A Barrett nyelőcső klinikai és kísérletes vizsgálata = Clinical and experimental investigation of Barrett's esophagus

Klinikai vizsgálatok Megvizsgáltuk a laparoscopos Nissen féle fundoplicatio hatékonyságát Barrett-nyelőcső (BNY) miatt operált betegeken (n=78). A műtét után 64 beteg utánkövetése történt, átlagosan 42±16.19 hónapig. Vizsgálataink szerint a low-grade dysplasia kialakulásában szerepet játszik a súlyos epés reflux. A kontroll vizsgálatok 10 esetben mutatták a Barrett-metaplasia (BM) teljes regresszióját. Részleges regresszió 9 esetben volt, 34 betegnél nem volt progresszió, 11 esetben volt progresszió (cardiális vagy intestinális metaplasia kialakulása). Az antireflux műtétek a betegek nagy részében kontrollálják a reflux betegséget, megakadályozzák a BM progresszióját és elősegítik a BM regresszióját. In vitro vizsgálatok Kísérleti rendszert dolgoztunk ki, amely alkalmas a humán nyelőcső epitél sejtek (NYES) iontranszport folyamatainak karakterizálására és toxikus ágensek NYES kifejtett hatásának a vizsgálatára. Kidolgoztunk egy új módszert, melynek során nyelőcső biopsziás mintákból enzimatikus úton NYESeket tudunk izolálni, mikrofluorometriás módszerrel karakterizáltuk a Na+/H+ és a Cl-/HCO3- kicserélő és a Na+/HCO3- kotranszporter jelenlétét. Humán NYES vonalon kimutattuk a pH regulációs transzporterek jelenlétét, megvizsgáltuk az epesav terhelés hatását a sejtek intracelluláris pH-jára, összehasonlítottuk a NYES ion transzportját más gasztrointesztinális epitél sejtek működésével. | Clinical studies: We investigated the efficacy of laparoscopic Nissen fundoplication in patients with Barrett’s esophagus (BE) (n=78). We assessed effect of fundoplication on symptoms of reflux disease, the changes of Barrett’s metaplasia (BM) in these patients. Clinical follow-up was available in the case of 64 patients at a mean of 42±16.19 months after surgery. Check-up examination revealed total regression of BM in 10 patients. Partial regression was seen in 9 cases, no further progression in 34 patients, and progression into cardiac or intestinal metaplasia in 11 patients. No cases of dysplastic or malignant transformation were registered. Severe biliary reflux is presumed to be a factor in the development of low grade dysplasia.Antireflux surgery can appropriately control the reflux disease and it may inhibit the progression and induce the regression of BM in these patients. In vitro studies: We developed a system for the characterization of ion transport mechanisms of human oesophageal epithelial cells (HOEC) and to study the effects of toxic agents on them. We used a novel method for the isolation of HOEC from oesophageal biopsy samples and characterized the presence of Na+/H+, Cl-/HCO3- exchanger and Na+/HCO3- cotransporter on HOEC. We confirmed the presence of pH regulatory transporters in HOEC line. We studied the effect of bile acids on the intracellular pH of HOEC and compared the HCO3- transport mechanisms of HOEC to those of other epithelial cells

Possible use of Digital Variance Angiography in Liver Transarterial Chemoembolization: A Retrospective Observational Study

Purpose Digital variance angiography (DVA), a recently developed image processing technology, provided higher contrast-to-noise ratio (CNR) and better image quality (IQ) during lower limb interventions than digital subtraction angiography (DSA). Our aim was to investigate whether this quality improvement can be observed also during liver transarterial chemoembolization (TACE).Materials and MethodsWe retrospectively compared the CNR and IQ parameters of DSA and DVA images from 25 patients (65% male, mean +/- SD age: 67.5 +/- 11.2 years) underwent TACE intervention at our institute. CNR was calculated on 50 images. IQ of every image set was evaluated by 5 experts using 4-grade Likert scales. Both single image evaluation and paired image comparison were performed in a blinded and randomized manner. The diagnostic value was evaluated based on the possibility to identify lesions and feeding arteries.ResultsDVA provided significantly higher CNR (mean CNRDVA/CNRDSA was 1.33). DVA images received significantly higher individual Likert score (mean +/- SEM 3.34 +/- 0,08 vs. 2.89 +/- 0.11, Wilcoxon signed-rank p < 0.001) and proved to be superior also in paired comparisons (median comparison score 1.60 [IQR:2.40], one sample Wilcoxon p < 0.001 compared to equal quality level). DSA could not detect lesion and feeding artery in 28 and 36% of cases, and allowed clear detection only in 22% and 16%, respectively. In contrast, DVA failed only in 8 and 18% and clearly revealed lesions and feeding arteries in 32 and 26%, respectively.ConclusionIn our study, DVA provided higher quality images and better diagnostic insight than DSA; therefore, DVA could represent a useful tool in liver TACE interventions

