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Rheumatoid Arthritis After SARS-CoV-2 Infection: A New Risk Factor?

Year 2022, Volume: 55 Issue: 3, 179 - 182, 31.12.2022
https://doi.org/10.20492/aeahtd.1072187

Abstract

OBJECTİVE: In rheumatoid arthritis (RA) etiopathogenesis, viral infections role as environmental trigger factors. The new corona virus SARS-COV-2 has been reported to trigger the autoimmunity and inflammatory arthritis. The aim of the study is to compare the patients diagnosed as RA after COVİD-19 with regular RA patients and to assess the possible mechanisms in RA development.
MATERİALS AND METHODS: Two groups were formed in newly diagnosed RA patients depending on COVİD-19 history before the initiation of joint symptoms. Gender, age, comorbidity, working status, smoking habits, family history, joint involvement pattern, symptom duration, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), disease activity scores (DAS28-ESR), rheumatoid factor (RF), anti-cyclic citrulline peptide (anti-CCP) was recorded. Wilcoxon test was used for data that does not show normal distribution, paired-t test used for data showing normal distribution, p <0.05 is considered statistically significant.
RESULTS: Of 61 newly diagnosed RA patients, 67.2% (n=41) had no previous history of COVID-19, and 32.8% (n=20) had a history of COVID-19 infection. There was no statistical difference in terms of age, gender, family history, smoking habit, working status and comorbidity between both groups. Symptom durations were statistically similar in both groups with and without a history of COVID-19, 24 weeks (2-62), 18 weeks (2-120), respectively. Joint involvement patterns were polysymmetric in 90% and oligoarticular in 10% in patients with COVID-19 history. Without COVID-19 group, 87.8% were polysymmetric and 12.2% were oligoarticular. ESR, CRP, DAS28-ESR levels and presence of RF and anti-CCP were also similar in both groups.
CONCLUSION: In this study, demographic, clinical and laboratory features were found to be similar with classical RA findings in patients who developed RA after COVID-19 infection. SARS-CoV-2 infection specifically targets the respiratory tract, thus may lead RA-associated autoimmunity. As a result; larger and prospective studies are needed to elucidate the relationship between RA and COVID-19.

