Minireviews Open Access
Copyright ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Feb 27, 2018; 10(2): 254-266
Published online Feb 27, 2018. doi: 10.4254/wjh.v10.i2.254
Spontaneous bacterial and fungal peritonitis in patients with liver cirrhosis: A literature review
Toru Shizuma
Toru Shizuma, Department of Physiology, Tokai University School of Medicine, Isehara 2591193, Japan
ORCID number: Toru Shizuma (0000-0003-4224-5834).
Author contributions: Shizuma T prepared the manuscript.
Conflict-of-interest statement: There is no conflict of interests to declare.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Toru Shizuma, MD, PhD, Associate Professor, Department of Physiology, Tokai University School of Medicine, 143, Shimokasuya, Isehara, Kanagawa 2591193, Japan. shizuma@is.icc.u-tokai.ac.jp
Telephone: +81-463-931121 Fax: +81-463-936684
Received: November 28, 2017
Peer-review started: November 28, 2017
First decision: December 18, 2017
Revised: December 31, 2017
Accepted: January 23, 2018
Article in press: January 23, 2018
Published online: February 27, 2018

Abstract

Spontaneous bacterial (SBP) and spontaneous fungal peritonitis (SFP) can be a life-threatening infection in patients with liver cirrhosis (LC) and ascites. One of the possible mechanisms of developing SBP is bacterial translocation. Although the number of polymorphonuclear cells in the culture of ascitic fluid is diagnostic for SBP, secondary bacterial peritonitis is necessary to exclude. The severity of underlying liver dysfunction is predictive of developing SBP; moreover, renal impairment and infections caused by multidrug-resistant (MDR) organism are associated with a fatal prognosis of SBP. SBP is treated by antimicrobials, but initial empirical treatment may not succeed because of the presence of MDR organisms, particularly in nosocomial infections. Antibiotic prophylaxis is recommended for patients with LC at a high risk of developing SBP, gastrointestinal bleeding, or a previous episode of SBP, but the increase in the risk of developing an infection caused by MDR organisms is a serious concern globally. Less is known about SFP in patients with LC, but the severity of underlying liver dysfunction may increase the hospital mortality. SFP mortality has been reported to be higher than that of SBP partially because the difficulty of early differentiation between SFP and SBP induces delayed antifungal therapy for SFP.

Key Words: Liver cirrhosis, Spontaneous bacterial peritonitis, Spontaneous fungal peritonitis, Bacterial infections

Core tip: Spontaneous bacterial (SBP) and spontaneous fungal peritonitis (SFP) are infectious complications in patients with liver cirrhosis (LC). Renal impairment, severity of underlying liver dysfunction, and infections caused by multidrug-resistant (MDR) organisms are associated with a fatal prognosis in SBP. Antibiotic prophylaxis is recommended for patients with LC and with a high risk of developing SBP, gastrointestinal bleeding, or a previous episode of SBP, but the increase in the risk of infections caused by MDR organisms is of concern. Increased mortality of SFP compared with that of SBP may partially result from delayed diagnosis and starting of antifungal therapy.



INTRODUCTION

Patients with liver cirrhosis (LC) are at a high risk of developing bacterial infections because of hypoactivity of phagocytic cells in the hepatic reticuloendothelial system, decreased production of complement, and bacterial influx into the general circulation through portacaval shunts[1]. The most common are spontaneous bacterial peritonitis (SBP), urinary tract infections, respiratory infections (pneumonia), soft tissue infections, and bacteremia[2].

SBP can be a life-threatening LC complication, and the severity of underlying liver dysfunction and renal impairment such as hepatorenal syndrome (HRS), are associated with poor prognosis[3]. An increasing prevalence of multidrug-resistant (MDR) bacterial infections has been associated with failure of empirical antibiotic therapy, and the prognosis of SBP caused by MDR bacteria is poor[4]. Less is known about spontaneous fungal peritonitis (SFP) in patients with LC[5,6], but the available case reports indicate that the mortality of SFP is worse than that of SBP.

This article reviews the published data on the incidence, diagnosis, causative organisms, treatment, prognosis, and prognostic factors of SBP and SFP in patients with LC.

BACTERIAL INFECTIONS IN PATIENTS WITH LIVER CIRRHOSIS
Possible mechanisms underlying bacterial infections including SBP

In cirrhosis with portal hypertension, the microcirculation in the intestinal mucosa is disturbed, resulting in a reduction of mucosal blood flow, intestinal bacterial overgrowth, and impaired mucosal integrity[7,8]. Intestinal bacterial overgrowth, impairment in permeability of the intestinal mucosal barrier, and deficiencies in local host immune defenses are estimated to the major mechanisms to promote bacterial translocation (BT or pathological BT) in LC[7,9]. BT may be involved in the onset or aggravation of bacterial infections such as SBP and or HRS in patients with LC[7,8,10]. Pijls et al[11] reported increased large and small intestine permeability in patients with LC, and BT has been reported to be associated with bacterial infections caused by aerobic Gram-negative bacteria in patients with LC and was found to be more frequent in experimental LC models with than in those without ascites[7].

Studies of BT and bacterial DNA (bact DNA) translocation are limited in humans[7], but acute-phase proteins such as C-reactive protein (CRP) or procalcitonin have been used as BT biomarker[7], and detection of bact DNA by polymerase chain reaction (PCR) in biologic fluid has been proposed as a useful surrogate biomarker of BT in patients with advanced LC[7]. The presence of bact DNA in ascites increases the risk of developing SBP and HRS[12] and is an indicator of poor prognosis[7,13]. Assay of bact DNA by PCR has low diagnostic accuracy for SBP because of possible contamination and has poor sensitivity[14]. In situ hybridization of bact DNA in leukocytes recovered from the ascitic fluid in patients with LC has high sensitivity and specificity even in patients with culture-negative SBP[14,15]. Proinflammatory cytokines or oxidative stress may be involved in the pathogenesis of BT, and anti-tumor necrosis factor (TNF) has been reported to be an effective treatment in an animal model of LC[8]. In addition to the severity of liver dysfunction, the genetic diversity and virulence of causative bacteria also may influence the development of BT[16]. Genetic variation of superoxide dismutase 1 may involve the development of SBP[17]. Bacterial metabolites that reach the liver through portal system activate toll-like receptors (TLRs)[18], and the genetic polymorphism of TLR and nucleotide-binding oligomerization domain 2 genes may also be involved in the pathogenesis of BT, thus increasing the risk of infection in patients with LC by altering TLR binding to lipopolysaccharides or endotoxins[13,16]. Finally, intestinal colonization and translocation of drug-resistant bacteria may induce MDR SBP infections[19,20].

Bacterial infections in patients with liver cirrhosis

It is estimated that 30%-60% of inpatients with LC will develop a bacterial infection[1,21], and that the occurrence of these infections is four to five times higher in patients with LC than that in the general population[21]. Bacterial infections can trigger rapid deterioration of liver function and are a common precipitating factor of acute-on-chronic liver failure in cirrhosis patients[10,16].

Mortality and the incidence of LC-related complications are both significantly higher in patients with than without bacterial infections[22].

Karvellas et al[23] reported that septic shock secondary to SBP has a high mortality rate of approximately 80% in patients with LC, and bloodstream infections occur in 4%-21% of patients with LC, which is 10-fold higher than the rate in noncirrhotic patients[24]. The mortality of bloodstream infections in patients with LC ranges from 23% to 58%[25].

The incidence of bacterial infections in patients with LC is significantly correlated with the severity of the underlying liver dysfunction[10,22,26,27]. However, a recent study by Dionigi et al[27] found that patients with LC who become infected had an increased risk of death independent of the severity of the underlying liver disease, even if they survived the acute infection. In patients with LC, infections caused by MDR bacteria are associated with a higher risk of mortality compared with those infections caused by susceptible bacteria[28,29]. An increased risk of MDR infections is a serious concern, is closely related to failure of antimicrobial therapy[29,30], and may induce deterioration of liver function[29]. MDR bacteria are resistant to at least three widely used antibiotic families[22]. These include the resistant bacteria that produce extended-spectrum β-lactamase (ESBL), such as Pseudomonas aeruginosa, and methicillin-resistant Staphylococcus aureus (MRSA)[31,32]. Recently, extensively drug-resistant (XDR) bacteria such as carbapenemase-producing Klebsiella pneumoniae and vancomycin-resistant Enterococci have been isolated from patients with LC[31]. The development of MDR infections is associated with suboptimal antibiotic use including antibiotic prophylaxis, nosocomial infection, recent infection with an MDR organism, current or recent hospitalization, exposure while receiving health care, and upper gastrointestinal bleeding in LC[33,34]. In a large prospective study, MDR bacteria were isolated in 4% of community-acquired infections, 14% of health care-associated infections, and 35% of nosocomial infections[33]. In two series of patients with LC evaluated in 2005-2007 and 2011-2012, Fernández et al[33] reported that MDR bacteria were more common in nosocomial infections and were associated with higher in-hospital mortality than in infections caused by antibiotic-susceptible bacteria. Pouriki et al[20] reported drug-resistant bacteria in intestinal cultures from 44% of uninfected patients with decompensated LC. Recent reports have found that asymptomatic intestinal colonization with MDR or XDR bacteria was an increased mortality risk in patients with LC in part because of BT of circulation of bacterial components[20].

SPONTANEOUS BACTERIAL PERITONITIS
Diagnosis

The development of ascites in patients with LC is a marker of poor prognosis and has been associated with high liver transplantation-free mortality ranging from 15% to 20% in 1 year and 40% to 60% in 5 year from the first onset[35].

SBP is as bacterial infection of the ascitic fluid with no apparent intraabdominal source of infection or malignancy[23]. A polymorphonuclear cell (PMN) count of ≥ 250 cells/mm3 in the ascitic fluid, regardless of the isolation of bacteria from the fluid[36], is diagnostic for SBP. PMN cell count is routinely performed by using the manual laboratory counting which is time-consuming and costly[37]. Some studies have reported that the manual and the automated counting methods have a good agreement in the determination of PMN in the ascitic fluid, and automated methods have the potential to replace the manual counting method[37,38]. Culture-negative SBP, also known as culture-negative neutrocytic ascites (CNNA), should be treated in the same way as culture-positive SBP[39]. Estimates of the mortality of culture-positive SBP and CNNA are conflicting. Some report a lower mortality for CNNA compared with culture-positive SBP[40]; others report comparable rates[41]. Bacterascites has also been diagnosed in patients with positive microbiological culture of ascites and a PMN count < 250 cells/mm3[36,42]. The incidence of bacterascites in inpatients with LC has been estimated at 3%-4%[42]. Most reports on bacterascites were published in the 1980s and early 1990s; very few are recent[43]. The diagnosis of SBP is necessary to distinguish from the cases with secondary bacterial peritonitis, partially because surgical treatments should be considered in secondary bacterial peritonitis but never in SBP[44,45]. Secondary bacterial peritonitis consists of ascitic fluid infection due to intraabdominal infections, for example, perforation of gastrointestinal tract or abscess[44,45]. It is much less frequent but has still high mortality rate compared with SBP in patients with LC[44,45].

Causative organisms

Ascitic fluid is culture positive in 35%-65% of patients with SBP[35,46-49]. The positive ascitic fluid bacterial cultures have been reported to increase by placement of the fluid directly into blood culture flasks at the bedside immediately after collection for a diagnosis of SBP[46,50]. BT from the intestinal tract is believed to be involved, as enterobacteria account for a relatively large percentage of the causative bacteria[8]. However, some reviews report a recent shift in the bacterial spectrum to include a high prevalence of Gram-positive bacteria (16.6%-68.3%) globally[32,51,52]. The change in etiology may have resulted from increases in the use of quinolones for bacterial prophylaxis and instrumentation in patients with LC[32]. The most frequently cultured organism in the ascitic fluid of patients with LC and SBP is Escherichia coli[18,30,52-56], followed by Gram-negative Klebsiella spp.. Streptococcus spp., Staphylococcus spp., and Enterococci are frequently isolated Gram-positive bacteria[30,53-56]. Kalvandi et al[57] reported E. coli, and Preto-Zamperlini et al[58] reported Streptococcus pneumoniae as the most frequent isolate in the ascitic fluid of children with SBP.

