Introduction: Sleep apnea (SA) is associated with metabolic and cardiovascular diseases, such as diabetes and myocardial infarction (MI). Insulin resistance is a key metabolic alteration in diabetes that also aggravates MI. Intermittent hypoxia (IH - one of the main consequences of SA) induces insulin resistance and increases infarct size following myocardial ischemia-reperfusion (I/R) in rodents. However, while SA affects both sexes, most pre-clinical data have been obtained on males, limiting our understanding of sex-specific responses to IH and of the roles of sex hormones in males and females. Objective: We investigated whether sex and sex hormones determine myocardial infract size following IH and a potential association with insulin resistance. METHOD: C57Bl/6J mice underwent orchiectomy (ORX – males), ovariectomy (OVX – female) or sham surgery, followed by a 2-week recovery period. Mice were then exposed to 21 days of IH (21-5% O2, 60 episodes/hour, 8 hours/day) or normoxia (Nx). At the end of the IH or Nx exposures, after 6 hours of fasting, blood samples were collected (n=6 mice/groups) to measure insulinemia and glycemia and calculate the homeostatic model assessment of insulin resistance (HOMA-IR). Myocardial I/R injuries were induced on anesthetized mice (n=16/groups) by occlusion of the left coronary artery (45 minutes), followed by reperfusion (90 minutes) then injection of Evans blue. The hearts were dissected and later analyzed to determine the occluded and infarcted regions using colorimetric staining and planimetric measurement techniques. Results: In sham males, IH slightly (but not significantly) increases glucose and insulin levels, resulting in a significantly higher HOMA-IR, but these effects are not observed in ORX males. Additionally, while the occluded area is similar across groups, IH increases the infarcted area in sham males, but the opposite effect occurred in ORX males with a reduced infarcted area after IH vs Nx exposures. In sham females IH slightly reduces glucose levels, without altering insulin levels and the HOMA-IR, while it increases the infarcted area following myocardial I/R. In females maintained under normoxia, OVX slightly reduces glucose levels, but almost doubles insulin levels and the HOMA-IR, without altering the infarcted area following myocardial I/R. In OVX females, IH reduces insulin and HOMA-IR, but has no effect on the infarcted area. Conclusion: There is an apparent correlation between insulin resistance and the size of the infarcted area following IH only in males, thus the mechanisms underlying the elevated infarct size induced by IH could differ between males and females. Sex and sex hormones appear to be fundamental determinants of metabolic and cardiac responses to IH. Agir pour les maladies chroniques, Fédération Française de Cardiologie, CIHR. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

Shape-controlled asymmetric bowl-like PDA@Au substrates for sensitive SERS detection of anabolic androgenic steroids.

