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Случай семейной транстиретиновой амилоидной полинейропатии с поздним дебютом
Случай семейной транстиретиновой амилоидной полинейропатии с поздним дебютом
Ковражкина Е.А., Смирнов А.П., Сердюк А.В. и др. Случай семейной транстиретиновой амилоидной полинейропатии с поздним дебютом. Consilium Medicum. 2020 (22); 2: 41–44. DOI: 10.26442/20751753.2020.2.200031
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Аннотация
Аннотация
Транстиретиновая семейная амилоидная полинейропатия (ТТР-САП) – прогрессирующее инвалидизирующее летальное нейродегенеративное заболевание, являющееся наиболее распространенным типом наследственного амилоидоза с аутосомно-доминантным типом наследования. Причиной ТТР-САП является мутация в гене транстиретина TTR. В настоящее время выявлены более 120 мутаций данного гена, наиболее частой является Val30Met. Выделяют ранний (до 50 лет) и поздний (старше 50 лет) дебюты заболевания. Поздний дебют более распространен в неэндемичных районах, такие пациенты часто не имеют наследственного анамнеза ТТР-САП. Представлен случай ТТР-САП с поздним, в 75 лет, дебютом с характерными особенностями этой формы заболевания.
Ключевые слова: транстиретиновая семейная амилоидная полинейропатия, клиническая гетерогенность, дифференциальный диагноз, поздний дебют.
Transthyretin familial amyloid polyneuropathy (TTR-FAP) is a progressive, disabling, fatal neurodegenerative disease, which is the most common type of hereditary amyloidosis with an autosomal dominant type of inheritance. The cause of TTR-FAP is a mutation in the transthyretin’s gene TTR. Currently, more than 120 mutations of this gene has been identified, the most common is Val30Met. There are early (up to 50 years) and and late (over 50 years) debuts of the disease. Late debut is more common in non-endemic areas, such patients often do not have a family history TTR-FAP. The case of TTR-FAP with a late, at 75 years old, debut with the characteristic features of this form of the disease is presented.
Key words: transthyretin familial amyloid polyneuropathy, clinical heterogeneity, differential diagnosis, late debut.
Транстиретиновая семейная амилоидная полинейропатия (ТТР-САП) – прогрессирующее инвалидизирующее летальное нейродегенеративное заболевание, являющееся наиболее распространенным типом наследственного амилоидоза с аутосомно-доминантным типом наследования. Причиной ТТР-САП является мутация в гене транстиретина TTR. В настоящее время выявлены более 120 мутаций данного гена, наиболее частой является Val30Met. Выделяют ранний (до 50 лет) и поздний (старше 50 лет) дебюты заболевания. Поздний дебют более распространен в неэндемичных районах, такие пациенты часто не имеют наследственного анамнеза ТТР-САП. Представлен случай ТТР-САП с поздним, в 75 лет, дебютом с характерными особенностями этой формы заболевания.
Ключевые слова: транстиретиновая семейная амилоидная полинейропатия, клиническая гетерогенность, дифференциальный диагноз, поздний дебют.
________________________________________________
Transthyretin familial amyloid polyneuropathy (TTR-FAP) is a progressive, disabling, fatal neurodegenerative disease, which is the most common type of hereditary amyloidosis with an autosomal dominant type of inheritance. The cause of TTR-FAP is a mutation in the transthyretin’s gene TTR. Currently, more than 120 mutations of this gene has been identified, the most common is Val30Met. There are early (up to 50 years) and and late (over 50 years) debuts of the disease. Late debut is more common in non-endemic areas, such patients often do not have a family history TTR-FAP. The case of TTR-FAP with a late, at 75 years old, debut with the characteristic features of this form of the disease is presented.
Key words: transthyretin familial amyloid polyneuropathy, clinical heterogeneity, differential diagnosis, late debut.
Полный текст
Список литературы
1. Зиновьева О.Е., Сафиулина Э.И. Транстиретиновая амилоидная полинейропатия: патогенез, клинические особенности, перспективы лечения. Manage pain. 2017; 4: 12–5.
[Zinov'eva O.E., Safiulina E.I. Transtiretinovaia amiloidnaia polineiropatiia: patogenez, klinicheskie osobennosti, perspektivy lecheniia. Manage pain. 2017; 4: 12–5 (in Russian).]
2. Benson MD, Kincaid JC. The molecular biology and clinical features of amyloid neuropathy. Muscle Nerve 2007; 36: 411–23.
