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Uvod: Friedewaldova formula (FF) se uobičajeno koristi za izračun LDL-kolesterola (LDL). Nedavne studije su pokazale da su novije formule kao Martin/Hopkins formula (M/HF) i Sampson formula (SF) točnije i usporedive s referentnom metodom za određivanje LDL-a, beta-kvantifikacijom. Cilj ove studije bio je usporediti izmjereni direktni LDL (dLDL) s računskim LDL-om (rLDL) koristeći FF, M/HF i SF te dobiti uvid mogu li se te nove formule primijeniti u našoj bolnici. Materijali i metode: Kolesterol (KOL), trigliceridi (TG), HDL-kolesterol (HDL) i LDL izmjereni su na AU5800 i DxC 700 AU analizatorima (Beckman Coulter, Brea, SAD) s pripadajućim reagensima kod 250 pacijenata iz Kliničke bolnice Dubrava. Samo rezultati s trigliceridima < 3, 5 mmol/L su bili uključeni u studiju. Korištene su sljedeće formule za rLDL: FF (rLDL = KOL – HDL - TG/2, 2) (mmol/L) ; M/HF (rLDL = KOL – HDL - TG/novi faktor) (mg/dL) ; SF (Rldl = KOL/0, 948 - HDL/0, 971 – (TG/8, 56 + (TG x (KOL - HDL))/2140 – TG x TG/16100) – 9, 44) (mg/dL), uz potrebne konverzije ovisno o mjernim jedinicama. Statistička analiza napravljena je u MedCalc statističkom softveru (verzija 14.8.1, Ostend, Belgija) s Bland-Altman analizom (BA), Passing-Bablok regresijom (PB) i Kruskal-Wallisovim testom (P < 0, 05). Rezultati: Rezultati BA analize (srednja razlika i 95% interval pouzdanosti) i PB regresije su bili kako slijedi: dLDL u odnosu na rLDL s FF (6, 9 (- 18, 6 do 32, 5%) ; (y = - 0, 69 (- 0, 79 do - 0, 58) + 1, 19 (1, 15 do 1, 22) x) ; s M/HF (5, 2 (- 17, 0 do 27, 5)%) ; (y = - 0, 57 (- 0, 65 do - 0, 49) + 1, 15 (1, 13 do 1, 18) x) ; sa SF (4, 9 (- 19, 5 do 29, 3)%), (y = - 0, 68 (- 0, 77 do - 0, 58) + 1, 20 (1, 17 to 1, 23) x). KruskalWallis test nije pokazao statistički značajnu razliku između dLDL-a i rLDL- a bez obzira na korištenu formulu (P = 0, 255). Zaključak: Nije nađena statistički značajna razlika između dLDL-a i rLDL-a sa FF, M/HF i SF. Međutim, prema usporedbi metoda s BA analizom SF za rLDL je pokazala najmanju prosječnu razliku u usporedbi s dLDL, stoga bi se SF mogla koristiti za izračun LDL-a umjesto dosadašnje FF.

BACKGROUND-AIM: The monitoring of COVID-19 patients has become a global challenge in many clinical laboratories, and there is anincreasing incidence of critical values in laboratory results as compared to other patients in intensive care units. Criticalvalues represent those laboratory results that indicate a life-threatening condition of the patient, and it is commonpractice in many laboratories to repeat critical results before reporting the value to the physician. Such results shouldbe reported within 30 minutes of confirmation, and waiting for a re-measurement may delay reporting. METHODS: Since it was noticed that COVID-19 patients had the highest percentage of critical values for potassium (K), sodium(Na), chloride (Cl) glucose (Glc), and lactate (Lac), the aim of this summary was to compare results obtained primarilyon a biochemical (Beckman Coulter DxC 700 AU) and repeatedly on a less time- consuming POCT (Siemens RapidLab1265) analyzer. For this purpose, 40 serum samples were used for the determination of K, Na, Cl and Glc and 10 plasmasamples for the determination of Lac. Statistical comparison of the results was performed using Passing-Bablock (forelectrolytes and Glc) and Deming regression analysis (for Lac). RESULTS: Analysis of the results revealed neither proportional, nor constant error for K [y = -0.15 (-0.29-0.02) + 1.03 (0.99-1.07)x], Na [y = -4.08 (-15.47-5.19) + 1.03 (0.96-1.11) x], Cl [y = 5.00 (-2.96-5.00) + 1.00 (1.00-1.08) x], and Glc [y = -0.10(-0.24-0.04) + 1.00 (0.98-1.02) x] determination on a biochemical analyzer as compared to the POCT instrument. Also, no proportional error [y = 0.17 (0.07-0.27) + 1.06 (0.99-1.13) x] was found in the determination of Lac on a biochemical(CV = 1.79%) vs. POCT (CV = 4.37%) analyzer. Although a constant error was observed, it had no clinical significance(mean BIAS = -17.4% ; calculated RCV = +/-75.9%) CONCLUSIONS: In conclusion, repeating the critical values of K, Na, Cl, Glc, and Lac on the POCT rather than on the biochemical analyzeris justified because the analytical process for determination on the POCT analyzer takes much less time and the criticalresults are reported to the physician much earlier.

