CLINICAL COURSE OF PERIMENOPAUSAL PERIOD IN WOMEN WITH HYPERANDROGENISM SYNDROME

2021 ◽  
Vol 2 (5) ◽  
pp. 25-29
Author(s):  
N.O. Azamkulova ◽  
◽  
Sevara Irgasheva
Keyword(s):  
Luteinizing Hormone ◽  
Female Body ◽  
Adrenal Glands ◽  
Clinical Course ◽  
Dehydroepiandrosterone Sulfate ◽  
Reproductive Disorders ◽  
Peripheral Tissues ◽  
Androgen Synthesis ◽  
Excess Production ◽  
Endocrine Status

Hyperandrogenism is a disorder of endocrine status caused by excess production of androgens. The syndrome is a consequence of increased androgen production both in the ovaries and adrenal glands. However, such a division is very arbitrary, as increased production of androgens in the adrenal glands may increase production in the ovaries and vice versa. Androgens in women are synthesized by ovaries, adrenal glands and peripheral tissues, which also participate in metabolism.The set of androgens in both womenand men includes dehydroepiandrosterone-sulfate, dehydroepiandrosterone, androstenedione, testosterone and 5-alpha-dihydrotestosterone (5-alpha-DHT). Still, unlike men, women have a higher concentration of the first three hormones than the lasttwo. Androgen synthesis in the adrenal glands in women is regulated by adrenocorticotropic and in the ovaries by luteinizing hormone (LH) and some other intraglandular autoparacrine mechanisms. According to recent studies, in addition to the basic biological, previously commonly known effects of androgens, their new mechanisms of influence on the female body have been discovered. Keywords: hyperandrogenism, hormones, ovaries, adrenal glands, reproductive disorders

scholarly journals Possible Relevance of Soluble Luteinizing Hormone Receptor during Development and Adulthood in Boys and Men

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1329
Author(s):  
Li Juel Mortensen ◽  
Mette Lorenzen ◽  
Anne Jørgensen ◽  
Jakob Albrethsen ◽  
Niels Jørgensen ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Hormone Receptor ◽  
Adrenal Glands ◽  
Seminal Fluid ◽  
Body Fluids ◽  
Luteinizing Hormone Receptor ◽  
Gonadal Function ◽  
Fetal Kidney ◽  
Healthy Men ◽  
Human Fetal Kidney

Luteinizing hormone (LH) and human chorionic gonadotropin (hCG) are agonists for the luteinizing hormone receptor (LHCGR) which regulates male reproductive function. LHCGR may be released into body fluids. We wish to determine whether soluble LHCGR is a marker for gonadal function. Cross-sectional, longitudinal, and intervention studies on 195 healthy boys and men and 396 men with infertility, anorchia, or Klinefelter Syndrome (KS) were used to correlate LHCGR measured in serum, seminal fluid, urine, and hepatic/renal artery and vein with gonadal function. LHCGR was determined in fluids from in vitro and in vivo models of human testicular tissue and cell lines, xenograft mouse models, and human fetal kidney and adrenal glands. Western blot showed LHCGR fragments in serum and gonadal tissue of similar size using three different antibodies. The LHCGR-ELISA had no species cross-reactivity or unspecific reaction in mouse serum even after human xenografting. Instead, sLHCGR was released into the media after the culture of a human fetal kidney and adrenal glands. Serum sLHCGR decreased markedly during puberty in healthy boys (p = 0.0001). In healthy men, serum sLHCGR was inversely associated with the Inhibin B/FSH ratio (β −0.004, p = 0.027). In infertile men, seminal fluid sLHCGR was inversely associated with serum FSH (β 0.006, p = 0.009), sperm concentration (β −3.5, p = 0.003) and total sperm count (β −3.2, p = 0.007). The injection of hCG lowered sLHCGR in serum and urine of healthy men (p < 0.01). In conclusion, sLHCGR is released into body-fluids and linked with pubertal development and gonadal function. Circulating sLHCGR in anorchid men suggests that sLHCGR in serum may originate from and possibly exert actions in non-gonadal tissues. (ClinicalTrials: NTC01411527, NCT01304927, NCT03418896).