3. Sekiijima Y, Kelly JW, Ikeda S. Pathogenesis of therapeutic strategies of ameliorate the transthyretin amyloidoses. Curr Pharm des 2008; 14 (30): 3219–30.
4. Sekijima Y. Transthyretin (ATTR) amyloidosis: clinical spectrum, molecular pathogenesis and disease-modifying treatments. J Neurol Neurosurg Psychiatry 2015; 86 (9): 1036–43.
5. Falk RH, Comenzo RL, Skinner M.The systemic amyloidoses. N Eng J Med 1997; 337: 898–909.
6. Plante-Bordeneuve V, Ferreira A, Lalu T et al. Diagnostic pitfalls in sporadic transthyretin familial amyloid polyneuropathy (TTR-FAP). Neurology 2007; 69: 693–8.
7. Adams D, Suhr OB, Hund E et al. for T.-F. First European consensus for diagnosis, management, and treatmentof transthyretin familial amyloid polyneuropathy. Curr Opin Neurol 2016; 29 (Suppl. 1): S14–26.
8. Benson MD et al. Transthyretin amyloidosis. Amyloid 1996; 3: 44–56.
9. Ando Y, Nakamura M, Araki S. Transthyretin-related familiar amyloidic polyneuropathy. Arch Neurol 2005; 62: 1057–62.
10. Ikeda S, Yanagisawa N, Hongo M, Ito N. Vagus nerve and celiac ganglion lesions in generalizedamyloidosis: a correlative study of familial amyloid polyneuropathy and AL-amyloidosis. J Neurol Sci 1987; 79 (1): 129–39.
11. Зиновьева О.Е., Умари Д., Солоха О., Яхно Н. Амилоидная невропатия у пациента с транстиретиновым семейным амилоидозом. Неврологический журнал. 2016; 5: 305–12.
[Zinov'eva O.E., Umari D., Solokha O., Iakhno N. Amiloidnaia nevropatiia u patsienta s transtiretinovym semeinym amiloidozom. Nevrologicheskii zhurnal. 2016; 5: 305–12 (in Russian).]
12. Adams D. Recent advances in the treatment of familial amyloid polyneuropathy. Ther Adv Neurol Disord 2013; 119: 129–39.
13. Sousa A, Andersson R, Drugge U et al. Familial amyloidotic polyneuropathy in Sweden: geographical distribution, age of onset, and prevalence. Human Heredity 1993; 43 (5): 288–94.
14. Theaudin M, Loseron P, Algalarrondo V et al, French FAB Network (CORNAMIL) Study Group. Upper limb onset of hereditary transthyretin amyloidosis is common in non-endemic areas. Eur J Neurol 2019; 26 (3): 497–e36. DOI: 10.1111/ene
15. Lee YJ, Oh J, Hwang SK, Lee EJ et al. Extremely Early Onset Transthyretin Familial Amyloid Polyneuropathy with a Leu55Pro Mutation: A Pediatric Case Report and Literature Review. Neuropediatrics 2019; 50 (5): 322–6. DOI: 10.1055/s-0039-1693145
16. Pinto MV, Pinto LF, Dias M et al. Late-onset hereditary ATTR V30M amyloidosis with polyneuropathy: Characterization of Brazilian subjects from the THAOS registry. J Neurol Sci 2019; 403: 1–6. DOI: 10.1016/j.jns.2019.05.030
17. Živković SA, Mnatsakanova D, Lacomis D. Phenotypes of late-onset transthyretin amyloid neuropathy: a diagnostic challenge. J Clin Neuromuscul Dis 2019; 21 (1): 1–6. DOI:10.1097/CND.0000000000000252
18. Nakano Y, Tadokoro K, Ohta Y et al. Two cases of late onset familial amyloid polyneuropathy with a Glu61Lys transthyretin variant. J Neurol Sci 2018; 390: 22–5. DOI: 10.1016/j.jns.2018.04.003
19. Ericzon BG, Wilczek HE, Larsson M et al. Liver transplantation for hereditary transthyretin amyloidosis: after 20 years still the best therapeutic alternative? Transplantation 2015; 99: 1847–54.
20. Coelho T, Maia LF, Martins da SA et al. Tadamidis for transthyretin familial amyloid polyneuropathy: a randomized, controlled trial. Neurology 2012; 79: 785–92.
