clinmedКлиническая медицинаClinical Medicine (Russian Journal)0023-21492412-1339ООО «Медицинское информационное агентство»10.30629/0023-2149-2020-98-9-10-691-698clinmed-145Research ArticleОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯORIGINAL INVESTIGATIONSЗначение обмена железа, цитокинов в патогенезе анемии у больных ревматологического профиляIron metabolism, cytokine secretion in patients with rheumatologic pathologyhttps://orcid.org/0000-0001-5445-6028СахинВ. Т.SakhinV. T.

Сахин Валерий Тимофеевич — канд. мед. наук, старший ординатор кардиологического отделения 1586

142110, Подольск

Valery Timofeevich Sakhin — PhD, a senior resident cardiology department FSI

142110, Podolsk

SahinVT@yandex.ruhttps://orcid.org/0000-0002-8396-1936КрюковЕ. В.KryukovE. V.

105229, Москва

105229, Moscow

https://orcid.org/0000-0003-3586-9067ГригорьевМ. А.GrigoryevM. A.

194291, Санкт-Петербург

194291, St. Petersburg

https://orcid.org/0000-0001-6528-1059КазаковС. П.KazakovS. P.

105229, Москва

105229, Moscow

https://orcid.org/0000-0002-5913-9088СотниковА. В.SotnikovA. V.

194044, Санкт-Петербург

194044, St. Petersburg

https://orcid.org/0000-0002-6901-6436ГордиенкоА. В.GordienkoA. V.

194044, Санкт-Петербург

194044, St. Petersburg

https://orcid.org/0000-0002-1309-7265РукавицынО. А.RukavitsynO. A.

105229, Москва

105229, Moscow

ФГКУ «1586 Военный клинический госпиталь» МО РФРоссия1586 Military Hospital of the Ministry of Defense of RussiaRussian FederationФГБУ «Главный военный клинический госпиталь имени Н.Н. Бурденко» МО РФРоссияMain Military Hospital named after Burdenko N.N.Russian FederationГБУЗ «Ленинградская областная клиническая больница»РоссияLeningrad Regional Clinical Hospital, St. PetersburgRussian FederationФГБВОУ ВО «Военно-медицинская академия имени С.М. Кирова» МО РФРоссияRussian Military Medical Academy of the Ministry of Defense of RussiaRussian Federation202026032021989-10691698Copyright © Сахин В.Т., Крюков Е.В., Григорьев М.А., Казаков С.П., Сотников А.В., Гордиенко А.В., Рукавицын О.А., 20212021Сахин В.Т., Крюков Е.В., Григорьев М.А., Казаков С.П., Сотников А.В., Гордиенко А.В., Рукавицын О.А.Sakhin V.T., Kryukov E.V., Grigoryev M.A., Kazakov S.P., Sotnikov A.V., Gordienko A.V., Rukavitsyn O.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.clinmedjournal.com/jour/article/view/145Цель

Цель. Изучить влияние гепцидина, растворимого рецептора трансферрина (sTfR ), цитокинов на обмен железа и развитие анемии у ревматологических больных, предложить рабочий вариант классификации анемии хронических заболеваний (АХЗ) по ведущему патогенетическому фактору.

Материал и методы

Материал и методы. Обследованы 126 ревматических больных: 34 мужчины (45,8 [36–54,9] года), 92 женщины (49,5 [38–60] года). В 1-ю группу вошел 41 пациент с АХЗ, во 2-ю — 29 с сочетанием АХЗ и ЖДА, в 3-ю — 34 с железодефицитной анемией (ЖДА), 22 пациента составили контрольную группу — без анемии. Выполнен сравнительный анализ между группами с анемией и без нее и корреляционный анализ показателей гемограммы, обмена железа, С-реактивного белка (СРБ), гепцидина, sTfR, интерлейкина-6 (ИЛ-6), ИЛ-1β, ИЛ-10, интерферона-гамма (ИНФ-γ), фактора некроза опухоли альфа (ФНО-α).