Background: Abundant basic and clinical evidence demonstrate a critical role of androgenic hormones in regulation of water-electrolyte transport in both proximal tubule and collecting duct system. This culminates in the notable differences in renal function with females producing lower urinary volume and having a greater urinary concentrating ability than males. At the same time, the key intermediate signaling pathways linking binding the androgenic hormones to their respective receptors with integrative water-solute handling by the kidney remain largely underexplored. Exchange proteins directly activated by cAMP isoform 1 and isoform 2 (Epac1 and Epac2, respectively) are known to mediate a plethora of intracellular signaling processes downstream of receptor-ligand triggered events. Epac isoforms are abundantly expressed in the kidney. We previously showed that deletion of Epac1 or Epac2 increases urinary volume and reduces urinary concentrating ability. Here, we aimed to explore the potential relevance of Epac signaling in the kidney in setting sex-dependent dimorphism in urinary production. Methods: Age-matched mice with global or kidney specific (KS) deletion of Epac1 and Epac2 underwent balance studies in metabolic cages and water deprivation tests with the goal to examine sex-dependent differences in urinary production. In addition, gonadectomy was performed in males and females to ablate the androgenic input. Isolated kidneys were subjected to biochemical and immunofluorescent microscopy assessment. Results: Western blot analysis of whole kidney lysates from wild type (WT) mice revealed over 2-fold greater expression of both Epac1 and Epac2 in females than in males pointing to a sex-dependent contribution of Epac signaling in regulation of urinary volume and osmolarity. Genetic deletion of Epac isoforms increased urinary volume and reduced urinary osmolarity in an additive manner. Importantly, females lacking both isoforms exhibited drastically larger polyuria than males (increases urinary volume by 320% versus 38%). In addition, urinary concentrating ability was significantly more compromised in Epac isoform deficient females than in males. The polyuric phenotype was also reproduced in mice with renal tubule specific deletion of Epac isoforms suggesting the central role of renal Epac expression in this pathology. At the molecular level, deletion of both Epac12 decreased NHE-3 expression by 90% in females, whereas only by 58% in males. The reduced NHE-3 expression was also associated with translocation to the base of brush border of proximal tubule cells and impaired Na + /H + transport suggesting an increased fluid flow to the loop of Henle with a greater extent in females. Consistently, we also observed a compensatory elevation of AQP2 water channel levels in the collecting duct, which was larger in females. Importantly, ovariectomy greatly reduced urinary volume and improved urinary concentrating ability in Epac1&2 -/- females, whilst castration led to only a mild antidiuresis in Epac1&2 -/- males. In fact, gonadectomy abolished sex-dependent differences in urinary production in the knockouts. Conclusions: Our findings demonstrate a novel role of Epac signaling cascade in establishing sex-dependent differences in urinary production. We propose that higher Epac isoform expression in females is instrumental to control NHE-3 expression and activity in the proximal tubule to a larger extent than in males. This allows more effective regulation of fluid flow to the medulla to preserve interstitial hypertonicity and reduce urinary volume at the baseline and in response to androgenic inputs especially in females. This research was supported by NIDDK DK117865, DK136462, AHA 20EIA35260097 (to O. Pochynyuk), AHA 24POST1191738 (to A. Atamanchuk) and AHA 24SCEFIA1259812 (to K. Pyrshev). This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

Stanozolol-induced Liver Injury: A Distinctive Cholestatic Clinical and Biochemical Phenotype at Presentation.

Abstract Introduction: Unregulated supplements and anabolic androgenic steroids (AAS) are increasingly used for athletic enhancement, often without understanding their severe health risks. Although AAS is linked to cardiovascular complications, cases of multi-organ failure, including biventricular failure, acute respiratory distress syndrome (ARDS), and disseminated intravascular coagulation (DIC), remain largely underreported.Case Presentation: A 51-year-old man with hypertension and hyperlipidemia presented with worsening nausea, vomiting, and muscle cramps. He was hypotensive (BP 75/45 mmHg) and tachycardic (HR 100 bpm). Lab results indicated renal dysfunction (creatinine 3.1 mg/dL) and lactic acidosis (lactate 9.1 mmol/L), while echocardiography showed a reduced ejection fraction (LVEF 35-40%) indicating biventricular failure. He was intubated as hypoxemic respiratory failure progressed to ARDS. Thrombocytopenia and prolonged clotting times suggested evolving DIC.An endocrine panel revealed elevated free testosterone (423 ng/dL), estrone (961 pg/mL), and estradiol (509 pg/mL). The patient's family reported unregulated testosterone injections and supplements, including Fadogia agrestis, trimethylglycine, and anastrozole. Despite vasopressors, dialysis, and consideration of ECMO, the patient's condition worsened, leading to pulseless cardiac arrests and ultimately, death.Discussion: Chronic AAS use contributes to cardiomyopathy through myocardial fibrosis and hypertrophy, resulting in impaired function. Elevated estrogen levels, due to aromatase inhibition, can induce fluid retention and metabolic stress on cardiac cells, worsening heart function. Compounds like Fadogia agrestis may further increase testosterone, yet animal studies suggest it has toxic effects on the kidneys and liver. In this case, the combined use of AAS, estrogen modulators, and unregulated supplements likely precipitated biventricular failure, ARDS, and DIC, all hallmarks of multi-organ failure.Conclusion: This case highlights the potentially fatal consequences of unregulated testosterone and AAS use, leading to catastrophic cardiovascular and multi-system collapse. Clinicians should routinely screen for supplement use in patients with acute cardiac or respiratory distress. Urgent research is needed to better understand the toxicology of supplements like Fadogia agrestis, and stricter regulatory guidelines are warranted to prevent such fatal outcomes.

