搜索结果：Hormones (Athens, Greece)

The association between serum vitamins and sex hormones has gained considerable research interest; however, studies focusing specifically on adolescent males remain limited. To analyze associations between key serum vitamins and sex hormone levels in adolescent males. This cross-sectional study utilized data from the National Health and Nutrition Examination Survey (NHANES) (2001-2004). Weighted generalized linear regression models were employed to examine associations between serum vitamins (D, B12, folate, A, and E) and sex hormones, namely, total testosterone (TT), sex hormone-binding globulin (SHBG), and estradiol (E2). The Bayesian kernel machine regression (BKMR) model was employed to account for the combined effects of vitamins, nonlinear exposure-outcome relationships, and interactions among vitamins. A total of 231 participants aged 12-18 years were included. In the generalized linear model, vitamin A was positively correlated with TT (&#x3b2;&#x2009;=&#x2009;0.421; 95% CI: 0.013, 0.829; P&#x2009;=&#x2009;0.028) and negatively correlated with SHBG (&#x3b2;=-0.372; 95% CI: -0.549, -0.195; P&#x2009;<&#x2009;0.001); folate was negatively correlated with both TT (&#x3b2;=-0.017; P&#x2009;<&#x2009;0.001) and E2 (&#x3b2;=-0.012; P&#x2009;<&#x2009;0.001). In the BKMR model, the combined effects of serum vitamins on TT and E2 showed a non-significant weak negative trend; no clear pattern was observed for SHBG. Folate was identified as the most important factor influencing all three sex hormones. Bivariate exposure-response functions indicated potential interactions of folate with vitamin B12 on TT and with vitamin D on E2; no vitamin interactions were observed for SHBG. Complex effects of vitamins on sex hormones in adolescent males were revealed. The mechanism(s) underlying the regulation and long-term health implications will be explored in the future.

Background/Objectives: Resting energy expenditure (REE) rises during critical illness, but its determinants and prognostic relevance remain incompletely characterized. Identifying a circulating signal that tracks REE could provide a bedside surrogate for metabolic demand where indirect calorimetry is unavailable. This prospective pilot study described longitudinal trajectories of indirect calorimetry-measured REE, Sequential Organ Failure Assessment (SOFA) score, serum cortisol and insulin-like growth factor-1 (IGF-1) over two weeks in the intensive care unit (ICU), examined whether the REE trajectory was attenuated by adjustment for these variables, and generated preliminary effect-size and variance estimates for mortality. Methods: This single-center pilot study enrolled 39 critically ill adults at Evangelismos General Hospital (Athens, Greece); sample size was pragmatic, not based on an a priori power calculation. REE (Q-NRG metabolic monitor), cortisol and IGF-1 were measured at admission and days 5-7, 10-11 and 13-14, alongside SOFA. Trajectories were modeled with linear mixed-effects models using all available repeated measures. Confounding was assessed by adding SOFA, cortisol and IGF-1 as covariates and evaluating attenuation of the time effect; no formal mediation analysis was performed. Causes of missing data were quantified and a completers-only sensitivity analysis was undertaken. Mortality was analyzed by Cox regression with ICU length of stay as the time variable. Estimation was emphasized throughout; point estimates and 95% confidence intervals (CIs) are reported in preference to significance testing. Results: Mean age was 54.6 &#xb1; 18.1 years; 69.2% were male; median admission SOFA was 6 (IQR 3-9). ICU and 28-day mortality were 20.5% (8/39) and 10.3% (4/39). REE/kg rose from 25.3 &#xb1; 3.7 to a peak of 27.2 &#xb1; 4.2 kcal/kg/day by days 10-11 (likelihood-ratio &#x3c7;2 = 17.2, p = 0.0006). Attrition was driven predominantly by discharge alive (18 of 23 patients missing at days 13-14) rather than death (n = 2), and the trajectory was preserved in a completers-only sensitivity analysis (&#x3c7;2 = 9.13, p = 0.028). Cortisol declined (21.1 to 13.4 &#x3bc;g/dL) and IGF-1 rose (80.0 to 105.4 ng/mL); SOFA was essentially unchanged. REE did not correlate with SOFA, cortisol or IGF-1 at any time-point, and the time effect was not attenuated by adjustment for them. Admission REE was not associated with ICU mortality (HR 1.00, 95% CI 1.00-1.00). Higher admission REE was associated with a longer ICU stay, and this persisted after adjustment for body mass index (p = 0.026) and fat-free mass (p = 0.001). Age (HR 1.04, 95% CI 1.00-1.09) and admission SOFA (HR 1.18, 95% CI 0.98-1.44) were the covariates most associated with ICU mortality. Conclusions: REE rose progressively over the first 10-11 days of critical illness. Its trajectory was not attenuated by adjustment for SOFA, cortisol or IGF-1, which is compatible with-but does not establish-independence from the adrenal and somatotropic markers measured here. Neither REE nor these hormones were associated with mortality; age and disease severity remained the dominant prognostic factors, supporting a larger confirmatory study.

