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Эндотелиальная дисфункция у пациентов с системным AL-амилоидозом - Журнал Терапевтический архив №12 Vario 2024
Эндотелиальная дисфункция у пациентов с системным AL-амилоидозом
Хышова В.А., Рехтина И.Г., Зозуля Н.И., Двирнык В.Н., Менделеева Л.П. Эндотелиальная дисфункция у пациентов с системным AL-амилоидозом. Терапевтический архив. 2024;96(12):1144–1150. DOI: 10.26442/00403660.2024.12.203005
© ООО «КОНСИЛИУМ МЕДИКУМ», 2024 г.
© ООО «КОНСИЛИУМ МЕДИКУМ», 2024 г.
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Аннотация
Исследования, касающиеся состояния сосудов при системном AL-амилоидозе (AL-A), в основном выполнены на экспериментальных моделях. У пациентов с AL-A патогенетическое и клиническое значение сосудистой дисфункции мало изучено.
Цель. Изучить содержание маркеров эндотелиальной дисфункции (ЭД) у пациентов с AL-А в дебюте заболевания и после противоопухолевой терапии.
Материалы и методы. В группу исследования вошли 30 пациентов с AL-А. Группу сравнения составили 10 пациентов с множественной миеломой (ММ), группу контроля – 10 здоровых лиц. Пациенты с AL-А разделены на 2 группы: в 1-ю группу вошли 20 пациентов, которым проведен полный объем запланированной индукционной терапии. Во 2-ю группу включены 10 больных, у которых в процессе лечения наблюдали значительное повышение содержания мозгового натрийуретического пептида (NTproBNP), что послужило причиной для прекращения терапии. Методом иммуноферментного анализа в сыворотке определяли содержание асимметричного диметиларгинина (АДМА), большого эндотелина (бЭТ) и Е-селектина до начала противоопухолевого лечения и после его окончания (или досрочного прекращения).
Результаты. У больных AL-А содержание в сыворотке Е-селектина и АДМА оказалось статистически значимо выше, чем у больных с ММ и здоровых лиц. Повышение хотя бы одного маркера ЭД (Е-селектина и АДМА) в дебюте заболевания наблюдали у 27 (90%) пациентов с AL-A. Различий в содержании бЭТ не получено. У всех больных 1-й группы при достижении гематологической ремиссии отмечали снижение содержания как Е-селектина, так и АДМА по сравнению с исходными значениями (p<0,001). У 5 (55%) из 9 больных с гематологическим и органным ответом концентрация АДМА снизилась до нормальных значений. У всех пациентов из 2-й группы нарастание NТproBNP сопровождалось значимым повышением содержания АДМА (p=0,005) и E-селектина (p=0,007) по сравнению с исходными значениями. У 80% пациентов с повышением NТproBNP наблюдали неблагоприятные сердечно-сосудистые события. Увеличение кардиомаркеров в процессе противоопухолевой терапии чаще наблюдали при более продвинутых стадиях поражения сердца. В 1-й группе IIIA-стадия AL-A встречалась у 23% больных, во 2-й группе – у 70% пациентов (p=0,003). После отмены терапии содержание кардиомаркеров снижалось до исходных значений, что исключало прогрессию AL-A.
Заключение. У 90% пациентов с AL-А выявлена выраженная ЭД. При достижении гематологического и органного ответа наблюдали снижение содержания маркеров ЭД. Противоопухолевая терапия у пациентов с амилоидной кардиомиопатией может вызывать дополнительное повреждение эндотелия, что сопряжено с нарастанием NTproBNP и сердечно-сосудистыми осложнениями.
Ключевые слова: AL-амилоидоз, эндотелиальная дисфункция, кардиотоксичность, ангиотоксичность
Aim. To study the levels of endothelial dysfunction markers in patients with AL-A at the onset of the disease and after anti-tumor therapy.
Materials and methods. The study group included 30 patients with AL-A. The comparison group consisted of 10 patients with multiple myeloma (MM), and the control group included 10 healthy individuals. Patients with AL-A were divided into 2 groups: the first group included 20 patients who underwent the full planned induction therapy, and the second group included 10 patients whose treatment was stopped due to a significant increase in N-terminal pro-brain natriuretic peptide (NTproBNP) levels. The levels of asymmetric dimethylarginine (ADMA), big endothelin (bET), and E-selectin were measured by enzyme-linked immunosorbent assay in serum before and after completion (or premature cessation) of anti-tumor therapy.
Results. Patients with AL-A had significantly higher levels of E-selectin and ADMA in serum compared to patients with MM and healthy individuals. An increase in at least one marker of endothelial dysfunction (E-selectin and ADMA) was observed in 27 (90%) patients with AL-A at disease onset. There were no differences in bET levels. In all patients in the first group, reaching hematologic remission was associated with a decrease in E-selectin and ADMA levels compared to baseline values (p<0.001). In 5 (55%) out of 9 patients with hematologic and organ response, ADMA levels decreased to normal values. In all patients of the second group, the increase in NTproBNP was accompanied by a significant increase in ADMA (p=0.005) and E-selectin (p=0.007) levels compared to baseline values. Adverse cardiovascular events were observed in 80% of patients with elevated NTproBNP levels. The increase in cardiac markers during anti-tumor therapy was more common in advanced stages of heart involvement. Stage IIIA AL-A was present in 23% of patients in the first group and 70% in the second group (p=0.003). After discontinuation of therapy, the levels of cardiac markers decreased to baseline values, which ruled out disease progression.
