Premature ovarian insufficiency: the context of long-term effects.

PURPOSE: Premature ovarian insufficiency (POI) is defined as the cessation of the ovarian function before the age of 40 years. POI aetiology may be related to iatrogenic or endogenous factors and in many cases remains unclear. The aim of this review was to characterize the long-term consequences of POI. METHODS: The available literature regarding the long-term consequences of POI from MEDLINE has been reviewed. RESULTS: Lack of ovarian steroids synthesis has serious consequences for women's health. The short-term effects are similar to spontaneous menopause and refer mainly to the climacteric syndrome. In a longer perspective, POI affects a variety of aspects. It obviously and drastically reduces the chances for spontaneous pregnancies. Oestrogen loss leads also to urogenital atrophy. The most common urogenital symptoms include vaginal dryness, vaginal irritation and itching. The urogenital atrophy and hypoestrogenism interferes also with sexual functioning. Patients with POI are threatened by a decrease in bone mineral density (BMD). POI women also experience psychological distress and some studies have shown an increased risk of neurodegenerating diseases. Overall, POI women have a shortened life expectancy, mainly due to cardiovascular disease. Some studies have reported a reduced risk of breast cancer in this group of patients. CONCLUSIONS: In conclusion there are several well-characterized health risks in POI women. With every patient, an individualized approach is required to properly recognize and prevent these risks.

Functional hypothalamic amenorrhea and its influence on women's health.

INTRODUCTION: Functional hypothalamic amenorrhea (FHA) is one of the most common causes of secondary amenorrhea. There are three types of FHA: weight loss-related, stress-related, and exercise-related amenorrhea. FHA results from the aberrations in pulsatile gonadotropin-releasing hormone (GnRH) secretion, which in turn causes impairment of the gonadotropins (follicle-stimulating hormone and luteinizing hormone). The final consequences are complex hormonal changes manifested by profound hypoestrogenism. Additionally, these patients present mild hypercortisolemia, low serum insulin levels, low insulin-like growth factor 1 (IGF-1) and low total triiodothyronine. AIM: The aim of this work is to review the available data concerning the effects of FHA on different aspects of women's health. RESULTS: Functional hypothalamic amenorrhea is related to profound impairment of reproductive functions including anovulation and infertility. Women's health in this disorder is disturbed in several aspects including the skeletal system, cardiovascular system, and mental problems. Patients manifest a decrease in bone mass density, which is related to an increase in fracture risk. Therefore, osteopenia and osteoporosis are the main long-term complications of FHA. Cardiovascular complications include endothelial dysfunction and abnormal changes in the lipid profile. FHA patients present significantly higher depression and anxiety and also sexual problems compared to healthy subjects. CONCLUSIONS: FHA patients should be carefully diagnosed and properly managed to prevent both short- and long-term medical consequences.

Bone mineral density in women with polycystic ovary syndrome.

PURPOSE: PCOS is a complex disorder and various features of this disorder may have great importance for bone metabolism. The aim of the study was to determine the relationship between existing hormonal disorders, and bone mineral density (BMD) in young women with PCOS. METHODS: 69 reproductive-aged PCOS women and 30 age-matched healthy controls were enrolled to the study women. In each individual we assessed the body mass index (BMI). We evaluated the serum concentrations of: gonadotropins, prolactin (PRL), estradiol (E2), dehydroepiandrosterone sulfate (DHEAS), testosterone (T), thyroid stimulating hormone (TSH), free thyroxine (fT4). We used the Homeostatic Model Assessment-Insulin Resistance Index (HOMA-IR) to diagnose insulin resistance. Bone mineral density in the lumbar spine was measured by dual-energy X-ray absorptiometry (DXA). RESULTS: The PCOS women had lower BMD values as compared to the controls (1.057 ± 0.1260 vs. 1.210 ± 0.1805 g/cm(2), p < 0.0002). In the analysis of PCOS patients according to BMI, only in the subgroup of the normal weight PCOS we find significantly lower BMD in comparison to controls (p = 0.0049). In patients with PCOS, BMD was positively correlated with insulin concentration and HOMA-IR. In the controls Z-score values were positively correlated with insulin concentration and HOMA-IR. CONCLUSIONS: The deleterious effect of estrogen deficiency on bones in PCOS is not balanced by androgen overproduction. Women with PCOS had significantly lower BMD of the lumbar spine compared to controls. Insulin seems to be one of the most important positive bone growth stimulators.

Cushing's syndrome in pregnancy: a case report and mini review of the literature.

