Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

IV (XXVII) Национальный конгресс эндокринологов с международным участием «ИННОВАЦИОННЫЕ ТЕХНОЛОГИИ В ЭНДОКРИНОЛОГИИ» 22-25 сентября 2021 года ТРАНЗИТОРНОЕ ИЗМЕНЕНИЕ ГЛИКИРОВАННОГО ГЕМОГЛОБИНА У ПАЦИЕНТОВ C COVID-19 БЕЗ САХАРНОГО ДИАБЕТА В АНАМНЕЗЕ Калмыкова З .А ., Кононенко И

Introduction: COVID-19 can trigger either transient stress-induced state, or newly onset diabetes mellitus (DM). It is well known that HbA1c serves as an indicator of glycemic status 12 weeks before the acute disease. Aim: To examine glycemic status at admission and 6 weeks after hospital discharge in patients with confirmed COVID-19 but no previous DM-history. Methods: Of 155 patients hospitalized with COVID-19 and pneumonia 111 persons had no previous DM-history. The levels of HbA1с, fasting and admission plasma glucose (FPG and APG) were measured at admission and 6 weeks after the discharge. The severity of COVID-19 was confirmed by CT scan, SpO2, serum IL-6, CRP, D-dimer. Results: All 111 patients had normal FPG and APG values. According to HbA1c level all the patients were divided into two groups: A) HbA1c≤6.0% (n=64, median 5,8%) and B) HbA1c>6,0% (n=47, median 6,4%). Our particular interest was focused on the group B due to the discrepancy of high HbA1c level and normal FPG and APG. Group B patients were retested for glycemic status in 6±1 week after the discharge. Surprisingly the median HbA1c level dropped down from 6,4% to 5,7% in such a short period of time with no antidiabetic drugs. COVID-19 severity markers were significantly higher in the group B. Conclusions: We suggest two explanations for this faster than expected HbA1c decrease: 1) patients with HbA1c>6,0% will progress to DM later, and, therefore, a longer follow-up is needed; 2) SARS-CoV-2 virus has extensively glycosylated spike(S)-protein that may bind to erythrocytes. High-pressure liquid chromatography (the standard method for HbA1c) probably fails to separate the glycated 1-β-chain of hemoglobin from glycated viral spikes. In this case, abnormally high HbA1c in COVID-19 patients with no DM-history may serve as a marker of severe viral erythrocyte damage rather than a marker for the glucose control. This hypothesis is confirmed by the prompt (in 6 weeks) normalization of HbA1c level following the virus elimination. Disclosure M. V. Shestakova: None. I. Kononenko: None. Z. Kalmykova: None. A. Zheleznyakova: None. N. Mokrysheva: None. Funding Ministry of Science and Higher Education of the Russian Federation (075-15-2020-899)

СБОРНИК ТЕЗИСОВКонференция по лечению и диагностике сахарного диабета «

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Type 2 diabetes mellitus (T2DM) is a multifactorial metabolic disease, the development of which is mediated by both genetic disorders and various intracellular and extracellular molecular processes. One of the main pathogenetic mechanisms for the development of T2DM is a progressive decrease in the mass and functional reserve of β-cells, which largely determines the course of T2DM. The mechanisms of action of most sugar-lowering drugs are associated with increased secretion of insulin, so it is obvious that the effectiveness of the therapy will also largely depend on the functional state of β-cells. All this explains the great interest in studying the mechanisms of damage of β-cells in T2DM and factors that can accelerate this process, leading to their death and the development of a relative and then absolute insulin deficiency. The mechanisms of dysfunction β-cells in T2DM have not been studied much. This article provides an overview of the data of domestic and foreign literature of recent years on the molecular, intracellular features of various mechanisms of damage and death of β-cells in type 2 diabetes. The results of studies aimed at studying the possible factors and processes leading to their launch are presented.