Conclusion. A pronounced endothelial dysfunction was observed in 90% of patients with AL-A. Reduction in endothelial dysfunction markers was observed upon achieving hematologic and organ response. Anti-tumor therapy in patients with amyloid cardiomyopathy can cause additional endothelial damage, resulting in increased NTproBNP levels and cardiovascular complications.
Keywords: AL amyloidosis, endothelial dysfunction, cardiotoxicity, angiotoxicicity
Цель. Изучить содержание маркеров эндотелиальной дисфункции (ЭД) у пациентов с AL-А в дебюте заболевания и после противоопухолевой терапии.
Материалы и методы. В группу исследования вошли 30 пациентов с AL-А. Группу сравнения составили 10 пациентов с множественной миеломой (ММ), группу контроля – 10 здоровых лиц. Пациенты с AL-А разделены на 2 группы: в 1-ю группу вошли 20 пациентов, которым проведен полный объем запланированной индукционной терапии. Во 2-ю группу включены 10 больных, у которых в процессе лечения наблюдали значительное повышение содержания мозгового натрийуретического пептида (NTproBNP), что послужило причиной для прекращения терапии. Методом иммуноферментного анализа в сыворотке определяли содержание асимметричного диметиларгинина (АДМА), большого эндотелина (бЭТ) и Е-селектина до начала противоопухолевого лечения и после его окончания (или досрочного прекращения).
Результаты. У больных AL-А содержание в сыворотке Е-селектина и АДМА оказалось статистически значимо выше, чем у больных с ММ и здоровых лиц. Повышение хотя бы одного маркера ЭД (Е-селектина и АДМА) в дебюте заболевания наблюдали у 27 (90%) пациентов с AL-A. Различий в содержании бЭТ не получено. У всех больных 1-й группы при достижении гематологической ремиссии отмечали снижение содержания как Е-селектина, так и АДМА по сравнению с исходными значениями (p<0,001). У 5 (55%) из 9 больных с гематологическим и органным ответом концентрация АДМА снизилась до нормальных значений. У всех пациентов из 2-й группы нарастание NТproBNP сопровождалось значимым повышением содержания АДМА (p=0,005) и E-селектина (p=0,007) по сравнению с исходными значениями. У 80% пациентов с повышением NТproBNP наблюдали неблагоприятные сердечно-сосудистые события. Увеличение кардиомаркеров в процессе противоопухолевой терапии чаще наблюдали при более продвинутых стадиях поражения сердца. В 1-й группе IIIA-стадия AL-A встречалась у 23% больных, во 2-й группе – у 70% пациентов (p=0,003). После отмены терапии содержание кардиомаркеров снижалось до исходных значений, что исключало прогрессию AL-A.
Заключение. У 90% пациентов с AL-А выявлена выраженная ЭД. При достижении гематологического и органного ответа наблюдали снижение содержания маркеров ЭД. Противоопухолевая терапия у пациентов с амилоидной кардиомиопатией может вызывать дополнительное повреждение эндотелия, что сопряжено с нарастанием NTproBNP и сердечно-сосудистыми осложнениями.
Ключевые слова: AL-амилоидоз, эндотелиальная дисфункция, кардиотоксичность, ангиотоксичность
________________________________________________
Aim. To study the levels of endothelial dysfunction markers in patients with AL-A at the onset of the disease and after anti-tumor therapy.
Materials and methods. The study group included 30 patients with AL-A. The comparison group consisted of 10 patients with multiple myeloma (MM), and the control group included 10 healthy individuals. Patients with AL-A were divided into 2 groups: the first group included 20 patients who underwent the full planned induction therapy, and the second group included 10 patients whose treatment was stopped due to a significant increase in N-terminal pro-brain natriuretic peptide (NTproBNP) levels. The levels of asymmetric dimethylarginine (ADMA), big endothelin (bET), and E-selectin were measured by enzyme-linked immunosorbent assay in serum before and after completion (or premature cessation) of anti-tumor therapy.
Results. Patients with AL-A had significantly higher levels of E-selectin and ADMA in serum compared to patients with MM and healthy individuals. An increase in at least one marker of endothelial dysfunction (E-selectin and ADMA) was observed in 27 (90%) patients with AL-A at disease onset. There were no differences in bET levels. In all patients in the first group, reaching hematologic remission was associated with a decrease in E-selectin and ADMA levels compared to baseline values (p<0.001). In 5 (55%) out of 9 patients with hematologic and organ response, ADMA levels decreased to normal values. In all patients of the second group, the increase in NTproBNP was accompanied by a significant increase in ADMA (p=0.005) and E-selectin (p=0.007) levels compared to baseline values. Adverse cardiovascular events were observed in 80% of patients with elevated NTproBNP levels. The increase in cardiac markers during anti-tumor therapy was more common in advanced stages of heart involvement. Stage IIIA AL-A was present in 23% of patients in the first group and 70% in the second group (p=0.003). After discontinuation of therapy, the levels of cardiac markers decreased to baseline values, which ruled out disease progression.
