diaendoСахарный диабетDiabetes mellitus2072-03512072-0378Endocrinology research centre10.14341/DM13294diaendo-13294Research ArticleОБЗОРЫREVIEWSПсихоорганический синдром при сахарном диабете 1 типа: осложнение диабета или сопутствующая патология? Обзор литературыPsychoorganic syndrome in type 1 diabetes mellitus: a concomitant disease or a complication of diabetes? (Review)https://orcid.org/0000-0002-3328-2812СтаростинаЕ. Г.StarostinaE. G.

Старостина Елена Георгиевна - д.м.н., профессор.

Москва

ResearcherID C-9409-2014; Scopus Author ID 7003980023

Elena G. Starostina - MD, PhD, Professor.

Moscow

ResearcherID C-9409-2014; Scopus Author ID 7003980023

elena.starostina@rambler.ruhttps://orcid.org/0009-0006-8873-5301КотоваТ. С.KotovaT. S.

Котова Татьяна Сергеевна – аспирант.

129110, Москва, ул. Щепкина, д. 61/2

Tatyana S. Kotova - PhD student.

61/2, Schepkina street, 129110 Moscow

dr.tanya@inbox.ruМосковский областной научно-исследовательский клинический институт им. М.Ф. ВладимирскогоРоссияMoscow Regional Clinical and Research InstituteRussian Federation202524072025283274283Copyright © Старостина Е.Г., Котова Т.С., 20252025Старостина Е.Г., Котова Т.С.Starostina E.G., Kotova T.S.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/13294

Психоорганический синдром (ПОС), также известный как энцефалопатия, характеризуется снижением когнитивных функций, недержанием эмоций (эмоциональной лабильностью) и астеническими симптомами. Он может развиваться вследствие целого ряда экзогенных и эндогенных факторов, и, несмотря на использование термина «диабетическая энцефалопатия», доказательства существования специфического диабетического генеза ПОС остаются ограниченными. В обзоре подробно рассмотрена история возникновения термина «ПОС» и его определение, компоненты ПОС и его возможные причины, «за» и «против» существования ПОС диабетического генеза. Обсуждены вероятность влияния дисгликемии на развитие ПОС и изменения в головном мозге у больных сахарным диабетом 1 типа (СД1) по данным нейровизуализации, а также их взаимосвязь друг с другом и с другими клиническими параметрами, в том числе с возрастом манифестации CД, длительностью заболевания, острыми осложнениями СД, диабетической ретинпатией как маркером длительного воздействия гипергликемии. У молодых взрослых с СД1 показатели когнитивных функций находятся в пределах возрастной нормы, а ассоциации с выраженностью гипергликемии или другими осложнениями диабета не воспроизводятся в крупных исследованиях. Анализ нейровизуализационных и патоморфологических данных также не дает убедительного подтверждения уникальных для СД1 изменений в структурах головного мозга. Таким образом, вопрос ПОС (энцефалопатии) при СД1 остается недостаточно изученным и противоречивым. Текущие данные не позволяют однозначно принять мнение о специфическом диабетическом характере ПОС при СД1. Необходимы дальнейшие исследования для определения вклада диабета и сопутствующих факторов в развитие ПОС, включая гистологические данные.

Psychoorganic syndrome (POS), also known as organic brain syndrome, or encephalopathy, is characterized by cognitive decline, emotional incontinence (emotional lability), and asthenic symptoms. It can develop due to a number of exogenous and endogenous factors, and despite the use of the term «diabetic encephalopathy», the evidence for a specific diabetic etiology of POS remains limited. The review provides a detailed history of the term POS and its definition, components and possible causes, pros and cons of the existence of POS of diabetic origin. The potential influence of dysglycemia on the development of POS and brain abnormalities in Type 1 diabetic patients (T1D) found at neuroimaging, as well as their associations between each other and with other clinical parameters, including the age at diabetes manifestation, disease duration, acute diabetic complications, and diabetic retinopathy as a marker of a long-term exposure to hyperglycemia, are discussed. In young adults with T1DM, cognitive function parameters fall within the age-related reference ranges, and their associations with the degree of hyperglycemia or severe hypoglycemia are not reproducible in larger samples. The analysis of neuroimaging and histological data also does not provide convincing evidence that brain abnormalities are unique to T1DM. Thus, the issue of POS (encephalopathy) in T1DM remains insufficiently studied and controversial. Current data does not allow to unequivocally accept the specific diabetic nature of POS/encephalopathy in T1D. Further studies are necessary to identify the contribution of diabetes and associated factors to the development of POS, including histological data.

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