CC BY
33
Section 8. Medical science
certain one-item questionnaires, including a question about of impressions resulting from changes after therapy.
the overall treatment satisfaction and characterization
References:
1. Althof S. E., Abdo C., Dean J., Carmitta H. N. et al. International Society for Sexual Medicine’s Guidelines for the diagnosis and treatment of premature ejaculation//J Sex Med. - 2010. - Vol. 7. - P. 2947-2969.
2. Montorsi F. Prevalence of premature ejaculation: A global and regional perspective//J Sex Med. - 2005. - Vol. 2 (s2). - P. 96-102.
3. McMahon C. G. Treatment of premature ejaculation with sertraline HCL: a single-blind placebo controlled crossover study//J Urol. - 1998. - Vol. 159. - P. 1935-1938.
4. Arafa M., Shamloul R. Development and evaluation of the Arabic Index of Premature Ejaculation (AIPE)//J Sex Med. -2007. - Vol. 4. - P. 1750-1756.
5. Vatsyayana M., Doniger W., Kakar S./Kamasutra. - 2009. - Oxford University Press.
6. Kaplan H. S. The New Sex Therapy//Brunner Mazel/New York Times, 1974. - P. 292.
7. Sharlip I. D., Hellstrom W. J., Broderick G. A. The ISSM definition of premature ejaculation: A contemporary, evidence-based definition//J Urology. - 2008. - Vol. 179 (suppl. 340) - P. 988.
8. Althof S. E. Treatment of rapid ejaculation: Psychotherapy, pharmacotherapy, and combined therapy/In S. R. Leiblum (Ed.), Principles and practice of sex therapy (4th ed.), NY: Guilford. - 2007. - P. 212-240.
9. McMahon C. G., Althof S. E., Waldinger M. D., Porst H., Dean J. et al. An evidence-based definition of lifelong premature ejaculation: Report of the International Society for Sexual Medicine (ISSM) ad hoc committee for the definition of premature ejaculation//J Sex Med. - 2008. - Vol. 5. - P. 1590-1606.
10. Vinarov A. Z., Akhvlediani N. D., Verce P. Premature Ejaculation//Urology today. - 2013. - №.4 (26). - www.urotoday.ru
11. Porst H. et al. The premature ejaculation prevalence and attitudes (PEPA) Survey: Prevalence, Co-morbidities, and Professional Help-Seeking//European Urology. - 2007. - Vol. 51 (3). - P. 816.
12. Strassberg D. S., Perelman M. A. Sexual dysfunctions/In P. H. Blaney, T. Millon (Eds.), Oxford textbook of psychopathology (2nd ed.). - NY: Oxford University Press, 2009. - P. 399-430.
13. Coolen L. M., Olivier B., Peters H. J., Veening J. G. Demonstration of ejaculation-induced neural activity in the male rat brain using 5-HT1A agonist 8-OH-DPAT//Physiol. Behav. - 1997. - Vol. 62 (4). - P. 881-891.
14. McMahon CG, Abdo C, Incrocci L, et al. Disorders of orgasm and ejaculation in men. J Sex Med 2004 Jul;1 (1):58-65. Godpodinoff M. L. Premature ejaculation: clinical subgroups and etiology//J Sex Marital Ther. - 1989. - Vol. 15. - P. 130.
15. Lue T. F., Giuliano F., Montorsi F., Rosen R. C., Andersson K. E., Althof S., Christ G., Hatzichristou D., Hirsch M., Kimoto Y., Lewis R., McKenna K., Mac-Mahon C., Morales M., MulcahyJ., Padma-Nathan H., Pryor J., de Tejada I., Shabsigh R., Wagner G. Summary of the recommendation on sexual dysfunctions in men//J Sex Med. - 2004. - Vol. 1. - P. 6-23.
16. Patrick D., AlthofS., Pryor J., Rosen R., Rowland D., Ho K., McNulty P., Rothman M., Jamieson C. Premature ejaculation: An observational study of men and their partners//J Sex Med. - 2005. - Vol. 2. - P. 358-367.
17. Yuan Y. M., Xin Z. C., Jiang H. et al. Sexual dysfunction of premature ejaculation patients assayed with Chinese Index of Premature Ejaculation//Asian J Androl. - 2004. - Vol. 6. - P. 121-126.
Nazhmetdinova Dilfuza Farhatovna, Senior Research Scientist — researcher, State Medical Institute. Abu Ali Ibn Sina, Department of Obstetrics and Gynecology, Ministry of Health of the Republic of Uzbekistan Bukhara E-mail: [email protected]
Features of change of lipid spectrum of blood serum at prolonged pregnancy
Abstract: In women with prolonged post-term pregnancy and notes mixed form dislipoproteinemia characterized by hypertriglyceridemia, hypercholesterolemia, and increased levels of cholesterol in lipoproteins of very low and low density, due to lower his level of HDL cholesterol, causing a high risk of atherogenic with a forecast for the development of placental insufficiency.
