The research was carried out as part of investigation work at the SI «V. Danilevsky Institute for Endocrine Pathology Problems of NAMS of Ukraine» «Development of the methodology for the screening of hormonal-active pitui tary tumors, taking into account their clinical and genetic features» (State registration number: 0117U007186).

Сравнительная оценка некоторых показателей углеводного обмена у больных с гормонально-активными аденомами гипофизаМикитюк М.Р., Хижняк О.О., Сулима Т.Н. Диагностика, контроль и лечение Сахарный диабет. 2014;(1):70-74 ГУ

Гіперурикемія, подагра, артеріальна гіпертензія (АГ) і метаболічний синдром (МС)-дуже поширені патологічні стани, що можуть поєднуватися в одного хворого. Результати досліджень дають все більше доказів, що порушення балансу сечової кислоти (СК) є важливим етіологічним фактором такої актуальної для сьогодення патології, як серцево-судинні захворювання (ССЗ), хронічна хвороба нирок, цукровий діабет 2-го типу, дисфункція щитоподібної залози, псоріаз тощо. Доведено, що гіперурикемія і подагра асоційовані з кардіоваску

The review contains updated information on the epidemiology, etiology, pathogenesis, diagnosis, treatment and prevention of non-alcoholic fatty liver disease (NAFLD). We searched for terms including NAFLD, non-alcoholic steatohepatitis (NASH), metabolic syndrome and type 2 diabetes mellitus in literature published over the past 5 years using the Scopus, Web of Science, CyberLeninka, PubMed databases. The concept of NAFLD includes two morphological forms of the disease with different prognosis: non-alcoholic fatty hepatosis and NASH. The severity of NASH is quite variable, including fibrosis, cirrhosis and hepatocellular carcinoma. NAFLD, a spectrum of fatty liver disorders of viral, autoimmune, drug-induced, and genetic origin, which are not caused by alcohol abuse, has recently been renamed as metabolic (dysfunction) associated fatty liver disease (MAFLD). The average prevalence of NAFLD is approximately 25 % among the adult population worldwide, and in some regions exceeds 30 %. An increase in the prevalence of this pathology is in parallel with the global epidemic of obesity and type 2 diabetes mellitus in the world. It is time to reach a general consensus in the scientific community on changing the nomenclature and moving from a negative to a positive definition of NAFLD/NASH. The new nomenclature points to the “positive” determinants of the disease, namely the close relationship with metabolic disorders, instead of defining it as what it is not (ie. non-alcoholic). The MAFLD abbreviation more accurately discloses existing knowledge about fatty liver diseases associated with metabolic dysfunction and should replace NAFLD/NASH, as this will stimulate the research community’s efforts to update the disease nomenclature and subphenotype and accelerate the transition to new treatments. It is important that primary care physicians, endocrinologists, and other specialists are aware of the extent and long-term consequences of NAFLD. Early identification of patients with NASH can help improve treatment outcomes, avoid liver transplantation in patients with decompensated cirrhosis. There are currently no effective treatments for NAFLD, so it is important to follow a multidisciplinary approach, which means using measures to improve prognosis, reduce the risk of death associated with NAFLD, the development of cirrhosis or hepatocellular carcinoma. Epidemiological data suggest a close relationship between unhealthy lifestyles and NAFLD, so lifestyle adjustments are needed to all patients. Insulin sensitizers, statins, ezetimibe, a cholesterol absorption inhibitor, hepatoprotectors, antioxidants, incretin analogues, dipeptidyl peptidase 4 inhibitors, pentoxifylline, probiotics, angiotensin-converting enzyme inhibitors, and endocannabinoid antagonists are used in the treatment of NAFLD.

* Роботу виконано в межах планової наукової тематики ДУ «Інститут проблем ендокринної патології ім. В. Я. Данилевського НАМН України» «Дослідження внеску порушень пуринового обміну у розвиток та прогресування цукрового діабету» (державний реєстраційний № 0116U007261). Установою, що фінансує дослідження, є НАМН України. 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 9.08.2019.

