 x 109/L), differential count normal. (3) No recurrence of fever or effusion after extubation. (4) Able to walk independently with crutches (partial weight-bearing), able to perform straight leg raises without significant pain, and active knee flexion ≥90°.
  2. Follow-up plan: (1) 2 weeks after discharge: Clinical examination including wound assessment, joint range of motion measurement, and pain assessment. Laboratory tests: Complete blood count, ESR, CRP, serum uric acid, and renal function. (2) 4 weeks after discharge: Clinical examination focusing on functional recovery, inflammatory markers, and uric acid level assessment. (3) 8 weeks post-discharge: A comprehensive assessment including clinical examination, inflammatory markers, uric acid levels, and liver and kidney function tests. Assess full functional recovery and the ability to resume normal activities. Discuss the long-term management plan, including continued uric acid-lowering therapy and monitoring protocols.

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Results

On initial admission, the patient exhibited right knee swelling, warmth, erythema, and pain rated 10/10. MRI revealed joint effusion and synovial thickening without bone destruction. Synovial fluid appeared turbid yellow, with a markedly elevated leukocyte count. Culture identified MRSA. Empirical antibiotics were adjusted to vancomycin, resulting in a gradual improvement of symptoms and normalization of inflammatory markers. The patient was discharged after 1 week of treatment.

At 2 weeks pos...

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Discussion

This case lacks the typical symptoms and signs of GA, which commonly affects the first metatarsophalangeal joint and is often associated with elevated serum uric acid levels17. This case presented with knee swelling and pain, normal serum uric acid levels, and although no urate crystals were identified in the joint aspirate, elevated white blood cells (WBC), CRP, and procalcitonin suggested infection. Antibiotic therapy was effective but incomplete, as persistent intra-articular inflammation persi...

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Disclosures

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The authors have nothing to disclose.

Acknowledgements

This work was supported by the National Natural Science Foundation of China (82074469). Natural Science Foundation of Zhejiang Province (LY21H270008). 2024 Zhejiang Chinese Medical University Cultivation Plan for Top Innovative Talents of Postgraduates (721100G00747)

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Materials

List of materials used in this article
NameCompanyCatalog NumberComments
1.5-Tesla MRI ScannerSiemens HealthineersMAGNETOM Essenza
Allopurinol TabletsGlaxoSmithKline500790
Antinuclear Antibody (ANA) AssayThermo Fisher Scientific2401-0001
Antistreptolysin O (ASO) TestAbbott Laboratories7D55-20
Arthroscopy ShaverStryker Corporation272-300-100
Blood Agar PlateBD Diagnostics221261
Blood Culture Bottle (Aerobic)BD Diagnostics442020
Blood Culture Bottle (Anaerobic)BD Diagnostics442021
CCP ELISAAxis-Shield DiagnosticsFCCP600
Chocolate Agar PlatebioMérieux43101
Complete Blood Count Reagent KitSysmex CorporationXN-9000 series
C-Reactive Protein (CRP) AssayRoche Diagnostics4628918190
Drainage Tube (Surgical)Medtronic8888173031
Erythrocyte Sedimentation Rate (ESR) KitStreck107760
Etoricoxib TabletsMerck & Co.100 mg, NDC 0006-0372
Formalin Solution (10%)Sigma-AldrichHT501128
Gram Stain KitHardy DiagnosticsG100
Hematoxylin and Eosin (H&E) StainSigma-AldrichHHS128 & HT110116
HLA-B27 Antibody ReagentBD Biosciences340183
Levofloxacin InjectionJanssen PharmaceuticalsNDC 50458-050-01
Linezolid InjectionPfizerNDC 0009-4992-01
Medication Catheter (Intra-articular)Smith & Nephew72202866
Paraffin WaxLeica Biosystems3801310
Procalcitonin (PCT) AssayBrahms GmbHKRYPTOR PCT
Rheumatoid Factor (RF) TestBeckman Coulter467858
Synovial Fluid Collection TubeSarstedt82.1190.001
Tuberculosis Antibody TestStandard DiagnosticsTB Ab Rapid 11FK10
Ultrasound MachineGE HealthcareLOGIQ E10
Vancomycin HydrochlorideMylan PharmaceuticalsNDC 67457-156-60
Xpert MTB/RIF AssayCepheidGXMTB/RIF-10