scholarly journals Alarin/FSH Ratio Might Be A New Biological Marker in Polycystic Ovary Syndrome Women with Normal and Women with Obese

2019 ◽  
Vol 3 (5) ◽  
Keyword(s):  
Luteinizing Hormone ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Density Lipoprotein ◽  
Biological Marker ◽  
Dehydroepiandrosterone Sulfate ◽  
Normal Weight ◽  
Control Group ◽  
Total Testosterone ◽  
Ovary Syndrome

Neuropeptides coordinate and regulate physiological processes in all animals. Alarin is a 25 amino acid neuropeptide which promotes the secretion of luteinizing hormone (LH). It has been known that serum luteinizing hormone levels are increased in women with polycystic ovary syndrome. Therefore, purpose of this was to examine the association of circulating gonadotropin secretions, and alarin with women with polycystic ovary syndrome, and to compare these findings with those of control subjects in an effort to better understand the pathophysiology of PCOS. 28 participants with a diagnosis of PCOS with normal weight and 28 participants with a diagnosis of PCOS with obese and 28 control group participants were included in this case-control study. Hormone profiles of the participants (alarin, insulin, estradiol (E2), follicle-stimulating hormone (FSH), luteinizing hormone (LH), dehydroepiandrosterone sulfate (DHEA-SO4 ), lipid profiles total testosterone, low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglyceride, cholesterol) and fasting blood sugar (FBS) values were measured. Results: Serum androgens were elevated in the PCOS. Blood LH was also elevated (P < 0.05) but was higher in PCOS than Control. Patients with PCOS had an increased alarin compared with controls. LH/FSH ratio and Alarin /FSH ratio were greater than 2.1, 2.4, respectively. The blood alarin levels were significantly correlated with the serum LH levels (r=0.492, p=0.002) and the LH/FSH ratios (r=0.450, p<0.001) and Alarin/ FSH ratios. The FSH/LH and alarin /FSH ratio were elevated in the PCOS. Based on these results, the FSH/LH and Alarin /FSH ratio appears to be a useful marker of PCOS.

STEROIDAL CONTROL OF THE RELEASE OF THE PREOVULATORY SURGE OF LUTEINIZING HORMONE IN THE RAT

1978 ◽  
Vol 79 (2) ◽  
pp. 223-234 ◽  
Author(s):  
CATHERINE A. WILSON ◽  
J. C. HADLEY ◽  
D. GILBERT ◽  
A. S. McNEILLY
Keyword(s):  
Plasma Concentration ◽  
Luteinizing Hormone ◽  
Critical Period ◽  
Adrenal Glands ◽  
Sham Operation ◽  
Late Afternoon ◽  
Immature Rats ◽  
Pregnant Mare Serum Gonadotrophin ◽  
Adrenalectomized Rats

Experiments were carried out on 4 day cyclic rats or immature rats induced to ovulate by administration of pregnant mare serum gonadotrophin. Removal of the ovaries and adrenal glands at 17.00 h of pro-oestrus, i.e. after the critical period, prevented the appearance of the surge of LH. Sham-operation or removal of only one of the sets of glands had no effect. This indicates that the preovulatory increase in the concentration of oestradiol is not solely responsible for the surge of LH; the presence of a steroid, secreted by the ovaries and adrenal glands in the late afternoon of pro-oestrus, is also required. Attempts were made to reinstate the surge of LH in ovariectomized, adrenalectomized rats by administration of one of the steroids normally secreted in late pro-oestrus. Corticosterone, 20α- and 20β-hydroxy-4-pregnen-3-one and 17α-hydroxyprogesterone all had no effect. Progesterone injected at the time of the operation stimulated the release of LH but only after the plasma concentration had reached its maximum 3–5 h after injection. Testosterone also stimulated the release of LH some hours after administration.

scholarly journals Non-Classic Disorder of Adrenal Steroidogenesis and Clinical Dilemmas in 21-Hydroxylase Deficiency Combined with Backdoor Androgen Pathway. Mini-Review and Case Report

