Non-alcoholic fatty liver disease: The diagnosis and management

El-Kader, Shehab M Abd; Ashmawy, Eman M

doi:10.4254/wjh.v7.i6.846

Cited by 326 publications

(291 citation statements)

References 122 publications

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“…NAFLD was diagnosed when there was: 1) heterogeneous appearance of the liver and echogenicity exceeding that of the renal cortex or spleen on abdominal ultrasound; and/or 2) lower attenuation of the liver parenchyma compared to the spleen and/or intrahepatic blood vessels on abdominal CT; and/or 3) signal intensity loss on opposed-phase images in comparison with in-phase images by MRI. This is in accordance with previous studies [17,18].…”

Section: Diagnosis Of Nafldsupporting

confidence: 82%

Small Intestinal Bacterial Overgrowth Is Associated with Non- Alcoholic Fatty Liver Disease

Fialho

André

Thota

et al. 2016

JGLD

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Background: Changes in gut bacteria play a role in type 2 diabetes mellitus (DM) and hepatic steatosis. There is a lack of studies evaluating the frequency and risk factors for non-alcoholic fatty liver disease (NAFLD) in patients tested for small intestinal bacterial overgrowth (SIBO). Aim: To evaluate the frequency of NAFLD and associated risk factors in patients tested for SIBO. Methods: In this case-control study, 372 eligible patients submitted to glucose hydrogen/methane breath test for SIBO who also had an abdominal imaging study were included. Patients were divided into SIBO-positive and SIBO-negative groups. Clinical, demographic and laboratory variables were evaluated in addition to the presence of NAFLD on abdominal imaging. Results: Of the 372 eligible patients, 141 (37.9%) were tested positive for SIBO (study group) and 231 (62.1%) were negative for it (control group). NAFLD occurred in 45.4% (64/141) of the study group compared to 17.3% (40/231) of the control group (p<0.001). Patients in the study group were found to have higher rates of elevated aspartate aminotransferase (AST) (20.6% vs. 11.3%; p=0.034) and alanine aminotransferase (ALT) levels (56.0% vs. 40.7%; p= 0.039), type 2 diabetes (23.4% vs. 13.9%; p=0.041), hypertension (54.6% vs. 40.3%; p=0.046) and metabolic syndrome (78.0% vs. 60.2%; p=0.020). In the multivariate analysis, SIBO (odds ratio [OR]: 1.95; 95% confidence interval [CI]: 1.14-3.31; p=0.014), type 2 DM (OR: 3.04; 95%CI: 1.57-5.90; p=0.001) and obesity (OR: 3.58; 95%CI: 1.70-7.54; p=0.001) remained associated with NAFLD.Conclusion: Patients with SIBO have an increased risk for hepatic steatosis and may benefit from aggressive control of the risk factors for NAFLD including metabolic syndrome. Abbreviations: ALT: alanine aminotransferase; AST: aspartate aminotransferase; BMI: body mass index; CTE: computed tomography enterography; DM: diabetes mellitus; ETOH: ethanol; IL: interleukin; LPS: lipopolysaccharide; NAFLD: non-alcoholic fatty liver disease; NASH: non-alcoholic steatohepatitis; PPI: proton pump inhibitor; SIBO: small intestinal bacterial overgrowth; TLR-4: toll-like receptor 4; TMAO: trimethylamine-N-oxide (TMAO); TNF-α: tumor necrosis factor alpha.

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Section: Diagnosis Of Nafldsupporting

confidence: 82%

Small Intestinal Bacterial Overgrowth Is Associated with Non- Alcoholic Fatty Liver Disease

Fialho

André

Thota

et al. 2016

JGLD

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“…[31] Cytokines and fatty liver disease Non-alcoholic fatty liver disease (NAFLD) is now the most frequent chronic liver disease that occurs across all age groups and is recognized to occur in 14-30% of the general population, representing a serious and growing clinical problem due to the growing prevalence of obesity and overweight. [32] The first manifestation of hepatic injury is the accumulation of fat within hepatocytes (steatosis), this is followed by the development of necroinflammatory (steatohepatitis) activity that leads to cirrhosis. [33] The importance of cytokines as molecular effectors in liver damage has been particularly well demonstrated in patients and animals ranging from steatosis to cirrhosis.…”

