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Bolest malih krvnih sudova mozga podrazumeva nekoliko kliničkih sindroma koji proističu iz oštećenja zida ili začepljenja malih krvnih sudova unutar moždanog tkiva. Udružena je sa faktorima rizika kao što su hipertenzija, dislipidemija, dijabetes, gojaznost, ishemijska bolest srca, pušenje i zloupotreba alkohola. Jedan od potencijalnih faktora rizika za nastanak bolesti malih krvnih sudova mozga je metabolički sindrom. Bolest se klinički manifestuje neuroškim simptomima, kognitivnim disfunkcijama i depresijom. Istraživanje je sprovedeno kod pacijenata koji su hospitalizovani na Klinici za neurologiju KC Kragujevcu u periodu od 01.02.2017. do 31.12.2017. godine, kod kojih je neuroradiološki potvrđena bolest malih krvnih sudova (magnetnom rezonancom endokranijuma). Bilo je uključeno 49 odraslih bolesnika sa bolešću malih krvnih sudova mozga (24 sa lakunarnim infarktima i 25 sa ishemijskim, hiperintenzivnim lezijama bele mase). Kontrolnu grupu činilo je 25 neuroloških pacijenata sa urednim nalazom na magnetnoj rezonanci endokranijuma, sličnog pola i starosti. Sa pacijentima je postupano prema lokalnim smernicama i kliničkim putevima koji nisu povezani sa ovom studijom, već predstavljaju deo rutinske nege neuroloških bolesnika u Kliničkom centru Kragujevac. Rezultati prikazani u ovom radu ukazuju da je bolest malih krvnih sudova mozga praćena slabljenjem kognitivne sposobnosti i depresivnim simptomima, pri čemu pacijenti sa lakunarnim infarktima imaju slabiju kogniciju i izraženije depresivne simptome od pacijenata sa hiperintenzivnim lezijama bele moždane mase. Takođe, pacijenti sa bolešću malih krvnih sudova mozga koji imaju i metabolički sindrom su više depresivni i manje kognitivno sposobni od pacijenata sa bolešću malih krvnih sudova mozga, ali bez metaboličkog sindroma. Disease of the small blood vessels of the brain involves several clinical syndromes arising from damage to the wall or obstruction of the small blood vessels inside the brain tissue. It is associated with risk factors such as hypertension, dyslipidemia, diabetes, obesity, ischemic heart disease, smoking and alcohol abuse .One of the potential risk factors for developing cerebral small vessels disease is the metabolic syndrome. The disease is clinically manifested by neurological symptoms, cognitive dysfunctions and depression. The study was conducted in patients hospitalized at the Kragujevac Clinic for Neurology in the period from 01.02.2017. to 31.12.2017, in which neuroradiologically confirmed disease of the small blood vessels (magnetic resonance imaging of the endocranium). There were 49 adult patients with small cerebral blood vessels disease (24 with lacunar infarctions and 25 with ischemic, hyper intense white mass lesions). The control group consisted of 25 neurological patients with neat endocranial magnetic resonance imaging, of similar sex and age. Patients were treated according to local guidelines and clinical pathways not associated with this study, but are part of the routine care of neurological patients at the Clinical Center Kragujevac. The results presented in this paper indicate that cerebral small vessels disease is accompanied by impaired cognitive ability and depressive symptoms, whereby patients with lacunar infarctions have poorer cognition and more severe depressive symptoms than patients with hyper intensive white brain lesions. Also, patients with cerebral small vessels disease who also have metabolic syndrome are more depressed and less cognitively able than patients with cerebrovascular disease but no metabolic syndrome.