The oxidative balance score (OBS) was developed to reflect the overall exposure of the body to antioxidants and pro-oxidants in the individual's lifestyle and diet. The research aims to explore the relationship between OBS and sex hormones, including total testosterone (TT) and estradiol (E2), as well as indices including sex hormone-binding globulin (SHBG), testosterone deficiency (TD), free testosterone, and the ratio of TT to E2. A total of 2464 male participants were enrolled in the study during the period 2013 to 2016. Multivariable regression analyses were performed to investigate the association between OBS and sex hormones. Stratified analysis was conducted in participants of different age, body mass index (BMI), poverty income ratio, smoking status, alcohol consumption, and diabetes mellitus (DM). We found that OBS (&#x3b2;&#x2009;=&#x2009;2.13, 95% CI: 0.17&#x2009;~&#x2009;4.09, P&#x2009;=&#x2009;0.030) and lifestyle OBS (&#x3b2;&#x2009;=&#x2009;21.09, 95% CI: 9.27&#x2009;~&#x2009;32.90, P&#x2009;=&#x2009;0.004) were significantly correlated with TT with full adjustment. We also found noteworthy relationships between lifestyle OBS and SHBG (&#x3b2;&#x2009;=&#x2009;2.55, 95% CI: 0.77&#x2009;~&#x2009;4.33, P&#x2009;=&#x2009;0.010), TD (OR&#x2009;=&#x2009;0.76, 95% CI: 0.58&#x2009;~&#x2009;1.00, P&#x2009;=&#x2009;0.045), and ratio of TT to E2 (&#x3b2;&#x2009;=&#x2009;1.10, 95% CI: 0.71&#x2009;~&#x2009;1.50, P&#x2009;<&#x2009;0.001). Stratified analyses by many covariates revealed that the results were basically stable across populations. The results showed that males who lead an antioxidant-rich lifestyle had increased serum TT levels and were less likely to develop TD. This suggests that antioxidant-rich lifestyle choices may additionally help to prevent disorders related to sex hormone imbalance.

Kisspeptin stimulates gonadotropin-releasing hormone (GnRH) release and, by extension, gonadotropin secretion. Although continuous kisspeptin administration has been shown to dampen kisspeptin-induced GnRH release in non-human primates [1, 2], this has not been replicated in the limited human studies reported to date. The objective of this study was to examine the effects of continuous kisspeptin administration on luteinizing hormone (LH) secretion in healthy men. Three healthy adult men received a continuous intravenous infusion of kisspeptin-10 at a dose of 12.5 mcg/kg/h for 24&#xa0;h and underwent frequent blood sampling to characterize the effect on reproductive hormones. Continuous administration of kisspeptin resulted in an immediate increase in LH concentrations, from a baseline of 2.8-3.8 mIU/mL to the highest values of 17.5-30.6 mIU/mL (5- to eightfold above baseline), reached within 12-20&#xa0;h of infusion onset. LH concentrations subsequently declined by 13-47% from max to end of the infusion, settling at 10.7-22.8 mIU/mL. FSH and testosterone rose modestly in parallel. While kisspeptin boluses have been employed to probe GnRH pulse generation, continuous infusion of kisspeptin is a complementary physiologic tool used to study dynamic changes in GnRH-induced LH secretion. Further studies are warranted to further elucidate the physiologic response of the kisspeptin receptor to non-pulsatile ligand administration. NCT01438073 (August 24, 2011).

