{"paper_id":"1e2b187b-9666-411f-aff7-e1f9bed33df1","body_text":"Journal of Science in                                             Volume: 2 Issue: 9 Year: 2024    \n                     Medicine and Life                                ISSN: 2992-9202 | http://journals.proindex.uz \n \n108 \n \n \nStudy Relationship between Some Biochemical Parameters in \nPatients with Polycystic Ovary \n \nSarah Ayad Mahmood, Hadil Khalid Turki, Jwan Ahmed Hussein,  \nFatima abdullah salman \n \n \n \nAbstract: The current study included (45) female samples whose ages ranged between (20 -40) \nyears. For the period from September to February of the year 2024, the samples were divided into \nthree groups: The group of healthy women: This group included (15) s amples of women who did \nnot suffer from polycystic ovary syndrome (PCOS) as a control group, a group of women with the \nsyndrome, and a group Women with endometriosis: This group included (15) women with \npolycystic ovary syndrome (PCOS) and (15) women with endometriosis. The results of the current \nstudy showed that there was a significant change in the level of FSH at the probability level \n(P≤0.0001) between the patient groups and the healthy group, as its level increased significantly in \nwomen with endometr iosis (11.619±0.479) and decreased significantly in women patients with \nPCOS (7.624±0.293). ) compared to its level in the healthy group (9.133±0.247), and it also \ndecreased significantly in women with polycystic ovary syndrome compared to the group with \nendometriosis. \nThe statistical results also showed a significant difference in the level of the LH hormone between \nthe groups of patients and the healthy group at the probability level (P ≤0.0001), as it showed a \nsignificant decrease in women suffering from Endometriosis (1.109±0.318) compared to the healthy \ngroup, while its level increased in women with polycystic ovary syndrome (15.815). PCOS \n(±0.289) compared to its level in the group of healthy people (6.925±0.407) and those with \nendometriosis (P≤0.0001). Conclusion: Disturbances in the level of sexual and gonadal hormones \nplay a major role in causing the pathological conditions leading to polycystic ovary syndrome and \nendometriosis. \n \n \nIntroduction \nPolycystic ovary syndrome (PCOS) is a common endocrine disorder in women who suffer from it. \nThis disease is characterized by excessive secretion of androgens and gonadotropin. Previous \nstudies have shown that the percentage of women suffering from this disease ranges between 6-20% \nof women of reproductive age . The main cause of this syndrome is not clear, but there is some \nevidence that indicates that the disease is genetically related and may occur due to a disorder in the \npituitary gland, and it may be due to the ovaries not responding properly to pituitary hormones. \nThere is a theory that indicates that this disease It occurs due to a decrease in dopamine secretion in \nthe upper center of the brain (1). \nThere are some studies that indicate that an increase in the luteinizing hormone (LH) leads to a \ndecrease in the secretion of estrogen, which causes an irregular response by the cysts in the ovaries. \nSome studies indicate that this syndrome is related to the presence of a defect in the gene \nresponsible for the work of the hormone insulin, regardless of the dive rsity of the causes of this \ndisease. This disease must be dealt with.  Polycystic ovary syndrome (PCOS) is one of the most \nimportant causes of infertility, but this does not mean that the patient cannot become pregnant, as it \ncan be treated through medicati ons specialized in treating this disorder, such as anti -androgen \nmedications, and the patient may resort to cauterization of the ovaries (2). \n\n  Journal of Science in Medicine and Life, Volume: 2 Issue: 9 Year: 2024                                      ISSN: 2992-9202 \n109 \n \nPCOS is also closely associated with a wide range of metabolic disorders, such as hepatic steatosis, \nglucose intol erance, hypolipidemia, type 2 diabetes mellitus (T2DM), and hypertension with an \nincreased risk of developing impaired glucose tolerance and an increased risk of developing T2DM. \n(3). \nFollicle Stimulating Hormone (FSH) \nIt is a glycoprotein consisting of tw o polypeptide units (alpha and beta) and its molecular weight is \nabout 30 kDa. It is secreted by the cells of the anterior pituitary gland. The alpha unit consists of 92 \namino acids, and the beta unit consists of 111 amino acids, but the biological role an d \nimmunological properties depend on the beta units.  