S obzirom na visoku prevalencu metaboličkog sindroma (10-40% u svetskoj populaciji) i na činjenicu da prisustvo metaboličkog sindroma duplira rizik od nastanka aterosklerotske bolesti kardiovaskularnog sistema jasna je potreba za identifikacijom indivudualnih parametara koji doprinose njenom razvoju. Metabolički sindrom je klaster faktora rizika metaboličkog porekla koji je udružen sa povećanim rizikom za nastanak aterosklerotske bolesti kardiovaskularnog sistema i dijabetes melitusa tipa 2. Insulinska rezistencija, abdominalna gojaznost, aterogena dislipidemija, hipertenzija, proinflamatorno i protrombotično stanje su faktori koji su u osnovi metaboličkog sindroma a često su i praćeni nagomilavanjem masti u jetri. Cilj rada je bio da se utvrdi odnos između markera disfunkcije hepatocita (AST, ALT, GGT), serumskog nivoa inflamatornih biomarkera (broj leukocita, elektroforeza serumskih proteina, CRP, fibrinogen, TNF-α), biomarkera endotelne disfunkcije (ADMA i homocistein), kao i nivoa serumskih adipokina (leptin i adiponektin) i debljine intima-medija kompleksa (IMT) karotidne arterije kao pokazatelja prisustva aterosklerotskog procesa. Ispitivanje je dizajnirano kao studija preseka. U ispitivanje je uključeno 58 ispitanika oba pola sa karakteristikama metaboličkom sindroma (NCEP:ATP III kriterijumi). Odabir ispitanika je vršen u Odeljenju za pravilnu ishranu i zdravstvenu bezbednost hrane, Instituta za javno zdravlje Vojvodine. Kontrolnu grupu su sačinjavale 30 klinički i biohemijski zdravih ispitanika nepušača koji su prema polnoj i dobnoj strukturi odgovarali ispitivanim grupama bolesnika. Iz ispitivanja su isključene osobe koje konzumiraju više od 20g/dan alkohola, pušači, koji imaju dijagnostikovan virusni hepatitis B ili C ili pozitivan Hbs antigen, anti-Hbs antitela i anti-HCV antitela, osobe koje imaju verifikovana oboljenja kardiovaskularnog sistema, bubrega, CNS-a, infektivna, maligna i autoimuna oboljenja kao i druga oboljenja jetre i žučnih puteva, osobe koje su pod medikamentoznom terapijom koja može uticati na nivo serumskih biomarkera endotelne disfunckije, lipidni i lipoproteinski status, glikoregulaciju kao i menstruacioni ciklus. Sve laboratorijske analize su urađene u Centru za laboratorijsku medicinu, Kliničkog centra Vojvodine. Doppler ultrasonografski pregled karotidnih arterija i ultrazvuk abdomena i jetre je urađen u Centru za radiologiju Kliničkog centra Vojvodine. Signifikantna pozitivna korelacija niskog stepena je utvrđena između IMT zajedničke karotidne arterije i serumskih koncentracija GGT, hsCRP i leptina kao i odnosa neutrofili/limfociti. Prema prvom konstruisanom regresionom modelu u kojem je zavisna varijabla bila IMT preko 0,09 cm statistički značajan uticaj na predviđanje debljine IMT zajedničke karotidne arterije imaju hsCRP (Exp (B) 1,112 i glikemija (Exp (B) 1,973). Prema modelu neuronske mreže sa istom zavisnom varijablom najveću mogućnost predviđanja IMT imaju glikemija, AST i fibrinogen. Prema drugom konstruisanom regresionom modelu gde su zavisne varijable bile IMT zajedničke karotidne arterije preko 0,09 cm i prisutnost hepatične steatoze najveću mogućnost predviđanja imaju leptin Exp (B) 1,1022 i ALT Exp (B) 1,053. Prema modelu neuronske mreže sa istom zavisnom varijablom najveću mogućnost predviđanja IMT imaju ALT, ADMA i leptin., Given the high prevalence of metabolic syndrome (10-40% in the world population) and the fact that the presence of metabolic syndrome doubles the risk of atherosclerotic disease of the cardiovascular system, there is a clear need to identify individual parameters that contribute to its development. Metabolic syndrome is a cluster of the risk factors of metabolic origin that is associated with an increased risk for the onset of atherosclerotic disease of the cardiovascular system and type 2 diabetes mellitus. Insulin resistance, abdominal obesity, atherogenic dyslipidemia, hypertension, proinflammatory and prothrombotic conditions are the factors at the base of the metabolic syndrome and are often accompanied by fat accumulation in the liver. The aim of this work was to determine the relation between markers of hepatic dysfunction (AST, ALT and GGT), serum levels of inflammatory biomarkers (white blood cell count, electrophoresis of serum proteins, CRP, fibrinogen, TNF-α), biomarkers of endothelial dysfunction (ADMA and homocysteine) as well as levels of serum