Predictive Value of Tachycardia for Mortality in Trauma-Related Haemorrhagic Shock: A Systematic Review and Meta-Regression

OBJECTIVES: Heart rate (HR) is one of the physiological variables in the early assessment of trauma-related haemorrhagic shock, according to Advanced Trauma Life Support (ATLS). However, its efficiency as predictor of mortality is contradicted by several studies. Furthermore, the linear association between HR and the severity of shock and blood loss presented by ATLS is doubtful. This systematic review aims to update current knowledge on the role of HR in the initial haemodynamic assessment of patients who had a trauma. DESIGN: This study is a systematic review and meta-regression that follows the Preferred Reporting Items for Systematic Reviews and Meta-Analyses recommendations. DATA SOURCES: EMBASE, MEDLINE, CENTRAL and Web of Science databases were systematically searched through on 1 September 2020. ELIGIBILITY CRITERIA: Papers providing early HR and mortality data on bleeding patients who had a trauma were included. Patient cohorts were considered haemorrhagic if the inclusion criteria of the studies contained transfusion and/or positive focused assessment with sonography for trauma and/or postinjury haemodynamical instability and/or abdominal gunshot injury. Studies on burns, traumatic spinal or brain injuries were excluded. Papers published before January 2010 were not considered. DATA EXTRACTION AND SYNTHESIS: Data extraction and risk of bias were assessed by two independent investigators. The association between HR and mortality of patients who had a trauma was assessed using meta-regression analysis. As subgroup analysis, meta-regression was performed on patients who received blood products. RESULTS: From a total of 2017 papers, 19 studies met our eligibility criteria. Our primary meta-regression did not find a significant relation (p=0.847) between HR and mortality in patients who had a trauma with haemorrhage. Our subgroup analysis included 10 studies, and it could not reveal a linear association between HR and mortality rate. CONCLUSIONS: In accordance with the literature demonstrating the multiphasic response of HR to bleeding, our study presents the lack of linear association between postinjury HR and mortality. Modifying the pattern of HR derangements in the ATLS shock classification may result in a more precise teaching tool for young clinicians

Epidemiology and aetiology.

<p><b>A</b>. Sex distribution of AP cases. <b>B.</b> Age distribution of AP cases. <b>C.</b> AP severity groups. Mod: moderate; sev: severe. <b>D.</b> Age distribution of mild, moderate and severe AP cases and mortality. <b>E.</b> Overall mortality and distribution in the severity groups. p<0.001 was between the severe and other groups according to Fisher’s exact test. <b>F.</b> Days of hospitalization. Mann-Whitney U test with Bonferroni correction was used to compare the group pairs (p<0.001 between groups). <b>G.</b> Aetiology of AP. (<b>a:</b> p<0.001; <b>b:</b> p<0.001; <b>c:</b> p = 0.022, <b>d:</b> p = 0.030; <b>e:</b> p = 0.006; <b>f:</b> p<0.001; <b>g:</b> p = 0.011; <b>h:</b> p = 0.025).</p

Conservative therapy in AP.

<p><b>A.</b> Effect of fluid resuscitation on severity and mortality in the first 24 hours. The first dotted column represents the AP severity groups and mortality for each group in the entire cohort. Green: mild AP; yellow: moderate AP; red: severe AP; *: p = 0.030 (Fisher’s exact test on severity) versus the cohort (n = 8–185). A polynomial regression curve was fitted to demonstrate the mortality trend (n = 8–185). <b>B.</b> Enteral and parenteral feeding in AP. Mortality is shown for the severe AP group. NG: nasogastric feeding; NJ: nasojejunal feeding. <b>C.</b> Antibiotic therapy and its indications in AP. Table shows the indications for antibiotic therapy in the three severity groups. <b>D.</b> Probiotic therapy in AP.</p

Diagnosis, anamnestic data and symptoms at admission.