21. Berk JL, Suhr OB, Obici L et al, Diflunisal Trial Consortium. Repurposing diflunisal for familial amyloid polyneuropathy: a randomized clinical trial. JAMA 2013; 310: 2658–67.
22. Kapoor M, Rossor AM, Laura M, Reilly MM. Clinical presentation, diagnosis and treatment of TTR amyloidosis. J Neuromuscul Dis 2019; 6 (2): 189–99. DOI: 10.3233/JND-180371
23. Смирнов А.П., Сердюк А.В., Ковражкина Е.А. Случай транстиретиновой семейной амилоидной полинейропатии: диагностический поиск. Consilium Medicum. 2018; 20 (9): 58–62.
[Smirnov A.P., Serdyuk A.V., Kovrazhkina E.A. The case of transthyretin familial amyloid polyneuropathy: diagnostic search. Consilium Medicum. 2018; 20 (9): 58–62 (in Russian).]
2. Benson MD, Kincaid JC. The molecular biology and clinical features of amyloid neuropathy. Muscle Nerve 2007; 36: 411–23.
3. Sekiijima Y, Kelly JW, Ikeda S. Pathogenesis of therapeutic strategies of ameliorate the transthyretin amyloidoses. Curr Pharm des 2008; 14 (30): 3219–30.
4. Sekijima Y. Transthyretin (ATTR) amyloidosis: clinical spectrum, molecular pathogenesis and disease-modifying treatments. J Neurol Neurosurg Psychiatry 2015; 86 (9): 1036–43.
5. Falk RH, Comenzo RL, Skinner M.The systemic amyloidoses. N Eng J Med 1997; 337: 898–909.
6. Plante-Bordeneuve V, Ferreira A, Lalu T et al. Diagnostic pitfalls in sporadic transthyretin familial amyloid polyneuropathy (TTR-FAP). Neurology 2007; 69: 693–8.
7. Adams D, Suhr OB, Hund E et al. for T.-F. First European consensus for diagnosis, management, and treatmentof transthyretin familial amyloid polyneuropathy. Curr Opin Neurol 2016; 29 (Suppl. 1): S14–26.
8. Benson MD et al. Transthyretin amyloidosis. Amyloid 1996; 3: 44–56.
9. Ando Y, Nakamura M, Araki S. Transthyretin-related familiar amyloidic polyneuropathy. Arch Neurol 2005; 62: 1057–62.
10. Ikeda S, Yanagisawa N, Hongo M, Ito N. Vagus nerve and celiac ganglion lesions in generalizedamyloidosis: a correlative study of familial amyloid polyneuropathy and AL-amyloidosis. J Neurol Sci 1987; 79 (1): 129–39.
11. Zinov'eva O.E., Umari D., Solokha O., Iakhno N. Amiloidnaia nevropatiia u patsienta s transtiretinovym semeinym amiloidozom. Nevrologicheskii zhurnal. 2016; 5: 305–12 (in Russian).
12. Adams D. Recent advances in the treatment of familial amyloid polyneuropathy. Ther Adv Neurol Disord 2013; 119: 129–39.
13. Sousa A, Andersson R, Drugge U et al. Familial amyloidotic polyneuropathy in Sweden: geographical distribution, age of onset, and prevalence. Human Heredity 1993; 43 (5): 288–94.
14. Theaudin M, Loseron P, Algalarrondo V et al, French FAB Network (CORNAMIL) Study Group. Upper limb onset of hereditary transthyretin amyloidosis is common in non-endemic areas. Eur J Neurol 2019; 26 (3): 497–e36. DOI: 10.1111/ene
15. Lee YJ, Oh J, Hwang SK, Lee EJ et al. Extremely Early Onset Transthyretin Familial Amyloid Polyneuropathy with a Leu55Pro Mutation: A Pediatric Case Report and Literature Review. Neuropediatrics 2019; 50 (5): 322–6. DOI: 10.1055/s-0039-1693145
16. Pinto MV, Pinto LF, Dias M et al. Late-onset hereditary ATTR V30M amyloidosis with polyneuropathy: Characterization of Brazilian subjects from the THAOS registry. J Neurol Sci 2019; 403: 1–6. DOI: 10.1016/j.jns.2019.05.030
17. Živković SA, Mnatsakanova D, Lacomis D. Phenotypes of late-onset transthyretin amyloid neuropathy: a diagnostic challenge. J Clin Neuromuscul Dis 2019; 21 (1): 1–6. DOI:10.1097/CND.0000000000000252
18. Nakano Y, Tadokoro K, Ohta Y et al. Two cases of late onset familial amyloid polyneuropathy with a Glu61Lys transthyretin variant. J Neurol Sci 2018; 390: 22–5. DOI: 10.1016/j.jns.2018.04.003
19. Ericzon BG, Wilczek HE, Larsson M et al. Liver transplantation for hereditary transthyretin amyloidosis: after 20 years still the best therapeutic alternative? Transplantation 2015; 99: 1847–54.
