Coronavirus disease 2019 (COVID-19) and polyarthritis juvenile idiopathic arthritis (JIA) comorbidity in children at emergency Wisma Atlet Kemayoran: the first case report with two months follow up
Main Article Content
Keywords
COVID-19, JIA, comorbidity, hyperinflammation
Abstract
Background: Infection with SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) is often mild and asymptomatic in youngsters. However, in other circumstances, such as juvenile rheumatoid arthritis (JRA), COVID-19 necessitates special consideration because of the general immune system harm associated with autoimmune disorders and the iatrogenic side effects of corticosteroids. The multisystem inflammatory syndrome in children (MIS-C), which manifests 4-6 weeks after infection as a high fever, organ dysfunction, and markedly elevated markers of inflammation, is one manifestation of the COVID-19 disease that can cause secondary vasculitis or present with vasculitis or hyperinflammation manifestations. The association between MIS-C and SARS-CoV-2 infection shows that post-infectious immunological dysregulation plays a role in the pathogenesis. This study aimed to present a case of COVID-19 and JRA comorbidity in children at emergency Wisma Atlet Kemayoran.
Case Report: A 10-year-old boy was admitted to COVID-19 Emergency Hospital Wisma Atlet Kemayoran with complaints of anosmia. The patient had a history of polyarthritis JRA, has been diagnosed since January 2020 and has routinely received methylprednisolone 4 mg/day and one tablet of calcium lactate once daily. No abnormalities were discovered during a general physical examination or a Pediatric Gait, Arms, Legs, and Spine (pGALS) assessment. On laboratory testing, leukocytosis and thrombocytosis are present. Thorax and extremities were radiologically examined within acceptable bounds. According to national guidelines for mild COVID-19 in children, the patient got routine treatment, which included a multivitamin. The patient also continued receiving methylprednisolone and calcium lactate while he was treated. After 12 days of treatment, the patient tested negative for COVID-19. One month after treatment, there was no hyperinflammatory reaction or recurrence of JRA.
Conclusion: In pediatric patients diagnosed with COVID-19 and JRA, it is important to continue corticosteroid treatment with an adjusted dose. Even though this treatment has the possibility of causing immunosuppression which can complicate the healing process of COVID-19, we need to prevent the recurrence of JRA in patients.
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11. Misra DP, Agarwal V, Gasparyan AY, Zimba O. Rheumatologists’ perspective on coronavirus disease 19 (COVID-19) and potential therapeutic targets. Clin Rheumatol. 2020/04/10. 2020;39(7):2055–62. Available in: https://pubmed.ncbi.nlm.nih.gov/32277367
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21. Netea MG, Domínguez-Andrés J, Barreiro LB, Chavakis T, Divangahi M, Fuchs E, et al. Defining trained immunity and its role in health and disease. Nat Rev Immunol. 2020/03/04. 2020;20(6):375–88. Available in: https://pubmed.ncbi.nlm.nih.gov/32132681
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23. Arts RJW, Moorlag SJCFM, Novakovic B, Li Y, Wang S-Y, Oosting M, et al. BCG Vaccination Protects against Experimental Viral Infection in Humans through the Induction of Cytokines Associated with Trained Immunity. Cell Host & Microbe. 2018;23(1):89-100.e5. Available in: http://dx.doi.org/10.1016/j.chom.2017.12.010
24. Berg RE, Cordes CJ, Forman J. Contribution of CD8+ T cells to innate immunity: IFN-γ secretion induced by IL-12 and IL-18. Eur J Immunol. 2002;32(10):2807–16. Available in: http://dx.doi.org/10.1002/1521-4141(2002010)32:10%3C2807::aid-immu2807%3E3.0.co
25. Berg RE, Crossley E, Murray S, Forman J. Memory CD8+ T cells provide innate immune protection against Listeria monocytogenes in the absence of cognate antigen. J Exp Med. 2003;198(10):1583–93. Available in: https://pubmed.ncbi.nlm.nih.gov/14623912
26. Lertmemongkolchai G, Cai G, Hunter CA, Bancroft GJ. Bystander Activation of CD8+ T Cells Contributes to the Rapid Production of IFN-γ in Response to Bacterial Pathogens. J Immunol. 2001;166(2):1097–105. Available in: http://dx.doi.org/10.4049/jimmunol.166.2.1097
27. Mathurin KS, Martens GW, Kornfeld H, Welsh RM. CD4 T-cell-mediated heterologous immunity between mycobacteria and poxviruses. J Virol. 2009/02/04. 2009;83(8):3528–39. Available in: https://pubmed.ncbi.nlm.nih.gov/19193795
28. Kleinnijenhuis J, Quintin J, Preijers F, Joosten LAB, Ifrim DC, Saeed S, et al. Bacille Calmette-Guerin induces NOD2-dependent nonspecific protection from reinfection via epigenetic reprogramming of monocytes. Proc Natl Acad Sci U S A. 2012/09/17. 2012;109(43):17537–42. Available in: https://pubmed.ncbi.nlm.nih.gov/22988082
29. Teran R, Mitre E, Vaca M, Erazo S, Oviedo G, Hübner MP, et al. Immune system development during early childhood in tropical Latin America: evidence for the age-dependent down regulation of the innate immune response. Clin Immunol. 2011/01/17. 2011;138(3):299–310. Available in: https://pubmed.ncbi.nlm.nih.gov/21247809
30. Pou C, Nkulikiyimfura D, Henckel E, Olin A, Lakshmikanth T, Mikes J, et al. The repertoire of maternal anti-viral antibodies in human newborns. Nat Med. 2019;25(4):591–6. Available in: http://dx.doi.org/10.1038/s41591-019-0392-8
31. Meyer K. The Role of Immunity and Inflammation in Lung Senescence and Susceptibility to Infection in the Elderly. Semin Respir Crit Care Med. 2010;31(05):561–74. Available in: http://dx.doi.org/10.1055/s-0030-1265897
32. Lowery EM, Brubaker AL, Kuhlmann E, Kovacs EJ. The aging lung. Clin Interv Aging. 2013/11/06. 2013;8:1489–96. Available in: https://pubmed.ncbi.nlm.nih.gov/24235821
33. Favalli EG, Ingegnoli F, De Lucia O, Cincinelli G, Cimaz R, Caporali R. COVID-19 infection and rheumatoid arthritis: Faraway, so close! Autoimmun Rev. 2020/03/20. 2020;19(5):102523. Available in: https://pubmed.ncbi.nlm.nih.gov/32205186
34. Buch M, Emery P. The aetiology and pathogenesis of rheumatiod arthritis. Hosp Pharm. 2002;9(1):5–10.
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