{"title":"[Type 2 amiodarone-induced thyrotoxicosis: efficacy of glucocorticoid therapy, a retrospective analysis].","authors":"A S Ermolaeva, V V Fadeev","doi":"10.14341/probl13267","DOIUrl":"10.14341/probl13267","url":null,"abstract":"<p><strong>Background: </strong>Type 2 amiodarone-induced thyrotoxicosis remains a significant problem of endocrinology and cardiology. Due to the increase a life expectancy of the population, the prevalence of cardiac arrhythmias and prescribing of amiodarone are increasing. Thyrotoxicosis aggravates the existing cardiovascular disease in patients, leads to the progression of left ventricular dysfunction, relapses of arrhythmias, increasing the risk of adverse outcomes. The tactic of further management of patients is complicated: it is necessary to resolve the issue of canceling or continuing the use of antiarrhythmic drugs necessary for a patient with a history of cardiac arrhythmia, as well as competent therapy of the thyroid pathology that has arisen. Oral glucocorticoids are the first-line drugs for the treatment of patients with moderate and severe type 2 amiodarone-induced thyrotoxicosis. Despite the appearance of clinical recommendations, opinions on the management of patients are differ, both among cardiologists and among endocrinologists. Often thyrostatics are prescribed to patients simultaneously with glucocorticoids, although it doesn't have pathogenetic basis.</p><p><strong>Aim: </strong>To evaluate the efficacy of various therapy options in patients with type 2 amiodarone-induced thyrotoxicosis.</p><p><strong>Materials and methods: </strong>The retrospective study included 38 patients (20 men and 18 women aged 35 to 85 years) with type 2 amiodarone-induced thyrotoxicosis. All patients underwent an analysis of anamnestic, anthropometric data, complex laboratory and instrumental diagnostics. According to the treatment options, 3 groups were retrospectively formed: without therapy (n=19), taking glucocorticoids (n=11) and combination of glucocorticoids and thyrostatics (n=8). The follow-up period was 6-18 months, including the treatment. The efficacy of treatment in the groups was evaluated by the time of reaching euthyroidism on the background of glucocorticoid therapy and duration of thyrotoxicosis; the search was conducted for potential predictors of delayed response to glucocorticoid therapy and long-term course of thyrotoxicosis.</p><p><strong>Results: </strong>The average age was 62.0 [52.9; 66.3] years. The level of free thyroxine was significantly decreased after 1 month from the start of therapy in both groups: from 38.1 [32.1; 58.4] to 23.4 [19.6; 29.3] pmol/l (p<0.001) in the group taking glucocorticoids; from 73.9 [42.2; 75.6] to 39.3 [22.4; 47.2] pmol/l (p<0.001) in the combination therapy group. The time of reaching euthyroidism was longer in the combination therapy group (p=0.047), didn't depend on the dose (p=0.338) and duration of taking thiamazole (p=0.911), the delayed response to therapy correlated with age (p=-0.857; p=0.007) and time interval from the appearance of clinical symptoms of thyrotoxicosis to the start of glucocorticoid therapy (p=0.881; p<0.001).</p><p><strong>Conclusion: </strong>The result","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"69 6","pages":"17-27"},"PeriodicalIF":0.0,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10848191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139682283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
D V Kurkin, D A Bakulin, A I Robertus, Yu A Kolosov, I S Krysanov, E I Morkovin, A V Strygin, J V Gorbunova, I E Makarenko, R V Drai, E V Makarova, E V Pavlova, R А Kudrin, O V Ivanova
{"title":"[Evolution of insulin therapy: past, present, future].","authors":"D V Kurkin, D A Bakulin, A I Robertus, Yu A Kolosov, I S Krysanov, E I Morkovin, A V Strygin, J V Gorbunova, I E Makarenko, R V Drai, E V Makarova, E V Pavlova, R А Kudrin, O V Ivanova","doi":"10.14341/probl13251","DOIUrl":"10.14341/probl13251","url":null,"abstract":"<p><p>2021 marks the 100th anniversary of the discovery of insulin, an event that forever changed the lives of people with diabetes mellitus. At present patients around the world experience the miracle of insulin therapy every day. A disease that used to kill children and teenagers in 2 years in 1920 has become a disease that can be controlled with a possibility to lead a long productive life. Over the past century, the great discovery of Banting, Best and Collip has forever changed the world and saved millions of lives. This review is devoted to the history of the development of insulin and its further improvement: from the moment of discovery to the present days. Various generations of insulin are considered: from animals to modern ultrashort and basal analogues. The article ends with a brief review of current trends in the development of new delivery methods and the development of new insulin molecules. Over the past century, insulin therapy has come a long way, which has significantly improved the quality of life of our patients. But research is actively continuing, including in the field of alternative methods of insulin delivery, which are more convenient for the patient, as well as in the development of «smart» molecules that will have a glucose-dependent effect.