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The ANI scoring system may be used for the estimation of alcoholic origin of steatosis/steatohepatitis and may help in triaging patients for liver biopsy. ANI less than -0.66 indicates NAFLD, whereas ANI greater than -0.66 confirms the alcoholic etiology, but does not exclude the contribution of associated factors toward the development of fatty liver in a Serbian population.
Background: In multisystem inflammatory syndrome in children (MIS-C) temporarily associated with coronavirus disease-19 (COVID-19), myocardial damage has been reported. Materials and Methods: A retrospective observational cohort study included children under 18 who had a myocardial injury related to COVID-19 treated in mother and child health institute from April 2020 to August 2020. Myocardial injury related to COVID-19 was manifested by elevated serum cardiac troponin and NT-proBNP with LV dysfunction, arrhythmias, and coronary arteries (CAs) dilatation or aneurysms. During the short-term follow-up, cardiac testing (electrocardiography, laboratory analysis, echocardiography, 24-h Holter monitoring, exercise stress test, and cardiac magnetic resonance) was performed. Results: Six male adolescents (14.7 ± 2.4 years) were included in the analysis (2/6 had MIS-C shock syndrome). All patients had elevated acute-phase reactants and NT-proBNP, whereas troponins were elevated in 5/6 patients. Echocardiography revealed left ventricular (LV) systolic dysfunction (EF 45.2 ± 6.9%); 2/6 had dilated CAs. IVIG was prescribed to all patients with MIS-C. Four patients required inotropic drug support. During hospitalization, a significant reduction of CRP, LDH, NT-proBNP, and D-dimer ( P < 0.05) was registered. LV systolic function recovery was registered 3 days after applied therapy ( P < 0.001). None of the patients developed dilated cardiomyopathy or CA aneurysms. Conclusions: With early recognition and adequate MIS-C therapy, children recovered entirely, maintained in the short-term follow-up period.
Choline and methionine are precursors of acetylcholine, whose hydrolysis is catalyzed by acetylcholinesterase (AChE). Considering the possibility of their common deficiency, we investigated the influence of methionine-choline deprivation on AChE activity in liver and various brain regions (hypothalamus, hippocampus, cerebral cortex and striatum) in mice fed with methionine-choline deficient (MCD) diet. Male C57BL/6 mice (n = 28) were randomly and equally divided into following groups: control group fed with standard diet for 6 weeks (C) and groups fed with MCD diet for 2 weeks (MCD2), 4 weeks (MCD4) and for 6 weeks (MCD6). After the diet, mice were sacrificied and AChE activity in liver and brain was determined spectrophotometrically. Hepatic AChE activity was higher in MCD2, MCD4 and MCD6 compared to control (p < 0.01), with most prominent increase in MCD6. AChE activity in hypothalamus was higher in MCD4 and MCD6 vs. control (p < 0.05 and p < 0.01, respectively), as well as in MCD6 compared to MCD4 (p < 0.01). In hippocampus, increase in AChE activity was shown in MCD6 compared to control (p < 0.01). In cortex and striatum, increase in AChE activity was noted in MCD6 compared to control (p < 0.05). Our findings indicate the increase of hepatic and brain AChE activity in mice caused by methionine-choline deprivation.
Perinatal asphyxia (PA) is a condition characterized by a gas exchange disorder due to a lack of blood flow or gas exchange, with potential multiorgan dysfunction. Our study aimed to determine the correlation between biochemical markers and echocardiography findings in a group of asphyxiated newborns. The prospective cohort study included 120 neonates (52/120 with PA) treated at a tertial referral pediatric center, from 2012 to 2014. A moderate-strong positive correlation was recorded between the transtricuspid pressure gradient (TRPG) and serum lactate, and between TRPG and NT-proBNP in the PA group (P<0.001) on the 1st day of life. A moderate positive correlation was found between NT-proBNP, lactate and troponins on one side, and TRPG on the other in the PA group after the 2nd measurement. Multinomial regression analysis showed that the lactate level was an independent factor for survival on the 1st (odds ratio (OR) 41.3, 95%confidence interval (CI) 2.14-797.1) and 3rd (OR 136.4, 95% CI 2.27-8206.7) days. Our research confirmed a significant correlation between echocardiographic and biochemical parameters of the myocardial lesion and cardiac function. Due to their complementarity, the use of the biochemical and echocardiographic parameters may be conditioned by their availability.
ApstraktSindrom produženog QT intervala (engl. long QT syndrome, LQTS) je poremećaj repolarizacije komora miokarda koji se odlikuje produženjem QT intervala na elektrokardiogramu (EKG) i povećanim rizikom za nastanak ventrikularnih tahiaritmija i kardiogenih manifestacija. Može da bude stečeni ili kongenitalni, koji predstavlja skup kanalopatija usled mutacija u nekom od 15 do sada identifikovanih gena. Najčešći oblici kongenitalnog sindroma su LQT1, LQT2 i LQT3. Zbog produženja repolarizacije i, posledično, celog akcionog potencijala, stvaraju se uslovi za nastanak rane naknadne depolarizacije i izraženije transmuralne disperzije repolarizacije koje su, pojedinačno ili udruženo, osnova za nastanak Torsades de pointes ventrikularne tahikardije. Sindrom produženog QT intervala se klinički manifestuje palpitacijama, sinkopom, srčanim zastojem ili naprasnom srčanom smrću, a može da bude i asimptomatski. Provocirajući faktori za nastanak tegoba su specifični za određeni genotip. Ispitivanje LQTS obuhvata ličnu i porodičnu anamnezu sa naglaskom na karakteristične podatke (česte sinkope, iznenadna srčana smrt u porodici, nasledne aritmije), EKG u miru, test opterećenja i genetske analize, kao i druge dodatne metode (serijski EKG zapisi, 24h EKG holter, epinefrinski test). Za klinič-ko postavljanje dijagnoze koristi se Švarcov (Schwartz) skor, a kriterijumi za definitivno postavljanje dijagnoze zavise od Švar-covog skora, dužine QT intervala, postojanja mutacije i kliničke slike. Lečenje se zasniva na promeni životnih navika i terapiji β-blokatorima, a druge mogućnosti su ugradnja implantabilnog kardioverter-defibrilatora, permanentnog pejsmejkera ili hirurška simpatektomija. Sindrom produženog QT intervala je jedan od potencijalnih uzroka iznenadne srčane smrti koja čini 90% iznenadnih smrti mladih sportista. Kod dece sa LQTS preporuke za bavljenje sportom proizilaze iz preporuka za odrasle i podrazumevaju vrlo stroga ograničenja. Dalja istraživanja biće usmerena na bolje razumevanje genotip-fenotip korelacije kongenitalnih LQTS i očekuje se da će pružiti nove personalizovane terapijske mogućnosti i saznanja o ređim tipovima ovog sindroma, kao i jasnije preporuke za bavljenje fizičkom aktivnošću kod dece sa LQTS.Ključne reči: sindrom produženog QT intervala, deca, genetika, fizička aktivnost AbstractLong QT syndrome (LQTS) is a cardiac repolarization disorder characterized by prolonged QT interval on the electrocardiogram (ECG) and increased propensity to ventricular tachyarrhythmias and cardiac events. LQTS might be acquired or congenital, which presents a group of channelopathies that occur due to mutation in one of 15 so far identified genes. The most frequent types of congenital LTQS are LQT1, LQT2 and LQT3. Prolonged or delayed repolarization leads to the increase of action potential duration which predisposes early afterdepolarization, as well as the amplification of transmural dispersion of repolarization, both contributing to the development of Torsades de Pointes ventricular tachycardia. Clinical manifestatio...
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