Conclusion. A pronounced endothelial dysfunction was observed in 90% of patients with AL-A. Reduction in endothelial dysfunction markers was observed upon achieving hematologic and organ response. Anti-tumor therapy in patients with amyloid cardiomyopathy can cause additional endothelial damage, resulting in increased NTproBNP levels and cardiovascular complications.
Keywords: AL amyloidosis, endothelial dysfunction, cardiotoxicity, angiotoxicicity
Полный текст
Список литературы
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43. Tamura D, Arao T, Tanaka K, et al. Bortezomib potentially inhibits cellular growth of vascular endothelial cells through suppression of G2/M transition. Cancer Sci.
2010;101(6):1403-8. DOI:10.1111/j.1349-7006.2010.01544.x
44. Sahni A, Thomasson ED, Shah R, Sahni SK. Bortezomib effects on human microvascular endothelium in vitro. Pharmacology. 2016;98(5-6):272-8. DOI:10.1159/000448757
45. Aue G, Nelson Lozier J, Tian X, et al. Inflammation, TNFα and endothelial dysfunction link lenalidomide to venous thrombosis in chronic lymphocytic leukemia. Am J Hematol. 2011;86(10):835-40. DOI:10.1002/ajh.22114
46. Çaldır MV, Çelik GK, Çiftçi Ö, Müderrisoğlu İ H. The effect of high-dose steroid treatment used for the treatment of acute demyelinating diseases on endothelial and cardiac functions. Anatol J Cardiol. 2017;17(5):392. DOI:10.14744/AnatolJCardiol.2016.7425
47. Sidana S, Milani P, Binder M, et al. A validated composite organ and hematologic response model for early assessment of treatment outcomes in light chain amyloidosis. Blood Cancer J. 2020;10(4):41. DOI:10.1038/s41408-020-0306-5
48. Chung A, Kaufman GP, Sidana S, et al. Organ responses with daratumumab therapy in previously treated AL amyloidosis. Blood Advances. 2020;4(3):458-66. DOI:10.1182/bloodadvances.2019000776
49. Palladini G, Milani P, Merlini G. Management of AL amyloidosis in 2020. Blood. 2020;136(23):2620-7. DOI:10.1182/blood.2020006913
50. Palladini G, Paiva B, Wechalekar A, et al. Minimal residual disease negativity by next-generation flow cytometry is associated with improved organ response in AL amyloidosis. Blood Cancer J. 2021;11(2):34. DOI:10.1038/s41408-021-00428-0
2. Palladini G, Schönland S, Merlini G, et al. The management of light chain (AL) amyloidosis in Europe: clinical characteristics, treatment patterns, and efficacy outcomes between 2004 and 2018. Blood Cancer J. 2023;13(1):19. DOI:10.1038/s41408-023-00789-8
3. Muchtar E, Gertz MA, Kumar SK, et al. Improved outcomes for newly diagnosed AL amyloidosis between 2000 and 2014: cracking the glass ceiling of early death. Blood J Am Soc Hematol. 2017;129(15):2111-9. DOI:10.1182/blood-2016-11-751628
4. Khyshova VA, Rekhtina IG, Firsova MV, Mendeleeva LP. Difficulties in diagnosis of primary AL-amyloidosis. Oncohematology. 2021;16(3):74-82 (in Russian).
DOI:10.17650/1818-8346-2021-16-3-74-82
5. Niall S, Skinner M, O’Hara CJ. Bone marrow core biopsy specimens in AL (primary) amyloidosis: a morphologic and immunohistochemical study of 100 cases. Am J Clin Pathol. 2003;120(4):610-6. DOI:10.1309/PFUG-HBX0-TY20-E08U
6. Modesto KM, Dispenzieri A, Gertz, M, et al. Vascular abnormalities in primary amyloidosis. Eur Heart J. 2007;28(8):1019-24. DOI:10.1093/eurheartj/ehm066
7. Eirin A, Irazabal MV, Gertz MA, et al. Clinical features of patients with immunoglobulin light chain amyloidosis (AL) with vascular-limited deposition in the kidney. Nephrol Dialysis Transplant. 2012;27(3):1097-101. DOI:10.1093/ndt/gfr381
8. Gimbrone JR, Michael A. Vascular Endothelium: Nature's Blood-Compatible Container a. Ann N Y Acad Sci. 1987;516:5-11. DOI:10.1111/j.1749-6632.1987.tb33025.x
9. Strukova SM. Osnovy fiziologii gemostaza. Moscow: MGU, 2013 (in Russian).
10. Scherrer-Crosbie M, Ullrich R, Bloch KD, et al. Endothelial nitric oxide synthase limits left ventricular remodeling after myocardial infarction in mice. Circulation. 2001;104(11):1286-91. DOI:10.1161/hc3601.094298
11. Liu X, Hou L, Xu D, et al. Effect of asymmetric dimethylarginine (ADMA) on heart failure development. Nitric Oxide. 2017;54:73-81. DOI:10.1016/j.niox.2016.02.006
12. Stakhova TIu, Shcherbak AV, Kozlovskaia LV, et al. Clinical value of the determination of markers for endothelial dysfunction (endothelin-1, microalbuminuria) and tubulointerstitial tissue lesion (2-microglobulin, monocyte chemotactic protein-1) in hypertensive patients with uric acid metabolic disorders. Terapevticheskii Arkhiv (Ter. Arkh.). 2014;86(6):45‑51 (in Russian).
