Treatment method by correcting of purine metabolism in case of cardiovascular disease in the elderly patients
DOI:
https://doi.org/10.11603/mcch.2410-681X.2015.v17.i3.5052Abstract
A large number of metabolic diseases are the cause of their particular violation. One of these conditions is a
violation of purine metabolism substances. Meaning of purine bases in metabolizme is large since they are part of
purine nucleotides forming the nucleid acid (DNA and RNA). Purine nucleotides also have a part-energy compounds
(ATP, ADP) and certain regulatory coenzymes monophosphate (cAMP, cGMP and others). Normal flow of purine
metabolism underlies the optimum level update nucleic acids and proteins, stability in energy metabolism. Violation
of the synthesis of purine nucleotides leads to decreased tissue growth. Uric acid (UA) is the end product of purine
metabolism substances. Level of UA, which is formed during the reaction hypoxanthine qsantinoqsidase reaction
is a marker of activity of free radical processes – endotoxicoses that trigger damaging processes in the vessels
and myocardium. Thus, the UA is the main derivative of purine metabolism and an important mediator of catabolic
processes in stress and cardiovascular disease. Most studies have confirmed the role of UA as a risk factor for
cardiovascular disease. In fact, it turned out that the UA stronger predictor of results than the ejection fraction or
the oxygen uptake. Uric acid can be inserted in the adhesion and aggregation of platelets. This gave birth to the
hypothesis that hyperuricemia increases the risk of coronary thrombosis. It is believed that the increase of the UA
displays endothelial damage. An important mechanism of rapid progression of CHF in elderly patients who have
suffered myocardial infarction, there are systemic activation of apoptosis – cell death. A correlation revealed a high
index values between apoptosis and severity of CHF. An interesting fact is, that the use of pentoxifylline, a corrector
of the purine metabolism in patients with CHF improves the left ventricular function and prognosis of patients. Correction
of purine metabolism then acts as a correction of endotoxemia and apoptosis.
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