Abstract Rationale: The obesity-related asthma phenotype in children is often severe and difficult to control, in part due to a lack of understanding of its underlying pathophysiology. Given the distinct presentation of obese individuals with severe persistent asthma, we hypothesize that these patients have a unique dysregulated metabolomic profile compared to those with obesity or asthma alone. Identifying this profile may provide further insights into the mechanisms underlying this phenotype. Method: Data from the prospective observational NewYork-Presbyterian Pediatric Asthma Cohort Study of 73 participants, aged 7-21 years with physician-diagnosed severe persistent asthma and without asthma were analyzed. Mass spectrometry-based untargeted metabolomic profiling was performed on plasma samples. Participants had baseline determination of body mass index (BMI) percentile. A comprehensive survey was administered. Metabolites with less than 25% missing data were included; data were normalized and imputed. Linear regression was used to identify altered metabolomic pathways and metabolites, in obese participants with severe asthma, adjusting for age, sex, race/ethnicity, and atopic conditions. Significance was set at q<0.2 to account for the high dimensionality of metabolomic data. Results: Of 73 participants included in analyses: 62 were non-asthmatics (64% Hispanic, 16.1% Caucasian, 12.9% Black), 11 had severe persistent asthma (45% Hispanic, 36.4% Black, 9.1% Caucasian). Among severe asthmatics, 72.7% were obese and 27.3% healthy weight, and in non-asthmatic individuals, 62.9% were healthy weight and 37.1% obese. In asthmatics, 45.5% had eczema, 54.5% rhinitis, and 54.5% food allergies. Thirty-two metabolites from 17 sub-metabolic pathways were altered; 6 involved upregulated lipid pathways. The most impacted were branched fatty acid (75% of identified metabolites), followed by long-chain monosaturated (71%), long-chain saturated (71%), medium-chain (29%), long-chain polyunsaturated (n3 and n6) (24%), and mono-hydroxyl fatty acids (13%). Other sub-pathways impacted include fructose (25%), aspartate (11%), lysine (6%), histidine (6%), arginine (5%), and androgenic steroid metabolism (4%). Discussion: Findings reveal a high prevalence of obesity in severe asthmatics, suggesting a potential interaction between obesity and asthma severity, and a complex interplay of lipid metabolism. Children/adolescents with severe asthma and obesity demonstrated dysregulation in multiple metabolic lipid pathways, with a particular increase in those related to long-chain fatty acids. Some of these metabolites have been shown simultaneously to exhibit anti-inflammatory properties and contribute to airway remodeling and contraction. Additionally, a significant number of obese asthmatics were atopic. Further mechanistic studies are needed to understand whether Th2 and lipid pathways are linked.

BackgroundRecent years have brought significant development in athlete doping use detection with the implementation of the Athlete Biological Passport (ABP). The aim of this study was to explore if similar methods could also be used to detect non-medical use of anabolic androgenic steroids (AAS) among clinical patients. For this purpose, six elastic net regression models were trained in a sample of Finnish specialized health care male patients (N = 2918; no doping = 1911, AAS doping = 1007), using different approaches to longitudinal laboratory measurements as predictive variables. The laboratory data was retrieved from the Hospital District of Helsinki and Uusimaa (HUS) data lake, and doping use status was defined by patient disclosure, recorded in digital medical record free texts. Length of observation time (e.g., time between the first and last laboratory measurement) was used as weight. Model performance was tested with holdout cross-validation.ResultsAll the tested models showed promising discriminative ability. The best fit was achieved by using the existence of out-of-reference range measurements of 31 laboratory parameters as predictors of AAS doping, with test data area under the receiver operating characteristic curve (AUC) of 0.757 (95% CI 0.725–0.789).ConclusionsThe findings of this preliminary study suggest that AAS doping could be detected in clinical context using real-life longitudinal laboratory data. Further model development is encouraged, with added dimensions regarding the use of different AAS substances, length of doping use, and other background data that may further increase the diagnostic accuracy of these models.