13. Galliamov MG, Saginova EA, Severova MM, et al. Significance of the factors of hypoxia and endothelial dysfunction in kidney injury in the presence of obesity. Terapevticheskii Arkhiv (Ter. Arkh.). 2013;85(6):31‑7 (in Russian).
14. Böger RH, Bode-Böger SM, Szuba A, et al. Asymmetric dimethylarginine (ADMA): a novel risk factor for endothelial dysfunction: its role in hypercholesterolemia. Circulation. 1998;98(18):1842-7. DOI:10.1161/01.cir.98.18.1842
15. Abbasi F, Asagmi T, Cooke JP, et al. Plasma concentrations of asymmetric dimethylarginine are increased in patients with type 2 diabetes mellitus. Am J Cardiol. 2001;88(10):1201-3. DOI:10.1016/s0002-9149(01)02063-x
16. Stühlinger MC, Abbasi F, Chu JW, et al. Relationship between insulin resistance and an endogenous nitric oxide synthase inhibitor. Jama. 2002;287(11):1420-6. DOI:10.1001/jama.287.11.1420
17. Lundman P, Eriksson MJ, Stühlinger M, et al. Mild-to-moderate hypertriglyceridemia in young men is associated with endothelial dysfunction and increased plasma concentrations of asymmetric dimethylarginine. J Am Coll Cardiol. 2001;38(1):111-6. DOI:10.1016/s0735-1097(01)01318-3
18. Zoccali C, Bode-Böger SM, Mallamaci F, et al. Plasma concentration of asymmetrical dimethylarginine and mortality in patients with end-stage renal disease: a prospective study. Lancet. 2001;358(9299):2113-7. DOI:10.1016/s0140-6736(01)07217-8
19. Fleck C, Schweitzer F, Karge E, et al. Serum concentrations of asymmetric (ADMA) and symmetric (SDMA) dimethylarginine in patients with chronic kidney diseases. Clinica Chimica Acta. 2003;336(1-2):1-12. DOI:10.1016/s0009-8981(03)00338-3
20. Podzolkov VI, Safronova TA, Natkina DU. Endothelial dysfunction in patients with controlled and uncontrolled arterial hypertension. Terapevticheskii Arkhiv (Ter. Arkh.). 2019;91(9):108-14 (in Russian). DOI:10.26442/00403660.2019.09.000344
21. Pizov NA, Pizov AV, Skachkova OA, Pizova NV. Endothelial function in normal and pathological conditions. Meditsinsky Sovet. 2019;6:154-9 (in Russian).
DOI:10.21518/2079-701X-2019-6-154-159
22. Tomoda H. Plasma endothelin-1 in acute myocardial infarction with heart failure. Am Heart J. 1993;125(3):667-72. DOI:10.1016/0002-8703(93)90155-3
23. Haug C, Koenig W, Hoeher M, et al. Direct enzyme immunometric measurement of plasma big endothelin-1 concentrations and correlation with indicators of left ventricular function. Clinical Chem. 1998;44(2):239-43.
24. Goggins MG, Goh J, O’connell MA, et al. Soluble adhesion molecules in inflammatory bowel disease. Irish J Med Sci. 2001;170:107-11. DOI:10.1007/BF03168821
25. Zhang D, Liu L, Yuan Y, et al. Oxidative Phosphorylation-Mediated E-Selectin Upregulation Is Associated With Endothelia–Monocyte Adhesion in Human Coronary Artery Endothelial Cells Treated With Sera From Patients With Kawasaki Disease. Front Pediatr. 2021;9:618267. DOI:10.3389/fped.2021.618267
26. Zhong L, Simoneau B, Tremblay PL, et al. E-selectin-mediated adhesion and extravasation in cancer. Encycl Cancer. 2014:1618-24. DOI:10.1007/978-3-642-27841-9_1781-2
27. Kang SA, Blache CA, Bajana S, et al. The effect of soluble E-selectin on tumor progression and metastasis. BMC Cancer. 2016;16:1-13. DOI:10.1186/s12885-016-2366-2
28. Silva M, Videira PA, Sackstein R. E-selectin ligands in the human mononuclear phagocyte system: implications for infection, inflammation, and immunotherapy. Front Immunol. 2018;8:1878. DOI:10.3389/fimmu.2017.01878
29. Tsoref O, Tyomkin D, Amit U, et al. E-selectin-targeted copolymer reduces atherosclerotic lesions, adverse cardiac remodeling, and dysfunction. J Controll Release. 2018;288:136-47. DOI:10.1016/j.jconrel.2018.08.029
30. Berghoff M, Kathpal M, Khan F, et al. Endothelial dysfunction precedes C-fiber abnormalities in primary (AL) amyloidosis. Ann Neurol. 2003;53(6):725-30. DOI:10.1002/ana.10552
