İleri evre semptomatik diz osteoartritinde asemptomatik hiperürisemi sıklığı ve inflamatuar parametreler ile ilişkisi

Öz

Amaç: Hiperüriseminin diz OA gelişmesinde ve ilerlemesinde risk faktörü olduğu düşünülmektedir. Çalışmamızda ileri evre diz OA hastalarında asemptomatik hiperürisemi sıklığı ve sistemik inflamasyonla ilişkili olup olmadığının araştırılması amaçlandı. Gereç ve yöntem: Semptomatik diz OA olan ve radyografik Kellgren-Lawrence (K-L) sistemine göre derece 3 veya 4 olarak sınıflandırılan hastaları dahil eden tek merkezli, retrospektif bir çalışmadır. Yaş, cinsiyet, komorbiditeler, kullanılan ilaçlar, serum ürik asit (ÜA), hemogram parametreleri, eritrosit sedimantasyon hızı (ESH), C-reaktif protein (CRP) ve vücut kitle indeksi (VKİ) kaydedildi. Nötrofil/lenfosit oranı (NLO), trombosit/lenfosit oranı (TLO) ve sistemik immün-inflamasyon indeksi (Sİİ)=[(nötrofil sayısı × trombosit sayısı)/lenfosit sayısı] hesaplandı. Hiperürisemisi olan ve olmayan hastalar sırasıyla Grup 1 ve Grup 2 olarak tanımlandı ve gruplar arasında demografik ve laboratuvar veriler karşılaştırıldı. Bulgular: 240 hastanın 51’ inde hiperürisemi mevcuttu (%21). Grup 1’de yaş ortalaması 70.54±7.02, BKİ 34 kg/m2 (27.7-41), grup 2’ de yaş ortalaması 68.63±6.29, BKİ 32 kg/m2 (25- 51.5), gruplar arasında anlamlı fark yoktu. Grup 1 ve Grup 2 arasında NLO, TLO, Sİİ arasında fark yoktu (p=0.404, p=0.604, p=0.537). Her iki grup arasında ESH değerlerinde fark yokken (p=0.051), CRP düzeyleri grup 1’de anlamlı yüksek saptandı (p=0.007). Grup 2’ de ÜA düzeyi ile CRP (rho=0.243**, p<0.001), Sİİ (rho=0.173*, p=0.017), NLO (rho=0.154*, p=0.035) ve PLO (rho=0.166*, p=0.023) pozitif ilişki tespit edildi. Ancak Grup 1’ de ÜA düzeyi ile ESH, CRP, Sİİ, NLO, PLO ve VKİ arasında ilişki yoktu. Sonuç: Çalışmamızda ileri evre diz OA hastalarının yaklaşık 5’de 1’inin asemptomatik hiperürisemisinin olduğu gözlendi. Asemptomatik HÜ, diz OA’ da inflamasyona neden olabilir, sonuç olarak bu hastalarda serum ÜA seviyesinin normale çekilmesi gerekebilir.

Anahtar Kelimeler

• Asemptomatik hiperürisemi
• hiperürisemi
• diz osteoartriti
• sistemik inflamasyon

Frequency of asymptomatic hyperuricemia in advanced-stage symptomatic knee osteoarthritis and its relationship with inflammatory parameters