20. Coelho T, Maia LF, Martins da SA et al. Tadamidis for transthyretin familial amyloid polyneuropathy: a randomized, controlled trial. Neurology 2012; 79: 785–92.
21. Berk JL, Suhr OB, Obici L et al, Diflunisal Trial Consortium. Repurposing diflunisal for familial amyloid polyneuropathy: a randomized clinical trial. JAMA 2013; 310: 2658–67.
22. Kapoor M, Rossor AM, Laura M, Reilly MM. Clinical presentation, diagnosis and treatment of TTR amyloidosis. J Neuromuscul Dis 2019; 6 (2): 189–99. DOI: 10.3233/JND-180371
23. Smirnov A.P., Serdyuk A.V., Kovrazhkina E.A. The case of transthyretin familial amyloid polyneuropathy: diagnostic search. Consilium Medicum. 2018; 20 (9): 58–62 (in Russian).
[Zinov'eva O.E., Safiulina E.I. Transtiretinovaia amiloidnaia polineiropatiia: patogenez, klinicheskie osobennosti, perspektivy lecheniia. Manage pain. 2017; 4: 12–5 (in Russian).]
2. Benson MD, Kincaid JC. The molecular biology and clinical features of amyloid neuropathy. Muscle Nerve 2007; 36: 411–23.
3. Sekiijima Y, Kelly JW, Ikeda S. Pathogenesis of therapeutic strategies of ameliorate the transthyretin amyloidoses. Curr Pharm des 2008; 14 (30): 3219–30.
4. Sekijima Y. Transthyretin (ATTR) amyloidosis: clinical spectrum, molecular pathogenesis and disease-modifying treatments. J Neurol Neurosurg Psychiatry 2015; 86 (9): 1036–43.
5. Falk RH, Comenzo RL, Skinner M.The systemic amyloidoses. N Eng J Med 1997; 337: 898–909.
6. Plante-Bordeneuve V, Ferreira A, Lalu T et al. Diagnostic pitfalls in sporadic transthyretin familial amyloid polyneuropathy (TTR-FAP). Neurology 2007; 69: 693–8.
7. Adams D, Suhr OB, Hund E et al. for T.-F. First European consensus for diagnosis, management, and treatmentof transthyretin familial amyloid polyneuropathy. Curr Opin Neurol 2016; 29 (Suppl. 1): S14–26.
8. Benson MD et al. Transthyretin amyloidosis. Amyloid 1996; 3: 44–56.
9. Ando Y, Nakamura M, Araki S. Transthyretin-related familiar amyloidic polyneuropathy. Arch Neurol 2005; 62: 1057–62.
10. Ikeda S, Yanagisawa N, Hongo M, Ito N. Vagus nerve and celiac ganglion lesions in generalizedamyloidosis: a correlative study of familial amyloid polyneuropathy and AL-amyloidosis. J Neurol Sci 1987; 79 (1): 129–39.
11. Зиновьева О.Е., Умари Д., Солоха О., Яхно Н. Амилоидная невропатия у пациента с транстиретиновым семейным амилоидозом. Неврологический журнал. 2016; 5: 305–12.
[Zinov'eva O.E., Umari D., Solokha O., Iakhno N. Amiloidnaia nevropatiia u patsienta s transtiretinovym semeinym amiloidozom. Nevrologicheskii zhurnal. 2016; 5: 305–12 (in Russian).]
12. Adams D. Recent advances in the treatment of familial amyloid polyneuropathy. Ther Adv Neurol Disord 2013; 119: 129–39.
13. Sousa A, Andersson R, Drugge U et al. Familial amyloidotic polyneuropathy in Sweden: geographical distribution, age of onset, and prevalence. Human Heredity 1993; 43 (5): 288–94.
