Etiopathogenesis of systemic lupus erythematosus: molecular interactions and immune response
Keywords:
Systemic lupus erythematosus, Immune response, Amino acid metabolism, AutoantibodiesAbstract
Currently, establishing an accurate clinical diagnosis of systemic lupus erythematosus (SLE) represents a challenge in the Ecuadorian context, as in most cases, this is done when the disease has reached an advanced stage. Due to this situation, the medical community has directed its efforts to identify additional biomarkers in the bloodstream that facilitate early detection, beyond the presence of traditional antinuclear antibodies. In this study, adapted to the clinical reality of Ecuador, serum arginine levels were analyzed in clinically healthy individuals and in patients diagnosed with SLE at different referral hospitals in the country. The analyses revealed arginine concentrations ranging from 4 to 17 mg/dL in healthy individuals, while in SLE patients, levels ranged from 0.0 to 11 mg/dL. It is important to note that 77% of Ecuadorian patients diagnosed with SLE presented a significant reduction in arginine levels. Additionally, it was found that patients with arginine levels below 6 mg/dL also had elevated antinuclear antibody titers, suggesting a possible correlation between the two parameters. These findings represent a valuable contribution to the understanding of SLE in Ecuador and reinforce the hypothesis that serum arginine measurement may be a useful complementary tool in the comprehensive diagnosis of this autoimmune disease.
References
1. Ruiz, B. E., & Suarez, R. J. (1992). Lupus eritematoso sistémico. Acta Médica, 28, 93–102.
2. Manolios, N., & Schrieber, L. (1986). Current concepts in the etiopathogenesis and treatment of systemic lupus erythematosus (SLE). Australian and New Zealand Journal of Medicine, 16(5), 729–743.
3. Enriquez-Mejía, M. G. (2013). Fisiopatología del lupus eritematoso sistémico. Revista Medicina e Investigación, 1, 1–9.
4. Drayer, D. E., Reidenberg, M. M., & Reindenberg, M. M. (1977). Clinical consequences of polymorphic acetylation of basic drugs. Clinical Pharmacology & Therapeutics, 22(3), 251–258.
5. Zacharias, W., & Koopman, W. J. (1990). Lupus-inducing drugs alter the structure of supercoiled circular DNA domains. Arthritis & Rheumatism, 33(3), 366–374.
6. Dubroff, L. M., & Reid, R. J. Jr. (1980). Hydralazine-pyrimidine interactions may explain hydralazine-induced lupus erythematosus. Science, 208(4442), 404–406.
7. Ruiz, B. E., & Dionisio, A. M. (1996). Evaluación de los niveles de creatinina sérica en lupus eritematoso sistémico. Revista Mexicana de Patología Clínica, 43, 35–37.
8. Ruiz, B. E., & Bravo, M. J. (1997). Ornitina sérica en pacientes con lupus eritematoso sistémico. Revista Mexicana de Patología Clínica, 44, 217–221.
9. Ruiz, B. E. (2009). Arginasa sérica en pacientes con lupus eritematoso sistémico. Revista Mexicana de Patología Clínica, 56, 45–49.
10. Oginsky, E. L. (1957). Isolation and determination of arginine and citrulline. Methods in Enzymology, 3, 639–643.
11. Gonzalez, E. N., & Rothfield, N. F. (1966). Immunoglobulin class and pattern of nuclear fluorescence in systemic lupus erythematosus. New England Journal of Medicine, 274(24), 1333–1338.
12. Pegg, A. E. (1986). Recent advances in the biochemistry of polyamines in eukaryotes. Biochemical Journal, 234(2), 249–262.
13. Winfield, J. B., Faiferman, I., & Koffler, D. (1977). Avidity of anti-DNA antibodies in serum and IgG glomerular eluates from patients with systemic lupus erythematosus. Journal of Clinical Investigation, 59(1), 90–96.
14. Featherston, W. R., Rogers, Q. R., & Freedland, R. A. (1973). Relative importance of kidney and liver in synthesis of arginine by the rat. American Journal of Physiology, 224(1), 127–129.
15. Rahiala, E. L., Kekomäki, M., Jänne, J., et al. (1971). Inhibition of pyridoxal enzymes by L-canaline. Biochimica et Biophysica Acta, 227(2), 337–343.
16. Shih, V. E., Mandell, R., & Berson, E. L. (1988). Pyridoxine effects on ornithine ketoacid transaminase activity in fibroblasts from carriers of two forms of gyrate atrophy of the choroid and retina. American Journal of Human Genetics, 43(6), 929–933.
17. Kito, K., Sanada, Y., & Katunuma, N. (1978). Mode of inhibition of ornithine aminotransferase by L-canaline. Journal of Biochemistry, 83(1), 201–206.
18. Sipilä, I. (1980). Inhibition of arginine-glycine aminodiotransferase by ornithine. Biochimica et Biophysica Acta, 613, 79–83.
19. Morimoto, I., Shiozawa, S., Tanaka, Y., et al. (1990). L-canavanine acts on suppressor-inducer T cells to regulate antibody synthesis: lymphocytes of systemic lupus erythematosus patients are specifically unresponsive to L-canavanine. Clinical Immunology and Immunopathology, 55(1), 97–108.
20. Barbul, A., Sisto, D. A., Wasserkrug, H. L., et al. (1981). Arginine stimulates lymphocyte immune response in healthy human beings. Surgery, 90(2), 244–251.
21. Susskind, B. M., & Chandrasekaran, J. (1987). Inhibition of cytolytic T lymphocyte maturation with ornithine, arginine, and putrescine. Journal of Immunology, 139(3), 905–912.
22. Morris, D. R. (1991). A new perspective on ornithine decarboxylase regulation: prevention of polyamine toxicity is the overriding theme. Journal of Cellular Biochemistry, 46(2), 102–105.
23. Pisetsky, D. S., Grudier, J. P., & Gilkeson, G. S. (1990). A role for immunogenic DNA in the pathogenesis of systemic lupus erythematosus. Arthritis & Rheumatism, 33(2), 153–159.
24. Schwartz, R. S., & Stollar, B. D. (1985). Origins of anti-DNA autoantibodies. Journal of Clinical Investigation, 75(2), 321–327.
25. Portanova, J. P., Arndt, R. E., Tan, E. M., et al. (1987). Anti-histone antibodies in idiopathic and drug-induced lupus recognize distinct intrahistone regions. Journal of Immunology, 138(2), 446–451.
26. Tanner, J. J., Komissarov, A. A., & Deutscher, S. L. (2001). Crystal structure of an antigen-binding fragment bound to single-stranded DNA. Journal of Molecular Biology, 314(4), 807–822.
Downloads
Published
Issue
Section
License
Copyright (c) 2023 Sapiens in Health Sciences International Journal

This work is licensed under a Creative Commons Attribution 4.0 International License.
Articles published in this journal are available under the Creative Commons Attribution 4.0 International (CC BY 4.0) licence. This licence authorises third parties to download, copy, distribute, adapt and reuse the contents, including for commercial purposes, provided that credit is given to the original author of the work.