Cardiovascular disease (CVD) remains the leading cause of mortality in women, yet sex-specific risk factors are usually not included in conventional predictive models. Specifically, heart failure (HF) in women may be influenced by sex-specific hormones and pathologies that need to be addressed to improve prevention and treatment. This expert consensus statement aims to provide a comprehensive roadmap for HF prevention and management across specific conditions affecting women during their life-course. Each section focuses on the impact of a specific female condition on CVD and how to prevent and manage HF in specific settings: 1. Pregnancy with a specific focus on how to deal with hypertensive disorders in the acute and chronic setting and how to prevent and treat Peripartum Cardiomyopathy (PPCM); 2. Gynecological conditions predisposing to HF, such as Polycystic Ovary Syndrome (PCOS), endometriosis, and the menopausal transition. Emphasis is placed on chronic inflammation, metabolic dysfunction, and the "window of opportunity" for Menopausal Hormone Therapy (MHT); 3. Cardio-Oncology: mitigating Cancer Therapy-Related Cardiac Dysfunction (CTRCD) in breast and gynecological cancers, focusing on female-specific cardiotoxicity profiles, the importance of subclinical detection of cardiac dysfunction and the implementation of cardioprotective strategies (ACE-inhibitors, Beta-blockers, SGLT2 inhibitors) during cardiotoxic treatments. Lifestyle interventions such as the DASH diet and exercise-based rehabilitation are highlighted as essential for maintaining cardiac reserve.

Oocyte competency is a crucial determinant of fertilisation success and the initial development of embryos in assisted reproductive technologies. The metabolic and biochemical environment of the ovarian follicle is crucial for determining oocyte developmental potential, alongside genetic integrity. The follicular microenvironment includes a complex network of signalling chemicals that regulate mitochondrial activity, steroidogenesis, oxidative balance, and cellular energy metabolism. Recently, metabolic hormones originating from adipose tissue and skeletal muscle, namely, adipokines and myokines, have received considerable focus as crucial regulators of ovarian physiology. Adiponectin, irisin, and the recently identified hormone asprosin have emerged as crucial metabolic regulators influencing granulosa cell activity, mitochondrial bioenergetics, insulin signalling pathways, and redox homeostasis inside the follicular niche. Adiponectin mostly provides metabolic protection by activating AMP-activated protein kinase (AMPK) and improving insulin sensitivity, which in turn enhances mitochondrial efficiency and steroidogenic function in granulosa cells. Irisin, derived from the breakdown of fibronectin type III domain-containing protein 5 (FNDC5), aids the developing oocyte by facilitating mitochondrial biogenesis, augmenting oxidative phosphorylation, and altering cellular defence mechanisms against oxidative stress. Conversely, asprosin has been associated with glucogenic signalling, metabolic stress, and probable mitochondrial malfunction, suggesting a possible relationship between systemic metabolic problems and negative reproductive consequences. Clinical and experimental research indicate that the levels of these metabolic regulators in follicular fluid may correlate with ovarian response, oocyte quality, fertilisation rates, and embryo development during in vitro fertilisation cycles. This review consolidates current molecular, cellular, and clinical information, clarifying the pathways by which adipokines and myokines influence follicular metabolism and impact oocyte competency. Understanding the metabolic connections between systemic endocrine signals and the follicular milieu may provide novel indicators for reproductive prognosis and provide new treatment targets to improve assisted reproduction outcomes.