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"69 6","pages":"86-101"},"PeriodicalIF":0.0,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10848184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139682259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R K Mikheev, E N Andreeva, O R Grigoryan, E V Sheremetyeva, M S Pankratova, E V Loginova
{"title":"[Replicative and biochemical ageing mechanisms among females with Turner syndromes].","authors":"R K Mikheev, E N Andreeva, O R Grigoryan, E V Sheremetyeva, M S Pankratova, E V Loginova","doi":"10.14341/probl13256","DOIUrl":"10.14341/probl13256","url":null,"abstract":"<p><strong>Background: </strong>2025 is going to be the 100th anniversary of the first historical description of Turner syndrome - complex of genomic abnormalities, congenital gonadal disruption and hypergonadotropic hypogonadism. Total estrogenic deficiency triggers development of age-related comorbidities. There is no doubt that personalized search for replicative markers of cellular aging among females with Turner syndrome is needed.</p><p><strong>Aim: </strong>To evaluate features of replicative (telomere length) and biochemical (lipid profile, calcium-phosphate album, thyroid hormones, markers cytolysis and cholestasis, carbohydrate metabolism, nitrogenic metabolism, electrolytes, FSH) markers among females with Turner syndrome.</p><p><strong>Materials and methods: </strong>Research has been provided in collaboration between Endocrinology Research Centre of the Russian Ministry of Health and Lomonosov Moscow State University Medical Research and Educational Centre in the period since 10.01.2021 until 01.08.2022. Females with non-iatrogenic hypergonadotropic hypogonadism caused by Turner syndrome (45,X0; 45,X/46,XX; 45,X/46,X,r(X); 13-40 y.o.; n=26) and primary ovarian insufficiency (18-39 нyears=26); healthy females of reproductive age (15-49 y.o.; n=24). Patients have undergone laboratory genetic (leucocyte telomere length), biochemical (fasting glycaemia, urea, creatinine, common/conjugated bilirubin, ALT, AST, gamma-glutamyl transferase, triglycerides, HDL-P, LDL-P, common cholesterol, common/ionized calcium, phosphate, vitamin D, sodium/potassium/chlorides, FSH, HbA1c) analyses. Body measurements - body mass, body height. DNA extraction - provided with Qiagen DNA blood mini kit (Germany). Leukocyte telomere length - with real-time polymerase chain reaction PCR (Flow-fish). Soft program IBM SPSS Statistics (version 26,0 for Windows).</p><p><strong>Results: </strong>1. Females with Turner syndrome have significantly lower mean telomere length (8,22 kB [6,63-9,30]) than with primary ovarian insufficiency (10, 34 кБ [8,41-13,08], p<0,001) and healthy reproductive age females (10,77 kB [9,95-13,16], р>0,05).2. Telomere length correlates directly and significantly with longevity of menopausal hormonal therapy among females with primary ovarian insufficiency (ρ = 505; p<0,001).3. Patients with Turner syndrome are inclined to vitamin D deficiency (р<0,001), dyslipidemia (р=0,01); increase of levels of aminotransferases, cholestasis markers, phosphate and FSH (р<0,001).</p><p><strong>Conclusion: </strong>Turner syndrome is serious genetic disease that leads not only to infertility but to significant decrease of quality/life longevity out of \"healthy aging\" conception.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"69 6","pages":"113-120"},"PeriodicalIF":0.0,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10848188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139682282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
P A Zakharova, I A Ilovayskaya, S A Terpigorev, I V Komerdus, A Yu Lugovskaya