Öz

Purpose: Hyperuricemia (HU) is thought to be a risk factor in the development and progression of knee osteoarthritis (OA). We sought the frequency of asymptomatic HU in advanced knee OA patients and whether it was related to systemic inflammation. Materials and methods: This is a single-center, retrospective study including patients with symptomatic stage 3/4 knee OA classified based on Kellgren-Lawrence (K-L) system. Demographic data and serum uric acid (UA), hemogram parameters, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), body mass index (BMI) were recorded. Neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR) and systemic immune-inflammation index (SII)=[(neutrophil count × platelet count)/lymphocyte count] were calculated. Patients with/without hyperuricemia were defined as Group 1 and Group 2, respectively. Demographic and laboratory data were compared between the groups. Results: Hyperuricemia was present in 51 of 240 patients (21%). There was no significant difference between the groups based on age (Group1: 70.54±7.02, Group2: 68.63±6.29, p=0.07) and BMI (Group 1: 34 kg/m2 (27.7-41), Group2: 32 kg/m2 (25-51.5), p=0.107). NLR, PLR, and SII were similar between two groups (p=0.404, p=0.604, p=0.537). While there was no difference in ESR values between the two groups (p=0.051), CRP levels were found to be significantly higher in Group 1 (p=0.007). A positive correlation was detected between serum UA level and CRP (rho=0.243**, p<0.001), SII (rho=0.173*, p=0.017), NLR (rho=0.154*, p=0.035) and PLR (rho=0.166*, p=0.023) in Group 2. No correlation was detected between serum UA level and ESR, CRP, SII, NLR, PLR and BMI in Group 1. Conclusion: Asymptomatic HU was found 1 in 5 of advanced-stage knee OA patients and may contribute to inflammation in knee OA. Serum UA level may need to be reduced to normal level in these patients.

Anahtar Kelimeler

• Asymptomatic hyperuricemia
• hyperuricemia
• knee osteoarthritis
• systemic inflammation

Kaynakça

1. 1. Quicke JG, Conaghan PG, Corp N, Peat G. Osteoarthritis year in review 2021: epidemiology & therapy. Osteoarthritis Cartilage 2022;30:196-206. https://doi.org/10.1016/j.joca.2021.10.003
2. 2. Cui A, Li H, Wang D, Zhong J, Chen Y, Lu H. Global, regional prevalence, incidence and risk factors of knee osteoarthritis in population-based studies. EClinicalMedicine 2020;29-30:100587. https://doi.org/10.1016/j.eclinm.2020.100587
3. 3. Bardin T, Richette P. Definition of hyperuricemia and gouty conditions. Curr Opin Rheumatol 2014;26:186-191. https://doi.org/10.1097/BOR.0000000000000028
4. 4. FitzGerald JD, Dalbeth N, Mikuls T, et al. 2020 American College of Rheumatology Guideline for the Management of Gout. [published correction appears in Arthritis Care Res (Hoboken). 2020;72:1187] [published correction appears in Arthritis Care Res (Hoboken). 2021;73:458]. Arthritis Care Res (Hoboken) 2020;72:744-760. https://doi.org/10.1002/acr.24180
5. 5. Sun Y, Brenner H, Sauerland S, Günther KP, Puhl W, Stürmer T. Serum uric acid and patterns of radiographic osteoarthritis--the Ulm Osteoarthritis Study. Scand J Rheumatol 2000;29:380-386. https://doi.org/10.1080/030097400447589
6. 6. Lai JH, Luo SF, Hung LF, et al. Physiological concentrations of soluble uric acid are chondroprotective and anti-inflammatory. Sci Rep 2017;7:2359. https://doi.org/10.1038/s41598-017-02640-0
7. 7. Ma Q, Honarpisheh M, Li C, et al. Soluble uric acid is an intrinsic negative regulator of monocyte activation in monosodium urate crystal-induced tissue inflammation. J Immunol 2020;205:789-800. https://doi.org/10.4049/jimmunol.2000319
8. 8. Martinon F, Pétrilli V, Mayor A, Tardivel A, Tschopp J. Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature 2006;440:237-241. https://doi.org/10.1038/nature04516