Periodontal disease (PD) is associated with type 2 diabetes mellitus (T2DM), while periodontal treatment (PT) improves glycemic control in T2DM patients. Leptin and adiponectin belong to the adipokines family and have almost antagonistic functions in inflammatory processes and insulin sensitivity modulation. Hence, these hormones have been linked with both PD severity and glycemic control. This systematic review aims to assess the effect of PT on serum levels of leptin and adiponectin in patients with T2DM. PubMed, Cochrane Library, and Google Scholar databases and ClinicalTrials.gov website were searched up to January 5th, 2025. Randomized and non-randomized controlled clinical trials (RCTs and CCTs) including patients with T2DM and PD who underwent PT and evaluated serum levels of leptin and adiponectin were included. Assessments of risk of bias and of certainty of evidence were performed. Seven trials were eligible for qualitative synthesis. A statistically significant increase in serum adiponectin levels was observed across most studies, while no such consistency was observed for leptin. The overall level of certainty of evidence was judged low in the RCTs and very low in the CCTs. Meta-analysis could not be performed due to significant methodological heterogeneity. Preliminary findings suggest a potential increase in adiponectin levels in T2DM patients, with possible implications for glycemic control. However, these results should be interpreted with caution due to the small number of studies and important methodological limitations. Well-designed studies with larger sample sizes and adequate adjustment for confounders are necessary to verify this observation. People with type 2 diabetes often also have periodontitis, an inflammatory gum disease, which may affect their overall health. The aim of this study was to investigate whether treating periodontitis could help improve certain substances in the blood-called adiponectin and leptin-that are linked to blood sugar control and inflammation. Several studies that tested this in people with both diabetes and periodontitis were included and most of them showed that, after periodontal treatment, levels of adiponectin (which helps reduce inflammation and improve insulin sensitivity) increased. However, results for leptin were less clear. This suggests that taking care of gum health might support better diabetes management. The overall strength of evidence was low due to methodological limitations and heterogeneity among studies. Current findings should be interpreted cautiously, as available data remain preliminary. Still, more high-quality research is needed to fully understand how treating periodontitis may benefit people with diabetes.

Obesity is a major global health problem and is closely associated with a broad range of metabolic disorders, including metabolic syndrome (MetS), dyslipidemia, hypertension, atherosclerosis, type 2 diabetes mellitus, and cardiovascular disease. The gut microbiota plays a central role in maintaining intestinal epithelial integrity, regulating glucose and lipid metabolism, and modulating immune function. Through the gut-brain axis, it also contributes to appetite regulation and energy homeostasis by influencing the release of anorexigenic hormones. Dysbiosis, including alterations in the relative abundance of major bacterial phyla such as Firmicutes and Bacteroidetes, has been associated with increased intestinal permeability, metabolic endotoxemia, and chronic low-grade inflammation, all of which may contribute to the development of obesity and insulin resistance. Diets rich in plant-derived fiber can beneficially shape gut microbiota composition. Bacterial fermentation of dietary fiber produces short-chain fatty acids (SCFAs), including butyrate, acetate, and propionate, which contribute to intestinal barrier integrity, inflammatory regulation, immune regulation, and metabolic homeostasis. Overall, the interaction between gut microbiota, diet, and host metabolic pathways represents a promising field for therapeutic and nutritional interventions aimed at preventing and managing MetS and metabolic diseases.

Thyroid hormones play an important role in regulating the cardiovascular system. Thyroid dysfunction, which encompasses hypothyroidism and hyperthyroidism, is relatively common and has been linked to a range of cardiovascular manifestations, including dyslipidaemia, abnormal blood pressure regulation, endothelial dysfunction, impaired cardiac function, and arrhythmias. The effects of levothyroxine replacement therapy on cardiovascular endpoints in subclinical hypothyroidism remain uncertain. The largest randomized controlled trial (TRUST) to date was underpowered to assess cardiovascular outcomes, although the results demonstrated a pattern towards a beneficial effect of levothyroxine. The aim of this review was to provide a summary of current knowledge on the relationship between thyroid dysfunction and cardiovascular health, with a focus on molecular and pathophysiological mechanisms underlying thyroid dysfunction and cardiovascular disease. Evidence from recent omics and Mendelian randomization studies is discussed, alongside an overview of the epidemiology of thyroid diseases and the impact of levothyroxine treatment on cardiovascular outcomes in subclinical hypothyroidism.

