Russian Journal of Child NeurologyRussian Journal of Child NeurologyРусский журнал детской неврологии2073-88032412-9178Publishing House ABV Press49510.17650/2073-8803-2024-19-4-42-51CLINICAL OBSERVATIONSКЛИНИЧЕСКИЕ НАБЛЮДЕНИЯMoya-moya disease in a child with nephropatic cystinosis: a case report and literature reviewБолезнь мойя-мойя у ребенка с нефропатическим цистинозом: клиническое наблюдение и обзор литературыhttps://orcid.org/0000-0002-7520-1072PivovarovaA. M.ПивовароваА. М.
Russian Federation

Aleksandra Mikhaylovna Pivovarova 

2 Taldomskaya St., Moscow 125412

Александра Михайловна Пивоварова 

125412 Москва, ул. Талдомская, 2

ampivovarova@gmail.comhttps://orcid.org/0000-0001-6459-2795PapizhS. V.ПапижС. В.
Russian Federation

2 Taldomskaya St., Moscow 125412

125412 Москва, ул. Талдомская, 2

https://orcid.org/0000-0003-3071-578XKаzakovD. O.КазаковД. О.
Russian Federation

2 Taldomskaya St., Moscow 125412

125412 Москва, ул. Талдомская, 2

https://orcid.org/0000-0001-9286-7805GorchkhanovаK. Z.ГорчхановаЗ. К.
Russian Federation

2 Taldomskaya St., Moscow 125412

125412 Москва, ул. Талдомская, 2

https://orcid.org/0000-0002-2910-3711MelnikovI. A.МельниковИ. А.
Russian Federation

22 Bolshaya Polyanka St., Moscow 119180

119180 Москва, ул. Большая Полянка, 22

Yu.E. Veltischev Research and Clinical Institute for Pediatrics and Pediatric Surgery, N.I. Pirogov Russian National Research Medical University, Ministry of Health of RussiaНаучно-исследовательский клинический институт педиатрии и детской хирургии им. акад. Ю.Е. Вельтищева ФГАОУ ВО «Российский национальный исследовательский медицинский университет им. Н.И. Пирогова» Минздрава РоссииResearch Institute for Urgent Pediatric Surgery and Traumatology, Moscow Healthcare DepartmentГБУЗ «Научно-исследовательский институт неотложной детской хирургии и травматологии» Департамента здравоохранения г. Москвы1512202419442512201202522012025Copyright ©; 2024, ABV-PressCopyright ©; 2024, АБВ-пресс2024ABV-PressАБВ-прессhttps://rjdn.abvpress.ru/jour/about/editorialPolicieshttps://rjdn.abvpress.ru/jour/article/view/495

The article presents a case report of a child with a combination of two ultra rare diseases: nephropathic cystinosis and moya-moya disease.

Cystinosis is an autosomal recessive lysosomal storage disorder characterized by accumulation of cystine in lysosomes throughout the body. Cystinosis is caused by mutations in the CTNS gene that encodes the lysosomal cystine carrier protein cystinosin. The lack of functional cystinosin causes accumulation and crystallization of cystine within the lysosomes, which leads to apoptosis and tissue damage in all organs. The disease is characterized by renal (Fanconi syndrome with progressive decline in renal function) and extrarenal manifestations in the form of hypothyroidism, hypogonadism, insulin-dependent diabetes mellitus, coronary vascular calcification, metabolic bone disease, damage to the central nervous system with cortical atrophy, cerebral calcification and etc.

Moya-moya disease is a progressive condition that can lead to ischemic stroke or intracranial hemorrhage in children and adults. The following types of this condition are distinguished: moya-moya disease primary (idiopathic) refers to patients with angiographic evidence of the disease, who may have a genetic predisposition, but do not have concomitant diseases and moya-moya syndrome – angiographic changes in patients are the same as in patients with moya-moya disease, but there is an underlying disease that is the cause.

We analyzed the probable changes in the central nervous system during cystinosis and concluded that the underlying disease cannot be the cause of the identified changes and when observing this patient, we encountered two independent conditions, which required a team approach to determining treatment tactics and further observation.

Timely diagnosis made it possible to improve the further prognosis of the disease, but also the patient’s quality of life, stop episodes of cerebral ischemia, and prevent the development of neurological deficits.

В статье представлен клинический случай ребенка с сочетанием 2 очень редких заболеваний: нефропатического цистиноза и болезни мойя-мойя.

Нефропатический цистиноз – аутосомно-рецессивная лизосомальная болезнь накопления, характеризующаяся накоплением цистина во всех органах и тканях в результате мутаций гена CTNS, который кодирует лизосомальный транспортер цистина цистинозин. Нарушение функции цистинозина приводит к накоплению и кристаллизации цистина внутри лизосом, что, в свою очередь, приводит к апоптозу и повреждению тканей во всех органах. заболевание характеризуется ренальными (синдром Фанкони с прогрессирующим снижением функции почек) и экстраренальными проявлениями в виде гипотиреоза, гипогонадизма, инсулинзависимого сахарного диабета, кальцификации коронарных сосудов, метаболической болезни костей, поражения центральной нервной системы с атрофией коры, кальцификацией головного мозга и др. болезнь мойя-мойя – прогрессирующее заболевание, которое может привести к ишемическому инсульту или внутричерепному кровоизлиянию у детей и взрослых. Выделяют следующие виды этого состояния: болезнь мойя-мойя – первичное (идиопатическое) состояние, относящееся к пациентам с ангиографическими данными заболевания, которые могут иметь генетическую предрасположенность, но не иметь заболеваний, являющихся триггером для развития данного состояния, и синдром мойя-мойя – ангиографические изменения, которые аналогичны таковым у пациентов с болезнью мойя-мойя, но при этом имеется заболевание, которое является первопричиной развития данного состояния.

Нами были проанализированы вероятные изменения со стороны центральной нервной системы при нефропатическом цистинозе и был сделан вывод о том, что основное заболевание не может являться причиной выявленных изменений; при наблюдении данного пациента мы встретились с комбинацией 2 независимых состояний, что потребовало командного подхода к определению тактики лечения и дальнейшего наблюдения.

Своевременная верификация диагноза позволила улучшить дальнейший прогноз течения заболевания, а также качество жизни пациента, предотвратить дальнейшие эпизоды ишемии головного мозга и развитие неврологического дефицита. 

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