Pituitary gigantism is an extremely rare disorder: the incidence of pituitary tumors in children is approximately 0.1 in one million, and only about 1 to 10% of the pituitary tumors secrete the GH in childhood. Gigantism should be suspected if the patient's height is 3 standard deviations above the normal average height or 2 standard deviations above the corrected height of parents. When pituitary gigantism is suspected, the clinician should consider the presence of disorders, known to be associated with the GH-secreting pituitary tumors, including the McCune Albright syndrome (MAS), Carney complex (CNC), multiple endocrine neoplasia, types 1 and 4 (MEN 1, MEN 4), Familial isolated pituitary adenoma (FIPA), the paraganglioma, pheochromocytoma and pituitary adenoma association (PAA) due to succinate dehydrogenase defects, and X-linked acrogigantism (X-LAG). The molecular genetics of the AIP-associated FIPA, MAS, CNC, and MEN 1 has been extensively studied and reviewed, especially in children and young adults. The GH-secreting adenomas seem to be more invasive and aggressive in childhood than in adulthood. Data on a rare disease — gigantism combined with phenotypic signs of acromegaly in a young patient are presented. Clinical and laboratory parameters, data of histological and genetic analysis are described. Genetic analysis performed by AIP gene by Sequencing, proved a rare mutation in the locus of exons 1-6 of the AIP gene. The presented clinical case describes a rare fact of the AIP-gene mutation in the p.Cys238Tyr locus, which is associated with the occurrence of a giant pituitary adenoma in childhood. Aggressive growths of the pituitary tumor, its high proliferative and hormonal activity, clinical manifestations of gigantism in combination with severe phenotypic signs of acromegaly have also been noticed. Resistance to the therapy with somatostatin analogs has been revealed in this case. Considering the absence of genetic predisposition to a pituitary adenoma in the patient, this case can be regarded as a sporadic pituitary adenoma variant due to the abnormal AIP-gene expression and the disturbance of regulation during tumorigenesis.

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Background. The purpose of the study is to determine the associations between clinical and anthropometric parameters, glucose homeostasis and serum xanthinoxidase (XO) activity in patients with type 2 diabetes mellitus (T2DM) taking into account gender, glycemic control and serum XO activity. Materials and methods. One hundred and twenty-five T2DM patients aged 34 to 81 years were examined, with an average age of 58.9 ± 9.4 years, disease duration from 1 month to 29 years (average of 8.9 ± 6.6 years). The age of patients at the time of the disease manifestation in the general sample was from 29 to 71 years, on average 50.6 ± 9.1 years. Results. The authors have found a nonlinear dependence of serum XO activity on fasting insulin concentration in patients with T2DM in the total sample, described by the multiplicative model (r = 0.45; p = 0.001). Serum XO activity in patients with T2DM in the general sample increases with adaptive increase in secretory activity of β-cells on an empty stomach according to the HOMA_β%. Serum ХO activity was highest in T2DM patients with low fasting insulin sensitivity (HOMA_S% < 50 %). In addition, it has been determined that the serum ХО activity in the subjects is nonlinearly associated with the QUICKI (r = –0.35; p = 0.016) and Caro indices (r = –0.40; p = 0.007). We have found a nonlinear dependence of serum XO activity on fasting insulin (r = 0.50; p = 0.08), HOMA_β% (r = –0.53; p = 0.06), HOMA_S% (r = –0.48; p = 0.09), HOMA-IR (r = –0.48; p = 0.09) in men with optimal glycemic control (HbA1c < 7.5 %) at the trend level and Caro (r = –0.64; p = 0.02). In women of this group, there was a nonlinear dependence of serum XO activity on fasting insulin (r = 0.56; p = 0.004), HOMA_β% (r = 0.56; p = 0.003), HOMA_S% (r = –0.54; p = 0.005), HOMA-IR (r = 0.54; p = 0.005), QUICKI (r = –0.50; p = 0.01) and Caro (r = –0.61; p = 0.003). Conclusions. In patients with T2DM, the serum uric acid is linearly associated with the level of serum XO activity, which determines 34 % of its variability. In patients with T2DM, regardless of the state of glycemic control, serum XO activity is nonlinearly associated with parameters characterizing the state of glucose homeostasis (fasting insulin, HOMA_S%, HOMA_β%, QUICKI and Caro indices). Predictors of high serum XO activity in patients with T2DM are the level of postprandial blood glucose (t = –3.53; p = 0.004) and serum uric acid (t = 4.73; p = 0.0005).