Article
THE PATHOGENETIC SUBSTANTIATION OF THERAPY LEIOMYOMA OF UTERUS AT WOMEN OF REPRODUCTIVE AGE
| About the author: | Zaporozhchenko М. В. |
| Heading | CLINICAL MEDICINE |
| Type of article | Scentific article |
| Annotation | Complications at leiomyoma of uterus have the multifactor nature and pass determination by bunches of genes which can promote development of a myoma of a uterus as a result of hereditary predisposition. The genes endotelial dysfunction which are one of the main parts of the pathogenetic mechanism of occurrence of complications owing to dismetabolic infringements in an organism of the woman deserve of the special attention in obstetrics and gynecology practice. Function of the endotely is controlled by a gene endotelial cyntase oxide of nitrogen (eNOS3). Inhibitor of activators plazminogen-1 (PAI-1) is coded by gene РАІ-1 PLANH1. Concentration РАІ-1 at carriers of alleles 4G above, than at carriers of alleles 5G that leads to increase of risk of development of a myoma of a uterus. Dysfunction of metabolic processes of the gomocyteine and a lack of vitamins of bunch B leads to accumulation gomocyteine in cells, intercellular space, a blood plasma, promotes a lesion of an intrinsic surface of vessels and development of systemic endotelial dysfunction, hypercoagulation. The raised level of the gomocyteine in an organism of the woman is a pathogenetic part of occurrence of complications. The aim of the study:To estimate risk of genetical predisposition in points in mechanisms of development of a myoma of a uterus and gynecologic complications and to make a pathogenetic substantiation of their therapy on the basis of studying of polymorphism of genes of the endotelial cyntase oxide of nitrogen (eNOS3), inhibitor of the activator of a histic plasminogen of I type (PAI1), level of the gomocyteine. Materials and methods. The risk of genetical predisposition in points in mechanisms occurrence and development leiomyoma of uterus and bound with this disease of complications is estimated at 300 women. The pathogenetic substantiation of their preventive maintenance and therapy is made. Definition of alleles of genes of the endotelial cyntase oxide of nitrogen, inhibitor of the activator of a histic plasminogen of I type made a method polymerase chain reaction. Calculation of degree of risk of hereditary predisposition of development of the leiomyoma of uterus and gynecologic complications for everyone alleles of investigated genes was made in points. Quantitative definition of general gomocyteine in human blood or plasma was carried out by the test system of the method immuno-fermentic analysis. Results and discussion. Mutant variants of polymorphism eNOS3 а/а, a / b and РАІ-1 4G/4G, 5G / 4G its are defined at bunch А in 10,0%, 20,0% and 3,3%, 30,0% of cases, at bunch B - 67,4%, 21,5% and 65,9%, 25,2%, at bunch V - 66,7%, 33,3% and 66,7%, 33,3% accordingly. Concentration gomocyteine in blood of women of bunch B was in 3,2 times more (р <0,01) in relation to control bunch A, that was regarded as hypergomocysteinemia easy severity level. Level of gomocyteine in bunch V it was sustained on high bound of norm and was in 1,6 times more in relation to control bunch (р <0,01). The mechanisms occurrence and development leiomyoma of uterus and bound with this disease of complications probably to present as follows: L-arginin (the aid donor of oxide of nitrogen) is soaked up in small intestines, is transported in a liver and is substrate for production NO. Synthesis NO from L-arginina is provided eNOS3 with 5 cofactors. The cofactor flavinadenindinucleotid contains vitamins of grup "B", low level of vitamins promotes hypergomocysteinemia. Degree of risk of occurrence and development leiomyoma of uterus and bound with this disease of complications in bunch A was minimum (<0,9), in bunch V - not expressed (0,9-1,1), in bunch B - raised (> 1,1). Conclusions. 1. Leiomyoma a uterus falls into to the multifactor diseases, one of which causes of development is polymorphism of genes endotelial cyntase oxide of nitrogen, inhibitor of the activator of a histic plasminogen of I type, level increase of the gomocyteine. 2. Dismetabolizm NO it is caused by infringement of suction L-arginina in small intestines, its transportations in a liver, infringement of synthesis NO as a result of activity decrease endotelial cyntase oxide of nitrogen and flavinadenindinucleotid, containing bunch "B" vitamins. Low level of vitamins promotes to hypergomocysteinemia, to infringement of coagulability of blood which depends on a functional state of inhibitor of the activator of a histic plasminogen of I type. 3. Preventive maintenance and treatment of occurrence, development leiomyoma of uterus and bound with this disease of complications is added by appointment L-arginin (Tivortin), hepatoprotection (essenciale, chophitol, etc.), antioxidants, desagregants, vitamins of grup "B", a complex of trace elements (Fe, Ca, Zn), at a high risk thromboembolism - anticoagulants, proteincontents diets (except cases with hypergomocysteinemia). |
| Tags | leiomyoma, uterus, pathogeny, therapy |
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| Publication of the article | «World of Medicine and Biology» №4(47) 2 part 2014 year, 039-042 pages, index UDK 618.14-006.363.03-092-08 |