References

  • 1. https://covid19.who.int/ World Health Organization Coronavirus (COVID-19) Dashboard
  • 2. Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet Lond Engl 2020;395:497–506.
  • 3. Zhao Y, Zhao Z, Wang Y, Zhou Y, Ma Y, Zuo W. Single-cell RNA expression profiling of ACE2, the receptor of SARS-CoV-2. Am. J. Respir. Crit. Care Med.202(5), 756–759 (2020).
  • 4. Zou Z, Yan Y, Shu Y et al. Angiotensin-converting enzyme 2 protects from lethal avian influenza A H5N1 infections. Nat. Commun. 5(1), 1–7 (2014).
  • 5. Firestein GS, Mcinnes IB. Immunopathogenesis of rheumatoid arthritis. Immunity 46(2), 183–196 (2017).
  • 6. Caso F, Costa L, Ruscitti P, et al. Could Sars-coronavirus-2 trigger autoimmune and/or autoinflammatory mechanisms in genetically predisposed subjects? Autoimmun Rev 2020; 19:102524.
  • 7. Galeotti C, Bayry J. Autoimmune and inflammatory diseases following COVID-19. Nat Rev Rheumatol 2020;16:413–4.
  • 8. Lucchese G, Flöel A. SARS-CoV-2 and Guillain-Barré syndrome: molecular mimicry with human heat shock proteins as potential pathogenic mechanism. Cell Stress Chaperones 2020; 25:731–5.
  • 9. Gasparotto M, Framba V, Piovella C, Doria A, Iaccarino L. Post-COVID-19 arthritis: a case report and literature review. Clin Rheumatol. 2021;40(8):3357-3362.
  • 10. Conway R, Konig MF, Graef ER, Webb K, Yazdany J, Kim AHJ. Inflammatory arthritis in patients with COVID-19. Transl Res. 2021;232:49-59.
  • 11. Cincinelli G, Di Taranto R, Orsini F, Rindone A, Murgo A, Caporali R. A case report of monoarthritis in a COVID-19 patient and literature review: Simple actions for complex times. Medicine (Baltimore). 2021 Jun 11;100(23):e26089.
  • 12. Perrot L, Hemon M, Busnel J-M, et al. First flare of ACPA-positive rheumatoid arthritis after SARS-CoV-2 infection. Lancet Rheumatol 2021;3:e6–8.
  • 13. Aletaha D, Neogi T, Silman AJ, et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum. 2010 Sep;62(9):2569-81.
  • 14. Fujinami RS, von Herrath MG, Christen U, Whitton JL (2006) Molecular mimicry, bystander activation, or viral persistence: in- fections and autoimmune disease. Clin Microbiol Rev 19:80–94.
  • 15. Angileri F, Legare S, Marino Gammazza A, Conway de Macario E, Jl Macario A, Cappello F. Molecular mimicry may explain multi-organ damage in COVID-19. Autoimmun Rev 2020;19:102591.
  • 16. Derksen VFAM, Kissel T, Lamers-Karnebeek FBG, van der Bijl AE, Venhuizen AC, Huizinga TWJ, Toes REM, Roukens AHE, van der Woude D. Onset of rheumatoid arthritis after COVID-19: coincidence or connected? Ann Rheum Dis. 2021 Mar 1:annrheumdis-2021-219859.
  • 17. ,Roongta R, Chattopadhyay A, Ghosh A. Correspondence on 'Onset of rheumatoid arthritis after COVID-19: coincidence or connected?'. Ann Rheum Dis. 2021 Apr 27:annrheumdis-2021-220479.
  • 18. Elemam NM, Maghazachi AA, Hannawi S. COVID-19 infection and rheumatoid arthritis: mutual outburst cytokines and remedies. Curr Med Res Opin. 2021 Jun;37(6):929-938.
  • 19. Tripathy A, Swain N, Gupta B. The COVID-19 pandemic: an increased risk of rheumatoid arthritis. Future Virol. 2021 Jun:10.2217/fvl-2020-0393.
  • 20. Li F, Xu J, Zheng J, et al. Association between interleukin-6 gene polymorphisms and rheumatoid arthritis in Chinese Han population: a case-control study and a meta-analysis. Sci Rep. 2014;4:5714.
  • 21. Kirtipal N, Bharadwaj S. Interleukin 6 polymorphisms as an indicator of COVID-19 severity in humans. J Biomol Struct Dyn. 2020:1–3.
  • 22. Demoruelle MK, Solomon JJ, Fischer A, Deane KD. The lung may play a role in the pathogenesis of rheumatoid arthritis. Int J Clin Rheumtol. 2014;9(3):295-309.
  • 23. Demoruelle MK, Deane KD, Holers VM. When and where does inflammation begin in rheumatoid arthritis? Curr Opin Rheumatol. 2014 Jan;26(1):64-71.
  • 24. Chatzidionisyou A, Catrina AI. The lung in rheumatoid arthritis, cause or consequence? Curr Opin Rheumatol. 2016 Jan;28(1):76-82.

SARS-Cov-2 Enfeksiyonu Sonrası Gelişen Romatoid Artrit: Yeni Bir Risk Faktörü Mü?

Year 2022, Volume: 55 Issue: 3, 179 - 182, 31.12.2022
https://doi.org/10.20492/aeahtd.1072187

