I I Larina, N V Makazan, K V Ivashchenko, N M Platonova, E M Orlova, M A Kareva, L S Sozaeva, M Yu Yukina, A N Tulpakov, A S Dukhanin, N L Shimanovskii, E A Troshina
Primary glucocorticoid resistance (OMIM 615962) is a rare endocrinologic condition caused by resistance of the human glucocorticoid receptor (hGR) to glucocorticoids (GR) and characterised by general or partial insensitivity of target organs to GK. Compensatory activation of hypothalamic-pituitary-andrenal axis results in development of a various pathological conditions caused by overstimulation of adrenal glands. Clinical spectrum may range from asymptomatic cases to severe cases of mineralocorticoid and/or androgen excess. At present time, primary generalized glucocorticoid resistance has been exclusively associated with defects in the NR3C1 gene. Here, we present a case report of an adolescent patient with clinical presentation of glucocorticoid resistance confirmed by detailed endocrinologic evaluation but no confirmed mutations in the NR3C1 gene.
{"title":"[Primary Generalized Glucocorticoid Resistance: a case report].","authors":"I I Larina, N V Makazan, K V Ivashchenko, N M Platonova, E M Orlova, M A Kareva, L S Sozaeva, M Yu Yukina, A N Tulpakov, A S Dukhanin, N L Shimanovskii, E A Troshina","doi":"10.14341/probl13321","DOIUrl":"10.14341/probl13321","url":null,"abstract":"<p><p>Primary glucocorticoid resistance (OMIM 615962) is a rare endocrinologic condition caused by resistance of the human glucocorticoid receptor (hGR) to glucocorticoids (GR) and characterised by general or partial insensitivity of target organs to GK. Compensatory activation of hypothalamic-pituitary-andrenal axis results in development of a various pathological conditions caused by overstimulation of adrenal glands. Clinical spectrum may range from asymptomatic cases to severe cases of mineralocorticoid and/or androgen excess. At present time, primary generalized glucocorticoid resistance has been exclusively associated with defects in the NR3C1 gene. Here, we present a case report of an adolescent patient with clinical presentation of glucocorticoid resistance confirmed by detailed endocrinologic evaluation but no confirmed mutations in the NR3C1 gene.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"70 1","pages":"30-37"},"PeriodicalIF":0.0,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10926243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140023908","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}
O A Malievskiy, R I Malievskaya, V A Malievskiy, A N Tulpakov
The description of the child aged 5 months with the von Hippel-Lindau syndrome without any manifestations of this syndrome is presented. The reason for the molecular genetic examination was the presence of cases of this syndrome in the family (mother and sister). The heterozygous variant c.355T>C p.F119L was found in the VHL gene. An objective examination revealed no pathology. A comprehensive laboratory and instrumental examination aimed at searching for components of the von Hippel-Lindau syndrome, including a blood test for metanephrines and normetanephrines, ultrasound of the abdominal organs, examination of the fundus, also did not reveal any abnormalities. Given the results of molecular genetic diagnosis, the child remains under observation and will undergo regular examinations to identify components of the von Hippel-Lindau syndrome, including blood/urine tests for normetanephrines.
{"title":"[Preclinical diagnostics of von Hippel-Lindau syndrome in a child].","authors":"O A Malievskiy, R I Malievskaya, V A Malievskiy, A N Tulpakov","doi":"10.14341/probl13280","DOIUrl":"10.14341/probl13280","url":null,"abstract":"<p><p>The description of the child aged 5 months with the von Hippel-Lindau syndrome without any manifestations of this syndrome is presented. The reason for the molecular genetic examination was the presence of cases of this syndrome in the family (mother and sister). The heterozygous variant c.355T>C p.F119L was found in the VHL gene. An objective examination revealed no pathology. A comprehensive laboratory and instrumental examination aimed at searching for components of the von Hippel-Lindau syndrome, including a blood test for metanephrines and normetanephrines, ultrasound of the abdominal organs, examination of the fundus, also did not reveal any abnormalities. Given the results of molecular genetic diagnosis, the child remains under observation and will undergo regular examinations to identify components of the von Hippel-Lindau syndrome, including blood/urine tests for normetanephrines.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"70 1","pages":"100-104"},"PeriodicalIF":0.0,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10926248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140023907","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 S Sheremeta, A A Trukhin, V D Yartsev, D V Yudakov, M O Korchagina, S A Gojaeva
Within the framework of the article, the authors analyzed the available information about the damage to the lacrimal apparatus during radionuclide therapy. In focus of article lesions of the lacrimal production system, the main and accessory lacrimal glands, as well as lacrimal drainage are considered. It was found that damage to the lacrimal apparatus is characteristic of 131I therapy for thyroid cancer, as well as for radioligand therapy using anti-PSMA antibodies labeled with 177Lu and 225Ac. 177Lu-PSMA and 225Ac-PSMA may damage the lacrimal gland with the formation of a clinically pronounced "dry eye syndrome". The pathogenesis of such lesions is associated with the accumulation of a radioisotope in the tissues of the lacrimal apparatus, while during therapy with 131I, accumulation is realized due to the expression of the sodium-iodine symporter in the nasolacrimal duct, and during therapy with 177Lu-PSMA and 225Ac-PSMA, the radiobiological effect is realized in connection with the expression PSMA by lacrimal tissue. An analysis of the available sources showed that to date there are no results of systematic studies on the problem, there is a lack of knowledge regarding the individual risks of developing these complications, methods for their prevention that have proven effectiveness have not been developed, and the treatment methods used, having relatively low efficiency, are not specialized. The authors concluded that the strengthening of interdisciplinary interaction, as well as the organization verification methodology and correct studies, can contribute to solving problems related to the study of the complications under consideration.