BACKGROUND: Less than a year has passed since the start of the new coronavirus infection COVID-19 pandemic caused by SARS-CoV-2. First published research results demonstrate a frequent increase in glycemia in patients without previously diagnosed carbohydrate metabolism disorders. A possible relationship between the carbohydrate metabolism state and the course of COVID-19 is considered.AIM: To identify the incidence of known and newly diagnosed diabetes mellitus (DM) in hospitalized patients with COVID-19 and evaluate the relationship between glycated hemoglobin (HbA1c), inflammation markers and infectious disease severity.METHODS: A single-center, cross-sectional, retrospective study included 155 patients with confirmed COVID-19 and bi- lateral polysegmental viral pneumonia hospitalized in the Endocrinology Research Centre, Russian Federation. Diagnosis of carbohydrate metabolism disorders was based on the HbA1c level, blood glucose level at admission (BGA) and fasting plasma glucose (FPG). Patients were divided into 2 groups: without the previously diagnosed DM (n=129, 83.3%) and with known history of DM (n=26, 16,7%). Patients without previously diagnosed DM were divided into subgroups according to HbA1c levels: ≤6,0% (Group A), >6,0% HbA1c, <6.5% (Group B), ≥6,5% (Group C). Additionally, insulin, interleukin 6 (IL-6) and D-dimer levels were measured in all patients. Blood oxygen saturation (SpO2) was measured by pulsoximetry, computerized tomography of lungs with calculation of lung parenchyma damage percentage.RESULTS: Type 2 DM was previously established in 16.7% of all included patients. Among patients without DM history, DM was revealed in 8 patients (5.2%), based on HbA1c, FPG and BGA. In 66 patients (42.6%) we observed no changes in carbohydrate metabolism. In 55 patients, the interpretation of carbohydrate metabolism state was difficult due to inconsistency of HbA1c level with FPG and BGA: in particular, the level of HbA1c ≥ 6.5% (which corresponds to the diagnostic threshold of the DM) was detected in 19 patients (12,2%) with normal FPG and BGA. No true stress hyperglycemia on admission and according to FPG was reported. Despite the presence of confirmed DM, HbA1c levels positively correlated with inflammatory markers (erythro- cyte sedimentation rate, C-reactive protein, IL-6) and SpO2. Patients with a HbA1c ≥6.5% without DM history had the most severe course of the disease: longest duration of hospitalization, largest damage of the pulmonary tissue, and high lethality.CONCLUSION: The incidence of DM among patients hospitalized with COVID-19 was 21.9% (16.7% had previous diagnosis of DM, 5.2% — newly diagnosed), which is 1.5 times higher than in general population in a comparable age category. It is difficult to assess the carbohydrate metabolism disorders in patients in acute infectious period. An increased level of HbA1c (≥6.5%), first detected in the acute period of infection, in combination with normal FPG and BGA parameters, cannot be a diagnostic criterion and requires dynamic monitoring. HbA1c level can be considered as a predictive factor of COVID-19 severity, independent of DM.

Progressive decrease in the weight and functional reserve of -cells is one of the main pathogenetic mechanisms of development of type 2 diabetes mellitus (DM2). The rate of progression of these processes is strictly individual, which largely determines the course of DM2 and the effectiveness of the therapy. As a rule, apoptosis and necrosis are the main mechanisms of -cell damage and death in CD2. At the same time, recent studies allow us to consider the destruction and death of -cells as the outcome of other types of programmed cell death (PCG), the role of innate immunity in the Genesis of CD2 ISactively discussed. This article provides an overview of the data of domestic and foreign literature of recent years regarding the molecular, intracellular characteristics of different types of -cell PCG in CD2. The results of studies aimed at studying the possible factors and processes leading to their launch are presented.

BACKGROUND : Less than a year has passed since the start of the new coronavirus infection COVID-19 pandemic caused by SARS-CoV-2. First published research results demonstrate a frequent increase in glycemia in patients without previously diagnosed carbohydrate metabolism disorders. A possible relationship between the carbohydrate metabolism state and the course of COVID-19 is considered. AIM : To identify the incidence of known and newly diagnosed diabetes mellitus (DM) in hospitalized patients with COVID-19 and evaluate the relationship between glycated hemoglobin (HbA 1c ), inflammation markers and infectious disease severity. METHODS : A single-center, cross-sectional, retrospective study included 155 patients with confirmed COVID-19 and bi- lateral polysegmental viral pneumonia hospitalized in the Endocrinology Research Centre, Russian Federation. Diagnosis of carbohydrate metabolism disorders was based on the HbA 1c level, blood glucose level at admission (BGA) and fasting plasma glucose (FPG). Patients were divided into 2 groups: without the previously diagnosed DM (n=129, 83.3%) and with known history of DM (n=26, 16,7%). Patients without previously diagnosed DM were divided into subgroups according to HbA 1c levels: ≤6,0% (Group A), >6,0% HbA 1c , <6.5% (Group B), ≥6,5% (Group C). Additionally, insulin, interleukin 6 (IL-6) and D-dimer levels were measured in all patients. Blood oxygen saturation (SpO 2 ) was measured by pulsoximetry, computerized tomography of lungs with calculation of lung parenchyma damage percentage. RESULTS : Type 2 DM was previously established in 16.7% of all included patients. Among patients without DM history, DM was revealed in 8 patients (5.2%), based on HbA 1c , FPG and BGA. In 66 patients (42.6%) we observed no changes in carbohydrate metabolism. In 55 patients, the interpretation of carbohydrate metabolism state was difficult due to inconsistency of HbA 1c level with FPG and BGA: in particular, the level of HbA 1c ≥ 6.5% (which corresponds to the diagnostic threshold of the DM) was detected in 19 patients (12,2%) with normal FPG and BGA. No true stress hyperglycemia on admission and according to FPG was reported. Despite the presence of confirmed DM, HbA 1c levels positively correlated with inflammatory markers (erythro- cyte sedimentation rate, C-reactive protein, IL-6) and SpO 2 . Patients with a HbA 1c ≥6.5% without DM history had the most severe course of the disease: longest duration of hospitalization, largest damage of the pulmonary tissue, and high lethality. CONCLUSION : The incidence of DM among patients hospitalized with COVID-19 was 21.9% (16.7% had previous diagnosis of DM, 5.2% — newly diagnosed), which is 1.5 times higher than in general population in a comparable age category. It is difficult to assess the carbohydrate metabolism disorders in patients in acute infectious period. An increased level of HbA 1c (≥6.5%), first detected in the acute period of infection, in combination with normal FPG and BGA parameters, cannot be a diagnostic criterion and requires dynamic monitoring. HbA 1c level can be considered as a predictive factor of COVID-19 severity, independent of DM.