The incidence of recurrent SBP has decreased in parallel with the use of norfloxacin[59,60], but the increased prevalence of MDR bacteria in patients with SBP may be related to the use of long-term antibiotic prophylaxis or invasive procedures such as catheterization and ablation of hepatocellular carcinoma[61]. MDR bacteria are found frequently in nosocomial SBP (20%-35%)[61,62], but also occur in community-acquired SBP (4%-16%)[18]. Nosocomial SBP is also more likely to be antibiotic resistant. Balaraju et al[63] reported that up to 48% of the E. coli in patients with nosocomial SBP were resistant to third-generation cephalosporins. Li et al[62] found higher frequencies of ESBL-producing E. coli and Klebsiella spp. in cases of nosocomial compared with non-nosocomial SBP.

Diagnostic markers

The gold standard for a diagnosis of SBP is the PMN count in the ascetic fluid[36], but paracentesis is not always possible. Laboratory markers are useful for early diagnosis of SBP and early prediction of the response to initial treatment because a lack of response is a predictor of SBP mortality[64-66]. TNF-α and interleukin-6 are significantly higher in the ascitic fluid of patients with SBP than in those with sterile ascites[67,68], and increases of those proinflammatory cytokines have been associated with renal impairment complicated by SBP and with mortality[67,69]. The lactoferrin concentration is also higher in patients with SBP than in those with sterile ascites[70-72], and the lactoferrin level in ascitic fluid has shown high sensitivity and specificity for the diagnosis of SBP[39]. The optimal timing of lactoferrin assays is not yet clear, and diagnostic assay kits are not commercially available[39].

Procalcitonin, a prohormone of calcitonin synthesized in the C cells of the thyroid gland[73,74], is an acute-phase reactant protein that has been studied in patients with SBP. Seven studies assayed serum procalcitonin[69,75-80]; three assayed procalcitonin in ascitic fluid[75,76,80]. Serum procalcitonin was significantly higher in SBP than in sterile ascites in six of the seven[69,75,76,78-80], which supports use of serum procalcitonin as an SBP marker. In a review by Yang et al[81] of the available data from 339 patients with LC accompanied by SBP, it was concluded that serum procalcitonin was a relatively sensitive and specific marker for the diagnosis of SBP. It has been reported that serum procalcitonin was significantly higher in cirrhotic patients with culture-positive SBP than in those with CNNA[77,82]. Two of the three evaluations of procalcitonin in ascitic fluid found no significant differences in procalcitonin levels in patients with SBP and those with sterile ascites[76,80]. The usefulness of ascitic fluid procalcitonin to distinguish between SBP and sterile ascites has not been demonstrated.

Calprotectin is a calcium- and zinc-binding protein with antimicrobial and antiproliferative functions. It is almost exclusively expressed in neutrophils, and its level in body fluids is proportional to the influx of neutrophils[69,83]. Burri et al[83] reported that ascitic fluid calprotectin level was correlated with the PMN count and that it reliably predicted a count of ≥ 250 cells/mm3, which is the standard for a diagnosis of SBP. Subsequent studies found that ascites calprotectin is significantly higher in cirrhotic patients with SBP than in those without SBP[47,69]. Lutz et al[47] have shown that the ratio of calprotectin to total protein in ascitic fluid was a better diagnostic marker of SBP than calprotectin alone and that a high ratio was independently associated with 30-d mortality.

Leukocyte esterase activity, which can be assayed with commercially available reagent strips, may have diagnostic value[39]. Castellote et al[84] reported that the use of reagent strips is a rapid and inexpensive tool for the diagnosis of ascitic fluid infection and it had a high negative predictive value (99%), indicating that a negative result may be useful as screening to exclude SBP. Oey et al[85] reviewed 23 studies of leukocyte esterase in patients with SBP published between 2002 and 2015 and concluded that it had poor sensitivity and positive predictive value for the diagnosis of SBP. They found that the sensitivity of the reagent strips for diagnosing SBP was variable, and a negative test result strongly suggested the absence of SBP[85]. In another review of 26 studies published from 2002 to 2010, Koulaouzidis[86] confirmed the poor sensitivity and poor positive predictive value of leukocyte esterase activity as well as the high 93%-100% negative predictive value. A negative test result may thus indicate a high probability of the absence of SBP[84-86].

There is evidence for the diagnostic value of other markers including monocyte chemotactic protein-1 in serum[87] and ascitic fluid[88,89], lipopolysaccharide-binding protein in serum[90] and ascitic fluid[91], macrophage inflammatory protein type-1 beta in ascitic fluid[76], interferon-γ-induced protein-10 in serum[92] and ascitic fluid[92], triggering receptor expressed on myeloid cells-1 in ascitic fluid[93], high-sensitivity CRP in serum[94] and ascitic fluid[55], and neutrophil gelatinase-associated lipocalin in ascitic fluid[95]. Further study is needed to validate the diagnostic usefulness of these candidate markers.

Incidence

The incidence of SBP in LC with ascitic fluid has been estimated as 7%-30% in hospital inpatients[52,56] compared with 1.5%-3.5%[56,96,97] in outpatients with LC. The annual recurrence rate is approximately 70%[98], and the 1-year survival after recovery from the first episode of SBP is 30%-40%[99].

Prediction of incidence

Factors associated with the incidence of SBP in patients with LC and ascites include age, history of SBP[100], gastrointestinal bleeding[61,100], and endoscopic intervention for varix control[101]. Severity of liver dysfunction[42,54,56,61,102] including the Child-Pugh score or model for end-stage liver disease (MELD) score has been reported as a predictive factor, but few studies have not found an association of MELD score and the incidence of SBP[103] in patients with LC and refractory ascites. The MELD score does not include some clinical variables that are evaluated in the Child-Pugh score[104,105]. A PMN count[42,102] and a low protein concentration (< 1.5 g/dL) in the ascitic fluid, which may be related to decreased opsonic activity in the ascitic fluid[26,54,56], have also been reported as predictive factors, but the evidence for ascitic fluid protein is not conflicting[106]. The severity of liver dysfunction and serum and ascitic albumin levels have also been reported as risk factors for the recurrence of SBP[39].

Long-term use of proton pump inhibitors (PPIs) may increase the risk of SBP[107-110] because of facilitation of intestinal BT, but the association is controversial[26,111,112]. Multivariate analysis has identified the use of PPIs by patients with LC as an independent risk factor for the development of SBP[108,109], and Kwon et al[107] reported that PPI use was associated with the development of SBP and increased mortality, but other studies have not found a significant association of PPIs and development of SBP in patients with LC[112,113]. A recent meta-analysis by Yu et al[114] of 10 case-control and six cohort studies involving 8145 patients and published between 2008 and 2014 concluded that it is not possible to establish causality between PPI use and increased risk of SBP. A similar analysis by Khan et al[115] of six case-control and eight cohort studies concluded that there was a statistically significant association between PPI use and increased incidence of SBP, but that the difference in incidence was small. Kim et al[116] reported that PPI use was not associated with risk or SBP recurrence. PPI use may be associated with slightly increased risk for SBP[117], but the significance of the association has not been confirmed.

Mortality

SBP mortality has decreased in the four decades since it was first described as a result of early diagnosis and prompt treatment[56] and treatment by liver transplantation[103]. Hospital mortality is estimated as 10%-50% for the first episode and 31%-93% for the second or subsequent episodes[53,118]. Recent studies have estimated 1-mo mortality at > 20%[52,102], inpatient mortality at > 30%[61], and 1- and 2-year mortality following an SBP episode as 50%-70% and 70%-75%, respectively[23,39]. A recent nationwide cohort study in Taiwan reported that SBP mortality was 24.2% at 1 mo and 66.5% at 3 year[119].

Prediction of mortality

Predictors of mortality in SBP include severe underlying liver disease with a high Child-Pugh[48,52,64,96,100,102,104,105,120-122] or MELD score[47,48,52,104,121-123], renal impairment[16,52,54,64,65,96,100,124,125] such as HRS, and onset of severe sepsis[96]. Some studies did not find differences in the mortality of nosocomial and community-acquired SBP[63]; others have reported increased mortality in nosocomial compared with community-acquired SBP, which was correlated with the involvement of drug-resistant bacteria[4,21,63,65]. Other predictors of SBP mortality include old age[16,102], gastrointestinal bleeding[4,52], complications of shock[65], rapid deterioration of liver function[64], positive ascitic fluid culture[16,48], elevated blood leukocyte level[47,104,123], low serum sodium[63,102], complications of hepatic encephalopathy[52,63,122], presence of hepatocellular carcinoma[54], and complications of other infections, such as pneumonia[122]. Tandon et al[123] reported that peripheral blood leukocyte count ≥ 11 × 109 cells/L and MELD score ≥ 22 were independent predictors of 30-d mortality in patients with LC and SBP.

Renal impairment develops in 30%-40% of patients with LC and SBP[16] and is a significant prognostic factor in patients with LC and SBP. The available evidence strongly associates renal impairment with SBP mortality[16,52,54,64,65,96,100,124,125], but Lim et al[97] exceptionally reported that renal impairment, including HRS, was not predictive of mortality possibly because of early and effective treatment of SBP. Tandon et al[121] reported 67% mortality in patients with SBP and renal failure, but only 11% in patients with SBP and normal renal function. Some clinical studies indicated the use of intravenous albumin in addition to antibiotics for treatment of SBP[70,126-130]. Possible mechanisms of albumin use for improvement of SBP include its oncotic properties, immunomodulatory and antioxidant effects, and its endothelium stabilization capacity[131]. Dosage and duration of intravenous albumin in previous studies were as follows: (1) 1.5 g/kg body weight at the time of diagnosis and 1 g/kg body weight on day 3[126-128,130]; and (2) 20% 50 mL every day for 3 d[70]. Moreover, some clinical studies indicated that the use of intravenous albumin and antibiotics can reduce the incidence of renal impairment and mortality in patients with LC and SBP[126,129,130]. The efficacy of albumin treatment in patients with LC and other types of bacterial infection remains unknown. Thévenot et al[132] reported that albumin did not improve renal function or survival at 3 mo in patients with LC and non-SBP bacterial infections.

A meta-analysis of studies published between 2002 and 2011 identified a four-fold increased risk of mortality of patients with LC and SBP caused by MDR bacteria[133], and a retrospective multicenter study in Korea found that SBP caused by ESBL-producing bacteria was an independent prognostic factor of high in-hospital mortality[54,108]. Chon et al[4] reported that both in-hospital mortality and follow-up mortality after recovery from SBP were significantly higher in nosocomial SBP than in community-acquired SBP. Alexopoulou et al[31] did not find significant differences in the 30-d mortality of infections caused by MDR bacteria and nonresistant bacteria in 60 cases of culture-positive SBP and 70 cases of bacteremia without SBP.

However, 30-d mortality from infections caused by XDR bacteria was significantly higher than that of infections caused by MDR or nonresistant bacteria[31]. In another study, an overall 20% 30-d survival of nosocomial SBP was related to inadequate empirical antibiotic treatment[32].