{"title":"[The lacrimal apparatus as an organ at risk during radionuclide therapy].","authors":"M S Sheremeta, A A Trukhin, V D Yartsev, D V Yudakov, M O Korchagina, S A Gojaeva","doi":"10.14341/probl13163","DOIUrl":"10.14341/probl13163","url":null,"abstract":"<p><p>Within the framework of the article, the authors analyzed the available information about the damage to the lacrimal apparatus during radionuclide therapy. In focus of article lesions of the lacrimal production system, the main and accessory lacrimal glands, as well as lacrimal drainage are considered. It was found that damage to the lacrimal apparatus is characteristic of 131I therapy for thyroid cancer, as well as for radioligand therapy using anti-PSMA antibodies labeled with 177Lu and 225Ac. 177Lu-PSMA and 225Ac-PSMA may damage the lacrimal gland with the formation of a clinically pronounced \"dry eye syndrome\". The pathogenesis of such lesions is associated with the accumulation of a radioisotope in the tissues of the lacrimal apparatus, while during therapy with 131I, accumulation is realized due to the expression of the sodium-iodine symporter in the nasolacrimal duct, and during therapy with 177Lu-PSMA and 225Ac-PSMA, the radiobiological effect is realized in connection with the expression PSMA by lacrimal tissue. An analysis of the available sources showed that to date there are no results of systematic studies on the problem, there is a lack of knowledge regarding the individual risks of developing these complications, methods for their prevention that have proven effectiveness have not been developed, and the treatment methods used, having relatively low efficiency, are not specialized. The authors concluded that the strengthening of interdisciplinary interaction, as well as the organization verification methodology and correct studies, can contribute to solving problems related to the study of the complications under consideration.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"70 1","pages":"13-17"},"PeriodicalIF":0.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10926245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140023910","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}
O O Golounina, Zh E Belaya, K A Voronov, A G Solodovnikov, L Ya Rozhinskaya, G A Melnichenko, N G Mokrysheva, I I Dedov
Aim: To develop a noninvasive method of differential diagnosis of ACTH-dependent hypercortisolism, as well as to evaluate the effectiveness of an optimal algorithm for predicting the probability of ectopic ACTH syndrome (EAS) obtained using machine learning methods based on the analysis of clinical data.
Materials and methods: As part of a single-center, one-stage, cohort study, a retrospective prediction of the probability of EAS among patients with ACTH-dependent hypercortisolism was carried out. Patients were randomly stratified into 2 samples: training (80%) and test (20%). Eleven machine learning algorithms were used to develop predictive models: Linear Discriminant Analysis, Logistic Regression, elastic network (GLMNET), Support Vector machine (SVM Radial), k-nearest neighbors (kNN), Naive Bayes, binary decision tree (CART), C5.0 decision tree algorithms, Bagged CART, Random Forest, Gradient Boosting (Stochastic Gradient Boosting, GBM).
Results: The study included 223 patients (163 women, 60 men) with ACTH-dependent hypercortisolism, of which 175 patients with Cushing's disease (CD), 48 - with EAS. As a result of preliminary data processing and selection of the most informative signs, the final variables for the classification and prediction of EAS were selected: ACTH level at 08:00 hours, potassium level (the minimum value of potassium in the active stage of the disease), 24-h urinary free cortisol, late-night serum cortisol, late-night salivary cortisol, the largest size of pituitary adenoma according to MRI of the brain. The best predictive ability in a training sample of all trained machine learning models for all three final metrics (ROC-AUC (0.867), sensitivity (90%), specificity (56.4%)) demonstrated a model of gradient boosting (Generalized Boosted Modeling, GBM). In the test sample, the AUC, sensitivity and specificity of the model in predicting EAS were 0.920; 77.8% and 97.1%, respectively.
