Infections in Alcoholic Liver Disease

Kim, Angela C.; Epstein, Marcia; Gautam-Goyal, Pranisha; Doan, Thien-Ly

doi:10.1016/j.cld.2012.08.008

Cited by 5 publications

(6 citation statements)

References 75 publications

(79 reference statements)

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“…The mortality rate for sepsis caused by V. vulnificus infection is about 50%, of which, the morbidity and mortality in ALD patients are higher than others (2,11). Studies have shown that the immune function of patients with ALD is generally impaired (16). However, after infection with V. vulnificus, whether the immune response of ALD patients is different from others remains unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, elevated serum iron concentrations may not be the only factor causing ALD patients to be susceptible to V. vulnificus infection. It is important to acknowledge that in addition to being susceptible to V. vulnificus infection, ALD patients are also susceptible to infections with other microorganisms ( 16 ). Hence, the reason for their susceptibility may be related to other common factors such as the immune status of the patient.…”

Section: Introductionmentioning

confidence: 99%

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Analysis of Gene Expression Profiles, Cytokines, and Bacterial Loads Relevant to Alcoholic Liver Disease Mice Infected With V. vulnificus

Feng

Zhang

et al. 2021

Front. Immunol.

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Patients with liver disease are susceptible to infection with Vibrio vulnificus (V. vulnificus), but the specific reasons remain elusive. Through RNA-seq, we found that when mice with alcoholic liver disease (ALD) were infected with V. vulnificus by gavage, compared with the Pair group, the small intestinal genes affecting intestinal permeability were upregulated; and the number of differentially expressed genes related to immune functions (e.g., such as cell chemotaxis, leukocyte differentiation, and neutrophil degranulation) decreased in the liver, spleen, and blood. Further analysis showed that the number of white blood cells decreased in the Pair group, whereas those in the ALD mice did not change significantly. Interestingly, the blood bacterial load in the ALD mice was about 100 times higher than that of the Pair group. After the ALD mice were infected with V. vulnificus, the concentrations of T cell proliferation-promoting cytokines (IL-2, IL-23) decreased. Therefore, unlike the Pair group, ALD mice had weaker immune responses, lower T cell proliferation-promoting cytokines, and higher bacterial loads post-infection, possibly increasing their susceptibility to V. vulnificus infection. These new findings we presented here may help to advance the current understanding of the reasons why patients with liver disease are susceptible to V. vulnificus infection and provides potential targets for further investigation in the context of treatment options for V. vulnificus sepsis in liver disease patient.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Analysis of Gene Expression Profiles, Cytokines, and Bacterial Loads Relevant to Alcoholic Liver Disease Mice Infected With V. vulnificus

Feng

Zhang

et al. 2021

Front. Immunol.

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“…Given the side effects of alcohol use and altered sensorium, it may be unsurprising that patients with ALD are at risk for aspiration of gastric contents (89). This can lead to a multitude of other complications including pneumonia, empyema, and lung abscesses, traditionally stemming from pathogens endogenous to gastric or oropharyngeal flora (90). Furthermore, chronic alcohol abuse is a risk factor for transfusion-related acute lung injury (TRALI) and acute respiratory distress syndrome (ARDS) (91).…”

Section: Pulmonary Abnormalitiesmentioning

confidence: 99%

Nonalcoholic fatty liver disease and alcoholic liver disease: metabolic diseases with systemic manifestations

Kovalic¹,

Cholankeril²

2019

Transl. Gastroenterol. Hepatol

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The progression of liver disease is portrayed by several common, overarching signs and symptoms. Classically, these include findings such as spider angiomata, jaundice, palmar erythema, and as cirrhosis decompensates, ascites, variceal hemorrhage (VH), hepatic encephalopathy (HE), and hepatocellular carcinoma (HCC). Aside from these universal hallmarks among cirrhotics, patients with nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) harbor their own distinct systemic associations and manifestations. NAFLD is tightly linked to metabolic syndrome, which appears to be a driving force for a multitude of comorbidities, such as insulin resistance, cardiovascular disease, chronic kidney disease (CKD), obstructive sleep apnea (OSA), as well as increased malignancy risk. ALD also maintains a variety of comorbidities congruent with systemic effects of chronic alcohol use. These findings are highlighted by cardiovascular conditions, neuronal damage, myopathy, nutritional deficiencies, chronic pancreatitis, in addition to increased malignancy risk. While a general, guideline-driven management for all cirrhotic patients remains imperative for minimizing risk of complications, a tailored treatment strategy is useful for patients with NAFLD and ALD who entertain their own constellation of unique systemic manifestations.

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“…Hence, infectious diseases may cause or exacerbate hyponatremia in patients with hepatopathies. This fact should be taken into account in a patient with liver disease developing acute hyponatremia, since infections, such as spontaneous bacterial peritonitis, in these patients may have a vague clinical presentation and are often difficult to diagnose [45,46].…”

Section: Hyponatremia Related With Infections In Patients With Liver mentioning

confidence: 99%

Hyponatremia in patients with liver diseases: not just a cirrhosis-induced hemodynamic compromise

et al. 2016

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Hyponatremia (Na(+) <135 mmol/l) is the most common electrolyte disorder. Cirrhosis represents a rather frequent cause of hyponatremia mainly due to systemic and splanchnic vasodilation resulting in decreased effective arterial blood volume, which leads to excessive non-osmotic secretion of antidiuretic hormone. However, hyponatremia of multifactorial origin may be seen in patients with liver diseases. The review focuses on the factors and pathogenetic mechanisms of decreased sodium levels other than the hemodynamic compromise of cirrhosis in patients with liver diseases. The mechanisms and causal or contributing role of pseudohyponatremia, hyperglycemia, infections, drugs and toxins as well as of endocrine disorders, renal failure and cardiac disease in patients with liver disease are meticulously discussed. Hyponatremia of multifactorial origin is frequently observed in patients with liver diseases, and special efforts should be made to delineate the underlying causative and precipitating factors as well as the risk factors of the osmotic demyelination syndrome in order to properly manage this serious electrolyte disorder and avoid treatment pitfalls.

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Infections in Alcoholic Liver Disease

Cited by 5 publications

References 75 publications

Analysis of Gene Expression Profiles, Cytokines, and Bacterial Loads Relevant to Alcoholic Liver Disease Mice Infected With V. vulnificus

Analysis of Gene Expression Profiles, Cytokines, and Bacterial Loads Relevant to Alcoholic Liver Disease Mice Infected With V. vulnificus

Nonalcoholic fatty liver disease and alcoholic liver disease: metabolic diseases with systemic manifestations

Hyponatremia in patients with liver diseases: not just a cirrhosis-induced hemodynamic compromise

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