Hyperammonemia in the practice of a therapist and cardiologist: theoretical and practical significance


Citar

Texto integral

Acesso aberto Acesso aberto
Acesso é fechado Acesso está concedido
Acesso é fechado Acesso é pago ou somente para assinantes

Resumo

Hyperammonemia (HAM) is a metabolic disorder caused by excessive amounts of ammonia in the blood as a result of inherited, acquired and even functional causes of ammonia synthesis and excretion. Currently, the clinical-laboratory symptom complex (syndrome) of HAM is associated by clinicians predominantly with severe liver pathology, including cirrhotic and non-cyrrhotic forms of disease. However, in some cases, HAM may also have extrahepatic developmental genesis. The article presents an analysis of domestic and foreign sources of literature on data demonstrating the importance of studying the phenomenon of HAM in cardiological practice. Taking into account the pathogenetic and pathophysiological mechanisms of formation, GAM can be studied not only in hepatology, but also in clinical cardiology, as well as preventive and age-associated medicine.

Texto integral

Acesso é fechado

Sobre autores

Olga Khlynova

Academician E.A. Wagner Perm State Medical University of the Ministry of Healthcare of Russia

Email: olgakhlynova@mail.ru
MD, professor, corresponding member of RAS, head of the Department of hospital therapy and cardiology

Valeria Skachkova

Academician E.A. Wagner Perm State Medical University of the Ministry of Healthcare of Russia

Email: valerya1skachkova@yandex.ru
resident physician of the Department of hospital therapy and cardiology