BACKGROUND: Migraine burden is over twice as high among females than males. Although sex differences are recognized in migraine, robust sex-specific guidance for management remains limited. OBJECTIVE: To systematically review and synthesize current evidence on sex-related clinical differences in migraine, including treatment outcomes and reproductive management, and to provide evidence-based or expert consensus recommendations where high-quality data are lacking. METHODS: A systematic literature review using the PICO framework addressed 24 sex-specific questions across three domains: (1) biological sex differences across the lifespan, (2) sex-specific variations in treatment outcomes, and (3) fertility and reproduction-related management. To address anticipated evidence gaps, a structured Delphi consensus process complemented the review. The protocol was registered in PROSPERO (CRD420251058438). RESULTS: Thirty-seven studies informed 10 evidence summaries. Acute and preventive anti-CGRP therapies seem to show similar efficacy between sexes. For menstrual-related migraine attacks (MM), triptans and lasmiditan are effective, with frovatriptan being recommended for short-term prevention; long-term prevention include topiramate and anti-CGRP mAbs. In pregnancy triptans, greater occipital nerve (GON) blocks, and onabotulinumtoxinA are safe, with GON blocks showing potential efficacy. During breastfeeding, triptans appear to be safe. Anti-CGRP mAbs are equally effective in pre and postmenopausal women. Expert consensus emphasizes the influence of hormonal transitions on migraine expression across sexes and supports the use of acetaminophen, antiemetics, magnesium, NSAIDs, steroids, beta-blockers, amitriptyline, and calcium channel blockers as generally safe in WOCBP and during pregnancy, although some agents have trimester-specific limitations. Efficacy was noted for acetaminophen, sumatriptan, antiemetics, magnesium, propranolol, amitriptyline, and onabotulinumtoxinA. During breastfeeding, acetaminophen, NSAIDs, domperidone, prochlorperazine, magnesium, caffeine, beta-blockers, tricyclics, onabotulinumtoxinA, and GON blocks were considered safe. CONCLUSIONS: Evidence is limited, but sex (likely mediated by sex hormones) influence the clinical course of migraine, and likely treatment response. Limitations include absence of sex-specific analyses in older trials, underrepresentation of men, and scarce reproductive safety data. Integrating sex-based analyses and broadening trial inclusion and more reproductive safety evidence are essential for personalized, equitable migraine care.

We read with great interest the recent articles by Chandrabalan et al on diabetic ketoacidosis (DKA) in type 2 diabetes mellitus (T2DM) and by Kodiyatar et al on adjuvant herbal therapies. These articles provide important insights into DKA in T2DM, both at a clinical and experimental level. However, further endocrine aspects need to be addressed. In one study a paradoxical relationship between pre-admission metformin use and reduced in-hospital mortality from DKA was noted; this may be related to preserved beta-cell function and a more favorable incretin-glucagon axis rather than a pharmacological effect per se. However, important endocrine effectors such as C-peptide, glucagon, and incretin hormones were not measured. Furthermore, currently available antidiabetic agents, such as glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors, have not been taken into account despite their possible effects on ketogenesis. An additional and underappreciated complexity is the concurrent occurrence of acute pancreatitis (AP) in DKA patients (DKA-AP), a complication that may affect at least 15% of DKA cases and that can neutralize key clinical and biochemical features of each condition, confounding diagnosis and worsening prognosis. At the same time, studies on Gymnema sylvestre have shown promising effects on glycemia and metabolism, while their endocrine effects have not been fully characterized. Recent data have shown possible effects of this herbal preparation on glucocorticoid receptors, suggesting a possible impact on the hypothalamus-pituitary-adrenal axis. We propose that future studies take into account detailed hormonal profiles and systematic screening for concurrent AP, which could help to further clarify the pathophysiology and mechanisms of currently available agents in T2DM-associated DKA.

PURPOSE: Parathyroid carcinoma is a rare endocrine malignancy. This study aimed to evaluate the clinical characteristics, treatment approaches, and follow-up data of patients diagnosed with parathyroid carcinoma. Additionally, pathological findings were reassessed according to the 2022 World Health Organization (WHO) classification to examine its clinical implications. METHODS: The medical records of patients who were pathologically diagnosed with parathyroid carcinoma at the Endocrinology Clinic of a University Hospital between March 2013 and June 2024 were retrospectively reviewed. Clinical characteristics, demographic data, and laboratory findings were recorded. Pathological features were also obtained retrospectively from medical charts and records. RESULTS: We reported eight patients with surgical and pathological diagnoses of parathyroid carcinoma. Six of the patients were females and two were males. The ages of the patients ranged from 43 to 85, with a mean age of 61. The follow-up periods after diagnosis varied from 6 to 132 months. The calcium levels at diagnosis ranged from 11.7&#xa0;mg/dL to 18.4&#xa0;mg/dL, with a median of 16.0&#xa0;mg/dL (normal range 8.6&#x2013;10.2&#xa0;mg/dL). The median PTH level at admission was 1609 ng/L (487.7&#x2013;3035 ng/L) (normal range: 15&#x2013;65 ng/L). Re-evaluation of all patients based on the 2022 WHO classification revealed no changes in initial diagnoses. CONCLUSIONS: Surgical resection remains the cornerstone of effective treatment. Accurate preoperative assessment, including detailed clinical and biochemical evaluation, is essential for optimal management. Sharing comprehensive data with pathologists enhances diagnostic accuracy. This study emphasizes the relevance of preoperative indicators and highlights that the updated WHO classification supports existing diagnostic criteria without altering clinical practice.

