Bálint Erőss

Helicobacter pylori infection reduces the risk of Barrett's esophagus: A meta-analysis and systematic review

The prevalence of Helicobacter pylori infection (HPI) has been decreasing in developed countries, with an increasing prevalence of Barretts esophagus (BE) and esophageal adenocarcinoma (EAC) at the same time. The aim of our meta‐analysis was to quantify the risk of BE in the context of HPI.

Asymmetric dimethylarginine levels in preeclampsia – Systematic review and meta-analysis

OBJECTIVEnPreeclampsia (PE) is the leading cause of maternal and perinatal mortality around the world. The impaired function of fetal-placental vasculature is a key factor in PE. Several studies have investigated the connection between PE and endothelial dysfunction. Also, many authors have examined the changes in asymmetric dimethylarginine (ADMA) as a prominent marker of endothelial dysfunction. Our study aim is to review and analyse the connections between PE and ADMA levels.nnnMETHODSnTo obtain data we performed a comprehensive literature search in Pubmed, Embase and Web of Science. Standardized mean differences were used to estimate the differences in ADMA levels.nnnRESULTSnThe quantitative analysis included 10 studies reporting a total number of 631u202fPE and 498 healthy pregnant individuals. We found significantly higher ADMA levels in PE patients compared to controls, when comparing the ADMA levels of the patients to the ADMA levels of the controls (zu202f=u202f5.93, pu202f<u202f0.001). This difference was present regardless of the measurement method. Regarding the onset of PE, we found significantly higher ADMA levels in patients suffering from early-onset PE when comparing the ADMA levels of the early-onset PE patients to that of the controls (zu202f=u202f2.82, pu202f=u202f0.005). However, we did not find such difference when we compared late-onset PE patients ADMA levels to controls.nnnCONCLUSIONnADMA is significantly higher in PE patients than in the controls. Elevated ADMA levels can play a major role in the development of PE, but more research is needed to clarify the connection between the two.

Intralesional steroid is beneficial in benign refractory esophageal strictures: A meta-analysis

AIM To analyze the effect of intralesional steroid injections in addition to endoscopic dilation of benign refractory esophageal strictures. METHODS A comprehensive search was performed in three databases from inception to 10 April 2017 to identify trials, comparing the efficacy of endoscopic dilation to dilation combined with intralesional steroid injections. Following the data extraction, meta-analytical calculations were performed on measures of outcome by the random-effects method of DerSimonian and Laird. Heterogeneity of the studies was tested by Cochrane’s Q and I2 statistics. Risk of quality and bias was assessed by the Newcastle Ottawa Scale and JADAD assessment tools. RESULTS Eleven articles were identified suitable for analyses, involving 343 patients, 235 cases and 229 controls in total. Four studies used crossover design with 121 subjects enrolled. The periodic dilation index (PDI) was comparable in 4 studies, where the pooled result showed a significant improvement of PDI in the steroid group (MD: -1.12 dilation/month, 95%CI: -1.99 to -0.25 P = 0.012; I2 = 74.4%). The total number of repeat dilations (TNRD) was comparable in 5 studies and showed a non-significant decrease (MD: -1.17, 95%CI: -0.24-0.05, P = 0.057; I2 = 0), while the dysphagia score (DS) was comparable in 5 studies and did not improve (SMD: 0.35, 95%CI: -0.38, 1.08, P = 0.351; I2 = 83.98%) after intralesional steroid injection. CONCLUSION Intralesional steroid injection increases the time between endoscopic dilations of benign refractory esophageal strictures. However, its potential role needs further research.

The effect of serum triglyceride concentration on the outcome of acute pancreatitis: systematic review and meta-analysis

Elevated serum triglyceride concentration (seTG, >1.7u2009mM or >150u2009mg/dL) or in other words hypertriglyceridemia (HTG) is common in the populations of developed countries. This condition is accompanied by an increased risk for various diseases, such as acute pancreatitis (AP). It has been proposed that HTG could also worsen the course of AP. Therefore, in this meta-analysis, we aimed to compare the effects of various seTGs on the severity, mortality, local and systemic complications of AP, and on intensive care unit admission. 16 eligible studies, including 11,965 patients were retrieved from PubMed and Embase. The results showed that HTG significantly elevated the odds ratio (ORu2009=u20091.72) for severe AP when compared to patients with normal seTG (<1.7u2009mM). Furthermore, a significantly higher occurrence of pancreatic necrosis, persistent organ failure and renal failure was observed in groups with HTG. The rates of complications and mortality for AP were significantly increased in patients with seTG >5.6u2009mM or >11.3u2009mM versus <5.6u2009mM or <11.3u2009mM, respectively. We conclude that the presence of HTG worsens the course and outcome of AP, but we found no significant difference in AP severity based on the extent of HTG.