References

  1. Cha, Y., et al. Pathophysiology and treatment of gout arthritis; including gout arthritis of hip joint: A literature review. Hip Pelvis. 36 (1), 1-11 (2024).
  2. Wallace, S. L., et al. Preliminary criteria for the classification of the acute arthritis of primary gout. Arthritis Rheum. 20 (3), 895-900 (1977).
  3. Stewart, S., Dalbeth, N., Vandal, A. C., Rome, K. The first metatarsophalangeal joint in gout: A systematic review and meta-analysis. BMC Musculoskelet Disord. 17, 69(2016).
  4. Dalbeth, N., et al. Gout. Nat Rev Dis Primers. 5 (1), 69(2019).
  5. Chen-Xu, M., Yokose, C., Rai, S. K., Pillinger, M. H., Choi, H. K. Contemporary prevalence of gout and hyperuricemia in the united states and decadal trends: The national health and nutrition examination survey. Arthritis Rheumatol. 71 (6), 991-999 (2019).
  6. Richette, P., Bardin, T. Gout. Lancet. 375 (9711), 318-328 (2010).
  7. Zhang, J., et al. The impact of uric acid on musculoskeletal diseases: Clinical associations and underlying mechanisms. Front Endocrinol (Lausanne). 16, 1515176(2025).
  8. Shah, K., Spear, J., Nathanson, L. A., McCauley, J., Edlow, J. A. Does the presence of crystal arthritis rule out septic arthritis. J Emerg Med. 32 (1), 23-26 (2007).
  9. Wang, Y., Xu, Y. Coexistence of gouty and septic arthritis. J Clin Rheumatol. 30 (2), e67(2024).
  10. Ichiseki, T., Ueda, S., Matsumoto, T. Rare coexistence of gouty and septic arthritis after arthroscopic rotator cuff repair: A case report. Int J Clin Exp Med. 8 (3), 4718-4720 (2015).
  11. Panicker, V. N., Turner, J. K., Chehade, M. J. Concomitant septic arthritis and tophaceous gout of the knee managed with intermittent closed joint irrigation combined with negative pressure therapy: A case study and literature review. Open Orthop J. 8, 482-487 (2014).
  12. Papanicolas, L. E., Hakendorf, P., Gordon, D. L. Concomitant septic arthritis in crystal monoarthritis. J Rheumatol. 39 (1), 157-160 (2012).
  13. Yu, K. H., et al. Concomitant septic and gouty arthritis--an analysis of 30 cases. Rheumatology (Oxford). 42 (9), 1062-1066 (2003).
  14. Medina-Perez, R., Baajour, S. A., Gonzalez, S., Lopez, J. L., Campbell, D. J. Septic arthritis with superimposed acute gouty arthritis in a rheumatoid arthritis patient. Cureus. 14 (4), e24352(2022).
  15. Lim, S. Y., Lu, N., Choi, H. K. Septic arthritis in gout patients: A population-based cohort study. Rheumatology (Oxford). 54 (11), 2095-2099 (2015).
  16. Huskisson, E. C. Measurement of pain. Lancet. 2 (7889), 1127-1131 (1974).
  17. Lu, C., et al. Research hotspots and trends related to pain in gouty arthritis from 2014 to 2024: A bibliometric analysis. Medicine (Baltimore). 103 (46), e40525(2024).
  18. Smith, J. R., Phelps, P. Septic arthritis, gout, pseudogout and osteoarthritis in the knee of a patient with multiple myeloma. Arthritis Rheum. 15 (1), 89-96 (1972).
  19. Jarrett, M. P., Grayzel, A. I. Simultaneous gout, pseudogout, and septic arthritis. Arthritis Rheum. 23 (1), 128-129 (1980).
  20. Asghari, K. M., et al. Gout: Global epidemiology, risk factors, comorbidities and complications: A narrative review. BMC Musculoskelet Disord. 25 (1), 1047(2024).
  21. Poulsen, R., Dalbeth, N. Gout and nlrp3 inflammasome biology. Arthritis Rheumatol. 77 (10), 1317-1326 (2025).
  22. Zhong, L., et al. Ddx3x could regulate gouty inflammation via nlrp3 inflammasome activation and macrophage pyroptosis crosstalk. Int Immunopharmacol. 166, 115458(2025).
  23. Gaal, O. I., Joosten, L. aB., Crișan, T. O. Targeting innate immune memory: A new paradigm for gout treatment. Explorat Musculoskel Dis. 3, 1007103(2025).
  24. Liu, Y., et al. Serum levels of il-17 are elevated in patients with acute gouty arthritis. Biochem Biophys Res Commun. 497 (3), 897-902 (2018).
  25. Fan, Y., et al. To investigate the mechanism of qinpi tongfeng formula in treating acute gouty arthritis by uhplc-q-orbitrap-ms, network pharmacology and experimental validation. J Inflamm Res. 17, 3475-3498 (2024).
