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This comprehensive review article delves into the critical role of the human microbiota in the development and management of endocrine-related diseases. We explore the complex interactions between the microbiota and the endocrine system, emphasizing the implications of microbiota dysbiosis for the onset and progression of various endocrine disorders. The review aims to synthesize current knowledge, highlighting recent advancements and the potential of novel therapeutic approaches targeting microbiota-endocrine interactions. Key topics include the impact of microbiota on hormone regulation, its role in endocrine pathologies, and the promising avenues of microbiota modulation through diet, probiotics, prebiotics, and fecal microbiota transplantation. We underscore the importance of this research in advancing personalized medicine, offering insights for more tailored and effective treatments for endocrine-related diseases. [ABSTRACT FROM AUTHOR]

Method-related variations in the measurement of hormones and the reference intervals used in the clinical laboratory can have a significant, but often under-appreciated, impact on the diagnosis and management of endocrine disorders. This variation in laboratory practice has the potential to lead to an errant approach to patient care and thus could cause harm. It may also be the source of confusion or result in excessive or inadequate investigation. It is important that laboratory professionals and clinicians know about these impacts, their sources, and how to detect and mitigate them when they do arise. In this review article, we describe the historical and scientific context from which inconsistency in the clinical laboratory arises. Examples from the published literature of the impact of the method, reference interval, and clinical decision threshold-related discordances on the assessment and monitoring of various endocrine disorders are discussed to illustrate the sources, causes, and effects of this variability. Its potential impact on the evaluation of growth hormone deficiency and excess, thyroid and parathyroid disorders, hyperandrogenism, hypogonadism, glucocorticoid excess and deficiency, and diabetes mellitus is elaborated. Strategies for assessment and mitigation of the discordance are discussed. The clinical laboratory has a responsibility to recognise and address these issues, and although a lot has been accomplished in this area already, there remains more to be done. [ABSTRACT FROM AUTHOR]

The coronavirus 2019 (COVID-19) disease has long-term effects, known as post-COVID conditions (PCC) or long-COVID. Post-COVID-19 syndrome is defined by signs and symptoms that occur during or after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection which persist for more than 12 weeks and cannot be supported by an alternative diagnosis. The cardiovascular damage caused by COVID-19 in the severe forms of the disease is induced by severe systemic inflammation, considered to be one of the causes of myocardial lesions, with increased levels of circulating cytokines and toxic response mediators. We have focused on conditions that can induce long-COVID-19, or multisystem inflammatory syndrome in adults or children (MIS-C/MIS-A), with an emphasis on endocrinological and metabolic disorders. Although described less frequently in children than in adults, long-COVID syndrome should not be confused with MIS-C, which is an acute condition characterized by multisystem involvement and paraclinical evidence of inflammation in a pediatric patient who tested positive for SARS-CoV-2. At the same time, we mention that the MIS-A symptoms remit within a few weeks, while the duration of long-COVID is measured in months. Long-COVID syndrome, along with its complications, MIS-A and MIS-C, represents an important challenge in the medical community. Underlying comorbidities can expose both COVID-19 adult and pediatric patients to a higher risk of negative outcomes not only during, but in the aftermath of the SARS-CoV-2 infection as well. [ABSTRACT FROM AUTHOR]

This study aims to investigate the effects of a high-fat, high-fructose (HF/HFr) diet on metabolic/endocrine dysregulations associated with letrozole (LET)-induced Polycystic Ovarian Syndrome (PCOS) in prepubertal female mice. Thirty-two prepubertal C57BL/6 mice were randomly divided into four groups of eight and implanted with LET or a placebo, with simultaneous administration of an HF/HFr/standard diet for five weeks. After sacrifice, the liver and blood were collected for selected biochemical analyses. The ovaries were taken for histopathological examination. The LET+HF/HFr group gained significantly more weight than the LET-treated mice. Both the LET+HF/HFr and the placebo-treated mice on the HF/HFr diet developed polycystic ovaries. Moreover the LET+HF/HFr group had significantly elevated testosterone levels, worsened lipid profile and indices of insulin sensitivity. In turn, the HF/HFr diet alone led to similar changes in the LET-treated group, except for the indices of insulin sensitivity. Hepatic steatosis also occurred in both HF/HFr groups. The LET-treated group did not develop endocrine or metabolic abnormalities, but polycystic ovaries were seen. Since the HF/HFr diet can cause substantial metabolic and reproductive dysregulation in both LET-treated and placebo mice, food items rich in simple sugar—particularly fructose—and saturated fat, which have the potential to lead to PCOS progression, should be eliminated from the diet of young females. [ABSTRACT FROM AUTHOR]

Nonalcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease. NAFLD often occurs associated with endocrinopathies. Evidence suggests that endocrine dysfunction may play an important role in NAFLD development, progression, and severity. Our work aimed to explore and summarize the crosstalk between the liver and different endocrine organs, their hormones, and dysfunctions. For instance, our results show that hyperprolactinemia, hypercortisolemia, and polycystic ovary syndrome seem to worsen NAFLD's pathway. Hypothyroidism and low growth hormone levels also may contribute to NAFLD's progression, and a bidirectional association between hypercortisolism and hypogonadism and the NAFLD pathway looks likely, given the current evidence. Therefore, we concluded that it appears likely that there is a link between several endocrine disorders and NAFLD other than the typically known type 2 diabetes mellitus and metabolic syndrome (MS). Nevertheless, there is controversial and insufficient evidence in this area of knowledge. [ABSTRACT FROM AUTHOR]

Building on the seminal work by Geoffrey Harris in the 1970s, the neuroendocrinology field, having undergone spectacular growth, has endeavored to understand the mechanisms of hormonal connectivity between the brain and the rest of the body. Given the fundamental role of the brain in the orchestration of endocrine processes through interactions among neurohormones, it is thus not surprising that the structural and/or functional alterations following traumatic brain injury (TBI) can lead to endocrine changes affecting the whole organism. Taking into account that systemic hormones also act on the brain, modifying its structure and biochemistry, and can acutely and chronically affect several neurophysiological endpoints, the question is to what extent preexisting endocrine dysfunction may set the stage for an adverse outcome after TBI. In this review, we provide an overview of some aspects of three common metabolic endocrinopathies, e.g., diabetes mellitus, obesity, and thyroid dysfunction, and how these could be triggered by TBI. In addition, we discuss how the complex endocrine networks are woven into the responses to sudden changes after TBI, as well as some of the potential mechanisms that, separately or synergistically, can influence outcomes after TBI. [ABSTRACT FROM AUTHOR]

Simple Summary: Nonhuman primates (NHP) can become ill due to a variety of diseases and disorders, yet endocrine disorders remain underreported. Therefore, an exhaustive literature search on this subject via widely used academic search systems, peer-reviewed publications, proceedings, and newsletters was performed. Selected major endocrine entities will be described emphasizing clinical signs, morphologic features, concomitant diseases, as well as available treatment options. In most cases, no clinical signs were noted and on gross pathology, the endocrine organs were unremarkable. The diagnosis was frequently made as incidental findings after standard histological examination. Although the findings were frequently incidental many have the potential to impact studies. This review explains that there is no standard procedure for diagnosing, monitoring, or treating endocrine disorders in NHP. More research is needed to evaluate these procedures and establish risk factors. Literature concerning veterinary medicine of non-human primates is continuously updated, yet endocrine disorders remain underreported. While case or survey reports of individual endocrinopathies are available, a comprehensive review is not. An exhaustive literature search on this subject via widely used academic search systems, (e.g., Google Scholar, PubMed, BioOne complete and Web of Science), and peer-reviewed publications, proceedings, and newsletters was performed. Selected major endocrine entities will be described with emphasis on clinical signs, morphologic appearances, concomitant diseases, as well as available treatment options. Mostly, no clinical signs were noted and on gross pathology, the endocrine organs were unremarkable. An endocrine-related diagnosis was frequently made as an incidental finding after standard histopathological examination. During the review, the pancreas represented the most affected endocrine organ and diabetes mellitus represented the most clinically significant disorder. Currently, no standard procedure for diagnosing, monitoring, or treating endocrine disorders in non-human primates exists. [ABSTRACT FROM AUTHOR]