Adrenal diseases in pregnant women are diagnosed relatively rarely. The main cause of hypercortisolemia during pregnancy is Cushing's syndrome related to adrenal adenoma. It is important to diagnose Cushing's syndrome in pregnant women because it can lead to significant maternal and foetal complications and morbidity. However, due to physiological endocrine changes and symptoms in pregnant women the diagnosis of this disorder can be a challenge. One current case describes a 38-year-old pregnant woman with hypertension, oedema and an adrenal tumour. At the beginning, Conn syndrome was suspected, but after careful analysis Cushing's syndrome (with an adenoma of the right adrenal gland) was diagnosed. After delivery and 5 weeks of pharmacological treatment the patient underwent right side adrenalectomy by laparoscopy.

Gherlin expression in women with polycystic ovary syndrome--a preliminary study.

The etiology and pathogenesis of polycystic ovary syndrome (PCOS) is still unknown. Using real-time PCR, we detected that polycystic ovaries showed almost ten times lower expression of ghrelin mRNA than normal ovaries, whereas the mRNA levels in blood cells were similar in both study groups. This suggests that the presence of ghrelin in PCOS and normal ovaries may have an autocrine/paracrine modulatory effect on ovary functions and local significance in the etiology of PCOS.

[Molecular basis of polycystic ovarian syndrome]. / Podloze molekularne zespolu policystycznych jajników.

Polycystic ovarian syndrome (PCO) is a relatively poorly defined type of steroidogenic abnormality, dependent on an overproduction of lutropin (LH). The PCO is characterized by infertility, amenorrhea or oligomenorrhea, obesity and hirsutism. The clinical symptoms are associated with typical morphological changes of the ovaries. It has been suggested that hyperplastic secondary interstitial cells and theca cells are the main site of excess androgen production. In PCO the elevation of androgens is observed, while the estrogen level is normal or slightly decreased. In the ovarian sex steroidogenic pathways, 17 alpha-hydroxylase, which produces androgens and aromatase, which converts androgens to estrogens are important regulatory enzymes. Major components of 17 alpha-hydroxylase and aromatase are cytochromes P450 17 alpha and P450 arom. Histochemical investigations revealed increased immunoreactivity with the antibody directed against P450 17 alpha in theca cells. In this review data from literature are presented and discussed regarding endocrinological and molecular background of PCO.

[Molecular background of hyperandrogenism of ovarian origin]. / Podloze molekularne hyperandrogenizmu pochodzenia jajnikowego.

Ovarian androgens constitute substrates for estrogen formation, the key enzyme in androgen production being 17 alpha-hydroxylase/17,20 lyase, while in estrogen synthesis, aromatase. Both enzymes are constituents of a complex, comprising two proteins: cytochrome P450 reductase and respective cytochromes P450c17 or P450arom, whose expression play an important role in a proper function of the ovaries and its genetically determined abnormalities may lead to appearance of clinical symptoms. Although it is difficult to clearly define the genetic background of disturbances, leading to hyperandrogenism, metabolic abnormalities, resulting in excessive androgen production, were observed in polycystic ovarian syndrome, hyperthecosis and hyperinsulinemia. In this review data from literature were presented and discussed regarding endocrine and molecular background of hyperandrogenism of ovarian origin.

[Assessment of the bone mass density in young women with secondary amenorrhea]. / Ocena gestosci kosci u mlodych kobiet z wtórnym brakiem miesiaczki.

Analisys of results of bone mass density among 120 patients of Gynecological Endocrinology Clinic AM Poznan was presented. Endocrinological background of lowered bone mass density was viewed.

Typical hormonal profiles are accompanied by increased immunoreactivity of theca folliculi steroid 17 alpha-hydroxylase P450 in polycystic ovary syndrome.

The localisation and expression of steroid 17 alpha-hydroxylase had been studied in ovaries obtained from 40 patients in whom polycystic ovary syndrome (PCO) was diagnosed, and in 15 normal ovaries. In patients, elevated serum LH and testosterone and normal FSH, prolactin and dehydroepiandrosterone levels were recorded. Serum oestradiol concentration was slightly decreased. Immunohistochemical staining with the use of antibody directed against human cytochrome P450c17 (CYP17) revealed that in polycystic as well as in normal ovaries, steroid 17 alpha-hydroxylase is localised mainly in the thecal cells of atretic follicles and in the interstitial cells of the stroma. Greater intensity of the immunohistochemical reaction in the polycystic ovaries than in normal controls, indicates a higher concentration of CYP17 and suggests increased expression of steroid 17 alpha-hydroxylase. It is postulated that the increased expression of ovarian steroid 17 alpha-hydroxylase is an important contributory factor in the pathogenesis of PCO.