State cellular immunity in patients with diabetes mellitus depending on the balance of uric acid

Authors

  • Karachentsev Y. I. SI «V. Danilevsky Institute of Endocrine Pathology Problems of the NAMS of Ukraine», Kharkiv, Ukraine
  • Kravchun N. A. SI «V. Danilevsky Institute of Endocrine Pathology Problems of the NAMS of Ukraine», Kharkiv, Ukraine
  • Tykhonova T.M. SI «V. Danilevsky Institute of Endocrine Pathology Problems of the NAMS of Ukraine», Kharkiv, Ukraine
  • Cherniaieva A. A. SI «V. Danilevsky Institute of Endocrine Pathology Problems of the NAMS of Ukraine», Kharkiv, Ukraine
  • Chervenko H. L. SI «V. Danilevsky Institute of Endocrine Pathology Problems of the NAMS of Ukraine», Kharkiv, Ukraine

DOI:

https://doi.org/10.21856/j-PEP.2018.3.02

Keywords:

diabetes mellitus, uric acid, purine metabolism, cellular immunity

Abstract

91 patients with diabetes mellitus (DM), including 28 patients with type 1 diabetes, 37 patients with type 2 diabetes and 26 patients with type 2 diabetes with developed absolute insulin deficiency, were examined. Based on the results of monoclonal antibodies determination in patients with DM, regardless of the type of disease, a significant decrease in the CD8+ — T-suppressor / cytotoxic lymphocyte content was established in combination with a significant increase in the relative amount of CD16+ — T-natural killers and CD20+ B lymphocytes. In type 1 diabetes, violations of purine metabolism lead to a further statistically significant decrease in the relative amount of CD8+ — T suppressors / cytotoxic lymphocytes, as evidenced by the growth of IRI. In patients with type 2 diabetes, impairment of purine metabolism is accompanied by a significant increase in the relative amount of CD3+ — mature T lymphocytes, CD8+ — T-suppressors/cytotoxic lymphocytes and a decrease in the level of IRI compared to those in patients with type 2 diabetes with normal uric acid levels. However, these changes in patients with type 2 DM in the development of purine dismetabolism do not lead to the normalization of these indicators, and these disorders are combined with the subsequent significant increase in the relative amount of CD16+ — T-natural killers in this cohort of patients.

References

Bandaru P, Shankar A. Int J Endocrinol 2011; 2: 75-81.

Thakur P, Kumar A, Patra PK, Kumar AA. Adv Hum Biol 2017; 7: 124-129.

Li C, Hsieh MC, Chang SJ. Curr Opin Rheumatol 2013; 25 (2): 210-216. https://doi.org/10.1097/BOR.0b013e32835d951e

Bonakdaran S, Kharaqani B. Curr Diabetes Rev 2014; 10 (2): 113-117. https://doi.org/10.2174/1573399810666140228160938

Chou P, Lin KC, Lin HY, Tsai ST. J Rheumatol 2001; 28 (3): 571-576.

Barskova VG, Eliseev MS, Zilov AV, Nasonov EL. Ozhirenie i Metabolizm 2007; 1: 19-23.

Madjanov IV. Osobennosti purinovogo obmena na jetapah razvitija i progressirovanija saharnogo diabeta (diagnosticheskie, patogeneticheskie i lechebnye aspekty), Moskva, 1999: 45 p.

Ficociello LH, Rosolowsky ET, Niewczas MA, et al. Diabetes Care 2010; 33: 1337-1343. https://doi.org/10.2337/dc10-0227

Ng G, Chau EM. Arch Immunol Ther Exp (Warsz) 2010; 58 (4): 273-277. https://doi.org/10.1007/s00005-010-0082-1

Ghaemi-Oskouie F, Shi Y. Curr Rheumatol Rep 2011; 13 (2): 160-166. https://doi.org/10.1007/s11926-011-0162-1

Saicrian K. A Study on the Role of Genes of Innate Immunity in Type 1 Diabetes, Stocholm, 2010: 69 p.

Beljakova NA, Rudenko EV, Mihajlova DG, et al. Saharnyj Diabet 2011; 2: 9-11.

Downloads

Published

2021-07-06

How to Cite

Karachentsev , Y. I., Kravchun, N. A., Tykhonova, T., Cherniaieva, A. A., & Chervenko, H. L. (2021). State cellular immunity in patients with diabetes mellitus depending on the balance of uric acid. Problems of Endocrine Pathology, 65(3), 16-23. https://doi.org/10.21856/j-PEP.2018.3.02

Issue

Section

CLINICAL ENDOCRINOLOGY

Most read articles by the same author(s)

1 2 3 4 > >>