Cilj: Cilj istraživanja je utvrditi učestalost promjena funkcija štitnjače kod ispitanika s različitom težinom simptoma i u različitim fazama bolesti COVID-19 te istražiti postoji li povezanost koncentracija ispitivanih hormona s ishodom hospitaliziranih ispitanika. Materijali i metode: Određivana je koncentracija tireotropina (TSH), slobodnog tiroksina (fT4) i slobodnog trijodtironina (fT3) kod ispitanika s teškim simptomima hospitaliziranih u intenzivističkom centru (IC ; N=45), ispitanika sa srednje teškim simptomima hospitaliziranih u respiratornom centru (RC ; N=43), ispitanika koji su preboljeli COVID- 19 i koji se prate u post-COVID ambulanti (PCDB ; N=76) i zdravih ispitanika koji su dobrovoljno sudjelovali u istraživanju (H ; N=60). Za usporedbu koncentracija TSH, fT4 i fT3 između skupina korišten je test Kruskal-Wallis, a logističkom regresijom ispitana je povezanost biljega s ishodom u skupinama hospitaliziranih ispitanika. Za statističku obradu podataka korišten je MedCalc Statistical Software, verzija 14.8.1 (MedCalc Software bvba, Ostend, Belgija). Rezultati: Medijani i 95% intervali pouzdanosti za ispitivane skupine za TSH, fT4 i fT3 redom su bili: 1, 02 (0, 51 – 1, 87) mIU/L ; 13, 34(10, 97 – 15, 39) pmol/L ; 3, 28 (2, 74 – 3, 43) pmol/L. Dobivena je statistički značajna razlika u koncentracijama TSH, fT3 i fT4 između 4 ispitivane skupine (P