Abstract

AMAÇ: Romatoid artrit (RA) etyopatogenezinde viral enfeksiyonlar çevresel tetikleyici faktörler olarak rol almaktadır. Yeni corona virüs SARS-CoV-2’nin neden olduğu hastalığın (COVİD-19) otoimmüniteyi ve inflamatuar artritleri tetiklediği bildirilmiştir. Çalışmanın amacı, COVİD-19 sonrası RA tanısı alan hastaları klasik RA özellikleriyle karşılaştırmak ve RA gelişimindeki olası mekanizmaları irdelemektir.
GEREÇ VE YÖNTEM: Romatoloji polikliniğine başvurarak RA tanısı alan olgular retrospektif olarak çalışmaya dahil edildi. Eklem yakınmaları başlamadan önce COVİD-19 öyküsü olan ve olmayan hastalar olarak iki grup oluşturuldu. Cinsiyet, yaş, komorbidite, çalışma durumu, sigara, aile öyküsü, eklem tutulum paterni, semptom süresi, eritrosit sedimantasyon hızı (ESR) ve C-reaktif protein (CRP), hastalık aktivite skorları (DAS28-ESR), romatoid faktör (RF), anti-siklik sitrülline peptid (anti-CCP) kaydedildi. Normal dağılım göstermeyen veriler için Wilcoxon testi, normal dağılım gösteren veriler için paired-t testi kullanıldı, p <0.05 istatistiksel olarak anlamlı kabul edildi.
BULGULAR: 61 yeni tanı RA hastasının %67.2 si (n=41) önceden COVİD-19 öyküsü yoktu, %32.8’inde (n=20) COVİD-19 enfeksiyon öyküsü mevcuttu. Her iki grup arasında yaş, cinsiyet, aile öyküsü, sigara alışkanlığı, çalışma durumu, komorbidite açısından istatiksel fark saptanmadı. Her iki grupta semptom süreleri istatiksel açıdan benzerdi, COVİD-19 öyküsü olan ve olmayan grupta sırasıyla 24 hafta (2-62), 18 hafta (2-120) saptandı. Eklem tutulum paternleri COVİD-19 geçirmiş hastalarda %90’ı polisimetrik, %10’u oligoartikülerdi. COVİD-19 öyküsü olmayan hastalarda %87.8’i polisimetrik, %12.2’si oligoartikülerdi, her iki grup arasında fark saptanmadı. ESR, CRP, DAS28-ESR düzeyleri ve RF ve anti-CCP varlığı da her iki grupta benzerdi.
SONUÇ: Bu çalışmada klasik RA bulgularıyla COVİD-19 enfeksiyonu sonrası RA gelişen hastalarda demografik, klinik ve laboratuar özellikler benzer bulunmuştur. SARS-CoV-2 enfeksiyonun solunum yollarını özellikle hedef alması RA ilişkili otoimmünite gelişme ihtimalini düşündürmektedir. Sonuç olarak; RA ve COVİD-19 ilişkisini aydınlatmak için daha geniş çaplı ve ileriye dönük çalışmalara ihtiyaç vardır.

