Nucleotide-binding oligomerization domain containing 2 (NOD2) variants are genetic risk factors for death and spontaneous bacterial peritonitis in liver cirrhosis

Appenrodt, Beate; Grünhage, F; Gentemann, M.; Thyssen, L.; Sauerbruch, Tilman; Lammert, Frank

doi:10.1002/hep.23440

Cited by 127 publications

(113 citation statements)

References 40 publications

(58 reference statements)

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“…It seems that the presence of bacterial DNA in serum and ascitic fluid is an independent factor in noninfected patients with the cirrhosis and implies a poor prognosis [15,29]. Recent studies suggest that a genetic variant associated with impaired mucosal barrier function may also be involved in this process [30]. …”

Section: Discussionmentioning

confidence: 99%

Identification of Bacterial DNA in Noninfectious Pleural Fluid with a Highly Sensitive PCR Method

Cremades

Galiana²,

Rodrı́guez³

et al. 2010

Respiration

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Background: Bacterial DNA due to bacterial translocation has been identified in noninfectious ascitic fluid samples. Objective: This study investigated the possible presence of bacterial DNA in the pleural fluid of patients with pleural effusions of noninfectious origin, using a highly sensitive PCR-based method. Methods: Pleural fluid samples from 175 patients (average age ± SD: 69 ± 14 years) with noninfectious pleural effusion (62 transudates, 113 exudates) were analyzed. Bacterial DNA was detected using nested PCR with amplification of a fragment of the gene r16S, with 2 amplification protocols, i.e. low sensitivity (10 and 40 cycles) and high sensitivity (40 and 40 cycles). Results: With the less sensitive amplification process, only 1 sample was positive (Haemophilus parainfluenzae in a patient with hepatic hydrothorax). With the highly sensitive nested PCR method, bacterial DNA was identified in the pleural fluid, of both transudative and exudative origin, of 75 of the 175 patients (43%). In cases of isolation of a single bacterium, the more frequent were Escherichia coli, Salmonella enterica and Streptococcus pneumoniae.Conclusions: Regardless of its origin, bacterial DNA can be identified in almost half of noninfectious pleural effusions by using a highly sensitive PCR-based method. The possible clinical significance or prognostic value of these findings deserves to be evaluated.

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Section: Discussionmentioning

confidence: 99%

Identification of Bacterial DNA in Noninfectious Pleural Fluid with a Highly Sensitive PCR Method

Cremades

Galiana²,

Rodrı́guez³

et al. 2010

Respiration

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“…In addition, essentially all animal models of intestinal fibrosis appear to be dependent on the presence of a microflora to initiate or perpetuate gut inflammation and fibrosis [25]. Although direct evidence about the innate immunity gene variants in liver fibrosis is lacking, several studies have shown that NOD2 is associated with the increased mortality in nonalcoholic liver transplant patients [30] or the increased risk of spontaneous bacterial peritonitis in patients with liver cirrhosis [31,32]. …”

Section: Innate Immunitymentioning

confidence: 99%

Intestinal Fibrosis and Liver Fibrosis: Consequences of Chronic Inflammation or Independent Pathophysiology?

Rieder¹,

Bettenworth²,

Imai³

et al. 2016

Inflamm Intest Dis

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Background: Intestinal fibrosis and liver fibrosis represent a significant burden for our patients and health-care systems. Despite the severe clinical problem and the observation that fibrosis is reversible, no specific antifibrotic therapies exist. Summary: In this review, using an ‘East-West' scientific collaboration, we summarize the current knowledge on principal mechanisms shared by intestinal fibrosis and liver fibrosis. We furthermore discuss inflammation as the cause of fibrogenesis in both entities, depict unique features of intestinal and hepatic fibrosis, and provide a future outlook on the development of antifibrotic therapies. Key Messages: A collaborative effort in the field of fibrosis, covering multiple organ systems, will have the highest chance of leading to the development of a successful antifibrotic intervention.

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“…Genetic factors may be involved in the development of infection-related ACLF. Genetic variants commonly found in Crohn's disease occur in patients with cirrhosis [21]. An intriguing finding is that the presence of these genetic variants in cirrhotics is associated with a high risk of death [21].…”

Section: Mechanisms Of Infection-related Aclfmentioning

confidence: 99%

Role of Infections in Acute-on-Chronic Liver Failure

Moreau¹

2015

Dig Dis

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Patients with cirrhosis are prone to developing bacterial infections. Moreover, bacterial infection is the most common identifiable trigger of acute-on-chronic liver failure (ACLF), which is characterized by organ failures and a high risk of death. There is evidence of an excessive immune response of the host as a major mechanism leading to the development of organ failures in patients with cirrhosis. However, a role for direct tissue damage caused by bacterial toxins and virulence factors cannot be excluded. Failed tolerance mechanisms may also contribute to organ failures, although the involved mechanisms are unclear. A proportion of patients with infection-related ACLF have a prolonged stay in the intensive care unit. These patients have immune suppression, increased risk of superinfection and poor outcome. Immune suppression might be a consequence of the first infection episode that has led patients to be admitted to hospital.

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Nucleotide-binding oligomerization domain containing 2 (NOD2) variants are genetic risk factors for death and spontaneous bacterial peritonitis in liver cirrhosis

Cited by 127 publications

References 40 publications

Identification of Bacterial DNA in Noninfectious Pleural Fluid with a Highly Sensitive PCR Method

Identification of Bacterial DNA in Noninfectious Pleural Fluid with a Highly Sensitive PCR Method

Intestinal Fibrosis and Liver Fibrosis: Consequences of Chronic Inflammation or Independent Pathophysiology?

Role of Infections in Acute-on-Chronic Liver Failure

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