Alcohol-related liver disease (ALD) consists of a wide spectrum of clinical manifestations and pathological features, ranging from asymptomatic patients to decompensated cirrhosis and hepatocellular carcinoma. Patients with heavy alcohol intake and advanced fibrosis often develop a subacute form of liver failure called alcohol-induced hepatitis (AH). Globally, most patients with ALD are identified at late stages of the disease, limiting therapeutic interventions. Thus, there is a need for early detection of ALD patients, which is lacking in most countries. The identification of alcohol misuse is hampered by the existence of alcohol underreporting by many patients. There are useful biomarkers that can detect recent alcohol use. Moreover, there are several non-invasive techniques to assess the presence of advanced fibrosis among patients with alcohol misuse, which could identify patients at high risk of liver related events or early death. In this review, we discuss differences between early stages of ALD and AH as the cornerstone of advanced forms. A global overview of epidemiological, anthropometric, clinical, analytical, histological, and molecular differences is summarized in this article. We propose that campaigns aimed at identifying patients with subclinical forms can prevent the development of life-threatening forms.
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Alcohol-associated liver disease (ALD), which ranges from mild disease to alcohol-associated hepatitis and cirrhosis, is the most prevalent type of chronic liver disease and a leading cause of morbidity and mortality worldwide. Accumulating evidence reveals that programmed cell death (PCD) plays a crucial role in progression of ALD involving crosstalk between hepatocytes and immune cells. Multiple pathways of PCD, including apoptosis, necroptosis, autophagy, pyroptosis and ferroptosis, are reported in ALD. Interestingly, PCD pathways are intimately linked and interdependent, making it difficult to therapeutically target a single pathway. This review clarifies the multiple types of PCD occurring in liver and focuses on crosstalk between hepatocytes and innate immune cells in ALD.
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Sang Gyune Kim, M.D., Young Seok Kim, M.D., Seung Won Jung, M.D.,
Hee Kyung Kim, M.D.1, Jae Young Jang, M.D., Jong Ho Moon, M.D.,
Hong Soo Kim, M.D., Joon Seong Lee, M.D., Moon Sung Lee, M.D.,
Chan Sup Shim, M.D., Boo Sung Kim, M.D.
Korean J Hepatol 2009;15(1):42-51. Published online March 31, 2009
Backgrounds/Aims It is not easy to differentiate between patients with cirrhosis and those with alcoholic liver disease. Liver biopsy is generally considered the gold standard for assessing hepatic fibrosis; however, this protocol frequently carries a risk of severe complications and false-negative results. Transient elastography (Fibroscan, Echosens, Paris, France), which is a noninvasive method of measuring liver stiffness, has become available for assessing liver fibrosis. Liver stiffness reportedly differs markedly with the cirrhosis etiology. The aim of this study was thus to determine the diagnostic accuracy of the Fibroscan in the detection of cirrhosis in patients with alcoholic liver disease. Methods: We enrolled 45 patients with alcoholic liver disease. Fibroscan, abdominal ultrasonography, aspartate aminotransferase/platelet ratio index (APRI), and liver biopsy were performed on all patients. Fibrosis stage was assessed using the Batts-Ludwig scoring system. Results: The stage of fibrosis (F1-F4) was distributed among the cohort as follows: 5 patients at F1, 4 patients at F2, 7 patients at F3, and 29 patients at F4. Liver stiffness differed significantly between each fibrosis stage (P<0.001). For the diagnosis of cirrhosis, the area under the receiver operating characteristic curve was 0.97 for transient elastography (95% confidence interval, CI, 0.93-1.01), 0.81 for ultrasonography (95% CI, 0.68-0.94), and 0.83 for APRI score (95% CI, 0.70-0.95). The optimal cut-off value of liver stiffness for detecting cirrhosis was 25.8 kPa, with a sensitivity of 90% and a specificity of 87%. Conclusions: Transient elastography is a useful method for diagnosing cirrhosis in patients with alcoholic liver disease. (Korean J Hepatol 2008;15:42-51)
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