31. Migrino RQ, Truran S, Gutterman DD, et al. Human microvascular dysfunction and apoptotic injury induced by AL amyloidosis light chain proteins. Am J Physiol Heart Circ Physiol. 2011;301(6):H2305-12. DOI:10.1152/ajpheart.00503.2011
32. Migrino RQ, Hari P, Gutterman DD, et al. Systemic and microvascular oxidative stress induced by light chain amyloidosis. Int J Cardiol. 2010;145(1):67-8. DOI:10.1016/j.ijcard.2009.04.044
33. Dispenzieri A, Gertz MA, Kyle RA, et al. Serum cardiac troponins and N-terminal pro-brain natriuretic peptide: a staging system for primary systemic amyloidosis. J Clin Oncol. 2004;22(18):3751-7. DOI:10.1200/JCO.2004.03.029
34. Palladini G, Sachchithanantham S, Milani P, et al. A European collaborative study of cyclophosphamide, bortezomib, and dexamethasone in upfront treatment of systemic AL amyloidosis. Blood. 2015;126(5):612-5. DOI:10.1182/blood-2015-01-620302
35. Gertz MA, Comenzo R, Falk RH, et al. Definition of organ involvement and treatment response in immunoglobulin light chain amyloidosis (AL): a consensus opinion from the 10th International Symposium on Amyloid and Amyloidosis. Am J Hematol. 2005;79(4):319-28. DOI:10.1002/ajh.20381
36. Kumar S, Dispenzieri A, Lacy MQ, et al. Revised prognostic staging system for light chain amyloidosis incorporating cardiac biomarkers and serum free light chain measurements. J Clin Oncol. 2012;30(9):989. DOI:10.1200/JCO.2011.38.5724
37. Comenzo RL, Reece D, Palladini G, et al. Consensus guidelines for the conduct and reporting of clinical trials in systemic light-chain amyloidosis. Leukemia. 2012;26(11):2317-25. DOI:10.1038/leu.2012.100
38. Palladini G, Hegenbart U, Milani P, et al. A staging system for renal outcome and early markers of renal response to chemotherapy in AL amyloidosis. Blood. 2014;124(15):2325-32. DOI:10.1182/blood-2014-04-570010.
39. Dubrey SW, Reece DE, Sanchorawala V, et al. Bortezomib in a phase 1 trial for patients with relapsed AL amyloidosis: cardiac responses and overall effects. QJM: Int J Med. 2011;104(11):957-70. DOI:10.1093/qjmed/hcr105
40. Hussain AS, Hari P, Brazauskas R, et al. Changes in cardiac biomarkers with bortezomib treatment in patients with advanced cardiac amyloidosis. Am J Hematol. 2015;90(11):E212. DOI:10.1002/ajh.24176
41. Dispenzieri A, Dingli D, Kumar SK, et al. Discordance between serum cardiac biomarker and immunoglobulin-free light-chain response in patients with immunoglobulin light-chain amyloidosis treated with immune modulatory drugs. Am J Hematol. 2010;85(10):757-9. DOI:10.1002/ajh.21822
42. Dinner S, Witteles W, Afghahi A, et al. Lenalidomide, melphalan and dexamethasone in a population of patients with immunoglobulin light chain amyloidosis with high rates of advanced cardiac involvement. Haematologica. 2013;98(10):1593. DOI:10.3324/haematol.2013.084574
43. Tamura D, Arao T, Tanaka K, et al. Bortezomib potentially inhibits cellular growth of vascular endothelial cells through suppression of G2/M transition. Cancer Sci.
2010;101(6):1403-8. DOI:10.1111/j.1349-7006.2010.01544.x
44. Sahni A, Thomasson ED, Shah R, Sahni SK. Bortezomib effects on human microvascular endothelium in vitro. Pharmacology. 2016;98(5-6):272-8. DOI:10.1159/000448757
45. Aue G, Nelson Lozier J, Tian X, et al. Inflammation, TNFα and endothelial dysfunction link lenalidomide to venous thrombosis in chronic lymphocytic leukemia. Am J Hematol. 2011;86(10):835-40. DOI:10.1002/ajh.22114
46. Çaldır MV, Çelik GK, Çiftçi Ö, Müderrisoğlu İ H. The effect of high-dose steroid treatment used for the treatment of acute demyelinating diseases on endothelial and cardiac functions. Anatol J Cardiol. 2017;17(5):392. DOI:10.14744/AnatolJCardiol.2016.7425
47. Sidana S, Milani P, Binder M, et al. A validated composite organ and hematologic response model for early assessment of treatment outcomes in light chain amyloidosis. Blood Cancer J. 2020;10(4):41. DOI:10.1038/s41408-020-0306-5