Conclusion: The prognostic model based on machine learning methods makes it possible to differentiate patients with EAS and CD based on basic clinical results and can be used as a primary screening of patients with ACTH-dependent hypercortisolism.
目的:开发一种无创的ACTH依赖性皮质醇增多症鉴别诊断方法,并评估基于临床数据分析的机器学习方法预测异位ACTH综合征(EAS)概率的最佳算法的有效性:作为单中心、单阶段队列研究的一部分,对ACTH依赖性皮质醇增多症患者的EAS概率进行了回顾性预测。患者被随机分为两个样本:训练样本(80%)和测试样本(20%)。11 种机器学习算法被用于开发预测模型:线性判别分析、逻辑回归、弹性网络(GLMNET)、支持向量机(SVM Radial)、k-近邻(kNN)、Naive Bayes、二元决策树(CART)、C5.0决策树算法、袋装CART、随机森林、梯度提升(随机梯度提升,GBM):研究对象包括 223 名 ACTH 依赖性皮质醇增多症患者(163 名女性,60 名男性),其中 175 名患者患有库欣病(CD),48 名患者患有 EAS。经过初步数据处理和选择最有参考价值的体征,最终选定了用于 EAS 分类和预测的变量:08:00 时的促肾上腺皮质激素水平、血钾水平(疾病活动期血钾的最低值)、24 小时尿游离皮质醇、深夜血清皮质醇、深夜唾液皮质醇、脑部核磁共振成像显示的最大垂体腺瘤。在训练样本中,所有经过训练的机器学习模型对所有三个最终指标(ROC-AUC(0.867)、灵敏度(90%)、特异性(56.4%))的预测能力最佳的是梯度提升模型(广义提升模型,GBM)。在测试样本中,该模型预测 EAS 的 AUC、灵敏度和特异性分别为 0.920、77.8% 和 97.1%:基于机器学习方法的预后模型可以根据基本临床结果区分 EAS 和 CD 患者,可用作 ACTH 依赖性皮质醇增多症患者的初筛。
{"title":"[Machine learning methods in differential diagnosis of ACTH-dependent hypercortisolism].","authors":"O O Golounina, Zh E Belaya, K A Voronov, A G Solodovnikov, L Ya Rozhinskaya, G A Melnichenko, N G Mokrysheva, I I Dedov","doi":"10.14341/probl13342","DOIUrl":"10.14341/probl13342","url":null,"abstract":"<p><strong>Aim: </strong>To develop a noninvasive method of differential diagnosis of ACTH-dependent hypercortisolism, as well as to evaluate the effectiveness of an optimal algorithm for predicting the probability of ectopic ACTH syndrome (EAS) obtained using machine learning methods based on the analysis of clinical data.</p><p><strong>Materials and methods: </strong>As part of a single-center, one-stage, cohort study, a retrospective prediction of the probability of EAS among patients with ACTH-dependent hypercortisolism was carried out. Patients were randomly stratified into 2 samples: training (80%) and test (20%). Eleven machine learning algorithms were used to develop predictive models: Linear Discriminant Analysis, Logistic Regression, elastic network (GLMNET), Support Vector machine (SVM Radial), k-nearest neighbors (kNN), Naive Bayes, binary decision tree (CART), C5.0 decision tree algorithms, Bagged CART, Random Forest, Gradient Boosting (Stochastic Gradient Boosting, GBM).</p><p><strong>Results: </strong>The study included 223 patients (163 women, 60 men) with ACTH-dependent hypercortisolism, of which 175 patients with Cushing's disease (CD), 48 - with EAS. As a result of preliminary data processing and selection of the most informative signs, the final variables for the classification and prediction of EAS were selected: ACTH level at 08:00 hours, potassium level (the minimum value of potassium in the active stage of the disease), 24-h urinary free cortisol, late-night serum cortisol, late-night salivary cortisol, the largest size of pituitary adenoma according to MRI of the brain. The best predictive ability in a training sample of all trained machine learning models for all three final metrics (ROC-AUC (0.867), sensitivity (90%), specificity (56.4%)) demonstrated a model of gradient boosting (Generalized Boosted Modeling, GBM). In the test sample, the AUC, sensitivity and specificity of the model in predicting EAS were 0.920; 77.8% and 97.1%, respectively.</p><p><strong>Conclusion: </strong>The prognostic model based on machine learning methods makes it possible to differentiate patients with EAS and CD based on basic clinical results and can be used as a primary screening of patients with ACTH-dependent hypercortisolism.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"70 1","pages":"18-29"},"PeriodicalIF":0.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10926240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140023906","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}
I I Dedov, O B Bezlepkina, M S Pankratova, E V Nagaeva, E N Raykina, V A Peterkova
The recombinant technologies era, which began in the second half of the XX century, made it possible to produce recombinant growth hormone (rGH) necessary for the treatment of stunting of various genesis. The time of practically unlimited possibilities of rGH production has come, which served as a stimulus for studying the efficacy and safety of rGH application, searching for optimal ways of its use and dosing regimes. Many years of experience in the use of somatropin in clinical practice allowed us to obtain data on its effectiveness primarily in somatotropic insufficiency in children, to study its effect on the functional state of various organs and systems, and to expand the indications for the use of RGR.