{"title":"[Development of sarcoidosis after successful treatment of Cushing's disease].","authors":"P A Zakharova, I A Ilovayskaya, S A Terpigorev, I V Komerdus, A Yu Lugovskaya","doi":"10.14341/probl13203","DOIUrl":"10.14341/probl13203","url":null,"abstract":"<p><p>Cushing's disease is a rare severe neuroendocrine disorder caused by chronic overproduction of adrenocorticotropic hormone by a pituitary tumor. Supraphysiological concentrations of cortisol in endogenous hypercortisolism have an immunosuppressive and anti-inflammatory effect similar to therapy with systemic glucocorticosteroids. This may reduce the activity of the patient's concomitant autoimmune inflammatory diseases. On the other hand, a decrease in cortisol levels during treatment for Cushing's disease may be associated with a reactivation of the immune system that pose a risk of onset or recurrence of an autoimmune disorder. We present our own clinical case demonstrating the development of sarcoidosis after surgical treatment of Cushing's disease.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"69 6","pages":"47-53"},"PeriodicalIF":0.0,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10848190/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139682255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M A Tiulpakov, E V Nagaeva, N Y Kalinchenko, O B Bezlepkina
{"title":"[A promising approach for therapy control in congenital adrenal hyperplasia. Problems of Endocrinology].","authors":"M A Tiulpakov, E V Nagaeva, N Y Kalinchenko, O B Bezlepkina","doi":"10.14341/probl13328","DOIUrl":"10.14341/probl13328","url":null,"abstract":"<p><p>Congenital adrenal hyperplasia (CAH) is a group of autosomal recessive disorders requiring lifelong glucocorticoid replacement (GC) therapy. Lack of GC therapy leads to precocious puberty in boys, heterosexual development in girls, accelerated bone maturation and short final height in both sexes. In adolescence, the lack of GC therapy is the cause of menstrual disorders in girls and the development of TART in boys, as a result reducing the reproductive potential in both sexes. On the other hand, an overdose of GC leads to drug-induced Itsenko-Cushing's syndrome. In order to select adequate doses of GC in childhood and adolescence, multiple determinations of 17-hydroxyprogesterone, androstenedione, and testosterone in blood plasma, and thus multiple venous blood sampling are required. The blood sampling requires specially trained medical staff and can effect on the results due to stress reaction especially in young patients. Hence, the development and implementation of a non-invasive method for determining the steroid profile is extremely important in monitoring GC therapy in children. In addition, the currently used immunofluorescence assay cannot determine other adrenal steroids, has a high variation due to the «cross-reaction» of steroids that are similar in structure, which inflates the results. Unlike immunofluorescence assay, liquid chromatography and tandem mass spectrometry is more preferable method, since it is more specific and accurate. In this literature review, saliva presented as an alternative substrate and the non-invasive method for determining the steroid profile. This method can solve the above disadvantages, simplify and make more accurate the selection of GC therapy in patients with CAH, which is especially important in childhood.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"69 6","pages":"102-108"},"PeriodicalIF":0.0,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10848187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139682254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A S Shutova, E A Pigarova, L I Lepeshkina, V A Ioutsi, M Yu Drokov, S Y Vorotnikova, L I Astafyeva, L K Dzeranova
{"title":"[Overcoming therapy resistance in prolactinomas: from perspectives to real clinical practice].","authors":"A S Shutova, E A Pigarova, L I Lepeshkina, V A Ioutsi, M Yu Drokov, S Y Vorotnikova, L I Astafyeva, L K Dzeranova","doi":"10.14341/probl13351","DOIUrl":"10.14341/probl13351","url":null,"abstract":"<p><p>The main treatment option of prolactin-secreting pituitary adenomas is dopamine agonist therapy, which demonstrates prolactin level normalizing and reducing the size of an adenoma in the majority of cases. However, significant amount of patients - about 20% - poorly responds even to high doses of dopamine agonists that is explained by the resistance to therapy. The occurrence of pharmacodynamic characteristics is one of the causes responsible for the development of resistance to typical therapy. Clinical manifestations of persistent hyperprolactinemia are due to following pathological factors: hormonal hypersecretion and the mass-effect of pituitary adenoma. Prevention of irreversible changes is possible only with timely detection of resistance and determination of the optimal personalized treatment algorithm.We report a clinical case of dopamine-agonist resistant microprolactinoma. Patient's health stabilisation, normal level of prolactin and reduction in size of adenoma were achieved due to administration of combined treatment with tamoxifen and dopamine agonists. Hyperprolactinaemia occurring because of prolactin-secreting pituitary adenoma and associated adverse effects are significant problem, decreasing quality of life and demographics in general. This underlines the importance of figuring out causes and identifying predictors of the therapy resistance.The results of the study, illustrated by a clinical example, are presented in the present paper.