The global prevalence of type 2 diabetes mellitus (T2DM) is rising exponentially, with alarming projections from the International Diabetes Federation estimating 589 million affected individuals in 2024 and more than 850 million in 2050. This represents an economic burden of approximately &#x20ac;1,015 billion worldwide. Traditional explanations such as sedentary lifestyle and overeating are insufficient to explain such a rapid expansion of the disease. Increasing attention has therefore turned toward the role of environmental endocrine disruptors (EDs), and, in particular, of persistent organic pollutants (POPs).EDs are natural or synthetic molecules capable of altering endocrine function by interfering with biochemical pathways. They are omnipresent in daily life and have for several decades been implicated in reproductive or thyroid disorders, various hormone-dependent cancers (breast, prostate, testicular and colon cancers) and metabolic complications such as obesity.To better understand their diabetogenic potential, numerous experimental studies have been conducted. In vitro findings showed that certain POPs increase insulin resistance in cultured adipocytes or myocytes. Bisphenol A, widely used in plastic manufacturing, induces an initial hypersecretion of insulin in pancreatic islets, followed by a later decrease in insulin sensitivity. In vivo animal studies similarly demonstrate strong diabetogenic effects.In humans, epidemiological and longitudinal studies have revealed direct associations between exposure to POPs (e.g., organochlorine pesticides, dioxins, and polychlorinated biphenyls) and the onset of metabolic syndrome or T2DM. These effects were first observed after acute environmental exposure, such as the Seveso disaster. More recent large-scale studies confirm higher circulating levels of EDs in people living with obesity and/or T2DM, strongly demonstrating that these compounds are independent risk factors for insulin resistance.Collectively, the evidence now supports a central role of EDs in the global rise of obesity and T2DM. Their contribution to the epidemic is no longer speculative but increasingly recognized as scientifically established.

Diabetic retinopathy (DR) is one of the most common microvascular complications of diabetes mellitus and a leading cause of visual impairment among adults worldwide. While hyperglycemia and metabolic dysregulation are recognized contributors to DR pathogenesis, increasing attention has been directed toward the role of genetic factors. This review evaluates the association between specific single nucleotide polymorphisms (SNPs) and DR susceptibility within the Greek population, an underrepresented group in global genomic studies. The review synthesizes findings from population-specific research focused on eight genes, namely, ADIPOQ, AGER, ALDH2, UCHL3, HNMT, PAI-1 (SERPINE1), SLC2A1, and NOS3. Variants in these genes have been implicated in key pathways related to inflammation, oxidative stress, endothelial dysfunction, and glucose metabolism. Several polymorphisms, including ADIPOQ rs1501299, AGER rs1051993, ALDH2 rs671, and NOS3 rs1799983, were associated with increased DR risk, while others showed associations with disease progression or early onset. Importantly, some polymorphisms revealed ethnic-specific effects not observed in other populations, highlighting the importance of localized genetic studies. These findings are hypothesis-generating and further research is required to replicate these associations, clarify underlying mechanisms, and assess gene-environment interactions before considering any potential clinical translation.