adipokines (leptin and adiponectin) and intima-media thickness of carotid artery as indicators of atherosclerotic process in the patients with metabolic syndrome. Study was cross-sectional. It included 58 participants with metabolic syndrome (NCEP:ATP III criteria) as well as 30 clinically and biochemically healthy nonsmokers, age and gender matched controls. Participants were selected in the Department for Nutrition and Food Safety, Center of Hygiene and Human Ecology Institute of Public Health of Vojvodina. Patients that consumed alcohol more than 20g/day were excluded. Participants with positive HBsAg, anti-HBs-antibodies or anti- HCV antibodies were excluded also. Smokers were also excluded. Patients with cardiovascular diseases, renal diseases, infective, hepatic, malignant and autoimmune diseases were excluded from this study. Subjects which used drugs that could affect biomarker levels of endothelial dysfunction, lipid metabolism, glucose metabolism and menstrual cycle were also excluded. All laboratory analyzes were done in Centre for Laboratory Medicine, Clinical Centre of Vojvodina. Doppler ultrasonography of carotid arteries and ultrasound of abdomen and liver were done in Centre for Radiology, Clinical Centre of Vojvodina. Significant positive correlation of low degree was determined between IMT of common carotid artery and serum concentrations between GGT, hsCRP and leptin and relationship neutrophils/lymphocytes. According to the first constructed regression model where dependent variable was IMT of common carotid artery above 0.09 cm statistically significant influence on foreseeing IMT of common carotid artery have hsCRP (Exp (B) 1.112 and glycaemia (Exp (B) 1.973). According to the neuronal network with the same dependent variable greatest probability for foreseeing IMT have glycaemia, AST and fibrinogen. According to the second constructed regression model where dependent variable was IMT above 0.09 cm and present hepatic steatosis greatest probability for foreseeing IMT have leptin Exp (B) 1.1022 and ALT Exp (B) 1.053. According to the neuronal network with the same dependent variable greatest probability for foreseeing IMT have ALT, ADMA and leptin.

S obzirom na visoku prevalencu metaboličkog sindroma (10-40% u svetskoj populaciji) i na činjenicu da prisustvo metaboličkog sindroma duplira rizik od nastanka aterosklerotske bolesti kardiovaskularnog sistema jasna je potreba za identifikacijom indivudualnih parametara koji doprinose njenom razvoju. Metabolički sindrom je klaster faktora rizika metaboličkog porekla koji je udružen sa povećanim rizikom za nastanak aterosklerotske bolesti kardiovaskularnog sistema i dijabetes melitusa tipa 2. Insulinska rezistencija, abdominalna gojaznost, aterogena dislipidemija, hipertenzija, proinflamatorno i protrombotično stanje su faktori koji su u osnovi metaboličkog sindroma a često su i praćeni nagomilavanjem masti u jetri. Cilj rada je bio da se utvrdi odnos između markera disfunkcije hepatocita (AST, ALT, GGT), serumskog nivoa inflamatornih biomarkera (broj leukocita, elektroforeza serumskih proteina, CRP, fibrinogen, TNF-α), biomarkera endotelne disfunkcije (ADMA i homocistein), kao i nivoa serumskih adipokina (leptin i adiponektin) i debljine intima-medija kompleksa (IMT) karotidne arterije kao pokazatelja prisustva aterosklerotskog procesa. Ispitivanje je dizajnirano kao studija preseka. U ispitivanje je uključeno 58 ispitanika oba pola sa karakteristikama metaboličkom sindroma (NCEP:ATP III kriterijumi). Odabir ispitanika je vršen u Odeljenju za pravilnu ishranu i zdravstvenu bezbednost hrane, Instituta za javno zdravlje Vojvodine. Kontrolnu grupu su sačinjavale 30 klinički i biohemijski zdravih ispitanika nepušača koji su prema polnoj i dobnoj strukturi odgovarali ispitivanim grupama bolesnika. Iz ispitivanja su isključene osobe koje konzumiraju više od 20g/dan alkohola, pušači, koji imaju dijagnostikovan virusni hepatitis B ili C ili pozitivan Hbs antigen, anti-Hbs antitela i anti-HCV antitela, osobe koje imaju verifikovana oboljenja kardiovaskularnog sistema, bubrega, CNS-a, infektivna, maligna i autoimuna oboljenja kao i druga oboljenja jetre i žučnih puteva, osobe koje su pod medikamentoznom terapijom koja može uticati na nivo serumskih biomarkera endotelne disfunckije, lipidni i lipoproteinski status, glikoregulaciju kao i menstruacioni ciklus. Sve laboratorijske