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"69 6","pages":"63-69"},"PeriodicalIF":0.0,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10848183/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139682261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
B I Yalaev, A V Novikov, I R Minniakhmetov, R I Khusainova
{"title":"[Development of prognostic clinical and genetic models of the risk of low bone mineral density using neural network training].","authors":"B I Yalaev, A V Novikov, I R Minniakhmetov, R I Khusainova","doi":"10.14341/probl13421","DOIUrl":"10.14341/probl13421","url":null,"abstract":"<p><strong>Background: </strong>Osteoporosis is a common age-related disease with disabling consequences, the early diagnosis of which is difficult due to its long and hidden course, which often leads to diagnosis only after a fracture. In this regard, great expectations are placed on advanced developments in machine learning technologies aimed at predicting osteoporosis at an early stage of development, including the use of large data sets containing information on genetic and clinical predictors of the disease. Nevertheless, the inclusion of DNA markers in prediction models is fraught with a number of difficulties due to the complex polygenic and heterogeneous nature of the disease. Currently, the predictive power of neural network models is insufficient for their incorporation into modern osteoporosis diagnostic protocols. Studies in this area are sporadic, but are widely demanded, as their results are of great importance for preventive medicine. This leads to the need to search for the most effective machine learning approaches and optimise the selection of genetic markers as input parameters to neural network models.</p><p><strong>Aim: </strong>to evaluate the effectiveness of machine learning and neural network analysis to develop predictive risk models for osteoporosis based on clinical predictors and genetic markers of osteoporetic fractures.</p><p><strong>Materials and methods: </strong>The predictive models were trained using a database of genotyping and clinical characteristics of 701 women and 501 men living in the Volga-Ural region of Russia. Anthropometric parameters, data on gender, bone mineral density level, and the results of genotyping of 152 polymorphic loci of candidate genes and replication loci of the GEFOS consortium's full genome-wide association search were included as input parameters.</p><p><strong>Results: </strong>It was found that the model for predicting low bone mineral density, including 6 polymorphic variants of the OPG gene (rs2073618, rs2073617, rs7844539, rs3102735, rs3134069) and 5 polymorphic variants of microRNA binding sites in the mRNA of genes involved in bone metabolism (COL11A1 - rs1031820, FGF2 - rs6854081, miR-146 - rs2910164, ZNF239 - rs10793442, SPARC - rs1054204 and VDR - rs11540149) (AUC=0.81 for men and AUC=0.82 for women).</p><p><strong>Conclusion: </strong>The results confirm the promising application of machine learning to predict the risk of osteoporosis at the preclinical stage of the disease based on the analysis of clinical and genetic factors.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"70 6","pages":"67-82"},"PeriodicalIF":0.0,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11775677/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143049373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N N Katamadze, A A Tskaeva, E A Pigarova, L K Dzeranova, N V Tarbaeva