Hydroxyl-functionalized multi-walled carbon nanotube-coated pipette tips for extraction and determination of illegally adulterated androgenic steroids

The exposure to nandrolone changed the expression of genes associated with sexual differentiation and disrupted the levels of hormones in the hypothalamic-pituitary-gonadal (HPG) axis, ultimately inducing male differentiation in zebrafish (Danio rerio).

Studies exploring the relationship between male-specific factors and risks of cardiovascular disease (CVD) are limited and inconsistent. We aimed to examine the association of male hormone levels and sexual factors (e.g., onset of puberty and baldness pattern) with CVD events. This study included 154,970 men from the UK Biobank for prospective analyses. Cox proportional hazards regression was performed, with outcomes of CVD, coronary heart disease (CHD), stroke, and heart failure (HF), and adjusted for sociodemographics, lifestyle, and medical factors. Restricted cubic spline models assessed nonlinear associations between sex hormone levels and CVD risks. Over a median follow-up of 13.0 years, 20,216 men (13.0%) experienced a CVD event. Men in the highest quintile of total testosterone had increased stroke risk (HR 1.13, 95% CI: 1.04-1.23). A J-shaped relationship was found between sex hormone-binding globulin (SHBG) levels and CVD risk, with the highest risk in Q5 (1.08, 1.03-1.13). A U-shaped association was noted for free testosterone (FT), where Q3 had lower CVD risk (0.94, 0.90-0.98). Earlier onset of facial hair or voice breaking (< 13 years) correlated with higher CVD risks (HR 1.10, 95% CI: 1.04-1.16 and HR 1.14, 95% CI: 1.06-1.22, respectively). Vertex baldness was linked to increased CVD risk (1.05, 1.01-1.09) and CHD risk (1.06, 1.02-1.11). Elevated SHBG levels, earlier puberty onset, and vertex baldness were associated with increased CVD risks in men, highlighting the need for targeted prevention strategies.

Abstract Text While the importance of estrogen in driving ER+ breast cancer progression is clear, data from pre-clinical studies exploring the role of tumoral progesterone (PR) and androgen (AR) receptors are conflicting, likely due in part to the promiscuity of steroid receptor ligands, as well as relative levels of steroid hormone receptor expression and of steroid hormones within the tumor milieu. While bone is usually the first site of metastases in ER+ metastatic breast cancer, the roles of tumoral PR and AR (present in 58 percent and 86 percent of clinical ER+ bone metastases [BMET], respectively) in ER+ breast cancer progression at this site have not been well studied. Studies were undertaken to examine the effects of ovariectomy (OVX), a model of surgical menopause that significantly reduces endogenous progesterone and androgen levels, in a pre-clinical model of human ER+ bone metastases that is dependent on exogenous 17ß-estradiol (E2) supplementation. Effects of OVX (at 9-weeks of age) were ascertained using skeletally mature female nude mice supplemented with a modest dose of E2 (0.36 mg 60 day pellets) prior to intracardiac inoculation (at 10 weeks of age) with bone metastasis-derived MCF7 cells (43.4M cells) that form robust E2- and TGFß-dependent osteolytic metastasis in vivo, and express PR and AR in vitro. Osteolytic bone metastatic lesions in E2-supplemented mice were reduced in both incidence and size in OVX (vs ovary intact) mice. Anti-tumoral effects of OVX were not limited to bone; E2-driven orthotopic tumor progression was similarly reduced. Histologic assessment of cytokeratin-positive breast cancer tumor cells within bone revealed a small but statistically significant reduction in Ki67-positivity in OVX (vs ovary -intact) mice that correlated with osteolytic lesion size. In addition, PR and AR expression in BMET lesions, which was readily detected by IHC in ovary-intact mice, was markedly reduced in OVX mice. While additional experiments are underway to query possible roles of specific reproductive hormones altered in OVX mice, these results are consistent with the postulate that tumoral AR and PR signaling may promote ER+ bone metastases progression in this model. In addition, while ovariectomy is a common pre-clinical means of reducing estrogen to model natural menopause in women, resultant changes in steroid receptor signaling are clearly much more complex. Funding: NIH 5R25CA275753, 5P30CA023074 Date of Presentation October 17, 2024

