Olga S. Derevyanko
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Olga S. Derevyanko has a total of 20 co-authors. Here are the top co-authors by number of shared publications:
- Tatiana Vasil'Evna Nikonova
Endocrinology Research Centre
5 shared publications - Magomedkerim R. Ragimov
Endocrinology Research Centre
4 shared publications - Liudmila I. Ibragimova
Endocrinology Research Centre
3 shared publications - Natalia M. Malysheva
Endocrinology Research Centre
2 shared publications - Agunda V. Dzagaxova
Endocrinology Research Centre
1 shared publication - Aleksandr L. Tikhomirov
Russian University of Medicine, Ministry of Health of the Russian Federation
1 shared publication
Latest Publications
- Open Access
- 10 September 2025
- Published by IRBIS in Obstetrics, Gynecology and Reproduction
- Vol. 19 (4) , 561-573
The importance of iron deficiency and folic acid deficiency prevention upon pregnancy planning
Information published over the last decade on using iron supplements has been collected and systematized. The need for long-term iron supplementation and patient compliance has been updated and emphasized. The main requirements for current iron supplements today have been formulated, and the advantages of combining organic iron salts with folic acid as the most optimal and contemporary approach to the prevention and treatment of iron deficiency during pregnancy have been emphasized.
- 10 September 2025
- Published by IRBIS in Obstetrics, Gynecology and Reproduction
- Vol. 19 (4) , 561-573
Open AccessThe importance of iron deficiency and folic acid deficiency prevention upon pregnancy planning
Information published over the last decade on using iron supplements has been collected and systematized. The need for long-term iron supplementation and patient compliance has been updated and emphasized. The main requirements for current iron supplements today have been formulated, and the advantages of combining organic iron salts with folic acid as the most optimal and contemporary approach to the prevention and treatment of iron deficiency during pregnancy have been emphasized.
- Open Access
- 8 February 2023
- Published by Endocrinology Research Centre in Diabetes mellitus
- Vol. 26 (1) , 93-97
A clinical case of exocrine pancreatic insufficiency in a patient with type 1 diabetes mellitus
The pancreas belongs to the glands of mixed secretion and simultaneously performs both endo- and exocrine functions. Exocrine pancreatic insufficiency (EPI) is the general name for the malabsorption process caused by inadequate production and decreased activation of the enzymes of the pancreas acinar cells, such as amylase, lipase and protease, which are necessary for digestion. The prevalence of EPI in patients with type 1 diabetes, according to many authors, varies from 25 to 59%, which is determine by the data of pancreatic elastase-1. In this work, we present a clinical case of confirmed exocrine pancreatic insufficiency in a patient with a 6-year history of type 1 diabetes, which became the main cause of the development of episodes of hypoglycemia after meals. In the course of further studies, antibodies to lactoferrin and a reduced prostate volume, determined by MRI data, high levels of antibodies to glutamate decarboxylase and zinc co-transporter 8, as well as residual insulin secretion based on the level of C-peptide on an empty stomach detected.
- 8 February 2023
- Published by Endocrinology Research Centre in Diabetes mellitus
- Vol. 26 (1) , 93-97
Open AccessA clinical case of exocrine pancreatic insufficiency in a patient with type 1 diabetes mellitus
The pancreas belongs to the glands of mixed secretion and simultaneously performs both endo- and exocrine functions. Exocrine pancreatic insufficiency (EPI) is the general name for the malabsorption process caused by inadequate production and decreased activation of the enzymes of the pancreas acinar cells, such as amylase, lipase and protease, which are necessary for digestion. The prevalence of EPI in patients with type 1 diabetes, according to many authors, varies from 25 to 59%, which is determine by the data of pancreatic elastase-1. In this work, we present a clinical case of confirmed exocrine pancreatic insufficiency in a patient with a 6-year history of type 1 diabetes, which became the main cause of the development of episodes of hypoglycemia after meals. In the course of further studies, antibodies to lactoferrin and a reduced prostate volume, determined by MRI data, high levels of antibodies to glutamate decarboxylase and zinc co-transporter 8, as well as residual insulin secretion based on the level of C-peptide on an empty stomach detected.