Diabetes mellitus (DM) and chronic liver disease (CLD) are pathological conditions associated with each other and reaching epidemic proportions. There is a strong pathogenetic relationship of carbohydrate metabolism disorders and a number of CLD. Common mechanisms that provoke metabolic and autoimmune disorders in the development of various CLD, leading to steatosis, insulin resistance (IR), impaired glucose tolerance and the development of DM are described. Effective glycemic control can have a beneficial effect on the treatment of these patients, and, conversely, there is evidence of a positive effect of CLD therapy on carbohydrate metabolism. This review discusses the correction of carbohydrate metabolism in patients with CLD, the main groups of modern hypoglycemic drugs, mechanisms of their action, the impact on the physiology of the liver, the possibility of using each of these pharmacological groups in patients with impaired liver function. The modern approaches and possibilities of drug effects on the process of fibrogenesis in CLD, the effect of these drugs on carbohydrate metabolism are listed.

In recent years there has been an active discussion about the relationship between diabetes mellitus (DM) and chronic liver diseases (CLD). On the one hand, patients with diabetes have an increased risk of developing CLD. On the other hand, patients with CLD very often identify abnormal glucose metabolism which ultimately leads to impaired glucose tolerance and the development of diabetes. This review outlines potential causal relationships between some CLD and DM. Common mechanisms that provoke metabolic and autoimmune disorders in the development of various nosologies of the CKD group, leading to steatosis, insulin resistance, impaired glucose tolerance and the development of diabetes are described. Certain features of the assessment of carbohydrate metabolism compensation in patients with hepatic dysfunction, anemia and protein metabolism disorders are described.

Сахарный диабет и хронические заболевания печени. Обзор литературы (часть 2): особенности лечения Сахарный диабет (СД) и хронические заболевания печени (ХЗП) - патологические состояния, ассоциированные друг с другом и достигающие масштабов эпидемии. Существует сильная патогенетическая взаимосвязь нарушений углеводного обмена и ряда ХЗП. Описаны единые механизмы, провоцирующие метаболические и аутоиммунные нарушения при развитии различных ХЗП, приводящие к стеатозу, инсулинорезистентности (ИР), нарушению толерантности к глюкозе и развитию СД. Эффективный контроль гликемии может оказать благоприятное влияние на лечение этих пациентов, и наоборот - имеются данные о положительном влиянии терапии ХЗП на углеводный обмен. Рассматриваются вопросы коррекции углеводного обмена у пациентов с ХЗП, приведены основные группы современных сахароснижающих препаратов, механизмы их действия, влияние на физиологию печени, возможности использования каждой из этих фармакологических групп у пациентов с нарушенной функцией печени. Перечислены современные подходы и возможности медикаментозного воздействия на процесс фиброгенеза при ХЗП, влияние этих препаратов на углеводный обмен.

Hyperprolactinemia (HP) is one of the most common neuroendocrine disorders. In 60% of cases, pathological HP is caused by pituitary prolactin-secreting adenoma. Therapy with agonists of dopamine type 2 receptors (D2 receptor agonists) is a method of choice for the treatment of pathological HP which allows to achieve prolactin normalization and reduction of pituitary adenoma in most cases. However, 15-20% of patients are resistant to D2 receptor agonists, and the question of overcoming this resistance is highly relevant. Different approaches are considered to solve this problem, one - is to increase the dose of D2 receptor agonists up to the maximally tolerated. In this article, we present a clinical observation of a patient with a partial resistance to D2 receptor agonists who demonstrated a good response to treatment with high doses of cabergoline.