Antibiotic prophylaxis

Antibiotic prophylaxis is effective, but long-term antibiotic administration leads to the emergence of MDR, which is a serious concern worldwide[33,134-136]. The current practice guidelines of the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver recommendations[26] limit its recommended use to patients who are at the highest risk of developing a bacterial infection. However, some studies have reported significant decreases in the incidence of SBP in patients with antibiotic prophylaxis[18,137]. Patients with LC and low ascites protein concentrations of < 1.5 g/dL are at risk of developing a first episode of SBP[26,138]. Primary antibiotic prophylaxis is recommended in patients with LC and no history of SBP and low ascites protein plus other predisposing factors, such as severe liver failure (Child-Pugh score > 9), impaired renal function (serum creatinine > 1.2 g/dL or blood urea nitrogen > 25 mg/dL), or hyponatremia (≤ 130 mEq/L), are present[23,26,102]. Primary prophylaxis is also recommended in patients with LC and acute gastrointestinal bleeding[138] or to reduce the incidence of SBP after gastrointestinal bleeding[134]. Antibiotic prophylaxis has also been associated with reduced rebleeding within 7 d and to lower 28-d mortality[18,134]. The standard therapy in patients with LC and acute gastrointestinal bleeding is oral norfloxacin[18], but Fernández et al[139] reported that intravenous ceftriaxone is more effective than oral norfloxacin. A randomized, controlled trial demonstrated that primary prophylaxis with trimethoprim/sulfamethoxazole also decreased the risk of SBP[140]. Recurrence rates as high as 70% have been reported in patients with LC who have recovered from a previous episode of SBP without secondary antibiotic prophylaxis[61]. Secondary prophylaxis is indicated for patients with a previous episode of SBP[26,53]. Norfloxacin was shown to decrease overall recurrence from 68% to 20%[26] and recurrence with a Gram-negative microorganism from 60% to 3% in the first year[61]. However, studies published between 2010 and 2016 reported that the frequency of recurrence with bacteria resistant to quinolones was 30%-33%[52]. The efficacy and safety of rifaximin for primary prophylaxis for SBP and for prophylaxis of recurrent SBP have been studied[141-145]. A study of primary prophylaxis by Assem et al[141] demonstrated that alternating norfloxacin and rifaximin as combination therapy was remarkably more effective compared with norfloxacin monotherapy in part because of an increased incidence of quinolone-resistant and Gram-positive SBP. Mostafa et al[142] showed that rifaximin prophylaxis was more effective than norfloxacin in patients with LC and at least one previous episode of SBP. A randomized, controlled trial of secondary prophylaxis by Elfert et al[143] demonstrated that SBP recurrence and mortality were significantly lower with rifaximin than with norfloxacin.

A systematic review by Goel et al[144] concluded that rifaximin was as effective for both primary and secondary prophylaxis as other systemically absorbed antibiotic. Rifaximin might be considered, particularly in cases involving quinolone-resistant bacteria[18]. The optimal duration of prophylaxis is currently unclear[26], but secondary prophylaxis should be continued until the ascites is resolved or liver transplantation can be performed[3].

Empirical antibiotic treatment for spontaneous bacterial peritonitis

Empirical antibiotic treatment must be initiated immediately after the diagnosis of SBP[53]. If the ascites neutrophil count decreases to < 25% of the pretreatment value after 2 d of antibiotic treatment, then there is an increased probability of failure to respond to any treatment[66]. Third-generation cephalosporins have been the most frequently used antibiotics in the treatment of SBP since 1985[4] and were highly effective until about 10 year ago[64]. They are still effective for community-acquired infections in patients with LC, with resolution rates of around 80%[33], but the development of resistance to third-generation cephalosporins is of great concern. Resistance can result in failure to respond to initial empiric therapy with a third-generation cephalosporin in 33%-75% of cases, and failure to respond is associated with reduced survival[48,49]. Recent studies indicate that third-generation cephalosporins are not appropriate for the treatment of nosocomial infections in patients with LC[34] because of effectiveness as low as 40% related to an increase in the prevalence of MDR bacteria in nosocomial infections[61,64]. SBP treatment recommendations distinguish between nosocomial and community-acquired infections[61] following evidence from studies like that by Lutz et al[146] who reported that approximately one third of health care-related and nosocomial SBP infections were resistant to third-generation cephalosporins. They also found that patients with health care-related SBP infections resistant to first-line treatment had worse survival than were those with infections susceptible to first-line treatment[146]. Moreover, Ariza et al[147] reported that resistance to third-generation cephalosporins occurred in 7.1% community-acquired SBP, 21.1% health care-related SBP, and 40.9% nosocomial SBP among 246 episodes in 200 patients with LC and SBP (2001-2009). Some studies recommend that third-generation cephalosporins not be used for empirical treatment of health care-related SBP[136,146]; Lutz et al[146] recommend piperacillin-tazobactam rather than third-generation cephalosporins. The most recent recommendations restrict third-generation cephalosporins to selected patients, primarily those with community-acquired SBP[21,32].

Daptomycin is effective against Gram-positive Enterococci resistant to vancomycin and against MRSA. A recent randomized, controlled study reported that empirical treatment of nosocomial SBP with meropenem plus daptomycin was more effective in resolving SBP and had better 3-mo survival than did third-generation ceftazidime[31,64]. Piano et al[64] and European expert opinion[49] both recommend a combination regimen of meropenem and daptomycin for the management of nosocomial SBP. A randomized trial by Jindal et al[122] reported that cefepime, a fourth-generation cephalosporin with good activity against most nosocomial Gram-negative bacteria and Gram-positive cocci, was as effective as imipenem for resolution of SBP. Following evaluation of antibiotic susceptibility in 575 SBP cases, Shi et al[30] recommended cefoperazone/sulbactam or piperacillin/tazobactam for the empirical treatment of SBP.

SPONTANEOUS FUNGAL PERITONITIS

Patients with LC are at an increased risk of fungal infection[138] because the antibiotics used for prevention of SBP can select for excessive growth of fungi in the intestinal flora with subsequent fungal translocation into peritoneal cavity and development of SFP[6]. Fungi are much larger than bacteria, which makes fungal translocation across the gut mucosa more difficult than BT, and may require higher intestinal permeability, which is more common in patients with advanced LC[148,149]. Fungal translocation may be facilitated by upper gastrointestinal bleeding, which is also common in patients with advanced LC[150]. Immunosuppression and malnutrition in LC patients also promote this fungal translocation[6]. Direct percutaneous inoculation of fungi is the proposed route of fungal infection in patients with refractory ascites and a history of paracentesis[150].

There are few data on the characteristics of SFP in LC patients[5,6], but case studies are available. Fungal colonization in ascitic fluid is not a rare complication in end-stage liver disease[5], and studies of the clinical characteristics of SFP are becoming more frequent. SFP is defined as a fungal infection of ascitic fluid with no apparent intraabdominal source of infection or malignancy[148]. A PMN count of ≥ 250 cells/mm3 in the ascitic fluid with a positive fungal culture regardless of co-colonization of bacteria is diagnostic of SFP[151]. A positive fungal culture with a PMN count of < 250 cells/mm3 is diagnosed as fungiascites or fungal ascites[151]. Fungal ascites has a higher mortality rate than does bacterascites[151]. Of spontaneous peritonitis cases, 0%-7.2% are culture positive for fungus[6,30,32,62,82,148,152-154], and the most frequent isolate is Candida albicans[5,6,148,149,153-156]. Other causative fungi include Candida glabrata[30], Candida krusei[153], Cryptococcus spp.[148,157], Aspergillus spp.[150,154], and Penicillium spp.[154]. Polymicrobial infections, i.e., bacterial co-colonization, occurs in 32%-74% of SFP cases[148,149,153,154,156], but early diagnosis by conventional microbial culture is difficult because of the time required for growth[155], and the efficacy of PCR or assay of the fungal biomarker 1,3-beta-D-glucan in ascitic fluid has not been established[149,155].

High Child-Pugh or MELD scores increase the risk of SFP in patients with LC[5,6,148], and a retrospective case-control study by Gravito-Soares et al[153] found no significant difference in the Child-Pugh or MELD scores of patients with SFP and SBP. The risk of SFP is increased in patients with LC who undergo invasive procedures[153] and increases with the length of the hospital stay[153,156]. Some studies have reported that a significantly greater proportion of SFP infections than SBP infections were nosocomial[148,156], but the data are conflicting[6]. In previous studies of spontaneous peritonitis with ascitic culture-positive diagnosed between 2003 and 2016, nosocomial SFP was confirmed in 7.7% (53/689) of nosocomial spontaneous peritonitis, and non-nosocomial SFP was confirmed in 1.7% (17/1018) of non-nosocomial spontaneous peritonitis[156].

Risk factors associated with hospital mortality in SFP include severe underlying liver disease[148], Child-Pugh score[155], MELD score[149], antibacterial prophylaxis[6], incidence of HRS[6], low ascites protein concentration[6], Acute Physiology And Chronic Health Evaluation II score[149], and sepsis shock[153]. SFP mortality is estimated to be 56%-90%[5,148,149,151,153], and 1-mo mortality may[148,153] or may not be significantly higher than SBP mortality[149,157]. Hwang et al[148] reported a high SFP mortality that was related to unresponsiveness to initial empirical treatment for suspected SBP. The condition of nearly all the patients with SFP worsened after initial empirical treatment, and they died during the early stage of peritonitis regardless of undergoing antifungal treatment[148]. Some patients with SFP improved after receiving the initial empirical treatment without any antifungal agents[148]. Those patients may have had SBP and colonization by innocent fungi[148], as it was not possible to distinguish fungal colonization from true SFP in the clinical setting[148]. SFP is usually diagnosed after the identification of fungi in cultures of ascitic fluid. The mortality is high because of delayed diagnosis, lack of clinical signs, lack of suspicion of SFP, and delay in treatment with antifungal therapy[5,6,148,155,156,158]. Fungal resistance to empirical specific antifungal therapy together with delayed diagnosis and treatment is related to poor prognosis of SFP[153].

Recent treatment guidelines on management of infections in LC do not include antifungals for prophylaxis or optimum treatment but do include recommendations for fungal infections[138]. Echinocandins are recommended as first-line treatment for patients with LC and nosocomial SFP or critically ill patients with LC and community-acquired SFP[148]. Fluconazole is recommended for less severe infections[6,138,152]. De-escalation from echinocandins to fluconazole is advised in critically ill patients with LC and SFP when their condition is stable and sensitivity tests are available[6,152]. However, directed antifungal therapy may not improve the outcomes of some patients with SFP[149,156] because of lack of response to the administration of empirical treatment and delay in starting antifungal therapy[156].

Although early differentiation between SFP and SBP may be difficult partially because identification of fungi in cultures of ascitic fluid is time-consuming, clinician is able to suspect SFP or SBP due to MDR if spontaneous peritonitis is not improved after 48 h empirical antibiotic treatment[151]. Therefore, new cultures in ascitic fluid and blood may be performed in these patients[151]. Moreover, additional administration of antifungal agents or administration of antifungal agents and alternation of antibiotics may be considered in these patients[151,159].

CONCLUSION

The evidence of previous studies confirms that SBP and SFP in patients with LC is often life-threatening. The severity of liver dysfunction, the presence of renal impairment, and the emergence of MDR bacteria have a clinically significant influence on the prognosis of SBP. The efficacy of the recommended antibiotic therapy for SBP may be decreased in nosocomial infections because of increases in the prevalence of MDR bacteria. In SFP, mortality is associated not only with the severity of the underlying liver disease but also with delay in diagnosis and initiation of antifungal therapy. Further research is needed to better our understanding of the nature of SFP and improve the response to treatment with the available antifungal agents.