- Open Access
- 19 October 2021
- Published by Endocrinology Research Centre in Diabetes mellitus
- Vol. 24 (5) , 433-439
Long-term β-cells autoimmune destruction markers persistence and residual C-peptide secretion in type 1 diabetes mellitus
Backgraund: It believed that autoimmune process maintained only during the first 5 years of diabetes mellitus type 1 (T1D). Recently scientists discovered the high levels of islet autoantibodies (Ab) in long-standing T1D and some of these patients had residual insulin secretion, determined by the level of C-peptide. According to various sources, the prevalence of such observations ranges from 12 to 48%.Aims: The aim of our study was to assess the duration of autoimmune β-cells destruction markers persistence and residual fasting C-peptide secretion in the long-standing T1D, as well as to determine the possible causes and patterns of these processes.Materials and methods: In the study included 237 patients (91 men, 146 women) with T1D. Patients divided in 4 groups, according to disease duration: а — up to 1 year, n=69 (29%); b — 1–5 years, 52 (22%); c — 5–10 years, 57 (24%); d — more than 10 years, 59 (25%). Ab to glutamic acid decarboxylase (GADA), tyrosine phosphatase-like IA-2 (IA2) and zinc T8 (ZnT8A) were detected by Enzyme Immunoassay. Also detected C-peptide levels and retrospectively HbA1с.Results: Antibodies to antigens of β-cell components were detected in 26 (37%) patients in group A, in 17 patients (33%) in group B, in 15 (29%) in group C and in 14 (23%) — G.In the control group (n = 19), an increased level of antibodies was not revealed. Fasting C-peptide levels were as follows: in group «A» — 0.86 ng / ml [0.53; 1.4], «B» — 0.65 ng / ml [0.27; 0.98], « B «- 0.19 ng / ml [0.17; 0.33],» D «- 0.01 ng / ml [0.01; 0.01]. However, in 13 (22%) patients in group D, fasting C-peptide levels were more than 0.09 ng / ml.Conclusion: The data obtained indicate a long-term persistence of markers of the autoimmune process in patients with T1DM. In groups with a long (more than 5 years) course of T1DM, levels of fasting C-peptide more than 30 pmol/L (0.09 ng / ml or 0.03 nmol / L) were noted in 39 (33.6%) cases.
- 19 October 2021
- Published by Endocrinology Research Centre in Diabetes mellitus
- Vol. 24 (5) , 433-439
Open AccessLong-term β-cells autoimmune destruction markers persistence and residual C-peptide secretion in type 1 diabetes mellitus
Backgraund: It believed that autoimmune process maintained only during the first 5 years of diabetes mellitus type 1 (T1D). Recently scientists discovered the high levels of islet autoantibodies (Ab) in long-standing T1D and some of these patients had residual insulin secretion, determined by the level of C-peptide. According to various sources, the prevalence of such observations ranges from 12 to 48%.Aims: The aim of our study was to assess the duration of autoimmune β-cells destruction markers persistence and residual fasting C-peptide secretion in the long-standing T1D, as well as to determine the possible causes and patterns of these processes.Materials and methods: In the study included 237 patients (91 men, 146 women) with T1D. Patients divided in 4 groups, according to disease duration: а — up to 1 year, n=69 (29%); b — 1–5 years, 52 (22%); c — 5–10 years, 57 (24%); d — more than 10 years, 59 (25%). Ab to glutamic acid decarboxylase (GADA), tyrosine phosphatase-like IA-2 (IA2) and zinc T8 (ZnT8A) were detected by Enzyme Immunoassay. Also detected C-peptide levels and retrospectively HbA1с.Results: Antibodies to antigens of β-cell components were detected in 26 (37%) patients in group A, in 17 patients (33%) in group B, in 15 (29%) in group C and in 14 (23%) — G.In the control group (n = 19), an increased level of antibodies was not revealed. Fasting C-peptide levels were as follows: in group «A» — 0.86 ng / ml [0.53; 1.4], «B» — 0.65 ng / ml [0.27; 0.98], « B «- 0.19 ng / ml [0.17; 0.33],» D «- 0.01 ng / ml [0.01; 0.01]. However, in 13 (22%) patients in group D, fasting C-peptide levels were more than 0.09 ng / ml.Conclusion: The data obtained indicate a long-term persistence of markers of the autoimmune process in patients with T1DM. In groups with a long (more than 5 years) course of T1DM, levels of fasting C-peptide more than 30 pmol/L (0.09 ng / ml or 0.03 nmol / L) were noted in 39 (33.6%) cases.