Keywords: Prolonged pregnancy, lipid metabolism, placental insufficiency.
70
Features of change of lipid spectrum of blood serum at prolonged pregnancy
Post-term pregnancy (PB) is a problem of great scientific and practical interest in obstetrics. The urgency is due to its large number of complications in childbirth, a high percentage of rodorazreshayuschih operations, high prenatal mortality rate [3; 4].
Prolonged pregnancy prep resents a significant threat to the fetus and is characterized by a high rate of complications for mother and newborn. Prenatal mortality in true Prolonged pregnancy and belated delivery is 3-4 times higher than that at timely delivery (3, 6). The frequency of complications in childbirth and neonatal period in children is directly proportional term Prolonged pregnancy. Many issues of this disease have not yet been resolved. All midwives recognize the need to prevent post-term birth, but their number remains high. These wide variations are explained by the lack of consensus about the beginning Prolonged pregnancy and the difficulty in determining the true duration of pregnancy [1, 6]. So far, there is not even a clear definition of the concept of prolonged pregnancy is not completely understood etiology, pathogenesis and diagnosis of this form of disease, there is no single point of view on the tactics of pregnancy and childbirth.
The reasons are numerous prolonged pregnancies. The main etiological factors leading to prolonged pregnancy are functional changes in the central nervous system (CNS), autonomic and endocrine disorders in pregnant [1; 3].
A certain role in this pathology play changes in the uterus (inflammatory, degenerative, and others.), Reducing its excitability and contractile activity.
The study of membrane pathology broader direction of modern obstetrics. Lipid biosloy, part of cell membranes, determine their mechanical and physical — chemical properties, simulates the activity of membrane receptors. Changing the qualitative and quantitative composition of phospholipids of biological membranes, undoubtedly affect the functional activity of the cells. Intensification of lipid peroxidation (LPO), disintegrating the structural integrity of the membrane structures in the cell, is influenced by a variety of damaging factors and is a universal mechanism of the reaction in the cell damaging effects.
There are numerous publications on the study of the processes of lipid per oxidation and antioxidant defense system during normal and pathological pregnancies occurring. However, Prolonged pregnancy these changes are not well understood. In this regard, taking into account not breaking the connection with the occurrence of pregnancy Prolonged pregnancy metabolic disorders in the homeostasis, lipid per oxidation process changes can be regarded as one of the links in the multi pathological process.
Objective: To study the changes of lipid metabolism during prolonged pregnancy.
Materials and methods:
The work in the clinic of obstetrics and gynecology of the Bukhara Medical Institute at the City Maternity Hospital № 1 and in the maternity ward of the city hospital of Bukhara.
There were examined 200 pregnant control group (I) consisted of 50 pregnant women with full-term period, with sustained 75 (II group) and 75 with post-term pregnancy (III group). We observed the women were aged 18 to 37 years old. The highest percentage of pregnant women and mothers were aged 18-25let; 28.3% puerperal control group, 26% — II group, 16,6% — III group.
The vast majority of pregnant women surveyed were female with the number of births 1-2, only 14.4% had 2 or more parity. In women with prolonged post-term pregnancy, and often identified extra genital diseases. So, if women with full-term pregnancy revealed only mild anemia 60% of the patients, when prolonged pregnancy anemia in addition to medium and mild identified obesity (26.7%), pathology of the hepato — biliary system (10.6%), endemic goiter (16%). When prolonged pregnancy rate increased even more extra genital diseases: obesity (29.3%), pathology, hepato-biliary system (17.3%), endemic goiter (50%) patients.
Consequently, pregnant women surveyed mainly detected metabolic disease, which undoubtedly affects the course of metabolic processes.
One of the manifestations of a dyslipidemia. According to the recommendations of the Russian [9] we measured serum total cholesterol (TC), cholesterol transport in its forms: LDL cholesterol (LDL) and high (HDL) density, triglycerides (TG) on the automated biochemical processor “Autohumol-izer F1” (“Human”, Germany) c using a special reagent kits. Based on these data, calculated atherogenic ratio (CA). (2).
Results and discussion.
We have all studied groups of pregnant women was defined triglycerides in the blood serum.
Studies in this regard studies have shown the development of hypertriglyceridemia (TG) for prolonged pregnancy. Contents TG in the serum of women with prolonged pregnancy increased to 1,61 ± 0,11 mmol/l, with post-term — up to 1,68 ± 0,12 mmol/l, at a value of this indicator in women with full-term pregnancy 1.37 0.05 mmol/l. From the data, if the level of triglycerides in the prolonged pregnancy has a tendency to increase, when it is prolonged pregnancy significantly increases by 1.23 (P <0.05) times. The obtained results are consistent with a high incidence of obesity and diseases of the hepatobiliary system, as well as diffuse goiter. For these pathologies characterized by the development of hypertriglyceridemia, however, it should be noted that for these types of pathologies characterized by 4-5 dyslipoproteinemia.