48. Chung A, Kaufman GP, Sidana S, et al. Organ responses with daratumumab therapy in previously treated AL amyloidosis. Blood Advances. 2020;4(3):458-66. DOI:10.1182/bloodadvances.2019000776
49. Palladini G, Milani P, Merlini G. Management of AL amyloidosis in 2020. Blood. 2020;136(23):2620-7. DOI:10.1182/blood.2020006913
50. Palladini G, Paiva B, Wechalekar A, et al. Minimal residual disease negativity by next-generation flow cytometry is associated with improved organ response in AL amyloidosis. Blood Cancer J. 2021;11(2):34. DOI:10.1038/s41408-021-00428-0
2. Palladini G, Schönland S, Merlini G, et al. The management of light chain (AL) amyloidosis in Europe: clinical characteristics, treatment patterns, and efficacy outcomes between 2004 and 2018. Blood Cancer J. 2023;13(1):19. DOI:10.1038/s41408-023-00789-8
3. Muchtar E, Gertz MA, Kumar SK, et al. Improved outcomes for newly diagnosed AL amyloidosis between 2000 and 2014: cracking the glass ceiling of early death. Blood J Am Soc Hematol. 2017;129(15):2111-9. DOI:10.1182/blood-2016-11-751628
4. Хышова В.А., Рехтина И.Г., Фирсова М.В., Менделеева Л.П. Трудности в диагностике первичного AL-амилоидоза. Онкогематология. 2021;16(3):74-82 [Khyshova VA, Rekhtina IG, Firsova MV, Mendeleeva LP. Difficulties in diagnosis of primary AL-amyloidosis. Oncohematology. 2021;16(3):74-82 (in Russian)]. DOI:10.17650/1818-8346-2021-16-3-74-82
5. Niall S, Skinner M, O’Hara CJ. Bone marrow core biopsy specimens in AL (primary) amyloidosis: a morphologic and immunohistochemical study of 100 cases. Am J Clin Pathol. 2003;120(4):610-6. DOI:10.1309/PFUG-HBX0-TY20-E08U
6. Modesto KM, Dispenzieri A, Gertz, M, et al. Vascular abnormalities in primary amyloidosis. Eur Heart J. 2007;28(8):1019-24. DOI:10.1093/eurheartj/ehm066
7. Eirin A, Irazabal MV, Gertz MA, et al. Clinical features of patients with immunoglobulin light chain amyloidosis (AL) with vascular-limited deposition in the kidney. Nephrol Dialysis Transplant. 2012;27(3):1097-101. DOI:10.1093/ndt/gfr381
8. Gimbrone JR, Michael A. Vascular Endothelium: Nature's Blood-Compatible Container a. Ann N Y Acad Sci. 1987;516:5-11. DOI:10.1111/j.1749-6632.1987.tb33025.x
9. Струкова С.М. Основы физиологии гемостаза. М.: МГУ, 2013 [Strukova SM. Osnovy fiziologii gemostaza. Moscow: MGU, 2013 (in Russian)].
10. Scherrer-Crosbie M, Ullrich R, Bloch KD, et al. Endothelial nitric oxide synthase limits left ventricular remodeling after myocardial infarction in mice. Circulation. 2001;104(11):1286-91. DOI:10.1161/hc3601.094298
11. Liu X, Hou L, Xu D, et al. Effect of asymmetric dimethylarginine (ADMA) on heart failure development. Nitric Oxide. 2017;54:73-81. DOI:10.1016/j.niox.2016.02.006
12. Стахова Т.Ю., Щербак А.В., Козловская Л.В., и др. Клиническое значение определения маркеров дисфункции эндотелия (эндотелин-1, микроальбуминурия) и поражения тубулоинтерстициальной ткани (2-микроглобулин, моноцитарный хемотаксический белок-1) у пациентов с артериальной гипертонией и нарушением обмена мочевой кислоты. Терапевтический архив. 2014;86(6):45‑51 [Stakhova TIu, Shcherbak AV, Kozlovskaia LV, et al. Clinical value of the determination of markers for endothelial dysfunction (endothelin-1, microalbuminuria) and tubulointerstitial tissue lesion (2-microglobulin, monocyte chemotactic protein-1) in hypertensive patients with uric acid metabolic disorders. Terapevticheskii Arkhiv (Ter. Arkh.). 2014;86(6):45‑51 (in Russian)].
13. Галлямов М.Г., Сагинова Е.А., Северова М.М., и др. Значение факторов гипоксии и дисфункции эндотелия в поражении почек при ожирении. Терапевтический архив. 2013;85(6):31‑7 [Galliamov MG, Saginova EA, Severova MM, et al. Significance of the factors of hypoxia and endothelial dysfunction in kidney injury in the presence of obesity. Terapevticheskii Arkhiv (Ter. Arkh.). 2013;85(6):31‑7 (in Russian)].