14. Theaudin M, Loseron P, Algalarrondo V et al, French FAB Network (CORNAMIL) Study Group. Upper limb onset of hereditary transthyretin amyloidosis is common in non-endemic areas. Eur J Neurol 2019; 26 (3): 497–e36. DOI: 10.1111/ene
15. Lee YJ, Oh J, Hwang SK, Lee EJ et al. Extremely Early Onset Transthyretin Familial Amyloid Polyneuropathy with a Leu55Pro Mutation: A Pediatric Case Report and Literature Review. Neuropediatrics 2019; 50 (5): 322–6. DOI: 10.1055/s-0039-1693145
16. Pinto MV, Pinto LF, Dias M et al. Late-onset hereditary ATTR V30M amyloidosis with polyneuropathy: Characterization of Brazilian subjects from the THAOS registry. J Neurol Sci 2019; 403: 1–6. DOI: 10.1016/j.jns.2019.05.030
17. Živković SA, Mnatsakanova D, Lacomis D. Phenotypes of late-onset transthyretin amyloid neuropathy: a diagnostic challenge. J Clin Neuromuscul Dis 2019; 21 (1): 1–6. DOI:10.1097/CND.0000000000000252
18. Nakano Y, Tadokoro K, Ohta Y et al. Two cases of late onset familial amyloid polyneuropathy with a Glu61Lys transthyretin variant. J Neurol Sci 2018; 390: 22–5. DOI: 10.1016/j.jns.2018.04.003
19. Ericzon BG, Wilczek HE, Larsson M et al. Liver transplantation for hereditary transthyretin amyloidosis: after 20 years still the best therapeutic alternative? Transplantation 2015; 99: 1847–54.
20. Coelho T, Maia LF, Martins da SA et al. Tadamidis for transthyretin familial amyloid polyneuropathy: a randomized, controlled trial. Neurology 2012; 79: 785–92.
21. Berk JL, Suhr OB, Obici L et al, Diflunisal Trial Consortium. Repurposing diflunisal for familial amyloid polyneuropathy: a randomized clinical trial. JAMA 2013; 310: 2658–67.
22. Kapoor M, Rossor AM, Laura M, Reilly MM. Clinical presentation, diagnosis and treatment of TTR amyloidosis. J Neuromuscul Dis 2019; 6 (2): 189–99. DOI: 10.3233/JND-180371
23. Смирнов А.П., Сердюк А.В., Ковражкина Е.А. Случай транстиретиновой семейной амилоидной полинейропатии: диагностический поиск. Consilium Medicum. 2018; 20 (9): 58–62.
[Smirnov A.P., Serdyuk A.V., Kovrazhkina E.A. The case of transthyretin familial amyloid polyneuropathy: diagnostic search. Consilium Medicum. 2018; 20 (9): 58–62 (in Russian).]
________________________________________________
2. Benson MD, Kincaid JC. The molecular biology and clinical features of amyloid neuropathy. Muscle Nerve 2007; 36: 411–23.
3. Sekiijima Y, Kelly JW, Ikeda S. Pathogenesis of therapeutic strategies of ameliorate the transthyretin amyloidoses. Curr Pharm des 2008; 14 (30): 3219–30.
4. Sekijima Y. Transthyretin (ATTR) amyloidosis: clinical spectrum, molecular pathogenesis and disease-modifying treatments. J Neurol Neurosurg Psychiatry 2015; 86 (9): 1036–43.
5. Falk RH, Comenzo RL, Skinner M.The systemic amyloidoses. N Eng J Med 1997; 337: 898–909.
6. Plante-Bordeneuve V, Ferreira A, Lalu T et al. Diagnostic pitfalls in sporadic transthyretin familial amyloid polyneuropathy (TTR-FAP). Neurology 2007; 69: 693–8.
7. Adams D, Suhr OB, Hund E et al. for T.-F. First European consensus for diagnosis, management, and treatmentof transthyretin familial amyloid polyneuropathy. Curr Opin Neurol 2016; 29 (Suppl. 1): S14–26.
8. Benson MD et al. Transthyretin amyloidosis. Amyloid 1996; 3: 44–56.
9. Ando Y, Nakamura M, Araki S. Transthyretin-related familiar amyloidic polyneuropathy. Arch Neurol 2005; 62: 1057–62.
10. Ikeda S, Yanagisawa N, Hongo M, Ito N. Vagus nerve and celiac ganglion lesions in generalizedamyloidosis: a correlative study of familial amyloid polyneuropathy and AL-amyloidosis. J Neurol Sci 1987; 79 (1): 129–39.