{"title":"[Differential diagnosis and tactics of managing a patient with primary hypophysitis on the example of a clinical case].","authors":"N N Katamadze, A A Tskaeva, E A Pigarova, L K Dzeranova, N V Tarbaeva","doi":"10.14341/probl13311","DOIUrl":"10.14341/probl13311","url":null,"abstract":"<p><p>In recent years, there has been a significant increase in the prevalence of autoimmune endocrinopathies, which are known to affect various levels of the endocrine system, including the pituitary gland. Hypophysitis is a general term used to describe any form of sellar and suprasellar inflammation that leads to structural changes in the hypothalamic-pituitary region and manifests itself in varying degrees of hormonal deficiency of the anterior and posterior pituitary glands. To date, there is a primary form of hypophysitis, which occurs as a result of an autoimmune lesion directly to the pituitary gland, and a secondary form of hypophysitis, which occurs as a result of the presence of a systemic autoimmune disease. Regardless of the etiology, patients with hypophysitis show various signs and symptoms caused by an inflammatory process in the pituitary gland, which can lead to the development of hypopituitarism, compression of the sellar and parasellar structures. MRI is currently the best non-invasive diagnostic tool for diagnosing hypopituitarism, however, the diagnosis can be made with certainty only by histological examination of the pituitary tissue, which requires an invasive approach, which greatly reduces the feasibility of this procedure. In this article, we present a patient with MRI showing signs of hypophysitis in the absence of clear clinical symptoms.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"69 6","pages":"54-62"},"PeriodicalIF":0.0,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10851037/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139682257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N N Katamadze, E A Pigarova, L K Dzeranova, N G Mokrysheva
{"title":"[Features of water-electrolyte balance in persons of the older age group].","authors":"N N Katamadze, E A Pigarova, L K Dzeranova, N G Mokrysheva","doi":"10.14341/probl13214","DOIUrl":"10.14341/probl13214","url":null,"abstract":"<p><p>Age-related changes have a great influence on the regulation of water and electrolyte homeostasis in the body, which is regulated by a complex interaction of environmental factors, drinking behavior, the secretion of a number of hormones and hormone-like substances, as well as the innervation and functional state of the kidneys. It is well known that the changes that are part of physiological aging underlie fluid and electrolyte imbalances, exacerbated by the presence of age-related diseases, medications, or a number of external factors such as malnutrition, fluid intake, and the presence of dementia. This review considers literature data on the effect of normal aging on the development of pathology of the water-sodium balance, including dehydration of senile patients, hyponatremia, hypernatremia, changes in the secretion of antidiuretic hormone and the activity of elements of the renin-angiotensin-aldosterone system.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"69 6","pages":"28-36"},"PeriodicalIF":0.0,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10848185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139682260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Pituitary disorders in patients with end-stage chronic renal failure].","authors":"T N Markova, E V Kosova, N K Mishchenko","doi":"10.14341/probl13212","DOIUrl":"10.14341/probl13212","url":null,"abstract":"<p><p>Disorders in the kidneys lead to disturbance of homeostasis. As the glomerular filtration rate decreases, the metabolism of numerous biologically active substances, including pituitary hormones, decreases. The article presents an overview of pituitary dysfunction in patients with chronic kidney disease (CKD) and discusses the possible reasons of the pathogenetic mechanisms. Particular focus is being given to the assessment of changes in the concentration of pituitary hormones in patients with end-stage chronic kidney disease (CKD) and discusses the pathogenetic mechanisms of their formation. Particular attention is paid to the assessment of changes in the concentration of pituitary hormones in patients receiving renal replacement therapy (RRT). CKD leads to an increase in the level of prolactin, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Concentrations of growth hormone (GH), isulin-like growth factor-1 (IGF-1), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH) and vasopressin may remain within normal values or increase in this group of patients. RRT does not reduce the levels of prolactin, LH, FSH, while the concentration of growth hormone, IGF-1, TSH tends to normalize. The content of ACTH and vasopressin may remain unchanged or decrease. Kidney transplantation in most cases corrects hormonal disorders. Correction of hormonal changes can improve the clinical outcome and quality of life of patients with end stage CKD.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"69 6","pages":"37-46"},"PeriodicalIF":0.0,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10848192/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139682262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}