14. Böger RH, Bode-Böger SM, Szuba A, et al. Asymmetric dimethylarginine (ADMA): a novel risk factor for endothelial dysfunction: its role in hypercholesterolemia. Circulation. 1998;98(18):1842-7. DOI:10.1161/01.cir.98.18.1842
15. Abbasi F, Asagmi T, Cooke JP, et al. Plasma concentrations of asymmetric dimethylarginine are increased in patients with type 2 diabetes mellitus. Am J Cardiol. 2001;88(10):1201-3. DOI:10.1016/s0002-9149(01)02063-x
16. Stühlinger MC, Abbasi F, Chu JW, et al. Relationship between insulin resistance and an endogenous nitric oxide synthase inhibitor. Jama. 2002;287(11):1420-6. DOI:10.1001/jama.287.11.1420
17. Lundman P, Eriksson MJ, Stühlinger M, et al. Mild-to-moderate hypertriglyceridemia in young men is associated with endothelial dysfunction and increased plasma concentrations of asymmetric dimethylarginine. J Am Coll Cardiol. 2001;38(1):111-6. DOI:10.1016/s0735-1097(01)01318-3
18. Zoccali C, Bode-Böger SM, Mallamaci F, et al. Plasma concentration of asymmetrical dimethylarginine and mortality in patients with end-stage renal disease: a prospective study. Lancet. 2001;358(9299):2113-7. DOI:10.1016/s0140-6736(01)07217-8
19. Fleck C, Schweitzer F, Karge E, et al. Serum concentrations of asymmetric (ADMA) and symmetric (SDMA) dimethylarginine in patients with chronic kidney diseases. Clinica Chimica Acta. 2003;336(1-2):1-12. DOI:10.1016/s0009-8981(03)00338-3
20. Подзолков В.И., Сафронова Т.А., Наткина Д.У. Эндотелиальная дисфункция у больных с контролируемой и неконтролируемой артериальной гипертензией. Терапевтический архив. 2019;91(9):108-14 [Podzolkov VI, Safronova TA, Natkina DU. Endothelial dysfunction in patients with controlled and uncontrolled arterial hypertension. Terapevticheskii Arkhiv (Ter. Arkh.). 2019;91(9):108-14 (in Russian)]. DOI:10.26442/00403660.2019.09.000344
21. Пизов Н.А., Пизов А.В., Скачкова О.А., Пизова Н.В. Эндотелиальная функция в норме и при патологии. Медицинский совет. 2019;6:154-9 [Pizov NA, Pizov AV, Skachkova OA, Pizova NV. Endothelial function in normal and pathological conditions. Meditsinsky Sovet. 2019;6:154-9 (in Russian)]. DOI:10.21518/2079-701X-2019-6-154-159
22. Tomoda H. Plasma endothelin-1 in acute myocardial infarction with heart failure. Am Heart J. 1993;125(3):667-72. DOI:10.1016/0002-8703(93)90155-3
23. Haug C, Koenig W, Hoeher M, et al. Direct enzyme immunometric measurement of plasma big endothelin-1 concentrations and correlation with indicators of left ventricular function. Clinical Chem. 1998;44(2):239-43.
24. Goggins MG, Goh J, O’connell MA, et al. Soluble adhesion molecules in inflammatory bowel disease. Irish J Med Sci. 2001;170:107-11. DOI:10.1007/BF03168821
25. Zhang D, Liu L, Yuan Y, et al. Oxidative Phosphorylation-Mediated E-Selectin Upregulation Is Associated With Endothelia–Monocyte Adhesion in Human Coronary Artery Endothelial Cells Treated With Sera From Patients With Kawasaki Disease. Front Pediatr. 2021;9:618267. DOI:10.3389/fped.2021.618267
26. Zhong L, Simoneau B, Tremblay PL, et al. E-selectin-mediated adhesion and extravasation in cancer. Encycl Cancer. 2014:1618-24. DOI:10.1007/978-3-642-27841-9_1781-2
27. Kang SA, Blache CA, Bajana S, et al. The effect of soluble E-selectin on tumor progression and metastasis. BMC Cancer. 2016;16:1-13. DOI:10.1186/s12885-016-2366-2
28. Silva M, Videira PA, Sackstein R. E-selectin ligands in the human mononuclear phagocyte system: implications for infection, inflammation, and immunotherapy. Front Immunol. 2018;8:1878. DOI:10.3389/fimmu.2017.01878
29. Tsoref O, Tyomkin D, Amit U, et al. E-selectin-targeted copolymer reduces atherosclerotic lesions, adverse cardiac remodeling, and dysfunction. J Controll Release. 2018;288:136-47. DOI:10.1016/j.jconrel.2018.08.029
30. Berghoff M, Kathpal M, Khan F, et al. Endothelial dysfunction precedes C-fiber abnormalities in primary (AL) amyloidosis. Ann Neurol. 2003;53(6):725-30. DOI:10.1002/ana.10552
31. Migrino RQ, Truran S, Gutterman DD, et al. Human microvascular dysfunction and apoptotic injury induced by AL amyloidosis light chain proteins. Am J Physiol Heart Circ Physiol. 2011;301(6):H2305-12. DOI:10.1152/ajpheart.00503.2011
32. Migrino RQ, Hari P, Gutterman DD, et al. Systemic and microvascular oxidative stress induced by light chain amyloidosis. Int J Cardiol. 2010;145(1):67-8. DOI:10.1016/j.ijcard.2009.04.044
33. Dispenzieri A, Gertz MA, Kyle RA, et al. Serum cardiac troponins and N-terminal pro-brain natriuretic peptide: a staging system for primary systemic amyloidosis. J Clin Oncol. 2004;22(18):3751-7. DOI:10.1200/JCO.2004.03.029
34. Palladini G, Sachchithanantham S, Milani P, et al. A European collaborative study of cyclophosphamide, bortezomib, and dexamethasone in upfront treatment of systemic AL amyloidosis. Blood. 2015;126(5):612-5. DOI:10.1182/blood-2015-01-620302
35. Gertz MA, Comenzo R, Falk RH, et al. Definition of organ involvement and treatment response in immunoglobulin light chain amyloidosis (AL): a consensus opinion from the 10th International Symposium on Amyloid and Amyloidosis. Am J Hematol. 2005;79(4):319-28. DOI:10.1002/ajh.20381
36. Kumar S, Dispenzieri A, Lacy MQ, et al. Revised prognostic staging system for light chain amyloidosis incorporating cardiac biomarkers and serum free light chain measurements. J Clin Oncol. 2012;30(9):989. DOI:10.1200/JCO.2011.38.5724
37. Comenzo RL, Reece D, Palladini G, et al. Consensus guidelines for the conduct and reporting of clinical trials in systemic light-chain amyloidosis. Leukemia. 2012;26(11):2317-25. DOI:10.1038/leu.2012.100
38. Palladini G, Hegenbart U, Milani P, et al. A staging system for renal outcome and early markers of renal response to chemotherapy in AL amyloidosis. Blood. 2014;124(15):2325-32. DOI:10.1182/blood-2014-04-570010.
