Multisystem pediatric inflammatory syndrome associated with COVID-2019 in the Zaporizhzhia region

The aim is to familiarize with the clinical signs of the multisystem inflammatory syndrome associated with COVID-19, based on the analysis of its course in children of the Zaporizhzhia region of Ukraine. Materials and methods. A retrospective analysis of the medical histories of 16 children, aged from 1 to 16 years, who had a history of COVID-19 and/or who were in contact with patients with this disease and had a confirmed disease accompanied by fever, disorders of other organs and systems, was conducted. The methods of non-parametric statistics – descriptive statistics and statistical inference – were used for statistical processing of the results. All calculations were carried out using Microsoft Excel. Results. Symptoms found in the examined children met the following WHO diagnostic criteria for multisystem pediatric inflammatory syndrome associated with COVID-2019: the age ranged from 1 to 16 years. Fever lasting at least 3 days was observed in 100 % of the subjects. Evidence of multisystem disease occurred in all patients in particular: 8 children had tiny-dotted exanthema, 12 – pharyngitis; damage to the cardiovascular system in the form of cardiopathy was detected in 12 children, rhythm disorders in 15, dysmetabolic changes in the myocardium in 9; laboratory signs of coagulopathy in the form of an increased level of D-dimer were observed in 8 children, a decrease in thrombin time in 4; abdominal syndrome was found in 8 children. All patients had elevated levels of inflammatory markers. During the examinations, no convincing evidence of the presence of another disease that could cause these symptoms was found. All children had evidence of infection with the SARS-CoV-2 virus, namely, 9 had a history of COVID-19, 2 had a positive PCR test, 12 had IgG to COVID-19, and 5 had IgM to COVID-19. Conclusions. The article demonstrates the polymorphism of the clinical and laboratory manifestations of the multisystem pediatric inflammatory syndrome associated with COVID-2019; easy to use WHO criteria WHO criteria for diagnosing this syndrome; the need for every physician to be alert to this syndrome when in contact with a child who has fever for three or more days during the period of epidemic disorder due to coronavirus disease (COVID-19)

ЗМІНИ БІОФІЗИЧНИХ ТА МОРФОЛОГІЧНИХ ВЛАСТИВОСТЕЙ МІОКАРДА ПРИ ОЖИРІННІ

Obesity is often an additional and leading risk factor for arterial hypertension. The likelihood of hypertension development in individuals with obesity is 50% higher than that of people with normal body weight. Obesity provokes acceleration of the development of factors that make up the cardiovascular risk in general. In obese individuals, arterial hypertension is found 2.9 times more often than in people with normal body mass. In 80% of men and 61% of women included in the Framingham study, the cause of arterial hypertension was an increase in body weight. WHO experts draw the conclusion that in Western countries 1/3 of patients, on average, suffer from arterial hypertension due to excessive body weight, and in men up to 45 years this figure reaches 60%. Obesity and arterial hypertension potentiate each other in relation to the development of unfavorable effects on the structure and function of the heart; the level of pre- and after-load of the heart increases, especially in people with severe and prolonged (> 15 years) obesity. The risk of left ventricular myocardial hypertrophy (LVMH) formation rises from 5.5% in people with normal body weight up to 29.9% in obese people. Hypertension, when associated with obesity, increases the risk of heart hypertrophy more than 4 times. The problem of overweight is the scourge of our time. Obesity is diagnosed quite often. Therefore, a conservative approach is not always reasonable. Surgical treatments for obesity are rather relevant in turn. Objective: to establish morphological changes in the heart and vessels of the anterior abdominal wall and the small intestinal mucus in case of obesity and to establish their role in the occurrence of arterial hypertension. Materials and methods: obesity was modeled according to the standard method of high-calorie nutrition for a month. The weight of rats was 390-420 g. Results and Discussion: the changes in the heart and blood vessels in different areas developed as a result of obesity were examined. The samples of the heart walls are presented in all the layers – the epicardium, myocardium, and endocardium. The endocardium is of usual histological structure, represented by endothelial lining in the form of single layer flat epithelium and such underlying layers – loose connective tissue, muscular and elastic layer, and external connective tissue layer. On the longitudinal sections, cardiomyocytes are represented by cells of elongated rectangular shape with eosinophilic cytoplasm, rounded or oval nuclei, located centrally and paracentrally. The layers of loose connective tissue and vessels are located between the muscular elements of the myocardium. Diffusely located small eosinophilic grains in the cytoplasm of separate groups of cardiomyocytes are present (phenomena of granular myocardial dystrophy). The interstitial stroma is in moderate edema. The plethora of all the vessels of the myocardium (arteries, veins, microvasculature) is noticed and accompanied by erythrostasis phenomena; individual red blood cells are destroyed with the release of brown pigment in the lumen of the vessel. The walls of the vessels are swelled in some places, and the release of red blood cells from the vascular bed is marked around some of them. The anterior abdominal wall is represented by epidermis, dermis, underlying fatty tissue, and muscle layer. In the lumen of the vessels erythrostasis is manifested significantly. The mesentery is represented by the adipose tissue of a usual histological structure with regional lymph nodes. Vessels are full-blooded, in some places defibration and swelling of the muscular layer are present. Conclusions: As it is evident from the histological sections, the reaction of all the parts of the cardiovascular system is expressed in pathological changes that subsequently lead to arterial hypertension and cardiovascular insufficiency.Ожирение и артериальная гипертензия потенцируют друг друга по отношению к развитию неблагоприятного влияния на структуру и функцию сердца, увеличивается уровень пред- и постнагрузку на сердце. Нами проводилось моделирование ожирения по стандартной методике высококалорийного питания в течение месяца. Вес крыс составляла 390-420 гр. На гистологических срезах выраженный стаз эритроцитов в просветах капилляров с единичными мелкими периваскулярными кровоизлияниями, очаговые явления внутрисосудистого гемолиза, умеренно выраженное фибриноидное набухание стенок сосудов. Диффузный отек стромы. Умеренно выраженная зернистая дистрофия кардиомиоцитов. На гистологических срезах брыжейки кишечника, в просветах сосудов наблюдается выраженный стаз эритроцитов, очаговые явления внутрисосудистого гемолиза, в стенках сосудов - разволокнение мышечного слоя, отек. Фрагменты передней брюшной стенки: выраженный стаз эритроцитов в просветах сосудов, отек гиподермы. Все эти патологические изменения приводят к возникновению артериальной гипертензии и сердечно-сосудистой недостаточности.Ожиріння і артеріальна гіпертензія потенціюють одне одного стосовно до розвитку несприятливого впливу на структуру і функцію серця, збільшується рівень перед- і постнавантаження на серце. Нами проводилось моделювання ожиріння за стандартною методикою висококалорійного харчування, протягом місяця.  Вага щурів становить 390-420 гр. На гістологічних зрізах виражений стаз еритроцитів у просвітах капілярів з одиничними дрібними периваскулярними крововиливами, осередкові явища внутрішньосудинного гемолізу, помірно виражене фибриноидное набухання стінок судин. Дифузний набряк строми. Помірно виражена зерниста дистрофія кардіоміоцитів. На гістологічних зрізах брижі кишечнику, у просвітах судин спостерігається виражений стаз еритроцитів, осередкові явища внутрішньосудинного гемолізу, у стінках судин - разволокнение м'язового шару, набряк. Фрагменти передньої черевної стінки: виражений стаз еритроцитів у просвітах судин, набряк гіподерми. Усі ці патологічні зміни призводять до виникнення артеріальної гіпертензії та серцево — судинної недостатності