Search Results (9)

Background: Polycystic ovary syndrome (PCOS) and autoimmune thyroid disease (AITD) have a high prevalence in women of reproductive age. PCOS can lead to long-term adverse health effects such as obesity, diabetes, and increased metabolic and cardiovascular risk. Although it is known that subclinical and clinical hypothyroidism may also worsen body mass index (BMI), lipid profile, and metabolic risk, there are few studies on the impact of elevated thyroid autoantibodies alone and associated chronic inflammation on metabolic complications in women with PCOS. The main aim of the study was to assess the prevalence of AITD among Polish women with PCOS and the metabolic impact of the co-occurrence of both diseases in euthyroid individuals. The additional aim was a review of the literature on the prevalence of co-occurrence of PCOS and AITD and the metabolic consequences of this condition. Methods: A total of 424 women aged 16–46 years were recruited into the study—230 women diagnosed with PCOS and 194 women diagnosed with PCOS and co-occurrence of euthyroid AITD. Before participating in the study, patients signed a written informed consent. The study was approved by the local ethics committee. Statistical analysis was performed using IBM SPSS Statistics (v.25). A mini-review of the literature was performed using the PubMed database. Results: Women with co-occurrence of PCOS and euthyroid AITD had statistically significantly higher serum levels of total cholesterol (189.57 mg/dL vs. 180.16 mg/dL; p = 0.005; d Cohen’s = −0.278), LDL-cholesterol (109.80 mg/dL vs. 102.01 mg/dL; p = 0.009; d Cohen’s = −0.256), and triglycerides (107.77 mg/dL vs. 96.82 mg/dL; p = 0.027; d Cohen’s = −0.219) compared to women with PCOS. The difference was observed regardless of body weight. BMI was also statistically significantly higher in the PCOS-AITD group (27.55 kg/m² vs. 25.46 kg/m²; p = 0.003; d Cohen’s = −0.319), as was the prevalence of obesity (32.5% vs. 20.7%; Chi-square = 7.956; p = 0.047). The mini-review of the literature did not find many studies evaluating the impact of thyroid autoantibodies on metabolic outcomes in PCOS euthyroid women, and the data are still inconclusive. Conclusions: The presence of elevated serum concentrations of thyroid autoantibodies in euthyroid women with PCOS increases the risk of obesity and metabolic consequences. It is observed even in euthyroid and non-obese individuals. Consequently, the cardiovascular risk in these women may be higher than in PCOS women without elevated thyroid autoantibodies. It is important to assess thyroid autoantibodies in all women with PCOS. In euthyroid PCOS women with co-occurrence of elevated serum levels of thyroid autoantibodies, it is crucial to pay more attention to maintaining an appropriate body mass index. There is an urgent need for further studies in large groups of women assessing the impact of elevated thyroid autoantibodies alone on metabolic outcomes in euthyroid women with PCOS to confirm and clarify the results. Full article

Introduction: Currently, progesterone is notably absent from conventional feminizing hormone therapies for transgender women. Anecdotal reports indicate the potential for health advantages following the incorporation of progesterone into treatment regimens. The primarily female hormone, progesterone naturally surges in women during the menstrual luteal phase. When administered exogenously, it may expedite bodily changes that are pivotal for gender transition. Progesterone holds promise as a potential remedy for various health conditions prevalent in the transgender woman population. Methods: This narrative review synthesizes existing literature and presents a comprehensive account of the administration of exogenous progesterone in transgender women. A literature search was conducted using the PubMed, Embase, ScienceDirect, and ResearchGate databases. The following keywords were used in the search: progesterone, transgender, breast neoplasms, lactation, prostate, testicular neoplasms, and thrombosis. These terms were combined using Boolean operators. The results of the initial search were screened by three independent reviewers based on their relevance to the topic under study. Results: A total of 104 studies were initially identified as meeting the criteria for inclusion. Following an assessment based on the contents of the title, abstract, and full text, 39 studies were deemed eligible for inclusion. A critical examination of health outcomes was conducted across key sections, including breast development, mental health, lactation, cancer risk (breast and prostate), thrombosis, and nervous and other systems. Discussion: The use of progesterone in the transgender woman population is a topic that has yet to be sufficiently researched. The limited sample size, short follow-up periods, and lack of randomization restrict the potential for achieving a robust scientific evidence base. In order to gain a fuller understanding of this topic, findings from studies on contraception, hormone replacement therapy, and animal models were considered. Conclusions: Progesterone may have a beneficial effect on the bodies of transgender women without significant adverse health effects. Further investigation through well-designed studies is recommended. Randomized controlled trials that include various dosages, broad and long-term effects, and precise demographics are needed. There is an immediate need for more knowledge to create appropriate patent and clinical practice guidelines. Full article