Результаты

Результаты. В группе АХЗ повышены концентрации гепцидина, ферритина, СРБ, ИЛ-6 в сравнении с другими группами. Выявлена взаимосвязь между эритроцитами, гемоглобином и ИЛ-6 (r = −0,3 и −0,6), ИЛ-10 (r = −0,4 и −0,4), ИНФ-γ (r = −0,4 и −0,3), ФНО-α (r = −0,3 и −0,3), гепцидином (r = −0,5 и −0,7), sTfR (r = −0,5 и −0,7). Показана зависимость между ИЛ-6 и железом (r = −0,6), коэффициентом насыщения трансферрина (КНТ) (r = −0,5), ферритином (r = −0,5), СРБ (r = 0,5), между ФНО-α и ОЖСС (r = −0,6), трансферрином (r = −0,6), ферритином (r = −0,7), между ИЛ-1β и ОЖСС, ферритином, трансферрином (r = −0,4). Установлена взаимосвязь между гепцидином и ИЛ-6 (r = 0,5), ИЛ-10 (r = 0,4), между sTfR и ИЛ-6 (r = 0,4), ИЛ-10 (r = 0,6), ИНФ-γ (r = 0,4).

Заключение

Заключение. Показан многокомпонентный генез анемии у ревматологических больных. Установлено значение нарушений в обмене железа, влияния гепцидина, sTfR и цитокинов на развитие анемии. Предложен рабочий вариант классификации АХЗ (с преимущественным дефицитом железа, с нарушениями регуляторных механизмов эритропоэза, с недостаточной продукцией эритропоэтина).

Aim

Aim. To study the eff ect of hepcidin, soluble transferrin receptor (sTfR ), and cytokines on iron metabolism and the development of anemia in rheumatologic patients, to propose a working version of the classifi cation of anemia of chronic diseases (ACD) according to the major nosotropic factor.

Material and methods

Material and methods. 126 patients with rheumatic disease, 34 men (45.8 (36–54.9) years old), 92 women (49.5 (38–60) years old) were examined. Group 1 included 41 patients with ACD. Group 2 included 29 patients with the combination of ACD and IDA and 34 patients with iron defi ciency anemia (IDA). Group 3 included 34 patients with IDA and 29 — with the combination of ACD and IDA. Control group included 22 patients without anemia. Comparative analysis between groups with and without anemia and correlation analysis of hemogram parameters, iron metabolism, C-reactive protein (CRP), hepcidin, sTfR , interleukin-6 (IL-6), IL-1β, IL-10, interferon gamma (INF-γ) and tumor necrosis factor alpha (TNF-α) were performed.

Results

Results. In the ACD group, the concentrations of hepcidin, ferritin, CRP, IL-6 were increased in comparison with other groups. The correlation was revealed between erythrocytes, hemoglobin and IL-6 (r = −0.3 and −0.6), IL-10 (r = −0.4 and −0.4), INF-γ (r = −0.4 and −0.3), TNF-α (r = −0.3 and −0.3), hepcidin (r = −0.5 and −0.7), sTfR (r = −0.5 and −0.7). Dependence was shown between IL-6 and iron (r = –0.6), transferrin saturation index (TSI) (r = −0.5), ferritin (r = −0.5), CRP (r = 0.5), between TNF-α and TIBС (r = −0.6), transferrin (r = −0.6), ferritin (r = −0.7), between IL-1β and TIBC, ferritin, transferrin (r = −0.4). The correlation was noted between hepcidin and IL-6 (r = 0.5), IL-10 (r = 0.4), between sTfR and IL-6 (r = 0.4), IL-10 (r = 0.6), INF-γ (r = 0.4).

Conclusion

Conclusion. The multicomponent genesis of anemia in patients with rheumatologic disease was detected. The signifi cance of disorders in iron metabolism, the eff ect of hepcidin, sTfR and cytokines on the development of anemia was found. A working version of ACD classifi cation (with a predominant iron defi ciency, with violations of the regulatory mechanisms of erythropoiesis, with insuffi cient production of erythropoietin) has been put forward.

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The authors declare that there are no conflicts of interest present.