39. Dubrey SW, Reece DE, Sanchorawala V, et al. Bortezomib in a phase 1 trial for patients with relapsed AL amyloidosis: cardiac responses and overall effects. QJM: Int J Med. 2011;104(11):957-70. DOI:10.1093/qjmed/hcr105
40. Hussain AS, Hari P, Brazauskas R, et al. Changes in cardiac biomarkers with bortezomib treatment in patients with advanced cardiac amyloidosis. Am J Hematol. 2015;90(11):E212. DOI:10.1002/ajh.24176
41. Dispenzieri A, Dingli D, Kumar SK, et al. Discordance between serum cardiac biomarker and immunoglobulin-free light-chain response in patients with immunoglobulin light-chain amyloidosis treated with immune modulatory drugs. Am J Hematol. 2010;85(10):757-9. DOI:10.1002/ajh.21822
42. Dinner S, Witteles W, Afghahi A, et al. Lenalidomide, melphalan and dexamethasone in a population of patients with immunoglobulin light chain amyloidosis with high rates of advanced cardiac involvement. Haematologica. 2013;98(10):1593. DOI:10.3324/haematol.2013.084574
43. Tamura D, Arao T, Tanaka K, et al. Bortezomib potentially inhibits cellular growth of vascular endothelial cells through suppression of G2/M transition. Cancer Sci.
2010;101(6):1403-8. DOI:10.1111/j.1349-7006.2010.01544.x
44. Sahni A, Thomasson ED, Shah R, Sahni SK. Bortezomib effects on human microvascular endothelium in vitro. Pharmacology. 2016;98(5-6):272-8. DOI:10.1159/000448757
45. Aue G, Nelson Lozier J, Tian X, et al. Inflammation, TNFα and endothelial dysfunction link lenalidomide to venous thrombosis in chronic lymphocytic leukemia. Am J Hematol. 2011;86(10):835-40. DOI:10.1002/ajh.22114
46. Çaldır MV, Çelik GK, Çiftçi Ö, Müderrisoğlu İ H. The effect of high-dose steroid treatment used for the treatment of acute demyelinating diseases on endothelial and cardiac functions. Anatol J Cardiol. 2017;17(5):392. DOI:10.14744/AnatolJCardiol.2016.7425
47. Sidana S, Milani P, Binder M, et al. A validated composite organ and hematologic response model for early assessment of treatment outcomes in light chain amyloidosis. Blood Cancer J. 2020;10(4):41. DOI:10.1038/s41408-020-0306-5
48. Chung A, Kaufman GP, Sidana S, et al. Organ responses with daratumumab therapy in previously treated AL amyloidosis. Blood Advances. 2020;4(3):458-66. DOI:10.1182/bloodadvances.2019000776
49. Palladini G, Milani P, Merlini G. Management of AL amyloidosis in 2020. Blood. 2020;136(23):2620-7. DOI:10.1182/blood.2020006913
50. Palladini G, Paiva B, Wechalekar A, et al. Minimal residual disease negativity by next-generation flow cytometry is associated with improved organ response in AL amyloidosis. Blood Cancer J. 2021;11(2):34. DOI:10.1038/s41408-021-00428-0
________________________________________________
2. Palladini G, Schönland S, Merlini G, et al. The management of light chain (AL) amyloidosis in Europe: clinical characteristics, treatment patterns, and efficacy outcomes between 2004 and 2018. Blood Cancer J. 2023;13(1):19. DOI:10.1038/s41408-023-00789-8
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Авторы
В.А. Хышова*, И.Г. Рехтина, Н.И. Зозуля, В.Н. Двирнык, Л.П. Менделеева
ФГБУ «Национальный медицинский исследовательский центр гематологии» Минздрава России, Москва, Россия
*viktoria2102@icloud.com
National Medical Research Center for Hematology, Moscow, Russia
*viktoria2102@icloud.com
ФГБУ «Национальный медицинский исследовательский центр гематологии» Минздрава России, Москва, Россия
*viktoria2102@icloud.com
________________________________________________
National Medical Research Center for Hematology, Moscow, Russia
*viktoria2102@icloud.com
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