Section: Structural Organization Of the Liver And Cytokines Potentialmentioning

confidence: 99%

Physiological potential of cytokines and liver damages

Mannaa¹,

Abdel-Wahhab²

2016

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Cytokines are soluble extracellular small molecular weight protein or peptide. They are produced by virtually every nucleated cell type in response to injurious stimuli to control body metabolism, infection, inflammation and tissue or neuronal damage; therefore acting as messengers between tissues and the immune system; and participating in many physiological processes through their either anti-inflammatory or pro-inflammatory characteristics. Many cytokines have multiple cellular sources and targets, as well as many natural inducers and inhibitors. In pathophysiological conditions and during the early phase of chronic liver diseases, agent like virus, bacteria, parasites, ethanol, or toxins, induce secretion of cytokines at high levels. The presence of cytokine antagonists and soluble cytokine receptors, often released in concert with their respective cytokine agonist, presents additional complexity to interpretation.

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“…Pure motor neuropathies and autonomic neuropathies are rare in HCV [12] . Abd ElKader et al [93] estimated the prevalence of PN in patients with HCV related liver disorders based on complete neurologic examination and nerve conduction study [93] . Of the 50 subjects included in the study, 22% had sensory abnormalities, 18% had motor impairment while 10% had a combination of both.…”

Section: Peripheral Neuropathymentioning

confidence: 99%

Hepatitis C virus and neurological damage

Mathew

Faheem

Ibrahim

et al. 2016

WJH

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Author contributions: Mathew S and Faheem M contributed equally to this manuscript; Qadri I conceived and designed the topic; Mathew S, Faheem M, Ibrahim SM, Iqbal W and Rauff B contributed to materials and wrote the paper; Faheem M, Ibrahim SM, Iqbal W, Rauff B, Fatima K and Qadri I contributed to proof reading of the manuscript.Supported by KACST large R and D grant to Ishtiaq Qadri (#162-34).Conflict-of-interest statement: Authors declare no conflict of interests for this article. AbstractChronic hepatitis C virus (HCV) infection exhibits a wide range of extrahepatic complications, affecting various organs in the human body. Numerous HCV patients suffer neurological manifestations, ranging from cognitive impairment to peripheral neuropathy. Overexpression of the host immune response leads to the production of immune complexes, cryoglobulins, as well as autoantibodies, which is a major pathogenic mechanism responsible for nervous system dysfunction. Alternatively circulating inflammatory cytokines and chemokines and HCV replication in neurons is another factor that severely affects the nervous system. Furthermore, HCV infection causes both sensory and motor peripheral neuropathy in the mixed cryoglobulinemia as well as known as an important risk aspect for stroke. These extrahepatic manifestations are the reason behind underlying hepatic encephalopathy and chronic liver disease. The brain is an apt location for HCV replication, where the HCV virus may directly wield neurotoxicity. Other mechanisms that takes place by chronic HCV infection due the pathogenesis of neuropsychiatric disorders includes derangement of metabolic pathways of infected cells, autoimmune disorders, systemic or cerebral inflammation and alterations in neurotransmitter circuits. HCV and its pathogenic role is suggested by enhancement of psychiatric and neurological symptoms in patients attaining a sustained virologic response followed by treatment with interferon; however, further studies are required to fully assess the impact of HCV infection and its specific antiviral targets associated with neuropsychiatric disorders. REVIEWSubmit a

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Non-alcoholic fatty liver disease: The diagnosis and management

Cited by 326 publications

References 122 publications

Small Intestinal Bacterial Overgrowth Is Associated with Non- Alcoholic Fatty Liver Disease

Small Intestinal Bacterial Overgrowth Is Associated with Non- Alcoholic Fatty Liver Disease

Physiological potential of cytokines and liver damages

Hepatitis C virus and neurological damage

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