  26. Fattori, V., et al. Il-33 enhances macrophage release of il-1β and promotes pain and inflammation in gouty arthritis. Inflamm Res. 69 (12), 1271-1282 (2020).
  27. Rossato, M. F., et al. Monosodium urate crystal interleukin-1β release is dependent on toll-like receptor 4 and transient receptor potential v1 activation. Rheumatology (Oxford). 59 (1), 266(2020).
  28. Cavalcanti, N. G., et al. Cytokine profile in gout: Inflammation driven by il-6 and il-18. Immunol Invest. 45 (5), 383-395 (2016).
  29. Chen, C., et al. Monosodium urate crystal-induced pyroptotic cell death in neutrophil and macrophage facilitates the pathological progress of gout. Small. 20 (23), e2308749(2024).
  30. Gu, Y., et al. Curcumin analogue ai-44 alleviates msu-induced gouty arthritis in mice via inhibiting cathepsin b-mediated nlrp3 inflammasome activation. Int Immunopharmacol. 93, 107375(2021).
  31. Morgan, A. M., Ferati, S., Fong, C., Egol, K. Identifying septic arthritis superimposed on crystalline arthropathy: Is synovial cell count the answer. J Clin Orthop Trauma. 65, 102985(2025).
  32. Mcgillicuddy, D. C., Shah, K. H., Friedberg, R. P., Nathanson, L., Edlow, J. A. How sensitive is the synovial fluid white blood cell count in diagnosing septic arthritis. Am J Emerg Med. 25 (7), 749-752 (2007).
  33. Swisher, J., Sitton, Z., Burbank, K., Nelson, C. Acute monoarthritis: Diagnosis in adults. Am Fam Physician. 111 (6), 497-506 (2025).
  34. Vrancianu, C. O., et al. The challenge of periprosthetic joint infection diagnosis: From current methods to emerging biomarkers. Int J Mol Sci. 24 (5), 4320(2023).
  35. Carpenter, C. R., Schuur, J., Everett, W. W., Pines, J. M. Evidence-based diagnostics: Adult septic arthritis. Acad Emerg Med. 18 (8), 781-796 (2011).
  36. Lenski, M., Scherer, M. A. Analysis of synovial inflammatory markers to differ infectious from gouty arthritis. Clin Biochem. 47 (1-2), 49-55 (2014).
  37. Pyo, J. Y., et al. Clinical significance of delta neutrophil index in the differential diagnosis between septic arthritis and acute gout attack within 24 hours after hospitalization. Medicine (Baltimore). 96 (30), e7431(2017).
  38. Guillén-Astete, C. A., García-García, V., Vazquez-Díaz, M. Procalcitonin serum level is a specific marker to distinguish septic arthritis of the knee in patients with a previous diagnosis of gout. J Clin Rheumatol. 27 (8), e575-e579 (2021).
  39. Schultz, B. J., et al. Pilot study of a novel serum mrna gene panel for diagnosis of acute septic arthritis. World J Orthop. 10 (12), 424-433 (2019).
  40. Yang, W., Yang, C. Septic arthritis caused by gout progressed to sepsis and hemophagocytic syndrome. Heliyon. 10 (9), e30583(2024).
  41. Giarritiello, F., De La Motte, L. R., Drago, L. Viscosupplementation and synovial fluid rheology: A hidden risk for bacterial biofilm formation in joint infections. Microorganisms. 13 (4), 700(2025).
  42. Ansari, S. R., et al. Magnetic microfiber hyperthermia for synergistic antimicrobial activity against methicillin-resistant staphylococcus aureus. Mater Today Bio. 32, 101862(2025).
  43. Luan, Y., Gao, X. A study on the diagnostic value of dual-energy ct (dect) imaging in patients with gouty arthritis. Int J Rheum Dis. 27 (12), e15431(2024).
  44. Kravchenko, D., et al. The role of dual energy computed tomography in the differentiation of acute gout flares and acute calcium pyrophosphate crystal arthritis. Clin Rheumatol. 41 (1), 223-233 (2022).

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Erratum


Formal Correction: Case Report of Gouty Arthritis Complicated by Septic Arthritis
Posted by JoVE Editors on 6/24/2026. Citeable Link.

This corrects the article 10.3791/69787

Tags

Knee SwellingSynovial Fluid AnalysisJoint AspirationArthroscopic DebridementStaphylococcus AureusInflammatory MarkersCrystal DepositsAllopurinol Therapy

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