Footnotes

Manuscript source: Invited manuscript

Specialty type: Gastroenterology and hepatology

Country of origin: Japan

Peer-review report classification

Grade A (Excellent): 0

Grade B (Very good): B, B

Grade C (Good): 0

Grade D (Fair): D

Grade E (Poor): 0

P- Reviewer: Acevedo JG, Castellote J, Leone S S- Editor: Cui LJ L- Editor: A E- Editor: Li D

References
1.  Bunchorntavakul C, Chavalitdhamrong D. Bacterial infections other than spontaneous bacterial peritonitis in cirrhosis. World J Hepatol. 2012;4:158-168.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 25]  [Cited by in F6Publishing: 18]  [Article Influence: 2.8]  [Reference Citation Analysis (0)]
2.  Fernández J, Navasa M, Gómez J, Colmenero J, Vila J, Arroyo V, Rodés J. Bacterial infections in cirrhosis: epidemiological changes with invasive procedures and norfloxacin prophylaxis. Hepatology. 2002;35:140-148.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 606]  [Cited by in F6Publishing: 428]  [Article Influence: 31.9]  [Reference Citation Analysis (0)]
3.  Hsu SJ, Huang HC. Management of ascites in patients with liver cirrhosis: recent evidence and controversies. J Chin Med Assoc. 2013;76:123-130.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 7]  [Article Influence: 1.8]  [Reference Citation Analysis (0)]
4.  Chon YE, Kim SU, Lee CK, Park JY, Kim DY, Han KH, Chon CY, Kim S, Jung KS, Ahn SH. Community-acquired vs. nosocomial spontaneous bacterial peritonitis in patients with liver cirrhosis. Hepatogastroenterology. 2014;61:2283-2290.  [PubMed]  [DOI]  [Cited in This Article: ]
5.  Lahmer T, Brandl A, Rasch S, Schmid RM, Huber W. Fungal Peritonitis: Underestimated Disease in Critically Ill Patients with Liver Cirrhosis and Spontaneous Peritonitis. PLoS One. 2016;11:e0158389.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 17]  [Cited by in F6Publishing: 13]  [Article Influence: 3.4]  [Reference Citation Analysis (0)]
6.  Fiore M, Leone S. Spontaneous fungal peritonitis: Epidemiology, current evidence and future prospective. World J Gastroenterol. 2016;22:7742-7747.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 15]  [Cited by in F6Publishing: 16]  [Article Influence: 3.8]  [Reference Citation Analysis (0)]
7.  Alexopoulou A, Agiasotelli D, Vasilieva LE, Dourakis SP. Bacterial translocation markers in liver cirrhosis. Ann Gastroenterol. 2017;30:486-497.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 16]  [Article Influence: 3.5]  [Reference Citation Analysis (0)]
8.  Gómez-Hurtado I, Such J, Sanz Y, Francés R. Gut microbiota-related complications in cirrhosis. World J Gastroenterol. 2014;20:15624-15631.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 23]  [Cited by in F6Publishing: 22]  [Article Influence: 3.8]  [Reference Citation Analysis (0)]
9.  Guarner C, Soriano G. Bacterial translocation and its consequences in patients with cirrhosis. Eur J Gastroenterol Hepatol. 2005;17:27-31.  [PubMed]  [DOI]  [Cited in This Article: ]
10.  Gentile I, Buonomo AR, Scotto R, Zappulo E, Borgia G. Infections worsen prognosis of patients with cirrhosis irrespective of the liver disease stage. Eur J Intern Med. 2017;46:e45-e47.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 11]  [Article Influence: 3.0]  [Reference Citation Analysis (0)]
11.  Pijls KE, Koek GH, Elamin EE, de Vries H, Masclee AA, Jonkers DM. Large intestine permeability is increased in patients with compensated liver cirrhosis. Am J Physiol Gastrointest Liver Physiol. 2014;306:G147-G153.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 25]  [Cited by in F6Publishing: 21]  [Article Influence: 3.1]  [Reference Citation Analysis (0)]
12.  Zhang J, Gong F, Li L, Zhao M, Wu Z, Song J. The diagnostic value of neutrophil gelatinase-associated lipocalin and hepcidin in bacteria translocation of liver cirrhosis. Int J Clin Exp Med. 2015;8:16434-16444.  [PubMed]  [DOI]  [Cited in This Article: ]
13.  Harputluoglu MM, Dertli R, Otlu B, Demirel U, Yener O, Bilgic Y, Erdogan MA, Atayan Y, Cagin YF. Nucleotide-Binding Oligomerization Domain-Containing Protein 2 Variants in Patients with Spontaneous Bacterial Peritonitis. Dig Dis Sci. 2016;61:1545-1552.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 7]  [Cited by in F6Publishing: 6]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
14.  Kawaratani H, Fukui H, Yoshiji H. Treatment for cirrhotic ascites. Hepatol Res. 2017;47:166-177.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 5]  [Article Influence: 2.2]  [Reference Citation Analysis (0)]
15.  Usui S, Ebinuma H, Chu PS, Nakamoto N, Yamagishi Y, Saito H, Kanai T. Detection of bacterial DNA by in situ hybridization in patients with decompensated liver cirrhosis. BMC Gastroenterol. 2017;17:106.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 1]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
16.  Bunchorntavakul C, Chamroonkul N, Chavalitdhamrong D. Bacterial infections in cirrhosis: A critical review and practical guidance. World J Hepatol. 2016;8:307-321.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 92]  [Cited by in F6Publishing: 46]  [Article Influence: 18.4]  [Reference Citation Analysis (0)]
17.  Schwab S, Lehmann J, Lutz P, Jansen C, Appenrodt B, Lammert F, Strassburg CP, Spengler U, Nischalke HD, Trebicka J. Influence of genetic variations in the SOD1 gene on the development of ascites and spontaneous bacterial peritonitis in decompensated liver cirrhosis. Eur J Gastroenterol Hepatol. 2017;29:800-804.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 2]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
18.  Piotrowski D, Boroń-Kaczmarska A. Bacterial infections and hepatic encephalopathy in liver cirrhosis-prophylaxis and treatment. Adv Med Sci. 2017;62:345-356.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 8]  [Reference Citation Analysis (0)]
19.  Waidmann O, Kempf VA, Brandt C, Zeuzem S, Piiper A, Kronenberger B. Colonisation with multidrug-resistant bacteria is associated with increased mortality in patients with cirrhosis. Gut. 2015;64:1183-1184.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 7]  [Cited by in F6Publishing: 5]  [Article Influence: 1.2]  [Reference Citation Analysis (0)]
20.  Pouriki S, Vrioni G, Sambatakou H, Alexopoulou A, Vasilieva L, Mani I, Tsakris A, Dourakis SP. Intestinal colonization with resistant bacteria: a prognostic marker of mortality in decompensated cirrhosis. Eur J Clin Microbiol Infect Dis. 2018;37:127-134.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 2]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
21.  Jalan R, Fernandez J, Wiest R, Schnabl B, Moreau R, Angeli P, Stadlbauer V, Gustot T, Bernardi M, Canton R. Bacterial infections in cirrhosis: a position statement based on the EASL Special Conference 2013. J Hepatol. 2014;60:1310-1324.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 464]  [Cited by in F6Publishing: 315]  [Article Influence: 66.3]  [Reference Citation Analysis (0)]
22.  Kuo CH, Changchien CS, Yang CY, Sheen IS, Liaw YF. Bacteremia in patients with cirrhosis of the liver. Liver. 1991;11:334-339.  [PubMed]  [DOI]  [Cited in This Article: ]
23.  Karvellas CJ, Abraldes JG, Arabi YM, Kumar A; Cooperative Antimicrobial Therapy of Septic Shock (CATSS) Database Research Group. Appropriate and timely antimicrobial therapy in cirrhotic patients with spontaneous bacterial peritonitis-associated septic shock: a retrospective cohort study. Aliment Pharmacol Ther. 2015;41:747-757.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 52]  [Cited by in F6Publishing: 35]  [Article Influence: 8.7]  [Reference Citation Analysis (0)]
24.  Bartoletti M, Giannella M, Caraceni P, Domenicali M, Ambretti S, Tedeschi S, Verucchi G, Badia L, Lewis RE, Bernardi M. Epidemiology and outcomes of bloodstream infection in patients with cirrhosis. J Hepatol. 2014;61:51-58.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 71]  [Cited by in F6Publishing: 53]  [Article Influence: 10.1]  [Reference Citation Analysis (0)]
25.  Bartoletti M, Giannella M, Lewis R, Caraceni P, Tedeschi S, Paul M, Schramm C, Bruns T, Merli M, Cobos-Trigueros N. A prospective multicentre study of the epidemiology and outcomes of bloodstream infection in cirrhotic patients. Clin Microbiol Infect. 2017; Epub ahead of print.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 36]  [Cited by in F6Publishing: 27]  [Article Influence: 12.0]  [Reference Citation Analysis (0)]
26.  Fagiuoli S, Colli A, Bruno R, Craxì A, Gaeta GB, Grossi P, Mondelli MU, Puoti M, Sagnelli E, Stefani S. Management of infections pre- and post-liver transplantation: report of an AISF consensus conference. J Hepatol. 2014;60:1075-1089.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 52]  [Cited by in F6Publishing: 24]  [Article Influence: 7.4]  [Reference Citation Analysis (0)]
27.  Dionigi E, Garcovich M, Borzio M, Leandro G, Majumdar A, Tsami A, Arvaniti V, Roccarina D, Pinzani M, Burroughs AK. Bacterial Infections Change Natural History of Cirrhosis Irrespective of Liver Disease Severity. Am J Gastroenterol. 2017;112:588-596.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 53]  [Cited by in F6Publishing: 36]  [Article Influence: 13.3]  [Reference Citation Analysis (0)]
28.  Thulstrup AM, Sørensen HT, Schønheyder HC, Møller JK, Tage-Jensen U. Population-based study of the risk and short-term prognosis for bacteremia in patients with liver cirrhosis. Clin Infect Dis. 2000;31:1357-1361.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 83]  [Cited by in F6Publishing: 49]  [Article Influence: 4.0]  [Reference Citation Analysis (0)]
29.  Merli M, Lucidi C, Di Gregorio V, Falcone M, Giannelli V, Lattanzi B, Giusto M, Ceccarelli G, Farcomeni A, Riggio O. The spread of multi drug resistant infections is leading to an increase in the empirical antibiotic treatment failure in cirrhosis: a prospective survey. PLoS One. 2015;10:e0127448.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 51]  [Cited by in F6Publishing: 34]  [Article Influence: 8.5]  [Reference Citation Analysis (0)]
30.  Shi L, Wu D, Wei L, Liu S, Zhao P, Tu B, Xie Y, Liu Y, Wang X, Liu L. Corrigendum: Nosocomial and Community-Acquired Spontaneous Bacterial Peritonitis in patients with liver cirrhosis in China: Comparative Microbiology and Therapeutic Implications. Sci Rep. 2017;7:46868.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 1]  [Article Influence: 0.5]  [Reference Citation Analysis (0)]
31.  Alexopoulou A, Vasilieva L, Agiasotelli D, Siranidi K, Pouriki S, Tsiriga A, Toutouza M, Dourakis SP. Extensively drug-resistant bacteria are an independent predictive factor of mortality in 130 patients with spontaneous bacterial peritonitis or spontaneous bacteremia. World J Gastroenterol. 2016;22:4049-4056.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 33]  [Cited by in F6Publishing: 21]  [Article Influence: 8.3]  [Reference Citation Analysis (0)]