2020 ◽  
Vol 21 (13) ◽  
pp. 4622
Author(s):  
Marta Sumińska ◽  
Klaudia Bogusz-Górna ◽  
Dominika Wegner ◽  
Marta Fichna
Keyword(s):  
Dehydroepiandrosterone Sulfate ◽  
Childhood And Adolescence ◽  
Adrenal Androgen ◽  
Hydroxylase Deficiency ◽  
Cyp21a2 Gene ◽  
Peripheral Tissues ◽  
Biochemical Alterations ◽  
Genes Encoding ◽  
Classic Form ◽  
21 Hydroxylase Deficiency

Congenital adrenal hyperplasia (CAH) is the most common cause of primary adrenal insufficiency in children and adolescents. It comprises several clinical entities associated with mutations in genes, encoding enzymes involved in cortisol biosynthesis. The mutations lead to considerable (non-classic form) to almost complete (classic form) inhibition of enzymatic activity, reflected by different phenotypes and relevant biochemical alterations. Up to 95% cases of CAH are due to mutations in CYP21A2 gene and subsequent 21α-hydroxylase deficiency, characterized by impaired cortisol synthesis and adrenal androgen excess. In the past two decades an alternative (“backdoor”) pathway of androgens’ synthesis in which 5α-androstanediol, a precursor of the 5α-dihydrotestosterone, is produced from 17α-hydroxyprogesterone, with intermediate products 3α,5α-17OHP and androsterone, in the sequence and with roundabout of testosterone as an intermediate, was reported in some studies. This pathway is not always considered in the clinical assessment of patients with hyperandrogenism. The article describes the case of a 17-year-old female patient with menstrual disorders and androgenization (persistent acne, advanced hirsutism). Her serum dehydroepiandrosterone sulfate and testosterone were only slightly elevated, along with particularly high values for 5α-dihydrotestosterone. In 24 h urine collection, an increased excretion of 16α-OHDHEA—a dehydroepiandrosterone metabolite—and pregnanetriolone—a 17α-hydroxyprogesterone metabolite—were observed. The investigations that we undertook provided evidence that the girl suffered from non-classic 21α-hydroxylase deficiency with consequent enhancement of the androgen “backdoor” pathway in adrenals, peripheral tissues or both, using adrenal origin precursors. The paper presents diagnostic dilemmas and strategies to differentiate between various reasons for female hyperandrogenism, especially in childhood and adolescence.

The adaptive capacity of the female body after conducting medical abortion

2014 ◽  
Vol 20 (29) ◽  
pp. 0-0
Author(s):  
Алексеюк ◽  
Maksim Alekseyuk
Keyword(s):  
Menstrual Cycle ◽  
Adaptive Capacity ◽  
Female Body ◽  
Clinical Course ◽  
Medical Abortion ◽  
Second Phase ◽  
Vacuum Aspiration ◽  
Adaptive Capabilities ◽  
Manual Vacuum Aspiration ◽  
First Time

Based on the evaluation of the clinical course and the adaptive capabilities of the organism in the postabortion period after manual vacuum aspiration in 128 patients found that disorder of adaptation and the most frequent complications in the postabortion period observed in the production of abortion in the second phase of the suppositive menstrual cycle , especially in first time pregnant patients. In this way, the abortion in the first phase of &#34;suppositive&#34; menstrual cycle is the reserve for increasing the safety of abortion by MVA.

scholarly journals Adrenarche Results from Development of a 3β-Hydroxysteroid Dehydrogenase-Deficient Adrenal Reticularis1

1998 ◽  
Vol 83 (10) ◽  
pp. 3695-3701 ◽  
Author(s):  
Jennifer S. Gell ◽  
Bruce R. Carr ◽  
Hironobu Sasano ◽  
Baron Atkins ◽  
Linda Margraf ◽  
...  
Keyword(s):  
Adrenal Glands ◽  
Dehydroepiandrosterone Sulfate ◽  
Hydroxysteroid Dehydrogenase ◽  
Immunohistochemical Localization ◽  
The Other ◽  
Age Group ◽  
Other Hand ◽  
Significant Difference ◽  
Steroid Precursor