- Open Access
- 14 February 2021
- Published by Endocrinology Research Centre in Diabetes mellitus
- Vol. 24 (1) , 70-73
Slowly evolving, immune-mediated diabetes in 14-year-old patient: a case report
Slowly developing immune-mediated diabetes, often called latent autoimmune diabetes in adults, is characterized by the presence of autoantibodies (ATs) to glutamic acid decarboxylase (GADA), the patient's age at the onset over 35 years, and the absence of the need for insulin therapy for 6-12 months to 6 years from the moment of diagnosis, according to the WHO classification of 2019, refers to hybrid forms of diabetes mellitus (DM). In this article, we present a case history of slowly developing immune-mediated diabetes in a 14-year-old boy who was transferred from metformin monotherapy and a diet with restriction of digestible carbohydrates to the intensified insulin therapy only 4 years after the onset of diabetes mellitus with a glycated hemoglobin (HbA1c) level of less than 6.5% throughout the disease. As a result of the studies, the patient was found to have a homozygous genotype highly predisposing to the development of Type 1 Diabetes Mellitus (T1DM), as well as increased levels of ATs to GADA and tyrosine phosphatase (IA-2A). The initially preserved level of basal C-peptide and the clinical course of the disease in this patient do not allow us to classify this case as a classic variant of the course of Type 1 Diabetes Mellitus.
- 14 February 2021
- Published by Endocrinology Research Centre in Diabetes mellitus
- Vol. 24 (1) , 70-73
Open AccessSlowly evolving, immune-mediated diabetes in 14-year-old patient: a case report
Slowly developing immune-mediated diabetes, often called latent autoimmune diabetes in adults, is characterized by the presence of autoantibodies (ATs) to glutamic acid decarboxylase (GADA), the patient's age at the onset over 35 years, and the absence of the need for insulin therapy for 6-12 months to 6 years from the moment of diagnosis, according to the WHO classification of 2019, refers to hybrid forms of diabetes mellitus (DM). In this article, we present a case history of slowly developing immune-mediated diabetes in a 14-year-old boy who was transferred from metformin monotherapy and a diet with restriction of digestible carbohydrates to the intensified insulin therapy only 4 years after the onset of diabetes mellitus with a glycated hemoglobin (HbA1c) level of less than 6.5% throughout the disease. As a result of the studies, the patient was found to have a homozygous genotype highly predisposing to the development of Type 1 Diabetes Mellitus (T1DM), as well as increased levels of ATs to GADA and tyrosine phosphatase (IA-2A). The initially preserved level of basal C-peptide and the clinical course of the disease in this patient do not allow us to classify this case as a classic variant of the course of Type 1 Diabetes Mellitus.
- Open Access
- 14 February 2021
- Published by Endocrinology Research Centre in Diabetes mellitus
- Vol. 24 (1) , 62-69
The role of the gut microbiota in the development of type 1 diabetes mellitus
At the beginning of the XXI century, with the advent of technical capabilities and new methods of genes sequencing, the attention of researchers to the study of the human metagenome has significantly increased. The interaction between changes in the qualitative and quantitative composition of the gut microbiota (GM) and various diseases is being actively studied, a search for specific metabolites and genes of microorganisms that may be associated with the development, in particular, of immune-mediated diseases is underway. In recent years, a lot of new data have been published on the possible contribution of gut flora dysbiosis to the development of Type 1 Diabetes Mellitus (T1DM), while the first assumptions were put forward as far back as 1970s. The search for pathogenetic mechanisms of GM influence on the development and progression of T1DM is becoming an increasingly relevant objective, since in recent years the incidence of T1DM is rapidly increasing, which is a serious health problem throughout the world.This review discusses the current ideas about the role of GM in the immunopathogenesis of T1DM, new data on the near-term prospects in the study of the human macrogenome, current ideas about the role of GM in the immunopathogenesis of T1DM, and the possibility of applying this knowledge by the practitioner.