analize su urađene u Centru za laboratorijsku medicinu, Kliničkog centra Vojvodine. Doppler ultrasonografski pregled karotidnih arterija i ultrazvuk abdomena i jetre je urađen u Centru za radiologiju Kliničkog centra Vojvodine. Signifikantna pozitivna korelacija niskog stepena je utvrđena između IMT zajedničke karotidne arterije i serumskih koncentracija GGT, hsCRP i leptina kao i odnosa neutrofili/limfociti. Prema prvom konstruisanom regresionom modelu u kojem je zavisna varijabla bila IMT preko 0,09 cm statistički značajan uticaj na predviđanje debljine IMT zajedničke karotidne arterije imaju hsCRP (Exp (B) 1,112 i glikemija (Exp (B) 1,973). Prema modelu neuronske mreže sa istom zavisnom varijablom najveću mogućnost predviđanja IMT imaju glikemija, AST i fibrinogen. Prema drugom konstruisanom regresionom modelu gde su zavisne varijable bile IMT zajedničke karotidne arterije preko 0,09 cm i prisutnost hepatične steatoze najveću mogućnost predviđanja imaju leptin Exp (B) 1,1022 i ALT Exp (B) 1,053. Prema modelu neuronske mreže sa istom zavisnom varijablom najveću mogućnost predviđanja IMT imaju ALT, ADMA i leptin. Given the high prevalence of metabolic syndrome (10-40% in the world population) and the fact that the presence of metabolic syndrome doubles the risk of atherosclerotic disease of the cardiovascular system, there is a clear need to identify individual parameters that contribute to its development. Metabolic syndrome is a cluster of the risk factors of metabolic origin that is associated with an increased risk for the onset of atherosclerotic disease of the cardiovascular system and type 2 diabetes mellitus. Insulin resistance, abdominal obesity, atherogenic dyslipidemia, hypertension, proinflammatory and prothrombotic conditions are the factors at the base of the metabolic syndrome and are often accompanied by fat accumulation in the liver. The aim of this work was to determine the relation between markers of hepatic dysfunction (AST, ALT and GGT), serum levels of inflammatory biomarkers (white blood cell count, electrophoresis of serum proteins, CRP, fibrinogen, TNF-α), biomarkers of endothelial dysfunction (ADMA and homocysteine) as well as levels of serum adipokines (leptin and adiponectin) and intima-media thickness of carotid artery as indicators of atherosclerotic process in the patients with metabolic syndrome. Study was cross-sectional. It included 58 participants with metabolic syndrome (NCEP:ATP III criteria) as well as 30 clinically and biochemically healthy nonsmokers, age and gender matched controls. Participants were selected in the Department for Nutrition and Food Safety, Center of Hygiene and Human Ecology Institute of Public Health of Vojvodina. Patients that consumed alcohol more than 20g/day were excluded. Participants with positive HBsAg, anti-HBs-antibodies or anti- HCV antibodies were excluded also. Smokers were also excluded. Patients with cardiovascular diseases, renal diseases, infective, hepatic, malignant and autoimmune diseases were excluded from this study. Subjects which used drugs that could affect biomarker levels of endothelial dysfunction, lipid metabolism, glucose metabolism and menstrual cycle were also excluded. All laboratory analyzes were done in Centre for Laboratory Medicine, Clinical Centre of Vojvodina. Doppler ultrasonography of carotid arteries and ultrasound of abdomen and liver were done in Centre for Radiology, Clinical Centre of Vojvodina. Significant positive correlation of low degree was determined between IMT of common carotid artery and serum concentrations between GGT, hsCRP and leptin and relationship neutrophils/lymphocytes. According to the first constructed regression model where dependent variable was IMT of common carotid artery above 0.09 cm statistically significant influence on foreseeing IMT of common carotid artery have hsCRP (Exp (B) 1.112 and glycaemia (Exp (B) 1.973). According to the neuronal network with the same dependent variable greatest probability for foreseeing IMT have glycaemia, AST and fibrinogen. According to the second constructed regression model where dependent variable was IMT above 0.09 cm and present hepatic steatosis greatest probability for foreseeing IMT have leptin Exp (B) 1.1022 and ALT Exp (B) 1.053. According to the neuronal network with the same dependent variable greatest probability for foreseeing IMT have ALT, ADMA and leptin.