References

  • 1. https://covid19.who.int/ World Health Organization Coronavirus (COVID-19) Dashboard
  • 2. Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet Lond Engl 2020;395:497–506.
  • 3. Zhao Y, Zhao Z, Wang Y, Zhou Y, Ma Y, Zuo W. Single-cell RNA expression profiling of ACE2, the receptor of SARS-CoV-2. Am. J. Respir. Crit. Care Med.202(5), 756–759 (2020).
  • 4. Zou Z, Yan Y, Shu Y et al. Angiotensin-converting enzyme 2 protects from lethal avian influenza A H5N1 infections. Nat. Commun. 5(1), 1–7 (2014).
  • 5. Firestein GS, Mcinnes IB. Immunopathogenesis of rheumatoid arthritis. Immunity 46(2), 183–196 (2017).
  • 6. Caso F, Costa L, Ruscitti P, et al. Could Sars-coronavirus-2 trigger autoimmune and/or autoinflammatory mechanisms in genetically predisposed subjects? Autoimmun Rev 2020; 19:102524.
  • 7. Galeotti C, Bayry J. Autoimmune and inflammatory diseases following COVID-19. Nat Rev Rheumatol 2020;16:413–4.
  • 8. Lucchese G, Flöel A. SARS-CoV-2 and Guillain-Barré syndrome: molecular mimicry with human heat shock proteins as potential pathogenic mechanism. Cell Stress Chaperones 2020; 25:731–5.
  • 9. Gasparotto M, Framba V, Piovella C, Doria A, Iaccarino L. Post-COVID-19 arthritis: a case report and literature review. Clin Rheumatol. 2021;40(8):3357-3362.
  • 10. Conway R, Konig MF, Graef ER, Webb K, Yazdany J, Kim AHJ. Inflammatory arthritis in patients with COVID-19. Transl Res. 2021;232:49-59.
  • 11. Cincinelli G, Di Taranto R, Orsini F, Rindone A, Murgo A, Caporali R. A case report of monoarthritis in a COVID-19 patient and literature review: Simple actions for complex times. Medicine (Baltimore). 2021 Jun 11;100(23):e26089.
  • 12. Perrot L, Hemon M, Busnel J-M, et al. First flare of ACPA-positive rheumatoid arthritis after SARS-CoV-2 infection. Lancet Rheumatol 2021;3:e6–8.
  • 13. Aletaha D, Neogi T, Silman AJ, et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum. 2010 Sep;62(9):2569-81.
  • 14. Fujinami RS, von Herrath MG, Christen U, Whitton JL (2006) Molecular mimicry, bystander activation, or viral persistence: in- fections and autoimmune disease. Clin Microbiol Rev 19:80–94.
  • 15. Angileri F, Legare S, Marino Gammazza A, Conway de Macario E, Jl Macario A, Cappello F. Molecular mimicry may explain multi-organ damage in COVID-19. Autoimmun Rev 2020;19:102591.
  • 16. Derksen VFAM, Kissel T, Lamers-Karnebeek FBG, van der Bijl AE, Venhuizen AC, Huizinga TWJ, Toes REM, Roukens AHE, van der Woude D. Onset of rheumatoid arthritis after COVID-19: coincidence or connected? Ann Rheum Dis. 2021 Mar 1:annrheumdis-2021-219859.
  • 17. ,Roongta R, Chattopadhyay A, Ghosh A. Correspondence on 'Onset of rheumatoid arthritis after COVID-19: coincidence or connected?'. Ann Rheum Dis. 2021 Apr 27:annrheumdis-2021-220479.
  • 18. Elemam NM, Maghazachi AA, Hannawi S. COVID-19 infection and rheumatoid arthritis: mutual outburst cytokines and remedies. Curr Med Res Opin. 2021 Jun;37(6):929-938.
  • 19. Tripathy A, Swain N, Gupta B. The COVID-19 pandemic: an increased risk of rheumatoid arthritis. Future Virol. 2021 Jun:10.2217/fvl-2020-0393.
  • 20. Li F, Xu J, Zheng J, et al. Association between interleukin-6 gene polymorphisms and rheumatoid arthritis in Chinese Han population: a case-control study and a meta-analysis. Sci Rep. 2014;4:5714.
  • 21. Kirtipal N, Bharadwaj S. Interleukin 6 polymorphisms as an indicator of COVID-19 severity in humans. J Biomol Struct Dyn. 2020:1–3.
  • 22. Demoruelle MK, Solomon JJ, Fischer A, Deane KD. The lung may play a role in the pathogenesis of rheumatoid arthritis. Int J Clin Rheumtol. 2014;9(3):295-309.
  • 23. Demoruelle MK, Deane KD, Holers VM. When and where does inflammation begin in rheumatoid arthritis? Curr Opin Rheumatol. 2014 Jan;26(1):64-71.
  • 24. Chatzidionisyou A, Catrina AI. The lung in rheumatoid arthritis, cause or consequence? Curr Opin Rheumatol. 2016 Jan;28(1):76-82.
There are 24 citations in total.

Details

Primary Language Turkish
Subjects Clinical Sciences
Journal Section Original research article
Authors

Reyhan Köse Çobanoğlu 0000-0001-9017-8483

Publication Date December 31, 2022
Submission Date February 18, 2022
Published in Issue Year 2022 Volume: 55 Issue: 3

Cite

AMA Köse Çobanoğlu R. SARS-Cov-2 Enfeksiyonu Sonrası Gelişen Romatoid Artrit: Yeni Bir Risk Faktörü Mü?. Ankara Eğitim ve Araştırma Hastanesi Tıp Dergisi. December 2022;55(3):179-182. doi:10.20492/aeahtd.1072187