This hormone is measured at a specific time \nduring the woman ’s menstrual cycle (usually between 2 -4 days of menstruation) to be valid for \nmeasurement (4). \nA high level of FSH indicates a decrease in ovar ian reserve, while a decrease in the level of this \nhormone indicates disorders in the pituitary gland or hypothalamus. The function of this hormone \ndiffers between females and males, as this hormone stimulates the growth of immature follicles in \nthe ovarie s until the follicles mature. The secretion of this hormone during the menstrual cycle \nreaches its peak on day 14 of the cycle and begins to decline when ovulation occurs. FSH stimulates \ncertain cells to luteinize the follicle, leading to the production of inhibin. During menopause there is \na sharp decrease in inhibin production and a significant increase in serum FSH . The ratio of FSH to \nLH is a measure to determine the condition of infertile women with polycystic ovary syndrome. \nThis ratio is greater tha n 2 according to the standard criteria for diagnosing polycystic ovary \nsyndrome. A high ratio causes cessation of the ovulation process and plays a role in stopping the \nmaturation of follicles in polycystic ovary syndrome. Bags(5). \nMaterials and methods \nEquipment and Materials \nTable (1) shows the devices and tools used in the study \nOrigin الجهاز \nCHANGHOUH/ China Sringes \nG.L.G\\ U.S.A Centrifuge \nFISHER/ U.S.A Incubator \nARCELIK/ Turkey refrigerator \nSlamed/Germany Micro pipet \nGallenkamp/Germany vortex \nMindray/China Cl900i (Minividas) \nChina رtest tubes \n \nTable 2 shows the Laboratory Kits used in the study \nOrigin Laboratory Kits \nShenzhen Mindray Bio-Medical \nElectronics/ China FSH \nShenzhen Mindray Bio-Medical \nElectronics/ China LH \n \nStudy Subjects \nThe current study included (45) female samples whose ages ranged between (20 -40) years. For the \nperiod from September to February of the year 2024, the data of each woman was recorded in a \nquestionnaire (Appendix 1) prepared for this purpose, and the sampl es were divided into three \ngroups:  \nGroup of healthy women: This group included (15) samples of women who did not suffer from \npolycystic ovary syndrome (PCOS) as a control group, after ensuring that they were safe from \n\n  Journal of Science in Medicine and Life, Volume: 2 Issue: 9 Year: 2024                                      ISSN: 2992-9202 \n110 \n \nincontinence or menopause and the pre sence of ovarian cysts through the diagnosis of a specialist \ndoctor and Ultrasound examination and hormone examination. \nThe group of women with the syndrome and the group of women with endometriosis: This \ngroup included (15) women with polycystic ovary syn drome (PCOS) and (15) women with \nendometriosis after confirmation of the infection and diagnosis by the specialist doctor based on the \nappearance of two Less symptoms such as (menstrual disorders, biochemical or clinical increase in \nandrogen, presence of a number of cysts on one of the ovaries using ultrasound). \n(5) ml of venous blood was drawn from each woman from the group, during days (2 -5) of the \nmenstrual cycle and distributed to be placed in test tubes containing a silicone gel tube. Then it was \nseparated by a centrifuge at 3500 revolutions for 15 minutes to obtain The blood serum was then \ntransferred to Eppendorf test tubes. The samples were kept at a temperature of -20 degrees Celsius, \nand all information was recorded on them until they were used to begin conducting biochemical \ntests. \nLH and FSH hormonal measurements \nLuteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured using the Cl900i \ndevice and according to the working kit equipped from Shenzhen Mindray Bio-Medical Electronics. \nLuteinizing hormone (LH). \nProcedure \nLuteinizing hormone (LH) was measured by following the steps indicated in the hormone device \n(Cl900i), and it differs from one device to another and according to its manufacturer, as the work \nwas done according to a number of analyzes designated and prepared by the company and \naccording to the steps: \n1. Place 25µ of the sample in the designated place in the device \n2. Give a command to the device to calculate LH \n3. The results are calculated automatically and appear on the device panel. \nEstimating the level of follicle-stimulating hormone (FSH) in blood serum principle  \nThe follicle -stimulating hormone (FSH) was used according to the principle of action of the \nluteinizing hormone (LH) and by following the steps indicated in the hormone device (Cl900i).  \nStatistical analysis: \nThe Statistical Analysis System - SAS (2012) pro gram was used to detect the effect of various \nfactors on the study parameters. At least significant difference -LSD and (Analysis of Variation -\nANOV A). Chi-square test was used for significant comparison of percentages \nResults and discussion \nThe results of the current study, shown in Table (3), showed that there was a significant change in \nthe level of FSH at the probability level (P ≤0.0001) between the patient groups and the healthy \ngroup, as its level increased significantly in women with endometriosis (11 .619±0.479) and \ndecreased significantly in women with endometriosis. In women with PCOS (7.624±0.293) \ncompared to its level in the healthy group (9.133±0.247), it also decreased significantly in women \nwith polycystic ovary syndrome compared to the group with endometriosis.  \nThe statistical results also showed a significant difference in the level of the LH hormone between \nthe patient groups and the healthy group at the probability level (P ≤0.0001), which showed a \nsignificant decrease. Endometriosis (1.109±0.318) in sick women compared to the healthy group, \nwhile its level increased in women with polycystic ovary syndrome (15.815±0.289) PCOS \ncompared to its level in the healthy group (6.925±0.407) and those with endometriosis (P ≤0.0001), \nas shown in the table (3) \n\n  Journal of Science in Medicine and Life, Volume: 2 Issue: 9 Year: 2024                                      ISSN: 2992-9202 \n111 \n \nTable (3) represents the levels of LH and FSH hormone concentrations and the t-test and p-\nvalue values for the two study groups. \nLH \nMean ±SD mlU/ml \nFSH \nMean ± SD mlU/ml \nGroups \n \n6.925±0.407 \n \n9.133±0.247b (15)control group \n1.109±0.318 11. 619±0.479a Endometriosis \n15.815±0.289 \n \n±0.293c7.624 polycystic ovary (30) \nP≤0.0001 0.0001< p-value \n \nThe results of the current study for women with Endometriosis showed a significant decrease in \ntheir LH hormone levels, while their FSH levels increased  compared to a group. These results were \nconsistent with the results of a study (6). \nThe results of the study showed an increase in the level of LH and no significant differences in the \nlevel of FSH. This may be due to an imbalance in the secretion of the luteinizing hormone (LH) in \nrelation to the follicle -stimulating hormone (FSH). The luteinizing hormone (LH) rises and the \nfollicle-stimulating hormone (FSH) decreases (the LH/FSH ratio is more than 2.5 normal). (Which \nresults in the failure of ovulation i n the ovary and thus the egg to cyst and not be released, in \naddition to several other factors involved in the pathogenesis of polycystic ovary syndrome. (7) \nIndicated that the main mechanism of the syndrome is the abnormal secretion of gonadotropin, with \nan increase in the LH hormone in Circulation and low FSH. Also, excessive secretion of androgens \nby the ovaries and adrenal glands, which provide the substrate for peripheral levels of estrogen, also \nplays a role in the development of polycystic ovary synd rome (7) In addition, the patterns of FSH \nand LH secretion reflect the integration of complex signals sensitive to the hypothalamus, pituitary, \nand peripheral glands, and the amplitude and frequency of the GnRH pulse determine the \nphysiological patterns of LH and FSH secretion, as a decrease in the frequency of the GnRH pulse \nenhances the amplitude of the LH pulse (8). \n(9) Indicated in their research that women with polycystic ovary syndrome show a high average \nlevel of luteinizing hormone (LH), in addition  to a high frequency of pulsatile LH secretion. The \nabnormally high LH pulsation frequency indicates a reflection of an overactive neural circuit in the \nsecretion of gonadotropin hormone (GnRH). ), which give a neuroendocrine basis either as etiology \nor in  the phenotype of PCOS (13). A high pulse in the gonadotropin hormone (GnRH) leads to \nexcessive secretion of luteinizing hormone (LH), which has effects on the production of androgen \nin the ovary and the development of eggs (10). The study agreed with the studies of Ali and Moran, \nin which they found no significant differences between the group of infected women. With the \nsyndrome and insulin resistance and another group of women with the syndrome only. Moran \nsuggested that the resistance to insulin and gon adotropins associated with polycystic ovary \nsyndrome may be caused by other separate genetic diseases (11,12).  Likewise, the current study \nwith regard to the increase in LH levels is consistent with Alsaadi ’s findings regarding the increase \nin LH levels in  women with polycystic ovary syndrome (13), which is likely to be due to an \nincrease in androgens with a continuous increase in the pulse rate of gonadotropin -releasing \nhormone (GnRH). ), which was related to androgen -induced resistance to the GnRH pulsati on \nassociated with negative feedback of progesterone, as this imbalance can lead to an excessive \nincrease in LH secretion, which may also be responsible for ovarian androgen production and \novulatory dysfunction, which causes polycystic ovary syndrome in adults ( 14) \nConclusions \nDisturbances in the level of sex hormones and nutrients for the gonads play a major role in causing \npathological conditions that lead to polycystic ovary syndrome and endometriosis. \n \n\n  Journal of Science in Medicine and Life, Volume: 2 Issue: 9 Year: 2024                                      ISSN: 2992-9202 \n112 \n \nReferences \n1. 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Tumor Biology, 35, 4031-4040.","source_license":"CC0","license_restricted":false}