Skin manifestations of hyperandrogenism are common and clinically diverse findings, indicating the complex interplay between metabolic, endocrine, and dermatologic systems. The aim of this review was to collect and analyze data on skin manifestations of hyperandrogenism and review the current treatment options for these diseases. We conducted a narrative review of the current literature focusing on cutaneous manifestations associated with hyperandrogenism. A search was performed on PubMed/MEDLINE which includes relevant articles published until February 2026. The search strategy included combinations of MeSH keywords ("hyperandrogenism," "polycystic ovary syndrome," "skin diseases," "hirsutism," "acne Vulgaris," "alopecia," "acanthosis nigricans," "acrochordons," and "hyperhidrosis") and screening of reference lists of selected articles. Eligible articles were considered those addressing epidemiology, pathophysiology, clinical presentation, diagnosis, and treatment of dermatologic manifestations associated with hyperandrogenism, with an emphasis on more recent bibliographic evidence. The dermatologic spectrum of hyperandrogenism-induced manifestations primarily includes hirsutism, acne vulgaris, androgenetic alopecia, acanthosis nigricans, acrochordons, and hyperhidrosis. These cutaneous features are often the earliest clinical indicators of hyperandrogenism and are tightly associated with androgen receptor (AR) activation, local enzymatic conversion, and downstream metabolic and inflammatory pathways. Multiple therapeutic strategies were reviewed with an emphasis on hormonal agents which target AR in the skin. Hyperandrogenism and the expression of AR in the skin precipitate the development of androgen-associated dermatologic conditions. Androgen-targeted treatment appears to be more effective when compared with other non-androgen-targeted therapeutic options. Further research is required to analyze the existing treatments and develop new approaches.

Pheochromocytoma is a rare neuroendocrine tumor that may present with atypical and potentially life-threatening cardiovascular manifestations due to catecholamine excess. Reverse Takotsubo cardiomyopathy, a distinct form of stress-induced cardiomyopathy, has been strongly associated with catecholamine crisis but remains underrecognized. The purpose of this report is to describe a rare case of pheochromocytoma-induced reverse Takotsubo cardiomyopathy complicated by acute severe mitral regurgitation and to emphasize the importance of early endocrine recognition. A 40-year-old woman presented with hypertensive emergency, acute chest pain, electrocardiographic changes suggestive of acute coronary syndrome, and markedly elevated cardiac biomarkers. Transthoracic echocardiography revealed reduced left ventricular ejection fraction with basal and mid-ventricular akinesis, apical hyperkinesis, and acute severe mitral regurgitation consistent with reverse Takotsubo cardiomyopathy. Emergency coronary angiography demonstrated normal coronary arteries. Recurrent stress-induced cardiomyopathy in a young patient without conventional cardiovascular risk factors, accompanied by autonomic symptoms, hyperglycemia, and lactic acidosis, raised suspicion of pheochromocytoma-related catecholamine crisis. Cross-sectional imaging identified a left adrenal mass and biochemical testing confirmed markedly elevated plasma metanephrines. After appropriate preoperative &#x3b1;-adrenergic blockade, laparoscopic adrenalectomy resulted in complete clinical and biochemical remission with full recovery of cardiac function. Pheochromocytoma should be considered in younger patients presenting with recurrent or atypical Takotsubo cardiomyopathy, particularly in the case of reverse pattern and when associated with acute mitral regurgitation or hypertensive emergency. Early endocrine diagnosis is critical as definitive surgical treatment leads to complete resolution and prevents recurrence of severe cardiovascular complications.

Semaglutide, a glucagon-like peptide-1 receptor agonist (GLP-1 RA), is widely used for the management of type 2 diabetes, metabolic syndrome, and obesity. Concerns regarding its potential association with thyroid cancer, particularly medullary thyroid carcinoma, have emerged, although current human evidence remains inconclusive. Reports of papillary thyroid carcinoma (PTC) while using semaglutide therapy are exceedingly rare. We describe a 40-year-old man with metabolic syndrome and obesity who had been treated with semaglutide for several years before discontinuation. A routine chest computed tomography (CT) performed for an unrelated diaphragmatic hernia identified a suspicious thyroid lesion, later confirmed by ultrasound as a 1&#x2009;&#xd7;&#x2009;1&#xa0;cm irregular hypoechoic nodule in the left lobe with several small ipsilateral lymph nodes demonstrating suspicious features. Fine-needle aspiration cytology revealed classic PTC (Bethesda VI). The patient underwent total thyroidectomy with left selective neck dissection and central compartment dissection. Histopathology confirmed a unifocal classic variant PTC, 16&#xa0;mm in size, with negative margins, no lymph node involvement, and no extrathyroidal extension. After an uncomplicated postoperative course, he was prescribed levothyroxine for TSH suppression and discharged. This case of PTC discovered concomitantly while the patient was on semaglutide therapy highlights an important clinical scenario but does not provide evidence of causation. The totality of available human data continues to support the safety of semaglutide with respect to thyroid cancer risk. Further long-term surveillance and high-quality epidemiological studies remain warranted.