32.  Fiore M, Maraolo AE, Gentile I, Borgia G, Leone S, Sansone P, Passavanti MB, Aurilio C, Pace MC. Nosocomial spontaneous bacterial peritonitis antibiotic treatment in the era of multi-drug resistance pathogens: A systematic review. World J Gastroenterol. 2017;23:4654-4660.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 28]  [Cited by in F6Publishing: 15]  [Article Influence: 9.3]  [Reference Citation Analysis (0)]
33.  Fernández J, Acevedo J, Castro M, Garcia O, de Lope CR, Roca D, Pavesi M, Sola E, Moreira L, Silva A. Prevalence and risk factors of infections by multiresistant bacteria in cirrhosis: a prospective study. Hepatology. 2012;55:1551-1561.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 341]  [Cited by in F6Publishing: 226]  [Article Influence: 37.9]  [Reference Citation Analysis (0)]
34.  Acevedo J. Multiresistant bacterial infections in liver cirrhosis: Clinical impact and new empirical antibiotic treatment policies. World J Hepatol. 2015;7:916-921.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 12]  [Article Influence: 3.0]  [Reference Citation Analysis (0)]
35.  Pericleous M, Sarnowski A, Moore A, Fijten R, Zaman M. The clinical management of abdominal ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: a review of current guidelines and recommendations. Eur J Gastroenterol Hepatol. 2016;28:e10-e18.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 47]  [Cited by in F6Publishing: 10]  [Article Influence: 9.4]  [Reference Citation Analysis (0)]
36.  Rimola A, García-Tsao G, Navasa M, Piddock LJ, Planas R, Bernard B, Inadomi JM. Diagnosis, treatment and prophylaxis of spontaneous bacterial peritonitis: a consensus document. International Ascites Club. J Hepatol. 2000;32:142-153.  [PubMed]  [DOI]  [Cited in This Article: ]
37.  Riggio O, Angeloni S, Parente A, Leboffe C, Pinto G, Aronne T, Merli M. Accuracy of the automated cell counters for management of spontaneous bacterial peritonitis. World J Gastroenterol. 2008;14:5689-5694.  [PubMed]  [DOI]  [Cited in This Article: ]
38.  Cereto F, Genescà J, Segura R. Validation of automated blood cell counters for the diagnosis of spontaneous bacterial peritonitis. Am J Gastroenterol. 2004;99:1400.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10]  [Cited by in F6Publishing: 9]  [Article Influence: 0.6]  [Reference Citation Analysis (0)]
39.  Dever JB, Sheikh MY. Review article: spontaneous bacterial peritonitis--bacteriology, diagnosis, treatment, risk factors and prevention. Aliment Pharmacol Ther. 2015;41:1116-1131.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 83]  [Cited by in F6Publishing: 44]  [Article Influence: 13.8]  [Reference Citation Analysis (0)]
40.  Na SH, Kim EJ, Nam EY, Song KH, Choe PG, Park WB, Bang JH, Kim ES, Park SW, Kim HB. Comparison of clinical characteristics and outcomes of spontaneous bacterial peritonitis and culture negative neutrocytic ascites. Scand J Gastroenterol. 2017;52:199-203.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 11]  [Article Influence: 2.8]  [Reference Citation Analysis (0)]
41.  Bal CK, Bhatia V, Daman R. Predictors of fifty days in-hospital mortality in patients with culture negative neutrocytic ascites. BMC Gastroenterol. 2017;17:64.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 2]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
42.  Lutz P, Goeser F, Kaczmarek DJ, Schlabe S, Nischalke HD, Nattermann J, Hoerauf A, Strassburg CP, Spengler U. Relative Ascites Polymorphonuclear Cell Count Indicates Bacterascites and Risk of Spontaneous Bacterial Peritonitis. Dig Dis Sci. 2017;62:2558-2568.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 9]  [Cited by in F6Publishing: 6]  [Article Influence: 2.3]  [Reference Citation Analysis (0)]
43.  Shizuma T. Retrospective Investigation of Bacterascites and Spontaneous Bacterial Peritonitis in Liver Cirrhosis Patients Undergoing Paracentesis. J Clin Trials. 2014;4:166.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
44.  Soriano G, Castellote J, Alvarez C, Girbau A, Gordillo J, Baliellas C, Casas M, Pons C, Román EM, Maisterra S. Secondary bacterial peritonitis in cirrhosis: a retrospective study of clinical and analytical characteristics, diagnosis and management. J Hepatol. 2010;52:39-44.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 65]  [Cited by in F6Publishing: 34]  [Article Influence: 5.4]  [Reference Citation Analysis (0)]
45.  Krastev N, Djurkov V, Murdjeva M, Akrabova P, Karparova T, Penkov V, Kiprin G, Asenov K, Krastev N, Djurkov V. Diagnosis of spontaneous and secondary bacterial peritonitis in patients with hepatic cirrhosis and ascites. Khirurgiia (Sofiia). 2013;20-25.  [PubMed]  [DOI]  [Cited in This Article: ]
46.  Strauss E. The impact of bacterial infections on survival of patients with decompensated cirrhosis. Ann Hepatol. 2013;13:7-19.  [PubMed]  [DOI]  [Cited in This Article: ]
47.  Lutz P, Pfarr K, Nischalke HD, Krämer B, Goeser F, Glässner A, Wolter F, Kokordelis P, Nattermann J, Sauerbruch T. The ratio of calprotectin to total protein as a diagnostic and prognostic marker for spontaneous bacterial peritonitis in patients with liver cirrhosis and ascites. Clin Chem Lab Med. 2015;53:2031-2039.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 11]  [Article Influence: 4.2]  [Reference Citation Analysis (0)]
48.  Friedrich K, Nüssle S, Rehlen T, Stremmel W, Mischnik A, Eisenbach C. Microbiology and resistance in first episodes of spontaneous bacterial peritonitis: implications for management and prognosis. J Gastroenterol Hepatol. 2016;31:1191-1195.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 28]  [Cited by in F6Publishing: 20]  [Article Influence: 7.0]  [Reference Citation Analysis (0)]
49.  Ison MG. Empiric treatment of nosocomial spontaneous bacterial peritonitis: One size does not fit all. Hepatology. 2016;63:1083-1085.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 7]  [Article Influence: 1.6]  [Reference Citation Analysis (0)]
50.  Runyon BA, Antillon MR, Akriviadis EA, McHutchison JG. Bedside inoculation of blood culture bottles with ascitic fluid is superior to delayed inoculation in the detection of spontaneous bacterial peritonitis. J Clin Microbiol. 1990;28:2811-2812.  [PubMed]  [DOI]  [Cited in This Article: ]
51.  Fiore M, Maraolo AE, Gentile I, Borgia G, Leone S, Sansone P, Passavanti MB, Aurilio C, Pace MC. Current concepts and future strategies in the antimicrobial therapy of emerging Gram-positive spontaneous bacterial peritonitis. World J Hepatol. 2017;9:1166-1175.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 14]  [Article Influence: 4.5]  [Reference Citation Analysis (0)]
52.  Oliveira AM, Branco JC, Barosa R, Rodrigues JA, Ramos L, Martins A, Karvellas CJ, Cardoso FS. Clinical and microbiological characteristics associated with mortality in spontaneous bacterial peritonitis: a multicenter cohort study. Eur J Gastroenterol Hepatol. 2016;28:1216-1222.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 15]  [Cited by in F6Publishing: 10]  [Article Influence: 3.8]  [Reference Citation Analysis (0)]
53.  European Association for the Study of the Liver. EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. J Hepatol. 2010;53:397-417.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1002]  [Cited by in F6Publishing: 637]  [Article Influence: 91.1]  [Reference Citation Analysis (0)]
54.  Tsung PC, Ryu SH, Cha IH, Cho HW, Kim JN, Kim YS, Moon JS. Predictive factors that influence the survival rates in liver cirrhosis patients with spontaneous bacterial peritonitis. Clin Mol Hepatol. 2013;19:131-139.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 17]  [Article Influence: 3.4]  [Reference Citation Analysis (0)]
55.  Kadam N, Acharya S, Shukla S, Gupta K. Ascitic Fluid High Sensitive C-Reactive Protein (hs-CRP). A Prognostic Marker in Cirrhosis with Spontaneous Bacterial Peritonitis. J Clin Diagn Res. 2016;10:OC20-OC24.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 2]  [Article Influence: 0.8]  [Reference Citation Analysis (0)]
56.  Oladimeji AA, Temi AP, Adekunle AE, Taiwo RH, Ayokunle DS. Prevalence of spontaneous bacterial peritonitis in liver cirrhosis with ascites. Pan Afr Med J. 2013;15:128.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 6]  [Cited by in F6Publishing: 6]  [Article Influence: 0.8]  [Reference Citation Analysis (0)]
57.  Kalvandi G, Honar N, Geramizadeh B, Ataollahi M, Rahmani A, Javaherizadeh H. Serum C-Reactive Protein in Children with Liver Disease and Ascites. Hepat Mon. 2016;16:e38973.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 2]  [Article Influence: 0.8]  [Reference Citation Analysis (0)]
58.  Preto-Zamperlini M, Farhat SC, Perondi MB, Pestana AP, Cunha PS, Pugliese RP, Schvartsman C. Elevated C-reactive protein and spontaneous bacterial peritonitis in children with chronic liver disease and ascites. J Pediatr Gastroenterol Nutr. 2014;58:96-98.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 22]  [Cited by in F6Publishing: 4]  [Article Influence: 3.1]  [Reference Citation Analysis (0)]
59.  Inadomi J, Sonnenberg A. Cost-analysis of prophylactic antibiotics in spontaneous bacterial peritonitis. Gastroenterology. 1997;113:1289-1294.  [PubMed]  [DOI]  [Cited in This Article: ]
60.  Younossi ZM, McHutchison JG, Ganiats TG. An economic analysis of norfloxacin prophylaxis against spontaneous bacterial peritonitis. J Hepatol. 1997;27:295-298.  [PubMed]  [DOI]  [Cited in This Article: ]
61.  de Mattos AA, Costabeber AM, Lionço LC, Tovo CV. Multi-resistant bacteria in spontaneous bacterial peritonitis: a new step in management? World J Gastroenterol. 2014;20:14079-14086.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 20]  [Cited by in F6Publishing: 14]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
62.  Li YT, Yu CB, Huang JR, Qin ZJ, Li LJ. Pathogen profile and drug resistance analysis of spontaneous peritonitis in cirrhotic patients. World J Gastroenterol. 2015;21:10409-10417.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 21]  [Cited by in F6Publishing: 11]  [Article Influence: 4.2]  [Reference Citation Analysis (0)]
63.  Balaraju G, Patil M, Krishnamurthy AC, Karanth D, Devarbhavi H. Comparative Study of Community Acquired and Nosocomial Spontaneous Bacterial Peritonitis and its Variants in 150 Patients. J Clin Exp Hepatol. 2017;7:215-221.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 2]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
64.  Piano S, Fasolato S, Salinas F, Romano A, Tonon M, Morando F, Cavallin M, Gola E, Sticca A, Loregian A. The empirical antibiotic treatment of nosocomial spontaneous bacterial peritonitis: Results of a randomized, controlled clinical trial. Hepatology. 2016;63:1299-1309.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 107]  [Cited by in F6Publishing: 68]  [Article Influence: 17.8]  [Reference Citation Analysis (0)]