Uvod: Statini su inhibitori 3-hidroksi-3-metilglutaril koenzim A (HMG-CoA) reduktaze koji se primjenjuju za smanjenje sinteze endogenog kolesterola kod pojedinih vrsta hiperlipoproteinemija. Međutim, statini pokazuju i pleiotropne učinke te se smatra da utječu na upalu, oksidacijski stres, oslobađanje citokina i apoptozu pojedinih staničnih vrsta. Kronična opstrukcijska plućna bolest (KOPB) je kronična upalna bolest pluća sa sistemskom upalom te se smatra da bi lijekovi koji utječu na prisutni upalni proces mogli doprinjeti poboljšanju stanja u bolesnika s KOPBom. Hipoteza ovoga istraživanja je da statini posjeduju protuupalni učinak koji bi mogao usporiti progresiju KOPB-a. Metode: U istraživanje je bilo uključeno 100 bolesnika sa stabilnim KOPB-om, na terapiji statinima dulje od godinu dana (N=66) i bez terapije statinima (N=34). Svim bolesnicima je određena koncentracija citokina: IL-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12 p70, IFN-γ, TNF-α i TNF-β u plazmi metodom protočne citometrije. Relativni udio apoptoze i nekroze leukocita odnosno subpopulacija granulocita, limfocita i monocita određen je također metodom protočne citometrije. Spirometrijski, biokemijski i hematološki parametri određeni su u svih bolesnika. Rezultati: Citokini IL-1β, IL-2, IL-4, IL-8, IL-10, IL-12p70 i TNF-α pokazali su statistički značajno smanjenje koncentracije u bolesnika s KOPB-om na terapiji statinima u odnosu na bolesnike s KOPB-om bez terapije statinima. Hijerarhijska klasterska analiza pokazala je nekoliko klastera u bolesnika s KOPB-om u skladu s vrijednostima citokina. Citokinski uzorci bili su u velikoj skupini pacijenata slični s umjerenim povećanjem vrijednosti citokina. Bolesnici s KOPB-om koji su uzimali statine pokazali su različit obrazac/uzorak citokina s nižim vrijednostima citokina. Koncentracije citokina nisu pokazale statistički značajnu razliku ovisno o podjeli bolesnika prema težini oboljenja odnosno GOLD stadiju. Statistički značajno snižene koncentracije citokina IL-4, IL-8 i IL-10 su bile prisutne u bolesnika s KOPB-om s povišenim ITM-om (> 25 kg/m2) u odnosu na bolesnike s normalnim ITM-om (20 – 25 kg/m2). U perifernoj krvi relativni udio svih leukocita, te subpopulacije limfocita i monocita u apoptozi pokazali su statistički značajno smanjenje u bolesnika s KOPB-om na terapiji statinima u odnosu na bolesnike s KOPB-om bez terapije statinima. Zaključak: Rezultati istraživanja pružaju uvid u pleiotropne učinke statina u bolesnika s KOPB-om. U ovom radu u bolesnika s KOPB-om, pored djelovanja statina na smanjenje koncentracije kolesterola i LDL-kolesterola, pokazali smo i pleiotropne učinke statina na koncentracije citokina, koji su ključni medijatori lokalne i sistemske upale u KOPBu, te na apoptozu leukocita periferne krvi. Mjerenje panela citokina, a ne samo pojedinog citokina, pruža uvid u karakteristične obrasce citokina u bolesnika s KOPB-om. Postoji prisutan Th1 (IL-2 i TNF-α) i Th2 (IL-4, IL-5, IL- 10) citokinski obrazac kod stabilnih bolesnika s KOPB-om. Background: Statins are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors used to reduce the endogenous cholesterol synthesis in some types of hyperlipoproteinemia. However, statins also show pleiotropic effects and are thought to affect inflammation, oxidative stress, release of cytokines and apoptosis of certain cell types. Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the lungs with systemic inflammation and it is considered that drugs that affect the present inflammatory process could contribute to improving the condition in patients with COPD. The hypothesis of this study is that statins possess an anti-inflammatory effect that could slow the progression of COPD. Methods: The study included 100 patients with stable COPD, who received statin therapy for longer than one year (N = 66) and no statin therapy (N = 34). Cytokine concentration of IL-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12 p70, IFN-γ,TNF-α and TNF- β was measured in plasma by flow cytometry. The relative percentage of apoptotic and necrotic leukocytes, populations of granulocytes, lymphocytes and monocytes was determined by flow cytometry. Spirometry, biochemical and hematological parameters were determined in all patients. Results: Cytokines IL-1β, IL-2, IL-4, IL-8, IL-10, IL-12p70 and TNF-α showed a statistically significant decrease of concentrations in patients with COPD on statin therapy compared to patients without statin therapy. Hierarchical cluster analysis showed several clusters in COPD patients in accordance with cytokine values. Cytokine patterns were in a large group of patients similar with a moderate increase in the cytokine levels. COPD patients who received statins showed a different pattern of cytokines with lower cytokine values. Cytokine concentrations did not show a statistically significant difference depending on the severity of the disease, according to GOLD stages. A statistically significant decrease of cytokine levels IL-4, IL-8 and IL-10 was present in patients with COPD with a body mass index (BMI) > 25 kg/m2 compared to patients with normal BMI 20-25 kg/m2. In peripheral blood, the relative percentage of all leukocytes, as well as the lymphocyte and monocyte subpopulations in apoptosis, showed a statistically significant decrease in COPD patients on statin therapy compared with COPD patients without statin therapy. Conclusions: The results of the study provide an insight into pleiotropic effects of statins in patients with COPD. In our patients with COPD, the statins reduced cholesterol and LDL cholesterol levels, but we also demonstrated pleiotropic effects of statins on cytokines, both local and systemic inflammatory mediators in COPD as well as on apoptosis of peripheral blood leukocytes. The measurement of the cytokine panel, not just a single cytokine, provides an insight into cytokine patterns that are present in COPD patients. There is a Th1 (IL-2 i TNF-α) and Th2 (IL-4, IL- 5, IL-10) cytokine pattern present in stable COPD patients.