- 14 February 2021
- Published by Endocrinology Research Centre in Diabetes mellitus
- Vol. 24 (1) , 62-69
Open AccessThe role of the gut microbiota in the development of type 1 diabetes mellitus
At the beginning of the XXI century, with the advent of technical capabilities and new methods of genes sequencing, the attention of researchers to the study of the human metagenome has significantly increased. The interaction between changes in the qualitative and quantitative composition of the gut microbiota (GM) and various diseases is being actively studied, a search for specific metabolites and genes of microorganisms that may be associated with the development, in particular, of immune-mediated diseases is underway. In recent years, a lot of new data have been published on the possible contribution of gut flora dysbiosis to the development of Type 1 Diabetes Mellitus (T1DM), while the first assumptions were put forward as far back as 1970s. The search for pathogenetic mechanisms of GM influence on the development and progression of T1DM is becoming an increasingly relevant objective, since in recent years the incidence of T1DM is rapidly increasing, which is a serious health problem throughout the world.This review discusses the current ideas about the role of GM in the immunopathogenesis of T1DM, new data on the near-term prospects in the study of the human macrogenome, current ideas about the role of GM in the immunopathogenesis of T1DM, and the possibility of applying this knowledge by the practitioner.
- Open Access
- 29 November 2018
- Published by Endocrinology Research Centre in Diabetes mellitus
- Vol. 21 (5) , 404-408
Autoimmune gastritis: comorbid pathology in type 1 diabetes
In recent years noted an increased number of patients with autoimmune diseases (AID), and the special attention deserves combination of several autoimmune pathologies collected in one patient, because such patients requires special tactics of management. Autoimmune diseases of the gastrointestinal tract are less researched and, nevertheless, prognostically unfavorable. Autoimmune gastritis (AIG) has a special place in other stomach diseases, which develops in the aggregate with type 1 diabetes. AIG is a chronic inflammation of the mucous membrane of the body of the stomach, leading to the appearance of atrophy and hypoxecretion. AIG is found in 510% of individuals in general population, with a higher incidence of AIG in patients with diabetes and other established autoimmune pathology. AIG is asymptomatic at the early stage of the disease and clinical manifestations appear after the atrophic changes in the mucous membrane of the stomach develop. Since autoimmune gastritis does not have pathognomonic signs, it can manifest itself in hematological and oncological complications at later stages. This is why screening, early diagnosis, prevention and treatment are very important. Early diagnosis and prevention of AIG and its complications play the main role. This article provides an overview of the worldwide data dedicated to this issue.
- 29 November 2018
- Published by Endocrinology Research Centre in Diabetes mellitus
- Vol. 21 (5) , 404-408
Open AccessAutoimmune gastritis: comorbid pathology in type 1 diabetes
In recent years noted an increased number of patients with autoimmune diseases (AID), and the special attention deserves combination of several autoimmune pathologies collected in one patient, because such patients requires special tactics of management. Autoimmune diseases of the gastrointestinal tract are less researched and, nevertheless, prognostically unfavorable. Autoimmune gastritis (AIG) has a special place in other stomach diseases, which develops in the aggregate with type 1 diabetes. AIG is a chronic inflammation of the mucous membrane of the body of the stomach, leading to the appearance of atrophy and hypoxecretion. AIG is found in 510% of individuals in general population, with a higher incidence of AIG in patients with diabetes and other established autoimmune pathology. AIG is asymptomatic at the early stage of the disease and clinical manifestations appear after the atrophic changes in the mucous membrane of the stomach develop. Since autoimmune gastritis does not have pathognomonic signs, it can manifest itself in hematological and oncological complications at later stages. This is why screening, early diagnosis, prevention and treatment are very important. Early diagnosis and prevention of AIG and its complications play the main role. This article provides an overview of the worldwide data dedicated to this issue.