11. Zinov'eva O.E., Umari D., Solokha O., Iakhno N. Amiloidnaia nevropatiia u patsienta s transtiretinovym semeinym amiloidozom. Nevrologicheskii zhurnal. 2016; 5: 305–12 (in Russian).
12. Adams D. Recent advances in the treatment of familial amyloid polyneuropathy. Ther Adv Neurol Disord 2013; 119: 129–39.
13. Sousa A, Andersson R, Drugge U et al. Familial amyloidotic polyneuropathy in Sweden: geographical distribution, age of onset, and prevalence. Human Heredity 1993; 43 (5): 288–94.
14. Theaudin M, Loseron P, Algalarrondo V et al, French FAB Network (CORNAMIL) Study Group. Upper limb onset of hereditary transthyretin amyloidosis is common in non-endemic areas. Eur J Neurol 2019; 26 (3): 497–e36. DOI: 10.1111/ene
15. Lee YJ, Oh J, Hwang SK, Lee EJ et al. Extremely Early Onset Transthyretin Familial Amyloid Polyneuropathy with a Leu55Pro Mutation: A Pediatric Case Report and Literature Review. Neuropediatrics 2019; 50 (5): 322–6. DOI: 10.1055/s-0039-1693145
16. Pinto MV, Pinto LF, Dias M et al. Late-onset hereditary ATTR V30M amyloidosis with polyneuropathy: Characterization of Brazilian subjects from the THAOS registry. J Neurol Sci 2019; 403: 1–6. DOI: 10.1016/j.jns.2019.05.030
17. Živković SA, Mnatsakanova D, Lacomis D. Phenotypes of late-onset transthyretin amyloid neuropathy: a diagnostic challenge. J Clin Neuromuscul Dis 2019; 21 (1): 1–6. DOI:10.1097/CND.0000000000000252
18. Nakano Y, Tadokoro K, Ohta Y et al. Two cases of late onset familial amyloid polyneuropathy with a Glu61Lys transthyretin variant. J Neurol Sci 2018; 390: 22–5. DOI: 10.1016/j.jns.2018.04.003
19. Ericzon BG, Wilczek HE, Larsson M et al. Liver transplantation for hereditary transthyretin amyloidosis: after 20 years still the best therapeutic alternative? Transplantation 2015; 99: 1847–54.
20. Coelho T, Maia LF, Martins da SA et al. Tadamidis for transthyretin familial amyloid polyneuropathy: a randomized, controlled trial. Neurology 2012; 79: 785–92.
21. Berk JL, Suhr OB, Obici L et al, Diflunisal Trial Consortium. Repurposing diflunisal for familial amyloid polyneuropathy: a randomized clinical trial. JAMA 2013; 310: 2658–67.
22. Kapoor M, Rossor AM, Laura M, Reilly MM. Clinical presentation, diagnosis and treatment of TTR amyloidosis. J Neuromuscul Dis 2019; 6 (2): 189–99. DOI: 10.3233/JND-180371
23. Smirnov A.P., Serdyuk A.V., Kovrazhkina E.A. The case of transthyretin familial amyloid polyneuropathy: diagnostic search. Consilium Medicum. 2018; 20 (9): 58–62 (in Russian).
Авторы
Е.А. Ковражкина*1, А.П. Смирнов2, А.В. Сердюк2, В.Г. Лелюк1, Н.А. Шамалов1
1 ФГБУ «Федеральный центр мозга и нейротехнологий» Минздрава России, Москва, Россия;
2 ФГБОУ ВО «Российский национальный исследовательский медицинский университет им. Н.И. Пирогова» Минздрава России, Москва, Россия
*elekov2@yandex.ru
1 Federal center of brain and neurotechnologies, Moscow, Russia;
2 Pirogov Russian National Research Medical University, Moscow, Russia
*elekov2@yandex.ru
1 ФГБУ «Федеральный центр мозга и нейротехнологий» Минздрава России, Москва, Россия;
2 ФГБОУ ВО «Российский национальный исследовательский медицинский университет им. Н.И. Пирогова» Минздрава России, Москва, Россия
*elekov2@yandex.ru
________________________________________________
1 Federal center of brain and neurotechnologies, Moscow, Russia;
2 Pirogov Russian National Research Medical University, Moscow, Russia
*elekov2@yandex.ru
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