Background: Dyslipidemia has been described in treated HIV-patients as a side effect of antiretroviral therapy and therefore lipid status is an essential part of monitoring HIV- positive patients. In the present study we compared measured with calculated low density lipoprotein cholesterol (LDL-C) (Friedewald’s formula and a recently new Anandaraja’s formula) in HIV-positive patients. Materials and methods: Determination of triglycerides and cholesterol (Thermo Fisher Scientific, USA), direct LDL-C (D-LDL-C) and HDL-C (Dijagnostika d.o.o., Croatia) was done on Beckman Coulter AU400 analyzer in sera of HIV-positive patients (N = 98). Calculation of LDL-C with Friedewald’s and Anandaraja’s formulas was performed. Measured D-LDL-C was compared with calculated LDL-C. Statistical analysis was done with MedCalc software (version 12.7.0). Results: Mean and standard deviation for LDL-C concentrations were as follows: 2.53 ± 0.79 mmol/L (D-LDL-C), 3.15 ± 1.13 mmol/L calculated by Friedewald’s formula (F-LDL-C) and 3.46 ± 1.14 mmol/L calculated by Anandaraja’s formula (A-LDL-C). Passing-Bablok regression analysis showed a constant difference between D-LDL-C and F-LDL-C, but not between D-LDL-C and A-LDL- C and a proportional difference for measured D- LDL-C and both equations (D-LDL-C vs. F-LDL-C: y=-0.259 + 1.353 x ; D-LDL-C vs. A-LDL-C: y = -0.425 + 1.500 x). Bland-Altman plot showed a mean difference between methods: D-LDL-C vs. F-LDL-C -0.62 mmol/L (95% CI: -1.50 to 0.27) and D-LDL-C vs. A-LDL-C -0.93 mmol/L (95% CI: -2.07 to 0.21). Conclusion: According to our results, measured and calculated LDL-C should not be used interchangeably in HIV-postive patients. Friedewald’s and Anandaraja’s equation generally overestimate LDL-C in HIV patients.

This study shows correlation between procalcitonin and C-reactive protein in patients with local and systematic infectious disease.

U radu je opisan značaj određivanja CRP i PCT te njihova korelaciju u infektivnim bolestima. Također, opisane su metode određivanja PCT-a.

Background: N-terminal pro B-type natriuretic peptide (NTproBNP)was recognized as a marker of heart failure. But some researches showed its value in diagnosis of sepsis and predicting mortality. Methods: Levels of NT-proBNP were measured by Cardiac reader, Roche. Measurement range: 60 ng/L - 3000 ng/L. Results: Retrospectively, we tried to assess the usefulness of measuring NT-proBNP in predicting mortality of two infant patients. The first patient was a nine-months-old female infant with confirmed meningococcal sepsis, Glasgow coma score: 9. On the second day of admission, the level of NT-proBNP was higher than 3000 ng/L, with elevated level of hsCRP (159 mg/L). NT-proBNP was measured two more times and its levels decreased respectively 2053 ng/L and 299 ng/L. According to other results there was no organ failure. The second patient was a nine-months-old male infant, with Glasgow coma score 14, admitted with diagnosis of bronchitis caused by Mycoplasma pneumoniae. The patient had corrected aortic stenosis and during mild respiratory infection his condition worsened with heart decompensation, secondary pneumonia and sepsis. Levels of NT-proBNP were measured four times and in all measurements, the levels were >3000 ng/L. hsCRP levels were not so high, 11.6 mg/L and lower which indicates the possibility of a generalized viral infection that caused sepsis syndrome. Organ failure occurred in this patient resulting in lethal outcome. Conclusions: These two cases have shown that measuring NT-proBNP levels in infant patients can be useful in predicting mortality, which was previously described in some other larger studies.