Centralized care for acute pancreatitis significantly improves outcomes

AIMSnIn this observational study, we investigated whether specialized care improves outcomes for acute pancreatitis (AP).nnnMETHODSnConsecutive patients admitted to two university hospitals with AP were enrolled in this study between 1 January 2016 and 31 December 2016 (Center A: specialized center; Center B: general hospital). Data on demographic characteristics and AP etiology, severity, mortality and quality of care (enteral nutrition and antibiotic use) were extracted from the Hungarian Acute Pancreatitis Registry. An independent sample t-test, Mann-Whitney test, chi-squared test or Fishers test were used for statistical analyses. Costs of care were calculated and compared in the two models of care.nnnRESULTSnThere were 355 patients enrolled, 195 patients in the specialized center (Center A) and 160 patients in the general hospital (Center B). There was no difference in mean age (57.02 +/-17.16 vs. 57.31 +/-16.50 P=0.872) and sex ratio (56% males vs. 57% males, P=0.837) between centres, allowing a comparison without selection bias. Center A had lower mortality (n=2, 1.03% vs. n=16, 6.25%, p=0.007), more patients received enteral feeding (n=179, 91.8%, vs. n=36, 22.5%, p<0.001) and fewer patients were treated with antibiotics (n=85, 43.6% vs. n=123, 76.9%, p=0.001). In Center A the median length of hospitalization was shorter (Me 6, IQR 5-9 vs. Me 8, IQR 6-11, p=0.02) and the costs of care were by 25% lower.nnnCONCLUSIONnOur data suggests that treatment of AP in specialized centers reduces mortality, length of hospitalization and thus might reduce the costs.

Does Helicobacter pylori infection increase the risk of Barrett's esophagus and esophageal adenocarcinoma?

Dear Editor We appreciate the thoughts and comments of Doulberis et al on our study published in Helicobacter recently.1 Our metaanalysis concluded that H. pylori infection (HPI) reduces the risk of Barrett’s esophagus (BE), dysplasia and adenocarcinoma developing in BE. Doulberis et al outlined their theory why HPI increases the risk of BE and esophageal adenocarcinoma (EAC), which is the opposite of what we have found in our metaanalysis. They propose that the following chain of events leads to increased risk of BE and EAC. HPI is associated with increased insulin resistance, leading to metabolic syndrome, which, complicated by obesity, facilitates gastroesophgeal reflux and promotes oncogenic factors, increasing the risk of EAC.2 We would like to emphasize, as clearly stated in our article, that there is no evidence for the benefit of HPI with regard to the risk of BE and EAC, and we do not recommend that H. pylori should not be eradicated. However, the results of our findings could be used for the risk stratification of individuals undergoing surveillance for BE. Finally, there are very little original data on the relationship between H. pylori eradication and the risk of BE and the adenocarcinoma of the esophagus. We agree that the confounding factors and the high degree of heterogeneity among the studies included in our metaanalysis should caution us, and conclusions from the results should be carefully assessed. The review cited by Doulberis et al included 10 original studies and four metaanalyses.3 Five of the original studies found that HPI was inversely associated with the risk of EAC, the other five studies showed no association. There were no original studies in this review demonstrating direct association of HPI and EAC. The four metaanalyses identified in the review all proved an inverse relationship between HPI and EAC. In contrast, the review stipulates that the results are inconclusive and the opposite may be the case. In countries with increasing incidence of EAC, the prevalence of obesity and metabolic syndrome is increasing while HPI prevalence is decreasing, which suggests that only a fraction of metabolic syndrome and obesity is related to HPI. It may well be that the dynamic decrease of HPI prevalence increases the risk of BE and EAC in a certain population, rather than a stable low prevalence. That would explain the low prevalence of both HPI and EAC in the Malaysian population, in addition to explaining why we see a sharp increase in the incidence of EAC in North America and Northwestern Europe, where HPI prevalence has been decreasing for the past decades. In addition, preliminary unpublished results of our retrospective study in Hungary show that the incidence of EAC has been increasing, along with a decreasing prevalence of HPI for the past decades, replicating the trend detailed above.4 That said, subgroup analysis for the prevalence rates of HPI in the control groups of the studies included in our metaanalysis showed that the infection reduces the risk of BE in all subgroups bar the one with prevalence greater than 70%, where the relationship is neutral, Table 1. Doulberis et al cites Graham’s article from 2003 in which he states that “H. pylori is not ‘protective’ against anything, including GERD and possibly its related complications including BE and EAC.”5 We would rather agree with his 2013 opinion, when he said “Under certain conditions, H. pylori can act as a biological antisecretory agent. In those instances, the infection results in reduced acid secretion and even the development of atrophy and diseases related to an increased esophageal acid load, such as symptomatic gastroesophageal reflux and adenocarcinoma of the esophagus, become rare, as does duodenal ulcer.”6 In summary, there are many unanswered question both in the epidemiology and the pathomechanism of BE and EAC in relation to HPI. We agree that the relationship needs further in-depth investigations.