Obesity, which leads to metabolic dysregulation and body function impairment, emerges as one of the pressing health challenges worldwide. Excessive body fat deposits comprise a dynamic and biologically active organ possessing its own endocrine function. One of the mechanisms underlying the pathophysiology of obesity is low-grade systemic inflammation mediated by pro-inflammatory factors such as free fatty acids, lipopolysaccharides, adipokines (including leptin, resistin and visfatin) and cytokines (TNF-α, IL-1β, Il-6), which are secreted by adipose tissue. Together with obesity-induced insulin resistance and hyperandrogenism, the exacerbated immune response has a negative impact on the hypothalamic–pituitary–gonadal axis at all levels and directly affects reproduction. In women, it results in disrupted ovarian function, irregular menstrual cycles and anovulation, contributing to infertility. This review focuses on the abnormal intracellular communication, altered gene expression and signaling pathways activated in obesity, underscoring its multifactorial character and consequences at a molecular level. Extensive presentation of the complex interplay between adipokines, cytokines, immune cells and neurons may serve as a foundation for future studies in search of potential sites for more targeted treatment of reproductive disorders related to obesity. Full article

Bone has traditionally been viewed in the context of its structural contribution to the human body. Foremost providing necessary support for mobility, its roles in supporting calcium homeostasis and blood cell production are often afterthoughts. Recent research has further shed light on the ever-multifaceted role of bone and its importance not only for structure, but also as a complex endocrine organ producing hormones responsible for the autoregulation of bone metabolism. Osteocalcin is one of the most important substances produced in bone tissue. Osteocalcin in circulation increases insulin secretion and sensitivity, lowers blood glucose, and decreases visceral adipose tissue. In males, it has also been shown to enhance testosterone production by the testes. Neuropeptide Y is produced by various cell types including osteocytes and osteoblasts, and there is evidence suggesting that peripheral NPY is important for regulation of bone formation. Hormonal disorders are often associated with abnormal levels of bone turnover markers. These include commonly used bone formation markers (bone alkaline phosphatase, osteocalcin, and procollagen I N-propeptide) and commonly used resorption markers (serum C-telopeptides of type I collagen, urinary N-telopeptides of type I collagen, and tartrate-resistant acid phosphatase type 5b). Bone, however, is not exclusively comprised of osseous tissue. Bone marrow adipose tissue, an endocrine organ often compared to visceral adipose tissue, is found between trabecula in the bone cortex. It secretes a diverse range of hormones, lipid species, cytokines, and other factors to exert diverse local and systemic effects. Full article

The bony skeleton, as a structural foundation for the human body, is essential in providing mechanical function and movement. The human skeleton is a highly specialized and dynamic organ that undergoes continuous remodeling as it adapts to the demands of its environment. Advances in research over the last decade have shone light on the various hormones that influence this process, modulating the metabolism and structural integrity of bone. More recently, novel and non-traditional functions of hypothalamic, pituitary, and adipose hormones and their effects on bone homeostasis have been proposed. This review highlights recent work on physiological bone remodeling and discusses our knowledge, as it currently stands, on the systemic interplay of factors regulating this interaction. In this review, we provide a summary of the literature on the relationship between bone physiology and hormones including kisspeptin, neuropeptide Y, follicle-stimulating hormone (FSH), prolactin (PRL), adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), growth hormone (GH), leptin, and adiponectin. The discovery and understanding of this new functionality unveils an entirely new layer of physiologic circuitry. Full article

Lactation is a physiological state of hyperprolactinemia and associated amenorrhea. Despite the fact that exact mechanisms standing behind the hypothalamus–pituitary–ovarian axis during lactation are still not clear, a general overview of events leading to amenorrhea may be suggested. Suckling remains the most important stimulus maintaining suppressive effect on ovaries after pregnancy. Breastfeeding is accompanied by high levels of prolactin, which remain higher than normal until the frequency and duration of daily suckling decreases and allows normal menstrual function resumption. Hyperprolactinemia induces the suppression of hypothalamic Kiss1 neurons that directly control the pulsatile release of GnRH. Disruption in the pulsatile manner of GnRH secretion results in a strongly decreased frequency of corresponding LH pulses. Inadequate LH secretion and lack of pre-ovulatory surge inhibit the progression of the follicular phase of a menstrual cycle and result in anovulation and amenorrhea. The main consequences of lactational amenorrhea are connected with fertility issues and increased bone turnover. Provided the fulfillment of all the established conditions of its use, the lactational amenorrhea method (LAM) efficiently protects against pregnancy. Because of its accessibility and lack of additional associated costs, LAM might be especially beneficial in low-income, developing countries, where modern contraception is hard to obtain. Breastfeeding alone is not equal to the LAM method, and therefore, it is not enough to successfully protect against conception. That is why LAM promotion should primarily focus on conditions under which its use is safe and effective. More studies on larger study groups should be conducted to determine and confirm the impact of behavioral factors, like suckling parameters, on the LAM efficacy. Lactational bone loss is a physiologic mechanism that enables providing a sufficient amount of calcium to the newborn. Despite the decline in bone mass during breastfeeding, it rebuilds after weaning and is not associated with a postmenopausal decrease in BMD and osteoporosis risk. Therefore, it should be a matter of concern only for lactating women with additional risk factors or with low BMD before pregnancy. The review summarizes the effect that breastfeeding exerts on the hypothalamus–pituitary axis as well as fertility and bone turnover aspects of lactational amenorrhea. We discuss the possibility of the use of lactation as contraception, along with this method’s prevalence, efficacy, and influencing factors. We also review the literature on the topic of lactational bone loss: its mechanism, severity, and persistence throughout life. Full article