65.  Cheong HS, Kang CI, Lee JA, Moon SY, Joung MK, Chung DR, Koh KC, Lee NY, Song JH, Peck KR. Clinical significance and outcome of nosocomial acquisition of spontaneous bacterial peritonitis in patients with liver cirrhosis. Clin Infect Dis. 2009;48:1230-1236.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 115]  [Cited by in F6Publishing: 96]  [Article Influence: 9.6]  [Reference Citation Analysis (0)]
66.  Fong TL, Akriviadis EA, Runyon BA, Reynolds TB. Polymorphonuclear cell count response and duration of antibiotic therapy in spontaneous bacterial peritonitis. Hepatology. 1989;9:423-426.  [PubMed]  [DOI]  [Cited in This Article: ]
67.  Suliman MA, Khalil FM, Alkindi SS, Pathare AV, Almadhani AA, Soliman NA. Tumor necrosis factor-α and interleukin-6 in cirrhotic patients with spontaneous bacterial peritonitis. World J Gastrointest Pathophysiol. 2012;3:92-98.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 15]  [Cited by in F6Publishing: 9]  [Article Influence: 1.9]  [Reference Citation Analysis (0)]
68.  Chen TA, Tsao YC, Chen A, Lo GH, Lin CK, Yu HC, Cheng LC, Hsu PI, Tsai WL. Effect of intravenous albumin on endotoxin removal, cytokines, and nitric oxide production in patients with cirrhosis and spontaneous bacterial peritonitis. Scand J Gastroenterol. 2009;44:619-625.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 54]  [Cited by in F6Publishing: 33]  [Article Influence: 4.5]  [Reference Citation Analysis (0)]
69.  Abdel-Razik A, Mousa N, Elhammady D, Elhelaly R, Elzehery R, Elbaz S, Eissa M, El-Wakeel N, Eldars W. Ascitic Fluid Calprotectin and Serum Procalcitonin as Accurate Diagnostic Markers for Spontaneous Bacterial Peritonitis. Gut Liver. 2016;10:624-631.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 24]  [Cited by in F6Publishing: 10]  [Article Influence: 6.0]  [Reference Citation Analysis (0)]
70.  Parsi MA, Saadeh SN, Zein NN, Davis GL, Lopez R, Boone J, Lepe MR, Guo L, Ashfaq M, Klintmalm G. Ascitic fluid lactoferrin for diagnosis of spontaneous bacterial peritonitis. Gastroenterology. 2008;135:803-807.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 48]  [Cited by in F6Publishing: 28]  [Article Influence: 3.7]  [Reference Citation Analysis (0)]
71.  Lee SS, Min HJ, Choi JY, Cho HC, Kim JJ, Lee JM, Kim HJ, Ha CY, Kim HJ, Kim TH. Usefulness of ascitic fluid lactoferrin levels in patients with liver cirrhosis. BMC Gastroenterol. 2016;16:132.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 9]  [Cited by in F6Publishing: 7]  [Article Influence: 1.8]  [Reference Citation Analysis (0)]
72.  Ali FM, Shehata, IH Abd Elsalam, AE, El-Ansary, M. Diagnostic value of lactoferrin ascitic fluid levels in spontaneous bacterial peritonitis. Egyptian Liver J. 2013;3:54-61.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
73.  Connert S, Stremmel W, Elsing C. Procalcitonin is a valid marker of infection in decompensated cirrhosis. Z Gastroenterol. 2003;41:165-170.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 30]  [Cited by in F6Publishing: 30]  [Article Influence: 1.7]  [Reference Citation Analysis (0)]
74.  Bode-Jänisch S, Schütz S, Schmidt A, Tschernig T, Debertin AS, Fieguth A, Hagemeier L, Teske J, Suerbaum S, Klintschar M. Serum procalcitonin levels in the postmortem diagnosis of sepsis. Forensic Sci Int. 2013;226:266-272.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 8]  [Reference Citation Analysis (0)]
75.  Viallon A, Zeni F, Pouzet V, Lambert C, Quenet S, Aubert G, Guyomarch S, Tardy B, Bertrand JC. Serum and ascitic procalcitonin levels in cirrhotic patients with spontaneous bacterial peritonitis: diagnostic value and relationship to pro-inflammatory cytokines. Intensive Care Med. 2000;26:1082-1088.  [PubMed]  [DOI]  [Cited in This Article: ]
76.  Lesińska M, Hartleb M, Gutkowski K, Nowakowska-Duława E. Procalcitonin and macrophage inflammatory protein-1 beta (MIP-1β) in serum and peritoneal fluid of patients with decompensated cirrhosis and spontaneous bacterial peritonitis. Adv Med Sci. 2014;59:52-56.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 28]  [Cited by in F6Publishing: 11]  [Article Influence: 4.0]  [Reference Citation Analysis (0)]
77.  Cekin Y, Cekin AH, Duman A, Yilmaz U, Yesil B, Yolcular BO. The role of serum procalcitonin levels in predicting ascitic fluid infection in hospitalized cirrhotic and non-cirrhotic patients. Int J Med Sci. 2013;10:1367-1374.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 25]  [Cited by in F6Publishing: 19]  [Article Influence: 3.1]  [Reference Citation Analysis (0)]
78.  Yuan LY, Ke ZQ, Wang M, Li Y. Procalcitonin and C-reactive protein in the diagnosis and prediction of spontaneous bacterial peritonitis associated with chronic severe hepatitis B. Ann Lab Med. 2013;33:449-454.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 26]  [Cited by in F6Publishing: 15]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
79.  Wu J, Jiang F, Zeng T, Xu H, Lei Y, Zhong S, Zhou Z, Ren H. Role of serum procalcitonin assay for diagnosis of spontaneous bacterial peritonitis in end-stage liver diseases. Zhongguo Yixue Kexueyuan Xuebao. 2014;36:37-41.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 2]  [Reference Citation Analysis (0)]
80.  Spahr L, Morard I, Hadengue A, Vadas L, Pugin J. Procalcitonin is not an accurate marker of spontaneous bacterial peritonitis in patients with cirrhosis. Hepatogastroenterology. 2001;48:502-505.  [PubMed]  [DOI]  [Cited in This Article: ]
81.  Yang Y, Li L, Qu C, Zeng B, Liang S, Luo Z, Wang X, Zhong C. Diagnostic Accuracy of Serum Procalcitonin for Spontaneous Bacterial Peritonitis Due to End-stage Liver Disease: A Meta-analysis. Medicine (Baltimore). 2015;94:e2077.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 13]  [Cited by in F6Publishing: 6]  [Article Influence: 2.6]  [Reference Citation Analysis (0)]
82.  Wu H, Chen L, Sun Y, Meng C, Hou W. The role of serum procalcitonin and C-reactive protein levels in predicting spontaneous bacterial peritonitis in patients with advanced liver cirrhosis. Pak J Med Sci. 2016;32:1484-1488.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 5]  [Article Influence: 2.8]  [Reference Citation Analysis (0)]
83.  Burri E, Schulte F, Muser J, Meier R, Beglinger C. Measurement of calprotectin in ascitic fluid to identify elevated polymorphonuclear cell count. World J Gastroenterol. 2013;19:2028-2036.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 25]  [Cited by in F6Publishing: 14]  [Article Influence: 3.1]  [Reference Citation Analysis (0)]
84.  Castellote J, López C, Gornals J, Tremosa G, Fariña ER, Baliellas C, Domingo A, Xiol X. Rapid diagnosis of spontaneous bacterial peritonitis by use of reagent strips. Hepatology. 2003;37:893-896.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 96]  [Cited by in F6Publishing: 69]  [Article Influence: 5.3]  [Reference Citation Analysis (0)]
85.  Oey RC, Kuiper JJ, van Buuren HR, de Man RA. Reagent strips are efficient to rule out spontaneous bacterial peritonitis in cirrhotics. Neth J Med. 2016;74:257-261.  [PubMed]  [DOI]  [Cited in This Article: ]
86.  Koulaouzidis A. Diagnosis of spontaneous bacterial peritonitis: an update on leucocyte esterase reagent strips. World J Gastroenterol. 2011;17:1091-1094.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 22]  [Cited by in F6Publishing: 8]  [Article Influence: 2.2]  [Reference Citation Analysis (0)]
87.  Kim JK, Chon CY, Kim JH, Kim YJ, Cho JH, Bang SM, Ahn SH, Han KH, Moon YM. Changes in serum and ascitic monocyte chemotactic protein-1 (MCP-1) and IL-10 levels in cirrhotic patients with spontaneous bacterial peritonitis. J Interferon Cytokine Res. 2007;27:227-230.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 9]  [Article Influence: 1.5]  [Reference Citation Analysis (0)]
88.  Girón-González JA, Rodríguez-Ramos C, Elvira J, Galán F, Del Alamo CF, Díaz F, Martín-Herrera L. Serial analysis of serum and ascitic fluid levels of soluble adhesion molecules and chemokines in patients with spontaneous bacterial peritonitis. Clin Exp Immunol. 2001;123:56-61.  [PubMed]  [DOI]  [Cited in This Article: ]
89.  El-Toukhy N, Emam SM. Diagnostic and Prognostic Values of Monocyte Chemotactic Protein-1 in Ascitic Fluid of Patients with Spontaneous Bacterial Peritonitis. Egypt J Immunol. 2016;23:17-27.  [PubMed]  [DOI]  [Cited in This Article: ]
90.  Tang NY, Chen WQ. [Significance of lipopolysaccharide binding protein in serum and ascites of patients with hepatic cirrhosis complicated with spontaneous bacterial peritonitis]. Zhonghua Gan Zang Bing Za Zhi. 2012;20:492-496.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 3]  [Reference Citation Analysis (0)]
91.  Agiasotelli D, Alexopoulou A, Vasilieva L, Hadziyannis E, Goukos D, Daikos GL, Dourakis SP. High serum lipopolysaccharide binding protein is associated with increased mortality in patients with decompensated cirrhosis. Liver Int. 2017;37:576-582.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 7]  [Article Influence: 2.4]  [Reference Citation Analysis (0)]
92.  Abdel-Razik A, Mousa N, Elbaz S, Eissa M, Elhelaly R, Eldars W. Diagnostic utility of interferon gamma-induced protein 10 kDa in spontaneous bacterial peritonitis: single-center study. Eur J Gastroenterol Hepatol. 2015;27:1087-1093.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 15]  [Cited by in F6Publishing: 3]  [Article Influence: 3.0]  [Reference Citation Analysis (0)]
93.  Ichou L, Carbonell N, Rautou PE, Laurans L, Bourcier S, Pichereau C, Baudel JL, Nousbaum JB, Renou C, Anty R. Ascitic fluid TREM-1 for the diagnosis of spontaneous bacterial peritonitis. Gut. 2016;65:536-538.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10]  [Cited by in F6Publishing: 4]  [Article Influence: 1.7]  [Reference Citation Analysis (0)]
94.  Guler K, Vatansever S, Kayacan SM, Salmayenli N, Akkaya V, Erk O, Palanduz A. High sensitivity C-reactive protein in spontaneous bacterial peritonitis with nonneutrocytic ascites. Hepatogastroenterology. 2009;56:452-455.  [PubMed]  [DOI]  [Cited in This Article: ]
95.  Cullaro G, Kim G, Pereira MR, Brown RS Jr, Verna EC. Ascites Neutrophil Gelatinase-Associated Lipocalin Identifies Spontaneous Bacterial Peritonitis and Predicts Mortality in Hospitalized Patients with Cirrhosis. Dig Dis Sci. 2017;62:3487-3494.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 7]  [Cited by in F6Publishing: 5]  [Article Influence: 1.8]  [Reference Citation Analysis (0)]
96.  Bal CK, Daman R, Bhatia V. Predictors of fifty days in-hospital mortality in decompensated cirrhosis patients with spontaneous bacterial peritonitis. World J Hepatol. 2016;8:566-572.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 13]  [Cited by in F6Publishing: 12]  [Article Influence: 2.6]  [Reference Citation Analysis (0)]
97.  Lim KH, Potts JR, Chetwood J, Goubet S, Verma S. Long-term outcomes after hospitalization with spontaneous bacterial peritonitis. J Dig Dis. 2015;16:228-240.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 7]  [Article Influence: 2.4]  [Reference Citation Analysis (0)]
