diaendoСахарный диабетDiabetes mellitus2072-03512072-0378Endocrinology research centre10.14341/DM13249diaendo-13249Research ArticleОБЗОРЫREVIEWSРоль микроэлементов в патогенезе заболеваний глазной поверхности при сахарном диабете 2 типа: современные представления и клинические перспективыThe role of trace elements in the pathogenesis of ocular surface diseases in type 2 diabetes mellitus: current concepts and clinical perspectiveshttps://orcid.org/0000-0002-4601-0904СафоноваТ. Н.SafonovaT. N.

Сафонова Татьяна Николаевна, к.м.н., ведущий научный сотрудник отделения патологии слезного аппарата

WoS Researcher ID: HIA-059502022

Scopus Author ID: 7005163774

Москва 

Tatiana N. Safonova, MD, PhD

WoS Researcher ID: HIA-059502022

Scopus Author ID: 7005163774

Moscow

safotat@mail.ruhttps://orcid.org/0000-0001-8575-3076ЗайцеваГ. В.ZaytsevaG. V.

Зайцева Галина Валерьевна, к.м.н., научный сотрудник отделения патологии слезного аппарата

119021, г. Москва, ул. Россолимо 11 А, Б 

Galina V. Zaytseva, MD, PhD

WoS Researcher ID: AAO-6881-2021

Scopus Author ID: 57202792897

11 A, B Rossolimo street, 119021 Moscow

privezentseva.galya@mail.ruНаучно-исследовательский институт глазных болезней имени М.М. КрасноваРоссияKrasnov Research Institute of Eye DiseasesRussian Federation202626072026293277282Copyright © Сафонова Т.Н., Зайцева Г.В., 20262026Сафонова Т.Н., Зайцева Г.В.Safonova T.N., Zaytseva G.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.dia-endojournals.ru/jour/article/view/13249

Сахарный диабет 2 типа (СД2) представляет собой значимый фактор риска развития патологии глазной поверхности, с распространенностью синдрома сухого глаза, дисфункции мейбомиевых желез и хронического блефарита, превышающей таковую в общей популяции в 2–3 раза. В обзоре проведен комплексный анализ роли дисбаланса микроэлементов в формировании и прогрессировании заболеваний глазной поверхности при СД2. Особое внимание уделено аспектам влияния дефицита или избытка цинка, меди, селена, магния и железа на ключевые патогенетические звенья: оксидативный стресс, хроническое воспаление, микроангиопатию, нейропатию и нарушение репаративных процессов. Систематизированы современные данные об изменениях микроэлементного профиля в системном кровотоке, слезной жидкости, секрете мейбомиевых желез у пациентов с СД2. Рассмотрены взаимосвязи между специфическими нарушениями микроэлементного гомеостаза и клиническими фенотипами поражения глазной поверхности. Представлены доказательства, указывающие на то, что микроэлементный дисбаланс выступает не пассивным маркером, а активным участником патологического каскада, определяющего характер и тяжесть офтальмологических проявлений СД2. Определены перспективные направления исследований, включая разработку методов неинвазивной оценки микроэлементного статуса глазной поверхности, создание таргетных средств коррекции и интеграцию микроэлементного подхода в персонализированные алгоритмы ведения пациентов с диабетическим поражением.

Type 2 diabetes mellitus (T2DM) represents a significant risk factor for the development of ocular surface pathology, with the prevalence of dry eye syndrome, meibomian gland dysfunction, and chronic blepharitis exceeding that in the general population by 2–3 times. This review provides a comprehensive analysis of the role of trace element imbalance in the formation and progression of ocular surface diseases in T2DM. Particular attention is paid to the aspects of the influence of deficiency or excess of zinc, copper, selenium, magnesium, and iron on key pathogenetic links: oxidative stress, chronic inflammation, microangiopathy, neuropathy, and impaired reparative processes. Modern data on changes in the trace element profile in the systemic bloodstream, tear fluid, and meibomian gland secretion in patients with T2DM are systematized. The relationships between specific disorders of trace element homeostasis and clinical phenotypes of ocular surface damage are considered. Evidence is presented indicating that trace element imbalance acts not as a passive marker, but as an active participant in the pathological cascade, that determines the nature and severity of ophthalmic manifestations of T2DM. Promising research directions are outlined, including the development of methods for non-invasive assessment of the ocular surface trace element status, the creation of targeted correction tools, and the integration of the trace element approach into personalized algorithms for managing patients with diabetic eye involvement.

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