Background and objectives: To assess whether placental growth factor (PlGF) levels may have a predictive value for the onset of gestational diabetes mellitus (GDM) and thyroid dysfunction during pregnancy. Materials and Methods: This single-center retrospective analysis was conducted at the Specialized Hospital for Active Treatment in Obstetrics and Gynecology "Dr. Shterev", Sofia, Bulgaria, from December 2017 to December 2019. Using pregnant women's electronic records, we analyzed and compared the data of 412 women diagnosed with GDM and 250 women without evidence for carbohydrate disorders. Thyroid function was tested in all patients at the time of performing GDM screening. The following measurements were compared and assessed: body mass index (BMI), fasting blood glucose levels, thyroid-stimulating hormone levels (TSH), free thyroxine, and triiodothyronine (FT4 and FT3) levels, and serum placental growth factor (PlGF). The sensitivity and specificity of PlGF as a predictive marker for GDM and thyroid dysfunction were analyzed using receiver operating characteristic (ROC) curves. Results: There were no significant differences between GDM and control groups in terms of age and BMI (p > 0.05). In patients with established GDM, the PlGF corrected multiple of the median (MoM) was significantly higher compared to the control group (0.9 vs. 0.7, p < 0.001). The ROC-AUC for the prediction of GDM and thyroid dysfunction during pregnancy was 0.68 (95% CI 0.64–0.72) and 0.61 (95% CI 0.57–0.65), respectively. Conclusions: Our results underscore the potential role of PlGF as a biomarker in the prediction and diagnosis of GDM and thyroid dysfunction during pregnancy. [ABSTRACT FROM AUTHOR]

The management of patients with spinal muscular atrophy type 1 (SMA1) is constantly evolving. In just a few decades, the medical approach has switched from an exclusively palliative therapy to a targeted therapy, transforming the natural history of the disease, improving survival time and quality of life and creating new challenges and goals. Many nutritional problems, gastrointestinal disorders and metabolic and endocrine alterations are commonly identified in patients affected by SMA1 during childhood and adolescence. For this reason, a proper pediatric multidisciplinary approach is then required in the clinical care of these patients, with a specific focus on the prevention of most common complications. The purpose of this narrative review is to provide the clinician with a practical and usable tool about SMA1 patients care, through a comprehensive insight into the nutritional, gastroenterological, metabolic and endocrine management of SMA1. Considering the possible horizons opened thanks to new therapeutic frontiers, a nutritional and endo-metabolic surveillance is a crucial element to be considered for a proper clinical care of these patients. [ABSTRACT FROM AUTHOR]

Down syndrome is a genetic disorder caused by the presence of a third copy of chromosome 21, associated with intellectual disabilities. Down syndrome is associated with anomalies of both the nervous and endocrine systems. Over the past decades, dramatic advances in Down syndrome research and treatment have helped to extend the life expectancy of these patients. Improved life expectancy is obviously a positive outcome, but it is accompanied with the need to address previously overlooked complications and comorbidities of Down syndrome, including obesity and diabetes, in order to improve the quality of life of Down syndrome patients. In this focused review, we describe the associations between Down syndrome and comorbidities, obesity and diabetes, and we discuss the understanding of proposed mechanisms for the association of Down syndrome with metabolic disorders. Drawing molecular mechanisms through which Type 1 diabetes and Type 2 diabetes could be linked to Down syndrome could allow identification of novel drug targets and provide therapeutic solutions to limit the development of metabolic and cognitive disorders. [ABSTRACT FROM AUTHOR]