Polycystic ovary syndrome (PCOS) is a one of the most common endocrine disorders, with a prevalence rate of 5–10% in reproductive aged women. It’s characterized by (1) chronic anovulation, (2) biochemical and/or clinical hyperandrogenism, and (3) polycystic ovarian morphology. PCOS has significant clinical implications and can lead to health problems related to the accumulation of adipose tissue, such as obesity, insulin resistance, metabolic syndrome, and type 2 diabetes. There is also evidence that PCOS patients are at higher risk of cardiovascular diseases, atherosclerosis, and high blood pressure. Several studies have reported the association between polycystic ovary syndrome (PCOS) and low-grade chronic inflammation. According to known data, inflammatory markers or their gene markers are higher in PCOS patients. Correlations have been found between increased levels of C-reactive protein (CRP), interleukin 18 (IL-18), tumor necrosis factor (TNF-α), interleukin 6 (IL-6), white blood cell count (WBC), monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1α (MIP-1α) in the PCOS women compared with age- and BMI-matched controls. Women with PCOS present also elevated levels of AGEs and increased RAGE (receptor for advanced glycation end products) expression. This chronic inflammatory state is aggravating by obesity and hyperinsulinemia. There are studies describing mutual impact of hyperinsulinemia and obesity, hyperandrogenism, and inflammatory state. Endothelial cell dysfunction may be also triggered by inflammatory cytokines. Many factors involved in oxidative stress, inflammation, and thrombosis were proposed as cardiovascular risk markers showing the endothelial cell damage in PCOS. Those markers include asymmetric dimethylarginine (ADMA), C-reactive protein (CRP), homocysteine, plasminogen activator inhibitor-I (PAI-I), PAI-I activity, vascular endothelial growth factor (VEGF) etc. It was also proposed that the uterine hyperinflammatory state in polycystic ovary syndrome may be responsible for significant pregnancy complications ranging from miscarriage to placental insufficiency. In this review, we discuss the most importance evidence concerning the role of the process of chronic inflammation in pathogenesis of PCOS. Full article

Premature ovarian insufficiency (POI), previously known as premature ovarian failure or premature menopause, is defined as loss of ovarian function before the age of 40 years. The risk of POI before the age of 40 is 1%. Clinical symptoms develop as a result of estrogen deficiency and may include amenorrhea, oligomenorrhea, vasomotor instability (hot flushes, night sweats), sleep disturbances, vulvovaginal atrophy, altered urinary frequency, dyspareunia, low libido, and lack of energy. Most causes of POI remain undefined, however, it is estimated that anywhere from 4–30% of cases are autoimmune in origin. As the ovaries are a common target for autoimmune attacks, an autoimmune etiology of POI should always be considered, especially in the presence of anti-oocyte antibodies (AOAs), autoimmune diseases, or lymphocytic oophoritis in biopsy. POI can occur in isolation, but is often associated with other autoimmune conditions. Concordant thyroid disorders such as hypothyroidism, Hashimoto thyroiditis, and Grave’s disease are most commonly seen. Adrenal autoimmune disorders are the second most common disorders associated with POI. Among women with diabetes mellitus, POI develops in roughly 2.5%. Additionally, autoimmune-related POI can also present as part of autoimmune polyglandular syndrome (APS), a condition in which autoimmune activity causes specific endocrine organ damage. In its most common presentation (type-3), APS is associated with Hashomoto’s type thyroid antibodies and has a prevalence of 10–40%. 21OH-Antibodies in Addison’s disease (AD) can develop in association to APS-2. Full article

The hair cycle and hair follicle structure are highly affected by various hormones. Androgens—such as testosterone (T); dihydrotestosterone (DHT); and their prohormones, dehydroepiandrosterone sulfate (DHEAS) and androstendione (A)—are the key factors in terminal hair growth. They act on sex-specific areas of the body, converting small, straight, fair vellus hairs into larger darker terminal hairs. They bind to intracellular androgen receptors in the dermal papilla cells of the hair follicle. The majority of hair follicles also require the intracellular enzyme 5-alpha reductase to convert testosterone into DHT. Apart from androgens, the role of other hormones is also currently being researched—e.g., estradiol can significantly alter the hair follicle growth and cycle by binding to estrogen receptors and influencing aromatase activity, which is responsible for converting androgen into estrogen (E2). Progesterone, at the level of the hair follicle, decreases the conversion of testosterone into DHT. The influence of prolactin (PRL) on hair growth has also been intensively investigated, and PRL and PRL receptors were detected in human scalp skin. Our review includes results from many analyses and provides a comprehensive up-to-date understanding of the subject of the effects of hormonal changes on the hair follicle. Full article