98.  Ginés P, Rimola A, Planas R, Vargas V, Marco F, Almela M, Forné M, Miranda ML, Llach J, Salmerón JM. Norfloxacin prevents spontaneous bacterial peritonitis recurrence in cirrhosis: results of a double-blind, placebo-controlled trial. Hepatology. 1990;12:716-724.  [PubMed]  [DOI]  [Cited in This Article: ]
99.  Titó L, Rimola A, Ginès P, Llach J, Arroyo V, Rodés J. Recurrence of spontaneous bacterial peritonitis in cirrhosis: frequency and predictive factors. Hepatology. 1988;8:27-31.  [PubMed]  [DOI]  [Cited in This Article: ]
100.  Shizuma T, Obata H, Hashimoto E, Hayashi N. Clinical analysis of bacterial infections in cirrhotic patients with ascites. Acta Hepatologica Japonica. 2002;43:446-452.  [PubMed]  [DOI]  [Cited in This Article: ]
101.  Bae S, Kim T, Kim MC, Chong YP, Kim SH, Sung H, Lim YS, Lee SO, Kim MN, Kim YS. Clinical characteristics and outcomes of spontaneous bacterial peritonitis caused by Enterobacter species versus Escherichia coli: a matched case-control study. BMC Infect Dis. 2016;16:252.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 1]  [Article Influence: 0.8]  [Reference Citation Analysis (0)]
102.  Schwabl P, Bucsics T, Soucek K, Mandorfer M, Bota S, Blacky A, Hirschl AM, Ferlitsch A, Trauner M, Peck-Radosavljevic M. Risk factors for development of spontaneous bacterial peritonitis and subsequent mortality in cirrhotic patients with ascites. Liver Int. 2015;35:2121-2128.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 45]  [Cited by in F6Publishing: 32]  [Article Influence: 7.5]  [Reference Citation Analysis (0)]
103.  Haddad L, Conte TM, Ducatti L, Nacif L, D’Albuquerque LA, Andraus W. MELD Score Is Not Related to Spontaneous Bacterial Peritonitis. Gastroenterol Res Pract. 2015;2015:270456.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 3]  [Article Influence: 0.7]  [Reference Citation Analysis (0)]
104.  Poca M, Alvarado-Tapias E, Concepción M, Pérez-Cameo C, Cañete N, Gich I, Romero C, Casas M, Román E, Castells L. Predictive model of mortality in patients with spontaneous bacterial peritonitis. Aliment Pharmacol Ther. 2016;44:629-637.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 7]  [Article Influence: 1.6]  [Reference Citation Analysis (0)]
105.  Bernardi M, Gitto S, Biselli M. The MELD score in patients awaiting liver transplant: strengths and weaknesses. J Hepatol. 2011;54:1297-1306.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 85]  [Cited by in F6Publishing: 61]  [Article Influence: 7.7]  [Reference Citation Analysis (0)]
106.  Bruns T, Lutz P, Stallmach A, Nischalke HD. Low ascitic fluid protein does not indicate an increased risk for spontaneous bacterial peritonitis in current cohorts. J Hepatol. 2015;63:527-528.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 15]  [Cited by in F6Publishing: 7]  [Article Influence: 2.5]  [Reference Citation Analysis (0)]
107.  Kwon JH, Koh SJ, Kim W, Jung YJ, Kim JW, Kim BG, Lee KL, Im JP, Kim YJ, Kim JS. Mortality associated with proton pump inhibitors in cirrhotic patients with spontaneous bacterial peritonitis. J Gastroenterol Hepatol. 2014;29:775-781.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 37]  [Cited by in F6Publishing: 26]  [Article Influence: 5.3]  [Reference Citation Analysis (0)]
108.  Miura K, Tanaka A, Yamamoto T, Adachi M, Takikawa H. Proton pump inhibitor use is associated with spontaneous bacterial peritonitis in patients with liver cirrhosis. Intern Med. 2014;53:1037-1042.  [PubMed]  [DOI]  [Cited in This Article: ]
109.  Min YW, Lim KS, Min BH, Gwak GY, Paik YH, Choi MS, Lee JH, Kim JJ, Koh KC, Paik SW. Proton pump inhibitor use significantly increases the risk of spontaneous bacterial peritonitis in 1965 patients with cirrhosis and ascites: a propensity score matched cohort study. Aliment Pharmacol Ther. 2014;40:695-704.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 63]  [Cited by in F6Publishing: 36]  [Article Influence: 9.0]  [Reference Citation Analysis (0)]
110.  Dam G, Vilstrup H, Watson H, Jepsen P. Proton pump inhibitors as a risk factor for hepatic encephalopathy and spontaneous bacterial peritonitis in patients with cirrhosis with ascites. Hepatology. 2016;64:1265-1272.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 93]  [Cited by in F6Publishing: 56]  [Article Influence: 18.6]  [Reference Citation Analysis (0)]
111.  de Vos M, De Vroey B, Garcia BG, Roy C, Kidd F, Henrion J, Deltenre P. Role of proton pump inhibitors in the occurrence and the prognosis of spontaneous bacterial peritonitis in cirrhotic patients with ascites. Liver Int. 2013;33:1316-1323.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 42]  [Cited by in F6Publishing: 35]  [Article Influence: 5.3]  [Reference Citation Analysis (0)]
112.  Terg R, Casciato P, Garbe C, Cartier M, Stieben T, Mendizabal M, Niveyro C, Benavides J, Marino M, Colombato L. Proton pump inhibitor therapy does not increase the incidence of spontaneous bacterial peritonitis in cirrhosis: a multicenter prospective study. J Hepatol. 2015;62:1056-1060.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 72]  [Cited by in F6Publishing: 46]  [Article Influence: 12.0]  [Reference Citation Analysis (0)]
113.  Miozzo SA, Tovo CV, John JA, de Mattos AA. Proton pump inhibitor use and spontaneous bacterial peritonitis in cirrhosis: An undesirable association? J Hepatol. 2015;63:529-530.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 8]  [Article Influence: 2.0]  [Reference Citation Analysis (0)]
114.  Yu T, Tang Y, Jiang L, Zheng Y, Xiong W, Lin L. Proton pump inhibitor therapy and its association with spontaneous bacterial peritonitis incidence and mortality: A meta-analysis. Dig Liver Dis. 2016;48:353-359.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 37]  [Cited by in F6Publishing: 16]  [Article Influence: 6.2]  [Reference Citation Analysis (0)]
115.  Khan MA, Kamal S, Khan S, Lee WM, Howden CW. Systematic review and meta-analysis of the possible association between pharmacological gastric acid suppression and spontaneous bacterial peritonitis. Eur J Gastroenterol Hepatol. 2015;27:1327-1336.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 7]  [Article Influence: 4.0]  [Reference Citation Analysis (0)]
116.  Kim JH, Lim KS, Min YW, Lee H, Min BH, Rhee PL, Kim JJ, Koh KC, Paik SW. Proton pump inhibitors do not increase the risk for recurrent spontaneous bacterial peritonitis in patients with cirrhosis. J Gastroenterol Hepatol. 2017;32:1064-1070.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 19]  [Cited by in F6Publishing: 11]  [Article Influence: 4.8]  [Reference Citation Analysis (0)]
117.  Johnson DA, Katz PO, Armstrong D, Cohen H, Delaney BC, Howden CW, Katelaris P, Tutuian RI, Castell DO. The Safety of Appropriate Use of Over-the-Counter Proton Pump Inhibitors: An Evidence-Based Review and Delphi Consensus. Drugs. 2017;77:547-561.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 35]  [Cited by in F6Publishing: 13]  [Article Influence: 8.8]  [Reference Citation Analysis (0)]
118.  Jeffries MA, Stern MA, Gunaratnam NT, Fontana RJ. Unsuspected infection is infrequent in asymptomatic outpatients with refractory ascites undergoing therapeutic paracentesis. Am J Gastroenterol. 1999;94:2972-2976.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 49]  [Cited by in F6Publishing: 34]  [Article Influence: 2.2]  [Reference Citation Analysis (0)]
119.  Hung TH, Tsai CC, Hsieh YH, Tsai CC. The long-term mortality of spontaneous bacterial peritonitis in cirrhotic patients: A 3-year nationwide cohort study. Turk J Gastroenterol. 2015;26:159-162.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 7]  [Cited by in F6Publishing: 4]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
120.  Cho Y, Park SY, Lee JH, Lee DH, Lee M, Yoo JJ, Choi WM, Cho YY, Lee YB, Yoon JW. High-sensitivity C-reactive protein level is an independent predictor of poor prognosis in cirrhotic patients with spontaneous bacterial peritonitis. J Clin Gastroenterol. 2014;48:444-449.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 13]  [Cited by in F6Publishing: 4]  [Article Influence: 1.9]  [Reference Citation Analysis (0)]
121.  Tandon P, Garcia-Tsao G. Renal dysfunction is the most important independent predictor of mortality in cirrhotic patients with spontaneous bacterial peritonitis. Clin Gastroenterol Hepatol. 2011;9:260-265.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 105]  [Cited by in F6Publishing: 74]  [Article Influence: 9.5]  [Reference Citation Analysis (0)]
122.  Jindal A, Kumar M, Bhadoria AS, Maiwall R, Sarin SK. A randomized open label study of ‘imipenem vs. cefepime’ in spontaneous bacterial peritonitis. Liver Int. 2016;36:677-687.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 6]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
123.  Tandon P, Kumar D, Seo YS, Chang HJ, Chaulk J, Carbonneau M, Qamar H, Keough A, Mansoor N, Ma M. The 22/11 risk prediction model: a validated model for predicting 30-day mortality in patients with cirrhosis and spontaneous bacterial peritonitis. Am J Gastroenterol. 2013;108:1473-1479.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 21]  [Article Influence: 3.4]  [Reference Citation Analysis (0)]
124.  Toledo C, Salmerón JM, Rimola A, Navasa M, Arroyo V, Llach J, Ginès A, Ginès P, Rodés J. Spontaneous bacterial peritonitis in cirrhosis: predictive factors of infection resolution and survival in patients treated with cefotaxime. Hepatology. 1993;17:251-257.  [PubMed]  [DOI]  [Cited in This Article: ]
125.  Lippi G, Danese E, Cervellin G, Montagnana M. Laboratory diagnostics of spontaneous bacterial peritonitis. Clin Chim Acta. 2014;430:164-170.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 7]  [Article Influence: 1.7]  [Reference Citation Analysis (0)]
126.  Sort P, Navasa M, Arroyo V, Aldeguer X, Planas R, Ruiz-del-Arbol L, Castells L, Vargas V, Soriano G, Guevara M. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med. 1999;341:403-409.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1050]  [Cited by in F6Publishing: 200]  [Article Influence: 47.7]  [Reference Citation Analysis (0)]
127.  Fernández J, Monteagudo J, Bargallo X, Jiménez W, Bosch J, Arroyo V, Navasa M. A randomized unblinded pilot study comparing albumin versus hydroxyethyl starch in spontaneous bacterial peritonitis. Hepatology. 2005;42:627-634.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 152]  [Cited by in F6Publishing: 94]  [Article Influence: 9.5]  [Reference Citation Analysis (0)]
128.  Fernández J, Navasa M, Garcia-Pagan JC, G-Abraldes J, Jiménez W, Bosch J, Arroyo V. Effect of intravenous albumin on systemic and hepatic hemodynamics and vasoactive neurohormonal systems in patients with cirrhosis and spontaneous bacterial peritonitis. J Hepatol. 2004;41:384-390.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 101]  [Cited by in F6Publishing: 72]  [Article Influence: 6.3]  [Reference Citation Analysis (0)]