Endocrine disorders are common in obesity, including altered somatotropic axis. Obesity is characterized by reduced growth hormone (GH) secretion, although the insulin-like growth factor-1 (IGF-1) values are controversial. The aim of this study was to evaluate the effect of weight loss after bariatric surgery in the GH–IGF-1 axis in extreme obesity, in order to investigate IGF-1 values and the mechanism responsible for the alteration of the GH–IGF-1 axis in obesity. We performed an interventional trial in morbidly obese patients who underwent bariatric surgery. We included 116 patients (97 women) and 41 controls (30 women). The primary endpoint was circulating GH and IGF-1 values. Circulating IGF-1 values were lower in the obese patients than in the controls. Circulating GH and IGF-1 values increased significantly over time after surgery. Post-surgery changes in IGF-1 and GH values were significantly negatively correlated with changes in C-reactive protein (CRP) and free T4 values. After adjusting for preoperative body mass index (BMI), free T4 and CRP in a multivariate model, only CRP was independently associated with IGF-1 values in the follow-up. In summary, severe obesity is characterized by a functional hyposomatotropism at central and peripheral level that is progressively reversible with weight loss, and low-grade chronic inflammation could be the principal mediator. [ABSTRACT FROM AUTHOR]

Treatment with immune checkpoint inhibitors has shown efficacy against a variety of cancer types. The effects of nivolumab and pembrolizumab on lung cancer have been reported, and further therapeutic advances are ongoing. The side effects of immune checkpoint inhibitors are very different from those of conventional cytocidal anticancer drugs and molecular targeted drugs, and they involve various organs such as the digestive and respiratory organs, thyroid and pituitary glands, and skin. The generic term for such adverse events is immune-related adverse events (irAEs). They are relatively infrequent, and, if mild, treatment with immune checkpoint inhibitors can be continued with careful control. However, early detection and appropriate treatment are critical, as moderate-to-severe irAEs are associated with markedly reduced organ function and quality of life, with fatal consequences in some cases. Of these, endocrinopathies caused by immune checkpoint inhibitors are sometimes difficult to distinguish from nonspecific symptoms in patients with advanced cancer and may have serious outcomes when the diagnosis is delayed. Therefore, it is necessary to anticipate and appropriately address the onset of endocrinopathies during treatment with immune checkpoint inhibitors. Here, we present a review of endocrine disorders caused by immune checkpoint inhibitor treatment. [ABSTRACT FROM AUTHOR]

Tea made from Camellia sinensis leaves is one of the most consumed beverages worldwide. This systematic review aims to update Camellia sinensis pharmacological activity on metabolic and endocrine disorders. Inclusion criteria were preclinical and clinical studies of tea extracts and isolated compounds on osteoporosis, hypertension, diabetes, metabolic syndrome, hypercholesterolemia, and obesity written in English between 2014 and 2019 and published in Pubmed, Science Direct, and Scopus. From a total of 1384 studies, 80 reports met inclusion criteria. Most papers were published in 2015 (29.3%) and 2017 (20.6%), conducted in China (28.75%), US (12.5%), and South Korea (10%) and carried out with extracts (67.5%, especially green tea) and isolated compounds (41.25%, especially epigallocatechin gallate). Most pharmacological studies were in vitro and in vivo studies focused on diabetes and obesity. Clinical trials, although they have demonstrated promising results, are very limited. Future research should be aimed at providing more clinical evidence on less studied pathologies such as osteoporosis, hypertension, and metabolic syndrome. Given the close relationship among all endocrine disorders, it would be of interest to find a standard dose of tea or their bioactive constituents that would be beneficial for all of them. [ABSTRACT FROM AUTHOR]

The Republic of Ireland (RoI) is the only European Country with a mandatory national legislation requiring artificial fluoridation of drinking water and has the highest per capita consumption of black tea in the world. Tea is a hyperaccumulator of fluoride and chronic fluoride intake is associated with multiple negative health outcomes. In this study, fifty four brands of the commercially available black tea bag products were purchased and the fluoride level in tea infusions tested by an ion-selective electrode method. The fluoride content in all brands tested ranged from 1.6 to 6.1 mg/L, with a mean value of 3.3 mg/L. According to our risk assessment it is evident that the general population in the RoI is at a high risk of chronic fluoride exposure and associated adverse health effects based on established reference values. We conclude that the culture of habitual tea drinking in the RoI indicates that the total cumulative dietary fluoride intake in the general population could readily exceed the levels known to cause chronic fluoride intoxication. Evidence suggests that excessive fluoride intake may be contributing to a wide range of adverse health effects. Therefore from a public health perspective, it would seem prudent and sensible that risk reduction measures be implemented to reduce the total body burden of fluoride in the population.