Abstract Text While the importance of estrogen in driving ER+ breast cancer progression is clear, data from pre-clinical studies exploring the role of tumoral progesterone (PR) and androgen (AR) receptors are conflicting, likely due in part to the promiscuity of steroid receptor ligands, as well as relative levels of steroid hormone receptor expression and of steroid hormones within the tumor milieu. While bone is usually the first site of metastases in ER+ metastatic breast cancer, the roles of tumoral PR and AR (present in 58 percent and 86 percent of clinical ER+ bone metastases [BMET], respectively) in ER+ breast cancer progression at this site have not been well studied. Studies were undertaken to examine the effects of ovariectomy (OVX), a model of surgical menopause that significantly reduces endogenous progesterone and androgen levels, in a pre-clinical model of human ER+ bone metastases that is dependent on exogenous 17ß-estradiol (E2) supplementation. Effects of OVX (at 9-weeks of age) were ascertained using skeletally mature female nude mice supplemented with a modest dose of E2 (0.36 mg 60 day pellets) prior to intracardiac inoculation (at 10 weeks of age) with bone metastasis-derived MCF7 cells (43.4M cells) that form robust E2- and TGFß-dependent osteolytic metastasis in vivo, and express PR and AR in vitro. Osteolytic bone metastatic lesions in E2-supplemented mice were reduced in both incidence and size in OVX (vs ovary intact) mice. Anti-tumoral effects of OVX were not limited to bone; E2-driven orthotopic tumor progression was similarly reduced. Histologic assessment of cytokeratin-positive breast cancer tumor cells within bone revealed a small but statistically significant reduction in Ki67-positivity in OVX (vs ovary -intact) mice that correlated with osteolytic lesion size. In addition, PR and AR expression in BMET lesions, which was readily detected by IHC in ovary-intact mice, was markedly reduced in OVX mice. While additional experiments are underway to query possible roles of specific reproductive hormones altered in OVX mice, these results are consistent with the postulate that tumoral AR and PR signaling may promote ER+ bone metastases progression in this model. In addition, while ovariectomy is a common pre-clinical means of reducing estrogen to model natural menopause in women, resultant changes in steroid receptor signaling are clearly much more complex. Funding: NIH 5R25CA275753, 5P30CA023074 Date of Presentation October 17, 2024

The prevalence of dyslipidemia in the pediatric population continues to rise, increasing the future risk of atherosclerotic cardiovascular disease (ASCVD) as these children transition to adulthood. Timely diagnosis and intervention, beginning at a young age, is important in reducing the risk of ASCVD and preventing premature mortality in this vulnerable population. Implementation of a heart-healthy lifestyle should be encouraged in all children, and, when appropriate, the role of medication discussed in those at-risk. The purpose of this review is to discuss the impact of non-lipid lowering medications which affect lipid and lipoprotein metabolism in children (< 18 years-of-age). According to National Center of Health Statistics, there has been a steady rise of pediatric obesity and cardiovascular disease (CVD) risk amongst youth over the last 2 decades, with roughly 1 out of 5 children having a BMI > 95th percentile for their age and gender. Such a rise can contribute to an increase of CVD risk factors, which play a role in the development of atherosclerosis. Evidence of atherosclerosis appears as early as childhood, progresses throughout adolescences, and accelerates after 20 years-of-age. Although some children are genetically predisposed to dyslipidemia, many have elevated lipids and lipoproteins as a result of unhealthy lifestyles - high fat, high carbohydrate diets, lack of exercise, and use of medications for other health conditions. In a 2023 survey, it was predicted that approximately 40.1% of children < 17 years-of-age have had at least one medication prescribed for a short or long-term health condition within the past 12 months. Clinicians should be aware of health conditions and medications that can adversely affect lipid levels when evaluating and treating children with lipid disorders. With the increased prevalence of lipid disorders in the pediatric population, healthcare providers are searching for both primary and secondary causes including the influence of certain medications or drug classes known to cause lipid abnormalities in adults, identifying similar findings amongst children. These include but are not limited to corticosteroids, retinoid agents, beta blockers, oral contraceptives, chemotherapy agents, antiretroviral medications, androgenic steroids and behavioral medications.