{"title":"[Growth hormone - 30 years of clinical practice: past, present, future].","authors":"I I Dedov, O B Bezlepkina, M S Pankratova, E V Nagaeva, E N Raykina, V A Peterkova","doi":"10.14341/probl13432","DOIUrl":"10.14341/probl13432","url":null,"abstract":"<p><p>The recombinant technologies era, which began in the second half of the XX century, made it possible to produce recombinant growth hormone (rGH) necessary for the treatment of stunting of various genesis. The time of practically unlimited possibilities of rGH production has come, which served as a stimulus for studying the efficacy and safety of rGH application, searching for optimal ways of its use and dosing regimes. Many years of experience in the use of somatropin in clinical practice allowed us to obtain data on its effectiveness primarily in somatotropic insufficiency in children, to study its effect on the functional state of various organs and systems, and to expand the indications for the use of RGR.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"70 1","pages":"4-12"},"PeriodicalIF":0.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10926242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140023904","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}
E O Mamedova, E G Przhiyalkovskaya, S A Buryakina, E V Bondarenko, A M Lapshina, M Yu Pikunov, Zh E Belaya, G A Melnichenko
Acromegaly is a neuroendocrine disorder caused by excessive production of growth hormone (GH). In the majority of cases the cause of acromegaly is a pituitary tumor producing GH. Cases of ectopic acromegaly are much rarer. Ectopic acromegaly occurs in cases of tumors which produce growth hormone-releasing hormone (GHRH) or extrapituitary tumors which produce GH. The main sources of excessive GHRH production are neuroendocrine tumors (NETs) of the lung or pancreas. Treatment of ectopic acromegaly consists of surgical removal of the source of GHRH hyperproduction and in cases where surgery is not an option, somatostatin analogues, pegvisomant, chemotherapy, immunotherapy or radiation therapy are used.In this article three cases of ectopic acromegaly due to GHRH-producing lung NETs are presented, each of them being notable for a number of features. In the first two cases, clinical symptoms were mild, besides in the second case ectopic acromegaly was accompanied by primary hyperparathyroidism. In the third case ectopic acromegaly was accompanied by pituitary macroadenoma, and after surgical removal of the lung NET remission of acromegaly was not achieved. In all three cases, lung NETs were detected incidentally on radiologic chest screening for other conditions.
肢端肥大症是一种由生长激素(GH)分泌过多引起的神经内分泌疾病。在大多数情况下,肢端肥大症的病因是产生生长激素的垂体瘤。异位性肢端肥大症则更为罕见。异位性肢端肥大症发生于产生生长激素释放激素(GHRH)的肿瘤或产生 GH 的垂体外肿瘤。GHRH分泌过多的主要来源是肺部或胰腺的神经内分泌肿瘤(NET)。异位肢端肥大症的治疗包括手术切除 GHRH 过度分泌的来源,如果无法选择手术,则使用体生长激素类似物、培维索胺、化疗、免疫疗法或放射疗法。前两个病例的临床症状轻微,第二个病例的异位肢端肥大症伴有原发性甲状旁腺功能亢进。在第三个病例中,异位肢端肥大症伴有垂体大腺瘤,手术切除肺NET后,肢端肥大症仍未缓解。在这三个病例中,肺 NET 都是在其他疾病的胸部放射检查中偶然发现的。
{"title":"[Ectopic acromegaly due to bronchial neuroendocrine tumors: the first description in Russia of three clinical cases].","authors":"E O Mamedova, E G Przhiyalkovskaya, S A Buryakina, E V Bondarenko, A M Lapshina, M Yu Pikunov, Zh E Belaya, G A Melnichenko","doi":"10.14341/probl13346","DOIUrl":"10.14341/probl13346","url":null,"abstract":"<p><p> Acromegaly is a neuroendocrine disorder caused by excessive production of growth hormone (GH). In the majority of cases the cause of acromegaly is a pituitary tumor producing GH. Cases of ectopic acromegaly are much rarer. Ectopic acromegaly occurs in cases of tumors which produce growth hormone-releasing hormone (GHRH) or extrapituitary tumors which produce GH. The main sources of excessive GHRH production are neuroendocrine tumors (NETs) of the lung or pancreas. Treatment of ectopic acromegaly consists of surgical removal of the source of GHRH hyperproduction and in cases where surgery is not an option, somatostatin analogues, pegvisomant, chemotherapy, immunotherapy or radiation therapy are used.In this article three cases of ectopic acromegaly due to GHRH-producing lung NETs are presented, each of them being notable for a number of features. In the first two cases, clinical symptoms were mild, besides in the second case ectopic acromegaly was accompanied by primary hyperparathyroidism. In the third case ectopic acromegaly was accompanied by pituitary macroadenoma, and after surgical removal of the lung NET remission of acromegaly was not achieved. In all three cases, lung NETs were detected incidentally on radiologic chest screening for other conditions.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"70 1","pages":"66-80"},"PeriodicalIF":0.0,"publicationDate":"2024-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10926249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140023902","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}