Ulcerozni kolitis (engl. Ulcerative colitis- UC) je hronično oboljenje koje karakteriše zapaljenje sluznice digestivnog trakta, prvenstveno debelog creva. Metabolički sindrom je čest poremećaj značajno povezan sa UC. Veliki broj studija je pokazao značajan komorbiditet ovih poremećaja i njihovu genetsku povezanost. Cilj studije bio je da se ispita povezanost razvojnih faza metaboličkog sindroma sa težinom bolesti, te lokalnim i sistemskim imunskim odgovorom kod pacijenata sa ulceroznim kolitisom. Kod ispitanika sa ulceroznim kolitisom i metaboličkim sindromom zabeležena je klinički i patohistološki blaža bolest sa sistemskom i lokalnom predominacijom galektina 1, galektina 3 i imunosupresivnog citokina IL-10, uz sniženu koncentraciju proinflamacijskih citokina TNF-α, IL-6 i IL-17. Takođe je registrovana manja zastupljenost CD8+ T limfocita, a veća zastupljenost regulatornih CD4+Foxp3+ limfocita, kao i veća ekspresija galektina-3 na limfocitima i veća produkcija imunosupresivnog IL-10 u lamina propria-i obolelih od ulceroznog kolitisa sa metaboličkim sindromom. Kod ispitanika u terminalnoj fazi metaboličkog sindomoma zabeležena je klinički i patohistološki teža forma ulceroznog kolitisa. U ovoj grupi ispitanika nađena je sistemska i lokalna predominacija proinflamacijskih citokina TNF-α, IL-6 i IL-17 nad galektinom-1, galektina-3 nad proinflamacijskim medijatorima TNF-α i IL-17 kao i povećana ekspresija galektina-3 na imunokompetentnim ćelijama koje infiltrišu lamina propria-u. Lokalna i sistemska predominacija Gal-1 i Gal-3 nad proinflamacijskim citokinima kod obolelih sa metaboličkim sindromom može predstavljati mehanizam zaustavljanja i ograničavanja proinflamacijskog procesa i sprečiti oštećenje tkiva, ukazujući na imunosupresivnu ulogu Gal-1 i Gal-3 u biologiji ulceroznog kolitisa kod bolesnika sa metaboličkim sindromom. Sistemska i lokalna predominacija proinflamacijskih citokina TNF-α, IL-6 i IL-17 nad Gal-1 i Gal-3 u terminalnoj fazi metaboličkog sindroma pojačava zapaljenje i sledstveno oštećenje tkiva. Ulcerative colitis (UC) is a chronic disease characterized by inflammation of intestinal epithelium, primarily of the colon. Metabolic syndrome is a common disorder significantly associated with UC. A large number of studies have shown significant comorbidity of these disorders and their genetic linkage. The aim of the study was to examine the relationship between the developmental stages of the metabolic syndrome with the severity of the disease, and the local and systemic immune response in patients with ulcerative colitis. Clinical and pathohystologically mild disease with systemic and local prevalence of galectin 1, galectin 3 and immunosuppressive cytokine IL-10 was observed in subjects with ulcerative colitis and metabolic syndrome, with reduced concentration of proinflammatory cytokines TNF-α, IL-6, and IL-17. Further, we detected lower incidence of CD8+ T lymphocytes and enhanced accumulation of regulatory CD4+ Foxp3+ T cells, as well as increased expression of galectin-3 on lymphocytes and higher production of immunosuppressive IL-10 in lamina propria derived from UC patients with metabolic syndrome. Clinical and pathohystologically severe disease was observed in the patients with terminal phase of the metabolic syndrome. In this group of subjects, we found systemic and local prevalence of proinflammatory cytokines TNF-α, IL-6, and IL-17 over galectin-1; galectin-3 over TNF-α and IL-17; as well as increased expression of galectin-3 on immunocompetent cells infiltrating the lamina propria. Local and systemic dominance of Gal-1 and Gal-3 over proinflammatory cytokines in patients with metabolic syndrome may present a mechanism for stopping and limiting the proinflammatory process and preventing tissue damage, indicating the immunosuppressive role of Gal-1 and Gal-3 in the ulcerative colitis biology of patients with metabolic syndrome. Systemic and local prevalence of proinflammatory cytokines TNF-α, IL-6, and IL-17 over Gal-1 and Gal-3 in the terminal phase of the metabolic syndrome enhances inflammation and consequent tissue damage.