129.  Salerno F, Navickis RJ, Wilkes MM. Albumin infusion improves outcomes of patients with spontaneous bacterial peritonitis: a meta-analysis of randomized trials. Clin Gastroenterol Hepatol. 2013;11:123-130.e1.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 91]  [Cited by in F6Publishing: 55]  [Article Influence: 10.1]  [Reference Citation Analysis (0)]
130.  Poca M, Concepción M, Casas M, Alvarez-Urturi C, Gordillo J, Hernández-Gea V, Román E, Guarner-Argente C, Gich I, Soriano G. Role of albumin treatment in patients with spontaneous bacterial peritonitis. Clin Gastroenterol Hepatol. 2012;10:309-315.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 47]  [Cited by in F6Publishing: 23]  [Article Influence: 4.7]  [Reference Citation Analysis (0)]
131.  Garcia-Martinez R, Caraceni P, Bernardi M, Gines P, Arroyo V, Jalan R. Albumin: pathophysiologic basis of its role in the treatment of cirrhosis and its complications. Hepatology. 2013;58:1836-1846.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 189]  [Cited by in F6Publishing: 102]  [Article Influence: 23.6]  [Reference Citation Analysis (0)]
132.  Thévenot T, Bureau C, Oberti F, Anty R, Louvet A, Plessier A, Rudler M, Heurgué-Berlot A, Rosa I, Talbodec N. Effect of albumin in cirrhotic patients with infection other than spontaneous bacterial peritonitis. A randomized trial. J Hepatol. 2015;62:822-830.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 90]  [Cited by in F6Publishing: 51]  [Article Influence: 15.0]  [Reference Citation Analysis (0)]
133.  Wiest R, Krag A, Gerbes A. Spontaneous bacterial peritonitis: recent guidelines and beyond. Gut. 2012;61:297-310.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 211]  [Cited by in F6Publishing: 135]  [Article Influence: 21.1]  [Reference Citation Analysis (0)]
134.  Fernández J, Tandon P, Mensa J, Garcia-Tsao G. Antibiotic prophylaxis in cirrhosis: Good and bad. Hepatology. 2016;63:2019-2031.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 96]  [Cited by in F6Publishing: 60]  [Article Influence: 19.2]  [Reference Citation Analysis (0)]
135.  Loomba R, Wesley R, Bain A, Csako G, Pucino F. Role of fluoroquinolones in the primary prophylaxis of spontaneous bacterial peritonitis: meta-analysis. Clin Gastroenterol Hepatol. 2009;7:487-493.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 39]  [Cited by in F6Publishing: 25]  [Article Influence: 3.0]  [Reference Citation Analysis (0)]
136.  Tandon P, Delisle A, Topal JE, Garcia-Tsao G. High prevalence of antibiotic-resistant bacterial infections among patients with cirrhosis at a US liver center. Clin Gastroenterol Hepatol. 2012;10:1291-1298.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 105]  [Cited by in F6Publishing: 83]  [Article Influence: 11.7]  [Reference Citation Analysis (0)]
137.  Hanouneh MA, Hanouneh IA, Hashash JG, Law R, Esfeh JM, Lopez R, Hazratjee N, Smith T, Zein NN. The role of rifaximin in the primary prophylaxis of spontaneous bacterial peritonitis in patients with liver cirrhosis. J Clin Gastroenterol. 2012;46:709-715.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 65]  [Cited by in F6Publishing: 19]  [Article Influence: 8.1]  [Reference Citation Analysis (0)]
138.  Nadim MK, Durand F, Kellum JA, Levitsky J, O’Leary JG, Karvellas CJ, Bajaj JS, Davenport A, Jalan R, Angeli P. Management of the critically ill patient with cirrhosis: A multidisciplinary perspective. J Hepatol. 2016;64:717-735.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 150]  [Cited by in F6Publishing: 80]  [Article Influence: 30.0]  [Reference Citation Analysis (0)]
139.  Fernández J, Ruiz del Arbol L, Gómez C, Durandez R, Serradilla R, Guarner C, Planas R, Arroyo V, Navasa M. Norfloxacin vs ceftriaxone in the prophylaxis of infections in patients with advanced cirrhosis and hemorrhage. Gastroenterology. 2006;131:1049-1056; quiz 1285.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 289]  [Cited by in F6Publishing: 152]  [Article Influence: 19.3]  [Reference Citation Analysis (0)]
140.  Singh N, Gayowski T, Yu VL, Wagener MM. Trimethoprim-sulfamethoxazole for the prevention of spontaneous bacterial peritonitis in cirrhosis: a randomized trial. Ann Intern Med. 1995;122:595-598.  [PubMed]  [DOI]  [Cited in This Article: ]
141.  Assem M, Elsabaawy M, Abdelrashed M, Elemam S, Khodeer S, Hamed W, Abdelaziz A, El-Azab G. Efficacy and safety of alternating norfloxacin and rifaximin as primary prophylaxis for spontaneous bacterial peritonitis in cirrhotic ascites: a prospective randomized open-label comparative multicenter study. Hepatol Int. 2016;10:377-385.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 31]  [Cited by in F6Publishing: 16]  [Article Influence: 5.2]  [Reference Citation Analysis (0)]
142.  Mostafa T, Badra G, Abdallah M. The efficacy and the immunomodulatory effect of rifaximin in prophylaxis of spontaneous bacterial peritonitis in cirrhotic Egyptian patients. Turk J Gastroenterol. 2015;26:163-169.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 14]  [Article Influence: 4.2]  [Reference Citation Analysis (0)]
143.  Elfert A, Abo Ali L, Soliman S, Ibrahim S, Abd-Elsalam S. Randomized-controlled trial of rifaximin versus norfloxacin for secondary prophylaxis of spontaneous bacterial peritonitis. Eur J Gastroenterol Hepatol. 2016;28:1450-1454.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 43]  [Cited by in F6Publishing: 18]  [Article Influence: 10.8]  [Reference Citation Analysis (0)]
144.  Goel A, Rahim U, Nguyen LH, Stave C, Nguyen MH. Systematic review with meta-analysis: rifaximin for the prophylaxis of spontaneous bacterial peritonitis. Aliment Pharmacol Ther. 2017;46:1029-1036.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 38]  [Cited by in F6Publishing: 22]  [Article Influence: 9.5]  [Reference Citation Analysis (0)]
145.  Sidhu GS, Go A, Attar BM, Mutneja HR, Arora S, Patel SA. Rifaximin versus norfloxacin for prevention of spontaneous bacterial peritonitis: a systematic review. BMJ Open Gastroenterol. 2017;4:e000154.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10]  [Cited by in F6Publishing: 4]  [Article Influence: 2.5]  [Reference Citation Analysis (0)]
146.  Lutz P, Nischalke HD, Krämer B, Goeser F, Kaczmarek DJ, Schlabe S, Parcina M, Nattermann J, Hoerauf A, Strassburg CP. Antibiotic resistance in healthcare-related and nosocomial spontaneous bacterial peritonitis. Eur J Clin Invest. 2017;47:44-52.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 34]  [Cited by in F6Publishing: 22]  [Article Influence: 6.8]  [Reference Citation Analysis (0)]
147.  Ariza X, Castellote J, Lora-Tamayo J, Girbau A, Salord S, Rota R, Ariza J, Xiol X. Risk factors for resistance to ceftriaxone and its impact on mortality in community, healthcare and nosocomial spontaneous bacterial peritonitis. J Hepatol. 2012;56:825-832.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 100]  [Cited by in F6Publishing: 79]  [Article Influence: 10.0]  [Reference Citation Analysis (0)]
148.  Hwang SY, Yu SJ, Lee JH, Kim JS, Yoon JW, Kim YJ, Yoon JH, Kim EC, Lee HS. Spontaneous fungal peritonitis: a severe complication in patients with advanced liver cirrhosis. Eur J Clin Microbiol Infect Dis. 2014;33:259-264.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 52]  [Cited by in F6Publishing: 30]  [Article Influence: 6.5]  [Reference Citation Analysis (0)]
149.  Bremmer DN, Garavaglia JM, Shields RK. Spontaneous fungal peritonitis: a devastating complication of cirrhosis. Mycoses. 2015;58:387-393.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 10]  [Article Influence: 2.3]  [Reference Citation Analysis (0)]
150.  Hassan EA, Abd El-Rehim AS, Hassany SM, Ahmed AO, Elsherbiny NM, Mohammed MH. Fungal infection in patients with end-stage liver disease: low frequency or low index of suspicion. Int J Infect Dis. 2014;23:69-74.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 41]  [Cited by in F6Publishing: 25]  [Article Influence: 5.9]  [Reference Citation Analysis (0)]
151.  Fiore M, Maraolo AE, Leone S, Gentile I, Cuomo A, Schiavone V, Bimonte S, Pace MC, Cascella M. Spontaneous peritonitis in critically ill cirrhotic patients: a diagnostic algorithm for clinicians and future perspectives. Ther Clin Risk Manag. 2017;13:1409-1414.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 15]  [Cited by in F6Publishing: 7]  [Article Influence: 3.8]  [Reference Citation Analysis (0)]
152.  Fiore M, Leone S. Use of antifungals in critically ill cirrhotic patients with spontaneous peritonitis. J Hepatol. 2016;64:986-987.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 4]  [Article Influence: 0.6]  [Reference Citation Analysis (0)]
153.  Gravito-Soares M, Gravito-Soares E, Lopes S, Ribeiro G, Figueiredo P. Spontaneous fungal peritonitis: a rare but severe complication of liver cirrhosis. Eur J Gastroenterol Hepatol. 2017;29:1010-1016.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 6]  [Article Influence: 3.5]  [Reference Citation Analysis (0)]
154.  Bucsics T, Schwabl P, Mandorfer M, Peck-Radosavljevic M. Prognosis of cirrhotic patients with fungiascites and spontaneous fungal peritonitis (SFP). J Hepatol. 2016;64:1452-1454.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10]  [Cited by in F6Publishing: 6]  [Article Influence: 2.0]  [Reference Citation Analysis (0)]
155.  Elkhateeb SR, Gouda NS, Ibrahim AS, Anwar R, Eissa LA. PCR-detected fungal infection is associated with fatal outcomes in cirrhotic patients with spontaneous peritonitis. EJBAS. 2017;4:42-46.  [PubMed]  [DOI]  [Cited in This Article: ]
156.  Fiore M, Chiodini P, Pota V, Sansone P, Passavanti MB, Leone S, Aurilio C, Pace MC. Risk of spontaneous fungal peritonitis in hospitalized cirrhotic patients with ascites: a systematic review of observational studies and meta-analysis. Minerva Anestesiol. 2017;83:1309-1316.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 6]  [Reference Citation Analysis (0)]
157.  Bal CK, Bhatia V, Khillan V, Rathor N, Saini D, Daman R, Sarin SK. Spontaneous cryptococcal peritonitis with fungemia in patients with decompensated cirrhosis: Report of two cases. Indian J Crit Care Med. 2014;18:536-539.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10]  [Cited by in F6Publishing: 5]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
158.  Karvellas CJ, Abraldes JG, Arabi Y, Kumar A; Cooperative Anti-microbial Therapy of Septic Shock (CATSS) Database Research Group. Letter: what else can improve survival in cirrhotic patients with spontaneous bacterial peritonitis and associated septic shock? Authors’ reply. Aliment Pharmacol Ther. 2015;42:123-124.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 2]  [Reference Citation Analysis (0)]
159.  Alexopoulou A, Vasilieva L, Agiasotelli D, Dourakis SP. Fungal infections in patients with cirrhosis. J Hepatol. 2015;63:1043-1045.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 28]  [Cited by in F6Publishing: 20]  [Article Influence: 4.7]  [Reference Citation Analysis (0)]