Casual Blood-Ethanol' Estimations in Patients With Chronic Liver Disease

Hamlyn, A.N.; Sherlock, Sheila; Brown, Andrew; Baron, D N

doi:10.1016/s0140-6736(75)92781-6

Cited by 44 publications

(14 citation statements)

References 6 publications

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“…These concentrations of alcohol have been found in the blood of patients with alcoholic liver diseases (39,40) and are sufficient to generate hepatic vasoconstriction in rats (41,42). The levels of PCBP2 mRNA, collagen α1(I) mature mRNA, and collagen α1(I) pre-mRNA were determined using real-time RT-PCR (Fig.…”

Section: Resultsmentioning

confidence: 99%

PCBP2 siRNA Reverses the Alcohol-induced Pro-fibrogenic Effects in Hepatic Stellate Cells

et al. 2011

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Purpose Type I collagen accumulates during liver fibrosis primarily because α-complex protein-2 (αCP2), encoded by the poly(rC) binding protein 2 (PCBP2) gene, binds to the 3′ end of the collagen mRNA and increases its half-life. This study aimed to reverse the pro-fibrogenic effect of alcohol on hepatic stellate cells (HSCs) by silencing the PCBP2 gene with siRNA. Methods The silencing effects of a series of predesigned PCBP2 siRNAs were evaluated in the rat hepatic stellate cell line, HSC-T6. The pro-fibrogenic effects of alcohol on the expression levels of PCBP2 and type-I collagen were examined by several methods. The effect of PCBP2 siRNA on the stability of type I collagen α1(I) mRNA was investigated by an in vitro mRNA decay assay. Results We identified one potent PCBP2 siRNA that reversed the alcohol-induced expression of PCBP2 in HSCs. The decay rate of the collagen α1(I) mRNA increased significantly in HSCs treated with the PCBP2 siRNA. Conclusion This study provides the first evidence that alcohol up-regulates the expression of PCBP2, which subsequently increases the half-life of collagen α1(I) mRNA. Silencing of PCBP2 using siRNA may provide a promising strategy to reverse the alcohol-induced pro-fibrogenic effects in HSCs.

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Section: Resultsmentioning

confidence: 99%

PCBP2 siRNA Reverses the Alcohol-induced Pro-fibrogenic Effects in Hepatic Stellate Cells

et al. 2011

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“…In a previous study, we examined whether HepG2 cells had a metabolic pathway for ethanol as a normal hepatocyte function, and we showed that these cells had significantly high alcohol dehydrogenase (ADH) activity (similar to that in rat liver tissue), and this activity was similar to that in human liver in vivo. 16 In the present study, we incubated the HepG2 cells with 100 mM ethanol; as such a high blood level of ethanol has been found in patients with alcoholic liver disease, 24,25 this concentration seemed to be suitable for an in vitro experiment. This concentration had previously been used in an investigation of the effects of ethanol on human macrophage functions.…”

Section: Discussionmentioning

confidence: 82%

Suppressive effect of ethanol on the expression of hepatic asialoglycoprotein receptors augmented by interleukin-1β, interleukin-6, and tumor necrosis factor-α

Kato

Mogi

Kohgo

et al. 1998

Journal of Gastroenterology

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Blood levels of inflammatory-related cytokines, including interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha, are elevated in patients with alcoholic liver diseases. We investigated the effects of these cytokines and ethanol on the expression of hepatic asialoglycoprotein receptors (AGPRs) in a human hepatoblastoma cell line, HepG2. An [125I]-asialo-orosomucoid binding assay showed significant increases in surface AGPR numbers in HepG2 cells by treatment with IL-1beta, IL-6, and TNF-alpha, to levels which were approximately 130% of the values in untreated control cells. However, the enhanced AGPR numbers induced by treatment with these cytokines were markedly suppressed, to 70%-80% of the number in the untreated cells, by treatment with ethanol. Immunological detection of AGPR with a specific antibody demonstrated that the modulation of surface AGPR numbers was correlated with the cellular expression levels of AGPR. These results suggest that, although IL-1beta, IL-6, and TNF-alpha stimulate the synthesis of hepatic AGPR, ethanol suppresses the expression of AGPR augmented by these cytokines. This leads to an increase in serum asialo-orosomucoid levels caused by the disordered catabolism mediated by AGPR in patients with alcoholic liver disease.

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“…However, the four patients who showed zonal necrosis were on average 42.5 years old, with no evidence of cardiopulmonary dysfunction. Because liver microcirculation damage is caused by high doses of ethanol (Oshita et al, 1993) and blood ethanol level was found to be greater than 100 mM in cases of liver damages (Hamlyn et al, 1975), we assumed that liver circulatory disturbance caused by excessive alcohol consumption led to the observed acute parenchymal inflammation.…”

Section: Discussionmentioning

confidence: 99%

A Clinicopathological Study of Acute Hepatitis in Heavy Drinkers, Unrelated to Hepatitis A, B, or C Viruses

Miyano

Maeyama

Iwaba

et al. 2001

Alcoholism Clin & Exp Res

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Background: There are six histological classifications of alcoholic liver disease (ALD) in Japan. However, it is unclear whether all cases of the disease conform to these criteria. This study investigated the clinicopathological features of eight histologically unusual cases of ALD.Methods: The characteristic features of alcohol drinking behavior, subjective and objective symptoms, laboratory data on admission, and progress after admission were analyzed for eight patients with acuteonset hepatitis.Result: The eight patients showed histologically acute hepatitis, with much spotty necrosis that contained granular ceroid pigment by Kupffer cells, which indicated acute parenchymal damage of the liver, but with no Mallory bodies and unremarkable intrasinusoidal neutrophilic infiltration. The only etiological factor for all the cases was habitual alcohol consumption, with increased consumption just before the onset of symptoms. In five cases that were tested, the patients were negative for hepatic viral markers, which included hepatitis G virus RNA and TT virus DNA.Conclusion: Some cases of ALD may not conform to the current histological classifications in either Japan or Western countries. It seems natural to consider that these cases are developed by other, unknown causes that overlap with ALD rather than as a result of damage from alcoholic overload.

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Casual Blood-Ethanol' Estimations in Patients With Chronic Liver Disease

Cited by 44 publications

References 6 publications

PCBP2 siRNA Reverses the Alcohol-induced Pro-fibrogenic Effects in Hepatic Stellate Cells

PCBP2 siRNA Reverses the Alcohol-induced Pro-fibrogenic Effects in Hepatic Stellate Cells

Suppressive effect of ethanol on the expression of hepatic asialoglycoprotein receptors augmented by interleukin-1β, interleukin-6, and tumor necrosis factor-α

A Clinicopathological Study of Acute Hepatitis in Heavy Drinkers, Unrelated to Hepatitis A, B, or C Viruses

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