Pheochromocytomas and paragangliomas (PPGLs) can trigger major cardiovascular events (MACEs) due to unpredictable release of catecholamines. The aim of this systematic review and meta-analysis was to determine prognostic factors associated with MACEs in PPGLs patients. A literature search was conducted in PubMed and the Cochrane Library from January 1980 to March 2026. Assessment of clinical, laboratory, imaging, histological, and genetic parameters was performed on the pooled data. Nine retrospective cohort studies involving 1566 patients with PPGL were included. MACEs were observed in 302 patients [pooled estimate of 21% (95% CI 14-29%)], 95 of those having Takotsubo syndrome [pooled estimate 39% (95% CI 23-54%)]. Tumor necrosis/hemorrhage and diabetes were associated with increased risk of MACEs [71% (95% CI 25-115%, p&#x2009;<&#x2009;0.001) and 56% (95% CI 2-109%, p&#x2009;=&#x2009;0.02), respectively]; additional predictors of MACES were dyspnea and chest pain [5-fold (95% CI 3.3-7.4, p&#x2009;<&#x2009;0.001) and 2.7-fold (95% CI 1.5-4, p&#x2009;<&#x2009;0.001) increased risk of MACEs]. Patients with MACEs had an average maximum diastolic blood pressure increase of 19.3 mmHg (95% CI 2.5-36mmHg, p&#x2009;=&#x2009;0.02) and 9.4&#xa0;mm larger tumor size (95% CI 1.2-17.56, p&#x2009;=&#x2009;0.02) than those without. No significant associations between age, adrenergic-noradrenergic phenotype, metastatic disease, familial PPGLs, and MACEs were found. This is, to the best of our knowledge, the first meta-analysis of cohort studies of catecholamine-induced MACEs in patients with PPGL. 21% of PPGL cases developed MACEs. Necrosis/hemorrhage, dyspnea, chest pain, and diabetes were associated with an increased likelihood of development of MACEs. However, these results should be interpreted with caution due to statistical and methodological heterogeneity.

Topical corticosteroids (TCS) remain the first-line treatment for atopic dermatitis (AD) and related inflammatory skin diseases, yet no standardized definition of response exists. This gap contributes to heterogeneity in clinical practice and complicates trial design. We therefore aimed to develop consensus-based definitions of response and inadequate response to TCS therapy through a structured international eDelphi process. A PubMed search (1974-July 2025) identified 403 relevant publications. Candidate statements were drafted from the evidence and refined by the ADCARE Steering Committee, categorized into 3 domains (status quo, unmet need, proposals), and evaluated in a three-round eDelphi survey among certified ADCARE members. Eighty-four dermatologists and allergists from 32 countries participated (Round 1 response rate 98%; Round 2, 80%; Round 3, 76%). Statements were rated on a 5-point Likert scale; consensus was defined as &#x2265;75% agreement (scores 4 or 5). In total, 66 of 83 statements reached consensus. In the status quo domain, agreement centred on baseline severity, body surface area, and anatomical site as guiding factors for TCS choice, with potency and licensed duration considered central to safe prescribing. In the unmet-need domain, experts highlighted the absence of standardized definitions, variability in monitoring and escalation strategies, and gaps in long-term evidence and integration of patient-reported outcomes. In the proposal domain, consensus supported relative improvement thresholds (&#x2265;50% in EASI, SCORAD, itch NRS, IGA, PGA, POEM) and 14 days as a meaningful evaluation point. Absolute cut-offs, very short (7 days) or long (3 months) timeframes, and rigid escalation rules did not achieve consensus. These parameters were synthesized into concise and extended definitions of TCS response and inadequate response. This GA2LEN ADCARE initiative represents the first international consensus on defining TCS response and inadequate response, offering a framework to harmonize clinical practice, enhance trial comparability, and support guideline development.