The prostate is an organ prone to diseases typical of human aging, with benign and malignant prostatic disorders being among the most common diseases that affect men. There are a wide variety of treatment options for diagnosing prostate cancer in humans, depending on the risk category the disease falls into. The dog is the only mammal, besides man, that spontaneously develops canine prostatic hyperplasia (PH), prostatic atrophy and prostatic carcinoma (PCa), which are associated with age and androgenic hormones. However, unlike PCa in humans, PCa in dogs is not androgen dependent, therefore androgen deprivation therapy is not effective, and animals develop castration-resistant prostatic carcinoma (CRPC). Many treatment modalities usually for human PCa cannot be applied in CRPC. And regarding dogs, unfortunately, there is still no effective therapy for the treatment of these tumors. Available pharmacological treatments are scarce, based primarily on the prescription of anti-inflammatory drugs, with a low degree of survival. Therefore, we intend to carry out new translational studies on human and canine PCa samples, aiming to identify predictive markers and potential common therapeutic targets, to subsequently elucidate the antitumor effect of existing drugs, aiming to develop targeted therapies. The study included 20 animals, with 4 in the control group and 16 in the neoplasia group, under CEUA approval. Samples underwent proteomic analysis, RT-qPCR, RNA sequencing (RNAseq), and Next-Generation Sequencing (NGS) to evaluate gene expression patterns, tumor microenvironment interactions, and immune cell infiltrate estimates. Cross-validation with independent data from canine and human prostate carcinoma databases was performed. Biological triplicates were analyzed, and differential protein and gene expression were assessed using Student’s t-test (p &amp;lt; 0.05, expression change &amp;gt; 1.5x). A total of 44 proteins, including significantly elevated levels of Vimentin and Peptidase S1, were identified in the neoplasia group. Additionally, 1,412 differentially expressed genes were enriched in prostate cancer-related pathways, with 536,200 SNPs identified across 291 genes in the canine exome. Thirteen genes co-expressed in RNAseq and NGS analyses emerged as potential direct therapy targets. Increased secretion of Vimentin and Peptidase S1 in the neoplasia group highlighted their potential as tumor biomarkers. These findings reveal a significant overlap in tumor progression and biomarker expression between canine and human PCa, offering promising avenues for translational studies to develop effective diagnostic tools and targeted therapies for both species. Citation Format: Alexandre Matheus Baesso Cavalca, Marxa Leao Figueiredo, Maricy Apparício Ferreira, Carlos Eduardo Fonseca Alves. Diagnostic and predictive biomarkers for canine prostatic carcinoma: translational therapeutic insights [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 5693.

Ethylene oxide (EO) is a crucial organic compound commonly utilized in industrial and medical products. Food and Drug Administration (FDA)-approved EO sterilization sterilizes about 50% of sterile medical devices in the U.S. Animal and human studies have suggested that EO exposure may result in severe health problem. However, studies evaluating the relationship between EO exposure and sex hormones in human populations are still lacking. Therefore, further investigation into EO's effects on humans is essential. This cross-sectional study within the U.S. National Health and Nutrition Examination Survey (NHANES),2013-2016 examined the relationship between EO-hemoglobin adducts (HbEO) and sex hormones. HbEO was found to be inversely associated with estradiol (E2) and positively associated with the ratio of total testosterone (TT) to E2 and sex hormone-binding globulin (SHBG) levels in adult males. Such associations HbEO and E2 and SHBG were non-linear in male adults. However, no significant associations were found between HbEO and sex steroids across various age groups of females and all male age groups except for adults. Thus, our study provides evidence that EO may potentially serve as an endocrine disruptor in the environment, affecting the levels of sex hormones in adult males.