9. 9. Xiao L, Lin S, Zhan F. The association between serum uric acid level and changes of MRI findings in knee osteoarthritis: a retrospective study (A STROBE-compliant article). Medicine (Baltimore) 2019;98:e15819. https://doi.org/10.1097/MD.0000000000015819
10. 10. Cao TN, Huynh KN, Tran HT, Nguyen MD. Association between asymptomatic hyperuricemia and knee osteoarthritis in older outpatients. Eur Rev Med Pharmacol Sci 2022;26:6600-6607. https://doi.org/10.26355/eurrev_202209_29760
11. 11. Taşoğlu Ö, Bölük H, Şahin Onat Ş, Taşoğlu İ, Özgirgin N. Is blood neutrophil-lymphocyte ratio an independent predictor of knee osteoarthritis severity? Clin Rheumatol 2016;35:1579-1583. https://doi.org/10.1007/s10067-016-3170-8
12. 12. Büyükavcı R, Aktürk S, Sağ S. Comparison of blood platelet distribution width and neutrophil-lymphocyte ratio in patients with different grades of knee osteoarthritis. J Back Musculoskelet Rehabil 2018;31:1035-1039. https://doi.org/10.3233/BMR-171028
13. 13. Kelesoglu Dincer AB, Sezer S. Systemic immune inflammation index as a reliable disease activity marker in psoriatic arthritis. J Coll Physicians Surg Pak 2022;32:773-778. https://doi.org/10.29271/jcpsp.2022.06.773
14. 14. Kellgren Jh, Lawrence Js. Radiological assessment of osteoarthrosis. Ann Rheum Dis 1957;16:494-502. https://doi.org/10.1136/Ard.16.4.494
15. 15. Kapoor M, Martel Pelletier J, Lajeunesse D, Pelletier JP, Fahmi H. Role of proinflammatory cytokines in the pathophysiology of osteoarthritis. Nat Rev Rheumatol 2011;7:33-42. https://doi.org/10.1038/nrrheum.2010.196
16. 16. Liu Bryan R, Terkeltaub R. Emerging regulators of the inflammatory process in osteoarthritis. Nat Rev Rheumatol 2015;11:35-44. https://doi.org/10.1038/nrrheum.2014.162
17. 17. Stürmer T, Brenner H, Brenner RE, Günther KP. Non-insulin dependent diabetes mellitus (NIDDM) and patterns of osteoarthritis. The Ulm osteoarthritis study. Scand J Rheumatol 2001;30:169-171. https://doi.org/10.1080/030097401300162969
18. 18. Krasnokutsky S, Oshinsky C, Attur M, et al. Serum urate levels predict joint space narrowing in non-gout patients with medial knee osteoarthritis. Arthritis Rheumatol 2017;69:1213-1220. https://doi.org/10.1002/art.40069
19. 19. Wang S, Pillinger MH, Krasnokutsky S, Barbour KE. The association between asymptomatic hyperuricemia and knee osteoarthritis: data from the third National Health and Nutrition Examination Survey. Osteoarthritis Cartilage 2019;27:1301-1308. https://doi.org/10.1016/j.joca.2019.05.013
20. 20. Denoble AE, Huffman KM, Stabler TV, et al. Uric acid is a danger signal of increasing risk for osteoarthritis through inflammasome activation. Proc Natl Acad Sci U S A. 2011;108:2088-2093. https://doi.org/10.1073/pnas.1012743108
21. 21. Jarraya M, Roemer F, Kwoh CK, Guermazi A. Crystal arthropathies and osteoarthritis-where is the link? Skeletal Radiol 2023;52:2037-2043. https://doi.org/10.1007/s00256-022-04246-8
22. 22. Nowatzky J, Howard R, Pillinger MH, Krasnokutsky S. The role of uric acid and other crystals in osteoarthritis. Curr Rheumatol Rep 2010;12:142-148. https://doi.org/10.1007/s11926-010-0091-4
23. 23. Felson DT, Niu J, Neogi T, et al. Synovitis and the risk of knee osteoarthritis: the MOST study. Osteoarthritis Cartilage 2016;24:458-464. https://doi.org/10.1016/j.joca.2015.09.013
24. 24. Billiet L, Doaty S, Katz JD, Velasquez MT. Review of hyperuricemia as new marker for metabolic syndrome. ISRN Rheumatol 2014;2014:852954. https://doi.org/10.1155/2014/852954