Bibliografia

  1. Vilstrup H., Amodio P., Cordoba J. et al. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of Liver. Hepatology. 2014; 60(2): 715-35. doi: 10.1002/hep.27210.
  2. Плотникова Е.Ю., Макарова М.Р., Грачева Т.Ю. Возможности применения L-орнитина в спортивной медицине. Спортивная медицина. 2016; 4: 28-35.
  3. Thomas G.A.O., Jurewicz A., Williams O.M. et al. Non-hepatic hyperammonemia: an important, potentially reversible cause of encephalopathy. Postgrad Med J. 2001; 77(913): 717-22. doi: 10.1136/pmj.77.913.717.
  4. Welsh E., Kucera J., Perloff M.D. Iatrogenic hyperammonemia after anorexia. Arch Intern Med. 2010; 170(5): 486-88. doi: 10.1001/ archinternmed.2009.549.
  5. Summar M.L., Barr F., Dawling S. et al. Unmasked adult-onset urea cycle disorders in the critical care setting. Crit Care Clin. 2005; 21(4 Suppl): S1-8. doi: 10.1016/j.ccc.2005.05.002.
  6. Panlaqui O.M., Tran K., Johns A. et al. Acute hyperammonemic encephalopathy in adult onset ornithine transcarbamylase deficiency. Intensive Care Med. 2008; 34(10): 1922-24. doi: 10.1007/s00134-008-1217-2.
  7. Schultz R.E., Salo M.K. Under recognition of late onset ornithine transcarbamylase deficiency. Arch Dis Child. 2000; 82(5): 390-91. doi: 10.1136/adc.82.5.390.
  8. Плотникова Е.Ю., Сухих А.С. Различные варианты гипераммониемии в клинической практике. Медицинский совет. 2018; 14: 34-42. doi: https://doi.org/10.21518/2079-701X-2018-14-34-42.
  9. Walker V. Severe hyperammonaemia in adult snot explained by liver disease. Ann Clin Biochem. 2012; 49(Pt 3): 214-28. doi: 10.1258/ acb.2011.011206.
  10. Laish I., Ari Z.B. Non cirrhotic hyperammonaemic encephalopathy. Liver Int. 2011; 31: 1259-70. doi: 10.1111/j.1478-3231.2011.02550.x
  11. Алексеенко С.А., Агеева Е.А., Полковникова О.П. Современные подходы к диагностике и лечению гипераммониемии у пациентов с хроническими заболеваниями печени на доцирротической стадии. РМЖ. 2018; 7-1: 19-23.
  12. Lora-Tamayo J., Palom X., Sarra J. et al. Multiple myeloma and hyperammonemic encephalopathy: review of 27 cases. Clin Lymphoma Myeloma. 2008; 8(6): 363-69. doi: 10.3816/CLM.2008.n.054.
  13. Nott L., Price T.J., Pittman K. et al. Hyperammonemia encephalopathy: an important cause of neurological deterioration following chemotherapy. Leuk Lymphoma. 2007; 48(9): 1702-11. doi: 10.1080/10428190701509822.
  14. Kaveggia F.F., Thompson J.S., Schafer E.C. et al. Hyperammonemic encephalopathy in urinary diversion with urea-splitting urinary tract infection. Arch Intern Med. 1990; 150(11): 2389-92.
  15. Nunes V., Niinikoski H. Lysinuric protein intolerance. In: Adam M.P., Ardinger H.H., Pagon R.A., Wallace S.E., Bean L.J.H., Stephens K., Amemiya A., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2018. 2006 Dec 21
  16. Walker V. Severe hyperammonaemia in adults not explained by liver disease. Ann Clin Biochem. 2012; 49(Pt 3): 214-28. doi: 10.1258/ acb.2011.011206.
  17. Stefan M., Bavli S. Recurrent stupor associated with chronic valporic acid therapy and hyperammonemia. Hospital Physician. 2009; 45: 17-20.
  18. Bessman A.N., Evans J.M. The blood ammonia in congestive heart failure. Am Heart J. 1955; 50(5): 715-19. doi: 10.1016/0002-8703(55)90178-2.
  19. Calkins W.G., Delph M. Level of blood ammonia in congestive heart failure. Ariz Med. 1956; 13(11): 470-75.
  20. Ogino K., Osaki S., Kitamura H. et al. Ammonia response to exercise in patients with congestive heart failure. Heart. 1996; 75(4): 343-48. doi: 10.1136/hrt.75.4.343.
  21. Sullivan M.J., Green H.J., Cobb F.R. Altered skeletal muscle metabolic response to exercise in chronic heart failurerelation to skeletal muscle aerobic enzyme activity. Circulation. 1991; 84(4): 1597-607. doi: 10.1161/01.cir.84.4.1597.
  22. Lamotte M., Fleury F., Pirard M. et al. Acute cardiovascular response to resistance training during cardiac rehabilitation: Effect of repetition speed and rest periods. Eur J. Cardiovasc Prev Rehabil. 2010; 17(3): 329-36. doi: 10.1097/HJR.0b013e328332efdd.
  23. Andrews R., Walsh J.T., Evans A. et al. Abnormalities of skeletal muscle metabolism in patients with chronic heart failure: Evidence that they are present at rest. Heart. 1997; 77(2): 159-63. doi: 10.1136/hrt.77.2.159.
  24. Bjarnason-Wehrens B., Mayer-Berger W., Meister E.R. et al. Recommendations for resistance exercise in cardiac rehabilitation. Recommendations of the German Federation for CPR. Eur J. Cardiovasc Prev Rehabil. 2004; 11(4): 352-61. doi: 10.1097/01. hjr.0000137692.36013.27.
  25. Kinugawa T., Fujita M., Ogino K. et al. Catabolism of adenine nucleotides favors adenosine production following exercise in patients with chronic heart failure. J. Card Fail 2006; 12(9): 720-25. doi: 10.1016/j.cardfail.2006.08.215.
  26. Funaya H., Kitakaze M., Node K. et al. Plasma adenosine levels increase in patients with chronic heart failure. Circulation. 1997; 95(6): 1363-65. doi: 10.1161/01.cir.95.6.1363.
  27. Tesch P.A., Ploutz-Snyder L.L., Ystrom L. et al. Skeletal muscle glycogen loss evoked by resistance exercise. J. Strength Cond Res. 1998; 12: 67-73.
  28. Valero A., Alroy G., Eisenkraft B., Itskovitch J. Ammonia metabolism in chronic obstructive pulmonary disease with special reference to congestive right ventricular failure. Thorax. 1974; 29(6): 703-09. doi: 10.1136/thx.29.6.703.
  29. Clifford P.S. Local control of blood flow. Adv Physiol Educ. 2011; 35(1): 5-15. doi: 10.1152/advan.00074.2010.
  30. Medeiros W.M., Carvalho A.C., Peres P. et al. The dysfunction of ammonia in heart failure increases with an increase in the intensity of resistance exercise, even with the use of appropriate drug therapy. Eur J. Prev Cardiol. 2014; 21(2): 135-44. doi: 10.1177/2047487312460520.
  31. Clifford P.S. Skeletal muscle vasodilatation at the onset of exercise. J. Physiol. 2007; 583(Pt 3): 825-33. doi: 10.1113/jphysiol.2007.135673.
  32. Nardelli S., Lattanzi B., Merli M. et al. Muscle alterations are associated with minimal and overt hepatic encephalopathy in patients with liver cirrhosis. Hepatology. 2019; 70(5): 1704-13. doi: 10.1002/hep.30692.

Arquivos suplementares

Arquivos suplementares
Ação
1. JATS XML

Declaração de direitos autorais © Bionika Media, 2021

Este site utiliza cookies

Ao continuar usando nosso site, você concorda com o procedimento de cookies que mantêm o site funcionando normalmente.

Informação sobre cookies