Adrenarche is the increased adrenal production of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) that occurs during the prepubertal period. To date, the exact mechanism initiating adrenarche is unknown, although many factors have been postulated. In the present study, we examined the hypothesis that alterations in intra-adrenal expression of 3β-hydroxysteroid dehydrogenase (3βHSD) or 21-hydroxylase (CYP21) within the inner reticularis zone leads to the increased production of 19-carbon (C19) steroids. After conversion of cholesterol to pregnenolone, 17α-hydroxylase/17,20-lyase (CYP17) can metabolize pregnenolone through to DHEA. The enzyme 3βHSD competes for substrate with CYP17 and effectively removes steroid precursor from the pathway leading to DHEA. On the other hand, deficiency in CYP21 expression is known to cause excessive production of adrenal C19 steroids, suggesting that CYP21 could play a role in adrenarche. Thus, a decrease in 3βHSD or CYP21 expression would allow substrate to flow toward the synthesis of DHEA. To determine whether adrenarche results from a decreased expression of 3βHSD or CYP21 in the reticularis, immunohistochemical localization of 3βHSD and CYP21 was performed, and staining intensities compared using adrenal glands from children ages 4 months to 4 yr (n = 12), ages 5–7 yr (n = 9), ages 8–13 yr (n = 9), and adults ages 25–56 yr (n = 8). There were no differences in the zonal expression of CYP21. No difference in 3βHSD staining was observed between the glomerulosa and fasciculata from any age group. However, children age 8 yr and older show a significant decrease in 3βHSD expression in reticularis as compared with the fasciculata. No significant difference was noted for 3βHSD levels between the fasciculata and reticularis for children age 7 yr or younger. The level of 3βHSD expression in the reticularis continued to decrease in the adult adrenals examined. These findings suggest that as children mature there is a decreased level of 3βHSD in the adrenal reticularis that may contribute to the increased production of DHEA and DHEAS seen during adrenarche.

scholarly journals Is the metalloendopeptidase EC 3.4.24.15 (EP24.15), the enzyme that cleaves luteinizing hormone-releasing hormone (LHRH), an activating enzyme?

Reproduction ◽  
2010 ◽  
Vol 139 (2) ◽  
pp. 319-330 ◽  
Author(s):  
Kirsty Cleverly ◽  
T John Wu
Keyword(s):  
Gene Expression ◽  
Luteinizing Hormone ◽  
Peptide Fragment ◽  
Peptide Fragments ◽  
Structural Variants ◽  
Peripheral Tissues ◽  
Luteinizing Hormone Releasing Hormone ◽  
Active Peptide ◽  
Neuroendocrine Axis ◽  
The Brain

LHRH (GNRH) was first isolated in the mammalian hypothalamus and shown to be the primary regulator of the reproductive neuroendocrine axis comprising of the hypothalamus, pituitary and gonads. LHRH acts centrally through its initiation of pituitary gonadotrophin release. Since its discovery, this form of LHRH (LHRH-I) has been shown to be one of over 20 structural variants with a variety of roles in both the brain and peripheral tissues. LHRH-I is processed by a zinc metalloendopeptidase EC 3.4.24.15 (EP24.15) that cleaves the hormone at the fifth and sixth bond of the decapeptide (Tyr5-Gly6) to form LHRH-(1–5). We have previously reported that the auto-regulation of LHRH-I (GNRH1) gene expression and secretion can also be mediated by itself and its processed peptide, LHRH-(1–5), centrally and in peripheral tissues. In this review, we present the evidence that EP24.15 is the main enzyme of LHRH metabolism. Following this, we look at the metabolism of other neuropeptides where an active peptide fragments is formed during degradation and use this as a platform to postulate that EP24.15 may also produce an active peptide fragment in the process of breaking down LHRH. We close this review by the role EP24.15 may have in regulation of the complex LHRH system.

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