OncohematologyOncohematologyОнкогематология1818-83462413-4023Publishing House ABV Press83510.17650/1818-8346-2023-18-3-50-56NEW DIRECTIONS AND TREATMENT ADVANCESНОВЫЕ НАПРАВЛЕНИЯ И УСПЕХИ ЛЕЧЕНИЯRisk factors for a differentiation syndrome in patients with acute promyelocytic leukemiaФакторы риска развития дифференцировочного синдрома у пациентов с острым промиелоцитарным лейкозомhttps://orcid.org/0000-0002-0201-8680SemenovaA. A.СеменоваА. А.
Russian Federation

Arina Arkadevna Semenova

125167

4 Novyy Zykovskiy Proezd

Moscow

Арина Аркадьевна Семенова

125167

Новый Зыковский пр-д, 4

Москва

arinasemenovaa69@gmail.comhttps://orcid.org/0000-0002-4827-8947TroitskayaV. V.ТроицкаяВ. В.
Russian Federation

125167

4 Novyy Zykovskiy Proezd

Moscow

125167

Новый Зыковский пр-д, 4

Москва

https://orcid.org/0000-0002-8490-6066GaltsevaI. V.ГальцеваИ. В.
Russian Federation

125167

4 Novyy Zykovskiy Proezd

Moscow

125167

Новый Зыковский пр-д, 4

Москва

https://orcid.org/0000-0001-6177-3566ParovichnikovaE. N.ПаровичниковаЕ. Н.
Russian Federation

125167

4 Novyy Zykovskiy Proezd

Moscow

125167

Новый Зыковский пр-д, 4

Москва

National Medical Research Center for Hematology, Ministry of Health of RussiaФГБУ «Национальный медицинский исследовательский центр гематологии» Минздрава России1309202318350561209202312092023https://oncohematology.abvpress.ru/ongm/article/view/835

   Differentiation syndrome (DS) is a severe complication of acute promyelocytic leukemia and its treatment, which is one of the causes of high early mortality. the similarity of clinical manifestations of DS and other complications that may develop during acute promyelocytic leukemia therapy makes it difficult to diagnose ds. at the same time, untimely initiation of DS therapy with glucocorticosteroids can lead to the patient’s death. The only generally accepted risk factor for ds is initial leukocytosis. Specific markers confirming ds have not yet been found. A number of studies show that in patients with diagnosed DS, the expression of CD56, CD54, CD2, CD15, CD13, markers of immature granulocytes, β2-integrins was more often found on blast cells. exposure to tretinoin increased the expression of chemokine receptors, chemokines, and cytokines by blast cells and vascular endothelium. The influence exerted by atypical promyelocytes, due to their biological characteristics, on the coagulation system suggests an association between hemostasis state and ds development. However, the value of the above markers as predictors or signs of DS still needs to be tested, especially when it comes to non-chemotherapeutic treatment of acute promyelocytic leukemia with arsenic trioxide.

   Дифференцировочный синдром (ДС) – тяжелое осложнение острого промиелоцитарного лейкоза и его лечения, являющееся одной из причин высокой ранней летальности. Схожесть клинических проявлений ДС и других осложнений, которые могут развиться на фоне терапии острого промиелоцитарного лейкоза, затрудняет диагностику ДС. При этом несвоевременное начало терапии ДС глюкокортикостероидными гормонами может привести к гибели пациента. Единственный принятый фактор риска развития ДС – инициальный лейкоцитоз. Специфические маркеры, подтверждающие ДС, на сегодняшний день пока не обнаружены. В ряде исследований показано, что у пациентов с диагностированным дС чаще обнаруживали экспрессию на опухолевых клетках CD56, CD54, CD2, CD15, CD13, маркеров незрелых гранулоцитов, β2-интегринов. Воздействие третиноина повышало экспрессию хемокиновых рецепторов, хемокинов и цитокинов опухолевыми клетками и эндотелием сосудов. Влияние, оказываемое биологическими особенностями атипичных промиелоцитов на систему свертывания, позволяет предположить наличие ассоциации состояния гемостаза с развитием ДС. Однако ценность перечисленных маркеров в качестве предикторов или признаков ДС еще нуждается в проверке, особенно когда речь идет о нехимиотерапевтическом лечении острого промиелоцитарного лейкоза триоксидом мышьяка.

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