Associations between prenatal dioxin-like polychlorinated biphenyls exposure and glucocorticoid and androgenic hormones in umbilical cord blood.

Bisphenol A exposure alters hormonal modulation and responsivity in the prostate of aged female gerbils.

Upregulation of olfactory-related neuropeptide transcripts in male Macrobrachium rosenbergii in correlation to pheromone perception from molting females.

Knowledge, attitude and practice towards anabolic–androgenic steroids utilisation among gymnasium attendees in Al-Qassim Province, Saudi Arabia

Цель. Проанализировать и систематизировать имеющиеся сведения в доступной отечественной и зарубежной специальной литературе по вопросу влияния половых гормонов на этиологию развития воспалительных заболеваний кожи, в том числе фурункулов челюстно-лицевой области. Материалы и методы. Выполнен анализ специальной литературы за последние 25 лет при использовании поисковых систем eLibrary и PubMed с учетом публикаций, содержащих доказательную экспериментальную и клиническую базы по вопросам, касающимся исследования уровня половых гормонов у пациентов при инфекционно-воспалительных заболеваниях кожи, в том числе при фурункулах челюстно-лицевой области. Результаты. Влияние уровня половых гормонов на возникновение и развитие дерматозов описано в специальной литературе. Анализ уровня половых стероидных гормонов у пациентов с одиночным фурункулом и хроническим фурункулезом челюстно-лицевой области показал, что у лиц пубертатного и раннего репродуктивного периодов отмечается повышение содержания свободного тестостерона в сыворотке крови на фоне снижения уровня содержания эстрадиола и белка, связывающего половые стероиды. Повышение содержания свободного тестостерона в сыворотке крови лиц с фурункулом челюстно-лицевой области способствует усилению процесса образования кожного сала, что ведет к изменению уровня pH кожи и ее микробиоценоза. При этом в части публикаций отмечено, что гормональная теория развития гнойных поражений кожных покровов до настоящего времени не подтверждена. О влиянии андрогенных гормонов на риск развития и течение фурункулов челюстно-лицевой области имеются только единичные публикации. Заключение. Из изложенного очевидно, что до настоящего времени нет однозначного мнения врачей-специалистов о роли уровней содержания половых гормонов в возникновении, прогрессировании и развитии осложнений фурункулов челюстно-лицевой области, что является основанием для проведения исследований, устраняющих указанные пробелы в знаниях по данному вопросу. Purpose. To analyse and systematise the available data in the available domestic and foreign special literature on the influence of sex hormones on the etiology of the development of inflammatory skin diseases, including furuncles of the maxillofacial region. Materials and methods. We analysed the special literature for the last 25 years using the search systems "eLibrary" and "PubMed", taking into account the publications containing evidence-based experimental and clinical basis on the issues related to the study of sex hormone levels in patients with infectious-inflammatory skin diseases, including furuncles of the maxillofacial region. Results. The influence of sex hormone levels on the occurrence and development of dermatoses has been described in the special literature. The analysis of the level of sex steroid hormones in patients with solitary furuncle and chronic furunculosis of maxillofacial region has shown that the increase of free testosterone content in blood serum in pubertal and early reproductive periods against the background of decrease of estradiol and sex steroid-binding protein content is observed in pubertal and early reproductive periods. Increase of free testosterone content in blood serum of persons with furuncle of maxillofacial region contributes to strengthening of sebum formation process, which leads to changes in skin pH and its microbiocenosis. At the same time in some publications, it is noted that the hormonal theory of the development of purulent skin lesions has not been confirmed so far. There are only single publications regarding the influence of androgenic hormones on the risk of development and course of maxillofacial furuncles. Conclusion. From the above it is obvious that up to the present time there is no unambiguous opinion of doctors-specialists about the role of sex hormone levels in the occurrence, progression and development of complications of furuncles of the maxillofacial region, which is the basis for conducting studies to eliminate the gaps in knowledge on this issue.