Therefore, in the future, we studied the levels of total cholesterol and its transport forms with calculation atherogenic factor. Studies in this regard studies have shown a tendency to increase the level of total cholesterol and VLDL cholesterol in structure, whereas the LDL cholesterol was significantly increased by 1.3 (P <0.05) times. HDL cholesterol was significantly reduced by 1.36 (P <0.05) times the value of women with full-term pregnancy. Women with post-term pregnancy total cholesterol, VLDL cholesterol and LDL cholesterol were not significantly different from the values of the indicators of
71
Section 8. Medical science
women with full-term pregnancy. Only in HDL cholesterol was significantly decreased in 1.63 (P <0.01) times. It must be said that if the content of total cholesterol in serum ofwomen with prolonged term pregnancy and were not significantly different, the cholesterol in VLDL and LDL levels were slightly lower than those of women with prolonged pregnancy. Apparently, that was associated with an increased use of cholesterol for the synthesis of progesterone in women with post-term pregnancy. On the other hand, when perenashivanie notes increased use of cholesterol fruit.
The findings of our research have shown that as perenashivanie pregnancy progressively increase the risk of atherogenesis. Thus, the figure for women with prolonged and post-term pregnancy significantly increased from 3,29 ± 0,19 to 5,04 ± 0,33 and 6,07 ± 0,52, respectively. These rates exceed the regulatory value of 1.53 (P <0.05) and 1.84 (P <0.01) times, respectively, in prolonged and prolonged pregnancy. This was mainly due to the marked decrease in HDL cholesterol. Therefore, in women with post-term pregnancy, and prolonged notes mixed form dyslipoproteinemia characterized by hypertriglyceridemia, hypercholesterolemia, and increased levels of cholesterol and lipoproteins of very
low and low density, due to lower his level of HDL cholesterol, causing a high risk of atherogenic.
The lipid metabolism disorders, great importance is attached to the peroxide modification of lipoproteins, primarily LDL, obviously, due to the peculiarities of their lipid composition. Peroxide-modified LP may influence the development of steroid hormone imbalances in several ways: by virtue of their cytotoxicity damaging endothelial cover of the arteries, stimulate monocyte chemotaxis into the intima, delay the migration of macrophages of the intima and stimulate the formation of leukotrienes macrophages. A combined contribution of these processes may play an important role in the development of placental insufficiency and disturbance of the reception process. Peroxidation undergoes modification as VLDL and HDL, which also increases their atherogenic properties by changing microhemodynamics in fetoplacental system.
Thus, women with prolonged post-term pregnancy, and notes mixed form dyslipoproteinemia characterized by hypertriglyceridemia; hypercholesterolemia and increased cholesterol in the lipoproteins are very low and low density, due to lower level of HDL cholesterol, causing a high risk of atherogenic forecast on the development of placental insufficiency.
References:
1. Buynova O.E. Regulatory — adaptive status of women in the post-term and prolonged pregnancy: Author. dis ... cand. honey. Nauk. - M., 2013. - 24 c.
2. William James. Marshal. Clinical biohimiya. - M-SPb, 2009. - S. 245-251.
3. Zhabchenko IA The modern view of perenashivanie and prolongation of pregnancy.//Health Ukrainy. - 2014.№ 3. - S. 16-17.
4. Sticky O.P., Vesic TL Methods perenashivanie prevention of pregnancy in women with a high risk of perinatal//Collection of scientific works, 2012. - S. 265-266.
5. Panova O.V. The role of placental protein, lipid peroxidation and nitric oxide in pregnant women in preparation for childbirth. Author. dis. cand. honey. Nauk. - M., 2008. - 21 c.
6. Khomasuridze A.G. Induction of labor at antigestagens perenashivanie pregnancy.//Neonatology, surgery and perinatal meditsina.- 2012. T. II, № 2 (4). - S. 65-67.
7. Avogaro A., Armigiiato M., Cazzolato G. et al. Lipid peroxida-tion and LDL modifications in nondiabetic patients with ischemic heart disease: the role of insulin action//G. tal. Car-diol. - 1996. - Vol. 26. N 2. - P. 169-175.
8. Bressler P., Bailey SR, Matsuda M., DcFronzo RA Insulin resistance and coronary artery disease//Diabetologia.- 2010.-Vol. 39. - P. 1345-1350.
9. Cardiovascular therapy and prevention. - M., 2007. - № 6 Appendix 3. - S. 3-26.
72
