ABSTRACT
A falência ovariana prematura (FOP) acomete aproximadamente 1:1000 mulheres antes dos 30 anos, 1:250 em torno dos 35 anos e de 1:100 aos 40 anos. Manifesta-se como amenorréia primária ou amenorréia secundária, não podendo ser considerada definitiva em todas as pacientes, uma vez que a concepção espontânea pode ocorrer em até 5-10 por cento das FOP. Na maioria dos casos apresenta-se na forma esporádica, pois apenas 5 por cento apresentam história familial. Entre as causas conhecidas estão as alterações cromossômicas, dos genes ligados ao cromossomo X e cromossomos autossômicos, doenças autoimunes, alterações tóxicas e iatrogênicas. Com relativa freqüência, a causa etiológica não é obtida, sendo então denominada de idiopática. O diagnóstico da FOP é feito baseado na história clínica e níveis elevados do hormônio folículo estimulante (FSH), sendo posteriormente investigadas as causas mais específicas. O manejo clínico visa o suporte emocional, o tratamento hormonal com estrogênios e progestogênios, a abordagem da infertilidade e a prevenção de co-morbidades como a osteoporose e potencial maior risco cardiovascular.
Premature ovarian failure occurs in approximately 1:1000 women before 30 years, 1:250 by 35 years and 1:100 by the age of 40. It is characterized by primary or secondary amenorrhea and cannot be considered as definitive because spontaneous conception may occur in 5 to 10 percent of cases. In 95 percent of cases, premature ovarian failure is sporadic. The known causes of premature ovarian failure include chromosomal defects, autoimmune diseases, exposure to radiation or chemotherapy, surgical procedures, and certain drugs. Frequently, however, the etiology is not clear and these cases are considered to be idiopathic. Premature ovarian failure is defined by gonadal failure and high serum follicle-stimulating hormone (FSH) levels. Clinical approach includes emotional support, hormonal therapy with estrogens and progesterone or progestogens, infertility treatment, and prevention of osteoporosis and potential cardiovascular risk.
Subject(s)
Adult , Female , Humans , Autoimmune Diseases/complications , Follicular Atresia/genetics , Primary Ovarian Insufficiency/etiology , Amenorrhea/etiology , Biomarkers/blood , Estrogen Replacement Therapy , Estrogens/therapeutic use , Follicle Stimulating Hormone/blood , Hypogonadism/etiology , Infertility, Female/etiology , Mutation/genetics , Primary Ovarian Insufficiency/genetics , Primary Ovarian Insufficiency/therapy , Ovarian Follicle/abnormalities , Progesterone/therapeutic use , Progestins/therapeutic use , Receptors, FSH/geneticsABSTRACT
This study was conducted to determine the histogenesis, growth and atresia of ovarian follicles in Makuii sheep fetuses at different developmental stages. Forty fetuses in four age groups of = 35, 36-70, 71-100 and 101-150 intrauterine days old were taken for study. The fetuses were collected and preserved in 10% neutral buffered formalin solution. After recognition and harvesting of ovaries from fetuses, they were processed through routine paraffin embedding. Serial 5-7 micro m thick sections were taken and stained with Hematoxylin-Eosin, Verhoeff, Van Gieson, Toluidine blue and PAS. Histologic and histomorphometric [point count] studies were adopted. In fetuses = 35 days old, the necrotic primordial germ cells [PGCs] were identified by pyknotic, condensed or karyolytic nuclei. In these fetuses, the undifferentiated gonads were recognized at the caudal aspects of the developing metanephrous kidneys. The healthy PGCs, were large with euchromatic nuclei, without any somatic cell surrounding them. In 36-70 days old fetuses, the germ cells were observed in clusters, which were surrounded by simple squamous cells. The hilus cells were seen in mesovarium. In the 71-100 days old fetuses, primordial follicles were observed. In the 84 days old fetuses, primary follicles were seen for the first time. In the ovaries of 101-150 days old fetuses, the secondary follicles with zona pellucida and theca folliculi were seen. Tertiary follicles were not seen in any age groups. The mean number of germ cell population at 0.25 mm [2] surface area of ovary, was the highest in 36-70 days old and lowest in 101-150 days old age group fetuses. It was revealed that in all age groups, the population of healthy follicles and/or germ cells is higher than population of atretic follicles and that there was significant difference [P<0.001] between them. There were significant [P<0.001] differences in the mean distribution of healthy follicles and or germ cells among all age groups. There were significant [P< 0.001] differences in atretic follicles among all age groups, except between 36-70 days old and 71-100 days old fetuses. We concluded that by increasing age, a decrease in population of healthy as well as atretic follicles in fetuses takes place. However, in all age groups, the population of the healthy follicle is greater than the population of atretic follicles
Subject(s)
Animals , Ovarian Follicle/abnormalities , Fetus , Formaldehyde , Ovary/embryology , Germ Cells , Fertilization in VitroABSTRACT
Numerous models have been developed to study polycystic ovarian syndrome in rats. In the present study, the syndrome was induced by exposure to constant light. The histological structure and differential distribution of extracellular matrix (ECM) fibers as well as the glycosaminoglycans (GAGs) content and composition of the ovarian follicular wall of rats with polycystic syndrome were evaluated. Histochemical differences were observed in the graunlosa and theca externa of follicular cysts when compared to normal preovulatory follicles. The colagen content of the theca externa of follicular cysts, quantified by the picrosirius method, was higher than in the controls. The neural carbohydrate and acidic GAC levels were lower in the granulosa and higher in the theca externa of cyst follicles than in control ovaries. Histomorphometrically, the follicular diameter was both a convenient and appropriate measurement for describing the cyst status; there were no differences in the thickness of each follicular layer. In conclusion, differences in the components of ECM were observed in the follicular wall of ovarian cysts compared eith normal preovulatory follicles. Howere, sinde these changes did not occur uniformly in all layers of the follicular wall, their role in cyst development remains to be established.