COPD (chronic obstructive pulmonary disease) is a chronic progressive inflammatory disease characterised by limitations in lung airflow that is not fully reversible. The concentrations and correlations of TNF-alpha, CXCL8, big ET-1 and hsCRP were investigated in healthy non-smokers, healthy smokers and patients with COPD in order to study their possible role in the pathophysiology of COPD. The concentrations of TNF-á, CXCL8 and big ET-1 were not statistically different between the experimental groups. No significant differences for the measured analytes were found between smokers and the non-smokers in the control group. The Spearman coefficient of correlation between the concentrations of TNF-á and CXCL8 was r = 0.638 (p

COPD (chronic obstructive pulmonary disease) is a chronic progressive inflammatory disease characterised by limitations in lung airflow that is not fully reversible. The concentrations and correlations of TNF-á, CXCL8, big ET-1 and hsCRP were investigated in healthy non-smokers, healthy smokers and patients with COPD in order to study their possible role in the pathophysiology of COPD. The concentrations of TNF-á, CXCL8 and big ET-1 were not statistically different between the experimental groups. No significant differences for the measured analytes were found between smokers and the non-smokers in the control group. The Spearman coefficient of correlation between the concentrations of TNF-á and CXCL8 was r = 0.638 (p

Background. The most common cause of COPD (chronic obstructive pulmonary disease) is tobacco smoke. Tobacco smoke induces release of proinflammatory cytokine': TNF-a (tumor necrosis factor-a), that further induced IL-8 (interleukin-8), and eventually ET-1 and bigET-1. The latter are potent bronchoconstrictors. These mediators probably contribute to the patophysiology oi COPD. hsCRP (high sensitivity C-reactive protein) and Ot-AT (ai-antitrypsin) are acute phase proteins elevated in inflammatory diseases. The aim of our study was to investigate the influence of smoking habits on the concentrations of TNF-a, IL-8 and bigET-1 in patients with COPD and their correlation. Systemic inflammation was investigated with these parameters and arAT, hsCRP and total leukocyte count (WBC). Materials and methods. The analytes were measured in healthy non-smokers (n=23, control group), healthy smokers (n=30) and COPD patients (n=30). ELISA-s were performed for TNF-a and IL-8 (serum) and bigET-1 (plasma), a, -AT and hsCRP were measured in serum nephelometrically. Results. The COPD group had a higher median for cigarette packs/year than the control (p=0.0052). Concentrations of TNF-a (p=0.0788), IL-8 (p=0.4839), bigET-1 (p=0.3641) and arAT (p=0.0547) were not statistically different between COPD patients vs. control. No significant difference for these analytes was found between smokers vs. control. However, concentration of hsCRP (p=0.0004) and the WBC (p=0.0012) were higher in patients with COPD vs. control. Conclusions. Probably there is no long term increase in the measured analytas due to tobacco smoking. Measurement of hsCRP proved to be a more sensitive parameter than a, -AT, TNF-a, IL-8, ana bigET-1 for systemic inflammation in patients with COPD.

COPD (chronic obstructive pulmonary disease) is a chronic progressive inflammatory disease characterized by limitations in lung airflow that is not fully reversible. Although the pathophysiology of COPD is not understood completely, it is well known that various cells in the lungs are releasing inflammatory mediators. Tobacco smoke induces the release of a pro-inflammatory cytokine TNF-alpha (tumor necrosis factor-alfa) that might play a key role in COPD. TNF-alpha activates certain transcription factors and switches on the transcription of genes for cytokines, chemokines, proteases and endothelins. CXCL8 (interleukin-8) is a chemokine that attracts neutrophils to the inflammatory site. ET-1 (endothelin-1) and big ET-1 contribute to pulmonary vasoconstriction and pulmonary hypertension in COPD patients. hsCRP (highly sensitivity C-reactive protein) is an acute phase protein elevated in inflammatory diseases. The aim of this study was to investigate the concentrations and correlation of TNF-alpha, CXCL8, big ET-1 and hsCRP in healthy non-smokers, healthy smokers and patients with COPD. The concentration of TNF-alpha and CXCL8 in serum and big ET-1 in plasma was measured with an ELISA test in healthy non-smokers (n=23, control group), healthy smokers (n= 30) and COPD patients (n=30). hsCRP was measured in serum nephelometrically. The concentration of hsCRP was significantly higher in patients with COPD than in the control group (p=0.0004) but the concentrations of TNF-alpha (p=0.0788), CXCL8 (p=0.4839) and big ET-1 (p=0.3641) were not statistically different. There was no significant difference in the measured analytes between smokers and control group. Spearman coefficient of correlation between the concentrations of TNF- alpha and CXCL8 was r= 0.638 (P