Yu S Absatarova, E N Andreeva, Yu S Evseeva, T A Zelenkova-Zakharchuk, E V Sheremetyeva, O R Grigoryan, R K Mikheev
The article presents data on the relationship of pathogenetic mechanisms for the development of menstrual disorders of functional and organic origin in connection with mental disturbances from the point of view of the psychosomatic concept. According to the latter, functional disorders of the menstrual cycle are considered as psychosomatic, in which gynecological pathology develops as a result of psychopathological illness. A striking example of such a disorder is functional hypothalamic amenorrhea. At the same time, endocrinopathies, such as polycystic ovary syndrome and premature ovarian insufficiency, can also be considered in the paradigm of psychosomatic illnesses of ovarian function due to the high prevalence of anxiety and depressive disorders in this cohort of patients. This review highlights the importance of interdisciplinary collaboration between a gynecologist and a psychiatrist for the most effective reproductive rehabilitation of patients with amenorrhea. Literature search was carried out in national (eLibrary, CyberLeninka.ru) and international (PubMed, Cochrane Library) databases in Russian and English. The priority was free access to the full text of articles. The choice of sources was prioritized for the period from 2018 to 2023.However, taking into account the insufficient knowledge of the chosen topic, the choice of sources dates back to 1985.
{"title":"[Endocrine and psychosomatic disorders in patients with amenorrhea].","authors":"Yu S Absatarova, E N Andreeva, Yu S Evseeva, T A Zelenkova-Zakharchuk, E V Sheremetyeva, O R Grigoryan, R K Mikheev","doi":"10.14341/probl13366","DOIUrl":"10.14341/probl13366","url":null,"abstract":"<p><p>The article presents data on the relationship of pathogenetic mechanisms for the development of menstrual disorders of functional and organic origin in connection with mental disturbances from the point of view of the psychosomatic concept. According to the latter, functional disorders of the menstrual cycle are considered as psychosomatic, in which gynecological pathology develops as a result of psychopathological illness. A striking example of such a disorder is functional hypothalamic amenorrhea. At the same time, endocrinopathies, such as polycystic ovary syndrome and premature ovarian insufficiency, can also be considered in the paradigm of psychosomatic illnesses of ovarian function due to the high prevalence of anxiety and depressive disorders in this cohort of patients. This review highlights the importance of interdisciplinary collaboration between a gynecologist and a psychiatrist for the most effective reproductive rehabilitation of patients with amenorrhea. Literature search was carried out in national (eLibrary, CyberLeninka.ru) and international (PubMed, Cochrane Library) databases in Russian and English. The priority was free access to the full text of articles. The choice of sources was prioritized for the period from 2018 to 2023.However, taking into account the insufficient knowledge of the chosen topic, the choice of sources dates back to 1985.</p>","PeriodicalId":101419,"journal":{"name":"Problemy endokrinologii","volume":"69 6","pages":"121-131"},"PeriodicalIF":0.0,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10848186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139682258","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}
Background: 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.
Aim: To evaluate the efficacy of various therapy options in patients with type 2 amiodarone-induced thyrotoxicosis.
Materials and methods: 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.
Results: 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).
{"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}
P A Zakharova, I A Ilovayskaya, S A Terpigorev, I V Komerdus, A Yu Lugovskaya
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.
{"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}
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
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.
{"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}