Short-Course Antibiotic Treatment Is Not Inferior to a Long-Course One in Acute Cholangitis: A Systematic Review

AimsOur aim was to summarize the available literature on the effect of short- versus long-course antibiotic therapy on acute cholangitis.MethodsA systematic review was performed according to the PRISMA Statement. We searched three databases for papers discussing the length of ABT in acute cholangitis. Long and short therapy groups were defined based on the most recent guideline available at the time of publication of the articles. Primary outcomes were the rate of recurrent cholangitis and mortality; secondary outcomes included length of hospitalization and the duration of fever after ERCP. Data were extracted on these outcomes and on general characteristics. A narrative synthesis was then provided based on collected data.ResultsOut of 692 articles produced by our search, four met our inclusion and exclusion criteria. These contained 205 acute cholangitis patients, with 137 and 68 patients receiving short and long antibiotic therapy, respectively. No significant difference was observed in any of the studies on the outcomes of mortality and duration of fever after ERCP between the two groups. One out of four studies found the rate of recurrent cholangitis to be significantly lower in the short antibiotic therapy group (0.0% vs. 13.3%, pu2009=u20090.036). Length of hospitalization was only compared in the same retrospective article, where it was found to be significantly shorter in the short-term antibiotic therapy group (with a median of 14 vs. 17.5xa0days, pu2009<u20090.001).ConclusionsOur review suggests short-course antibiotic therapy is non-inferior to long-course treatment; however, several limitations underline the need for well-designed randomized trials.

Chronic kidney disease severely deteriorates the outcome of gastrointestinal bleeding: A meta-analysis

AIM To understand the influence of chronic kidney disease (CKD) on mortality, need for transfusion and rebleeding in gastrointestinal (GI) bleeding patients. METHODS A systematic search was conducted in three databases for studies on GI bleeding patients with CKD or end-stage renal disease (ESRD) with data on outcomes of mortality, transfusion requirement, rebleeding rate and length of hospitalization (LOH). Calculations were performed with Comprehensive Meta-Analysis software using the random effects model. Heterogeneity was tested by using Cochrane’s Q and I2 statistics. Mean difference (MD) and OR (odds ratio) were calculated. RESULTS 1063 articles (EMBASE: 589; PubMed: 459; Cochrane: 15) were found in total. 5 retrospective articles and 1 prospective study were available for analysis. These 6 articles contained data on 406035 patients, of whom 51315 had impaired renal function. The analysis showed a higher mortality in the CKD group (OR = 1.786, 95%CI: 1.689-1.888, P < 0.001) and the ESRD group (OR = 2.530, 95%CI: 1.386-4.616, P = 0.002), and a rebleeding rate (OR = 2.510, 95%CI: 1.521-4.144, P < 0.001) in patients with impaired renal function. CKD patients required more unit red blood cell transfusion (MD = 1.863, 95%CI: 0.812-2.915, P < 0.001) and spent more time in hospital (MD = 13.245, 95%CI: 6.886-19.623, P < 0.001) than the controls. CONCLUSION ESRD increases mortality, need for transfusion, rebleeding rate and LOH among GI bleeding patients. Prospective patient registries and observational clinical trials are crucially needed.