The article is devoted to the conservative treatment of hyperprolactinemia of tumor origin. Cabergoline is considered as an effective treatment not only for microadenomas but also for large pituitary tumors which is illustrated by the clinical case of the patient P. The most important effects of cabergoline demonstrated in this clinical case are reduction in the size of the adenoma from macro to micro, reverse development of chiasmal syndrome with restoration of visual functions, achievement and maintenance of the target level of prolactin. Besides the article focused on the possible development of primary and secondary resistance to dopamine analogues. One of such difficult clinical scenario is illustrated by clinical case of patient M., who was treated with different dopamine analogues with the development of secondary dopamine resistance. Along with described in literature possible mechanisms for its development in our patient we also suggest the role of prolonged inadequate therapy with dopamine agonists, when the dose of the drug was not properly adjusted, despite not reaching the target prolactin level. The literature considers several ways of optimization of treatment in resistant patients but despite of this fact it remains one of unresolved problems in the management of patients with hyperprolactinemia.

* Автори гарантують повну відповідальність за все, що опубліковано в статті. Автори гарантують відсутність конфлікту інтересів і власної фінансової зацікавленості при виконанні роботи та написанні статті. Рукопис надійшов до редакції 5.08.2019.

Автор гарантує повну відповідальність за все, що опубліковано в статті. Автор гарантує відсутність конфлікту інтересів і власної фінансової зацікавленості при виконанні роботи та написанні статті. Рукопис надійшов до редакції 8.01.2019.

The article is dedicated to the problems of differentiated diagnostics of conditions, which are accompanied by the development of hypoglycemia. In clinical practice hypoglycemic syndrome usually associated with diabetes mellitus and considered as consequences of hypoglycemic treatment but causes of this conditions can be different. In the review possible causes of low blood sugar of endocrine and non-endocrine genesis are discussed, their pathogenetic mechanisms are explained.It is emphasized that often hypoglycemic states remain undiagnosed on the background of existing severe somatic pathology, while they can be the cause of deterioration, coma, and sometimes even death of the patient. Among the causes of hypoglycemic states of non-endocrine origin, malignant tumors occupy a special place, as illustrated by the clinical case from personal experience presented in the article.Analyzing this medical history, it should be noted that not always the diagnosis, which seemed obvious at first, is confirmed after a thorough examination of the patient. In addition, the genesis of hypoglycemic seizures often cannot be established as quickly as in our clinical case, especially in oncologic pathology. It may be due to the small size of the malignancy, difficult availability of the tumor for imaging by instrumental methods and other factors. Numerous diagnostic algorithms for determining the cause of hypoglycemic states have been described in the literature, but each of the following algorithms only complements the previous one, taking into account the results of new clinical trials. The article emphasizes that strict adherence to modern guidelines for the management of patients with hypoglycemia will not only promote the timely establishment of the etiological factor of this condition and adequate treatment of the underlying disease, but also improve the quality and sometimes save the patient’s life.

It were examined 262 patients, among which there were 121 patients with low-progressive autoimmune diabetes of adults (LADA), 60 patients with type 1 diabetes mellitus (DM) and 81 patients with diagnosed type 2 DM. It was performed comparative analysis of C-peptide level and indicators of insulin resistance (IR) in patients in the monitoring groups. It was installed the authentic reduction of C-peptide level in the blood of LADA patients and type 1 DM patients compared with type 2 DM patients. It wasn’t established in the absence of significant differences on this index between LADA patients and type 1 DM patients, despite on a significant reduction in C-peptide in patients LADA compared with controls, significant differences in this case. According to the results of calculating several coefficients, that are recommended for the determination of IR, it was confirmed the presence of this state in patients LADA. At the same time indicators of IR in LADA patients were significantly lower than in type 2 DM patients. These data indicate that the disorders of carbohydrate metabolism in LADA patients are caused by the decrease in the insulin secretion in pancreas β-cells, and also by the presence of IR.

The aim: To establish diagnostic markers of LADA at the stage of manifestation based on the analysis of clinical and anamnestic data, the results of immunological examination of patients with different types of DM. Materials and methods: Study included 121 patients with LADA (1st (main) group), 60 patients with type 1 DM (2nd group), 81 patients with type 2 DM (3d group). The examination included analysis of complaints, medical history, determination of anthropometric data, studies of the level of antibodies to glutamic acid decarboxylase (GAD ab), cytoplasmic antigen (ICA ab), tyrosine phosphatase (IA-2 ab). Results: Criteria of LADA diagnosis included slow nature of DM course, the average age of the disease onset (45,02±9,96) years, combination of diabetic complaints with gradual weight loss, frequent detection of DM (64,46%) on request, fairly high level of glycemia at diagnosis ((14,12±4,57) mmol/l)), the possibility of ketonuria episodes in a certain amount (23,14%) of cases in the absence of acute ketoacidotic states. The presence of excess body weight and even obesity is not a criterion for excluding LADA. Conclusions: To verify the diagnosis of LADA it is necessary to study of at least two types of antibodies. The most conclusive is the determination of GAD ab and IA-2 ab.

Introduction. Among medical and social problems, obesity (Ob) occupies one of the leading places. This is related to the established pathogenetic connection of Ob with type 2 diabetes mellitus, arterial hypertension, acute vascular events, dementia, osteoarthritis, obstructive sleep apnea and some forms of cancer. Ob is also associated with social problems and reduced work capacity. Despite numerous studies on the study of Ob, a number of unresolved issues and controversial points of view remain. The aim – is to analyze the currently existing data on the heterogeneity of Ob and the main pathogenetic factors of its development based on the study of literary sources, mainly for a period of 10 years. Materials and methods – an electronic search was carried out in MEDLINE/PubMed, Google Scholar and Web of Science databases using the keywords "obesity", "obesity heterogeneity", "obesity etiopathogenesis" with subsequent analysis of literature sources published mainly in the last 10 years. The results. To date, there is no single universally accepted classification of Ob, and those currently used in clinical practice and during scientific research are based on one or another criterion. Such criteria include etiopathogenetic factors, type of adipose tissue deposition, degree of weight gain, etc. The use of bioimpedancemetry became the basis for the assertion about the heterogeneity of Ob with the selection of its separate forms, namely: metabolically healthy Ob; metabolic Ob with normal body weight, sarcopenic and metabolically unhealthy Ob. Despite the lack of clear diagnostic criteria for each of these forms, their differences in clinical course, pathogenetic factors of development and degree of cardiovascular risk have been established. Considering the indicated heterogeneity, the selection of the leading etiological factor of Ob remains a rather controversial and difficult issue. The exceptions, obviously, should include cases of the secondary form of this pathology, when Ob is one of the symptoms and is pathogenetically related to the underlying disease. In general, it is believed that, being hereditary, Ob is the result of the interaction between genetic, hormonal-metabolic, behavioral and environmental factors. Conclusions. Ob is a chronic multifactorial and heterogeneous disease, the individual clinical forms of which differ in the course and level of metabolic disorders. Etiopathogenetic factors of the development and progression of Ob are multifactorial and include genetic predisposition, factors of the external and internal environment, eating behavior and hormonal and metabolic shifts. According to the data obtained today regarding the heterogeneity of Ob and the pathogenetic mechanisms of its development, a new generally accepted characteristic and classification of this pathology should be accepted.

* Автори гарантують повну відповідальність за все, що опубліковано в статті. Автори гарантують відсутність конфлікту інтересів і власної фінансової зацікавленості при виконанні роботи та написанні статті. Рукопис надійшов до редакції 29.08.2018.