<p><b>A.</b> Anamnestic data. The percentages of severe AP and mortality in severe AP are also shown in relation to alcohol consumption, smoking, diabetes and history of earlier AP. <b>B.</b> Relationship between time of onset of abdominal pain and presentation at ER units. <b>C.</b> Time of onset of abdominal pain and presentation at ER in the three severity groups and association with mortality in the severe group. <b>D.</b> Diagnosis. Distribution of diagnostic criteria in the overall cohort (pie chart) and in the three severity groups (table) and association with mortality in severe AP (table). P: pain; E: enzyme elevation; I: imaging alteration. ^O p = 0.189 (Fisher’s exact test) * p = 0.005 (Chi-square test) *** p<0.001 (Chi-square test). <b>E.</b> Type and localisation of abdominal pain. EPI: epigastric pain; URA: upper right abdomen; ULA: upper left abdomen; MD: middle abdomen; L: lower abdomen; D: diffuse. <b>F.</b> Symptoms in the entire cohort and in the severe AP group and association with mortality in the severe AP group. ^O p = 0.189 (Fisher’s exact test) ^OO p = 0.051 (Chi-square test) * p = 0.029 (Chi-square test).</p

Laboratory parameters in AP.

<p>The only parameters shown are where statistical differences were found between the AP severity groups. Green: mild AP; yellow: moderate AP; red: severe AP; <b>ns:</b> no significant difference (p>0.05); <b>+:</b> significant difference (p<0.05). In the left-hand panel of graphs, laboratory parameters were analysed by distinct values, grouped in ranges. The first dotted column represents the AP severity groups of the entire cohort. Here, the Chi-square test was employed. In the right-hand panel of graphs, the average laboratory parameters were compared in the three AP severity groups. Here, we used the Kruskal–Wallis test and Mann–Whitney U test with a Bonferroni correction to compare the pairs of groups under examination. <b>A.</b> White blood cell count (WBC, n = 21–204). A WBC count above 23,000/μL was associated with elevated risk of severe AP (<b>a:</b> p = 0.020), and the average WBC counts also showed significant differences between the mild versus moderate and mild versus severe AP groups (p<0.001). <b>B.</b> C-reactive protein (CRP: n = 32–144). CRP above 200 mg/L was associated with severe AP (<b>b:</b> p = 0.007). In addition, average CRP levels differed significantly between the mild versus moderate and mild versus severe AP groups (p<0.001). <b>C.</b> Procalcitonin (PCT, n = 5–54). PCT levels above 10 U/L were associated with elevated risk of severe AP (<b>c:</b> p<0.001); however, average PCT levels did not differ significantly between the three AP severity groups (p = 0.143). <b>D.</b> Calcium (Ca, n = 12–40). Ca levels below 2 mmol/L were associated with a heightened risk of severe AP (<b>d:</b> p = 0.004); however, the average calcium levels did not differ significantly between the three AP severity groups (p = 0.077). <b>E.</b> Triglycerides (Tg: n = 10–48). Tg levels above 41 mmol/L were associated with greater risk of severe AP (<b>e:</b> p = 0.012); however, average Tg levels did not differ significantly between the three AP severity groups (p = 0.153). <b>F.</b> Glucose. (n = 3–175). Significant differences in severity associated with particular glucose levels were not found (<b>f:</b> p = 0.191); however, average glucose levels differed significantly between the mild versus moderate and mild versus severe AP groups (p<0.001).</p

Type, indication and outcome of interventions in AP.

<p>Data show the mortality differences between early and late interventions in AP.</p

Frequency of organ failure and mortality in AP.

<p><b>A.</b> Frequency of individual organ failure (pancreas, lung, cardiac, kidney and brain) and mortality in severe AP. <b>B.</b> Frequency of combined organ failure and mortality in severe AP. <b>C.</b> Frequency of pancreatic complications and mortality in AP. Mortality was only calculated in severe AP. <b>a:</b> p = 0.020 (Fisher’s exact test); <b>b:</b> p = 0.002 (Chi-square test); <b>c:</b> p = 0.043 (Fisher’s exact test); <b>d:</b> p = 0.003 (Chi-square test); <b>e:</b> p = 0.030 (Fisher’s exact test).</p