ssmuБюллетень сибирской медициныBulletin of Siberian Medicine1682-03631819-3684Siberian State Medical University, the Ministry of Healthcare of the Russian Federation10.20538/1682-0363-2023-3-132-140ssmu-5319Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEW AND LECTURESДиабетический кетоацидоз и когнитивные нарушения у детей и подростковDiabetic ketoacidosis and cognitive impairment in children and adolescentshttps://orcid.org/0000-0003-1167-9074МагомедоваК. Ш.MagomedovaK. Sh.

Магомедова Камила Шамхаловна – врач-терапевт

357930, Ставропольский край, Степновский район, с. Степное, ул. Додонова, 52а

52а, Dodonova Str., Stepnoye village, Stavropol Region, 357930

kamilla.2017@bk.ruhttps://orcid.org/0000-0003-4705-3823БыковЮ. В.BykovYu. V.

Быков Юрий Витальевич – кандидат медицинских наук, ассистент, кафедра анестезиологии и реаниматологии с курсом ДПО, СтГМУ; Детская городская клиническая больница им. Г.К. Филиппского

355017, г. Ставрополь, ул. Мира, 310,

355002, г. Ставрополь, ул. Пономарева, 5

310, Mira Str., Stavropol, 355017,

5, Ponomareva Str., Stavropol, 355002

yubykov@gmail.comhttps://orcid.org/0000-0002-6892-3552БатуринВ. А.BaturinV. A.

Батурин Владимир Александрович – доктор медицинских наук, профессор, кафедра клинической фармакологии с курсом ДПО

355017, г. Ставрополь, ул. Мира, 310

310, Mira Str., Stavropol, 355017

prof.baturin@gmail.comСтепновская районная больницаРоссияStepnovskaya District HospitalRussian FederationСтавропольский государственный медицинский университет (СтГМУ) ; Детская городская клиническая больница им. Г.К. ФилиппскогоРоссияStavropol State Medical University; Children’s City Clinical Hospital named G. K. FilippskyRussian FederationСтавропольский государственный медицинский университет (СтГМУ)РоссияStavropol State Medical UniversityRussian Federation202318102023223132140Copyright © Магомедова К.Ш., Быков Ю.В., Батурин В.А., 20232023Магомедова К.Ш., Быков Ю.В., Батурин В.А.Magomedova K.S., Bykov Y.V., Baturin V.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://bulletin.ssmu.ru/jour/article/view/5319

Цель исследования – освещение современных научных источников по вопросам формирования и клиническим проявлениям когнитивных нарушений у детей и подростков с сахарным диабетом (СД) 1-го типа после перенесенного диабетического кетоацидоза (ДКА). СД 1-го типа является одним из распространенных эндокринных заболеваний в детском и подростковом возрасте. ДКА – наиболее частое острое осложнение СД 1-го типа, который может вызывать когнитивные нарушения. Отек головного мозга при ДКА является основной причиной, приводящей к церебральной недостаточности. Механизмы формирования когнитивной дисфункции при ДКА полностью не выяснены.

Ведущими гипотезами являются: возникновение нейровоспаления, оксидативный стресс, нарушение процессов нейрогенеза и нейродегенерация. Гипоксически-ишемические нарушения и изменения в нейроанатомии головного мозга также могут являться причинами когнитивной дисфункции. Отмечено нарушение некоторых структур головного мозга после ДКА, в первую очередь белого вещества. Клинические исследования, проведенные в педиатрической популяции, подтверждают корреляцию между тяжестью и частотой ДКА и выраженностью когнитивных нарушений. Когнитивная дисфункция у детей и подростков после ДКА может проявляться в снижении внимания, нарушении памяти и исполнительной функции, а также в низком уровне IQ. Максимально ранняя диагностика когнитивных нарушений в педиатрической практике при СД 1-го типа с проявлениями ДКА может улучшить терапевтический прогноз при лечении данной эндокринопатии.

 

The aim of the literature review was to highlight modern scientific sources on the formation and clinical manifestations of cognitive impairment in children and adolescents with type 1 diabetes mellitus (DM) after diabetic ketoacidosis (DKA). Type 1 DM is one of the most prevalent endocrine disorders in childhood and adolescence. DKA is the most common acute complication of type 1 DM that may cause cognitive impairment. Cerebral edema is the main cause of cerebral vascular insufficiency in patients with DKA. However, the mechanisms underlying the development of cognitive dysfunction in DKA have not been fully elucidated.

The leading hypotheses include development of neuroinflammation, oxidative stress, disruption of neurogenesis, and neurodegeneration. Hypoxic – ischemic injury and changes in the brain neuroanatomy may also cause cognitive dysfunction. Disruption of some brain structures has been reported after DKA episodes, primarily affecting the white matter. Clinical studies in the pediatric population support the presence of a correlation between the severity and frequency of DKA and the severity of cognitive impairment. Cognitive dysfunction in children and adolescents after a DKA episode can manifest through decreased attention, impaired memory and executive function, and reduced IQ. The earliest possible diagnosis of cognitive impairment in pediatric patients with symptoms of DKA in the context of type 1 DM can improve the treatment prognosis for this endocrinopathy.

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