Alcoholic foamy degeneration and alcoholic fatty liver with jaundice: Often overlooked causes of jaundice and hepatic decompensation that can mimic alcoholic hepatitis

Roth, Nitzan; Kanel, Gary C.; Kaplowitz, Neil

doi:10.1002/cld.520

Cited by 13 publications

(16 citation statements)

References 12 publications

(20 reference statements)

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“…In this study, biopsy revealed a different diagnosis in 13% of patients with a clinical diagnosis of severe AH. This proportion, while lower than reported, nonetheless highlights the important role of liver biopsy in distinguishing AH from other causes of acute‐on‐chronic liver injury in heavy drinkers …”

Section: Discussionmentioning

confidence: 53%

“…This proportion, while lower than reported, (5)(6)(7) nonetheless highlights the important role of liver biopsy in distinguishing AH from other causes of acute-onchronic liver injury in heavy drinkers. (10) We evaluated the relationships of clinical parameters and obtained histology in a large cohort of patients with clinically apparent severe AH. Results were used to develop and validate a novel model that can be used to noninvasively diagnose AH with near-perfect specificity.…”

Section: Discussionmentioning

confidence: 99%

“…Misdiagnosis potentially leads to unwarranted treatment and increases the risk of type II error in clinical studies . A recent expert consensus statement recommended confirmatory biopsy for patients being considered for inclusion in AH clinical trials if they have “potential confounding factors,” such as possible drug‐induced liver injury, ischemic hepatitis, or “atypical laboratory tests.” The statement did not address the potential role of biopsy in differentiating between AH and non‐necroinflammatory variants of acute alcoholic liver injury, specifically alcoholic foamy degeneration, alcoholic fatty liver with jaundice, and acute‐on‐chronic liver injury due to other causes . Distinguishing between AH and other histologic phenotypes of alcohol‐related liver disease was recently identified as a major gap in knowledge and research priority …”

Section: Introductionmentioning

confidence: 99%

“…(9) The statement did not address the potential role of biopsy in differentiating between AH and non-necroinflammatory variants of acute alcoholic liver injury, specifically alcoholic foamy degeneration, alcoholic fatty liver with jaundice, and acute-on-chronic liver injury due to other causes. (10) Distinguishing between AH and other histologic phenotypes of alcoholrelated liver disease was recently identified as a major gap in knowledge and research priority. (11) The primary aim of this study was to identify clinical predictors of histologically confirmed AH and to use these to develop and validate a clinical model capable of differentiating histologic AH from other forms of alcoholic liver disease.…”

Section: Introductionmentioning

confidence: 99%

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Prediction of histologic alcoholic hepatitis based on clinical presentation limits the need for liver biopsy

Roth

Saberi

Macklin

et al. 2017

Hepatology Communications

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The clinical presentation of alcoholic hepatitis (AH) can be mimicked by other alcoholic liver diseases. The aim of this study was to identify clinical features that predict AH on liver biopsy. Biopsies from patients hospitalized for presumed severe AH were used to identify a derivation cohort (101 patients) and validation cohort (71 patients). Using histologic scores for hepatocyte ballooning, Mallory‐Denk bodies, and lobular inflammation, 95 patient biopsies (55%) were classified as definite AH, 55 (32%) as possible AH, and 22 (13%) as no AH. Survival was similar among the groups, but mortality was significantly increased for patients with fatty change ≤50% on initial liver biopsy. An analysis limited to uninfected patients with definite AH or no AH in the derivation cohort identified a greater leukocyte count at admission and radiographic evidence of liver surface nodularity as independent predictors of definite AH on biopsy (P < 0.05). In the derivation cohort, the leukocyte count thresholds for ensuring 100% specificity for diagnosing definite AH were 10 × 109/L if the liver surface was nodular and 14 × 109/L if the liver surface was smooth, with a sensitivity of 76% and an area under the receiver operator characteristic curve of 0.88. In the validation cohort, these thresholds had a specificity of 86%, a sensitivity of 59%, and an area under the receiver operator characteristic curve of 0.72. Conclusion: The combination of an elevated leukocyte count and a nodular liver surface in the absence of active infection retrospectively identified patients with a high likelihood of histologic AH for whom liver biopsy may not be necessary. For patients with suspected severe AH who do not fulfill these criteria, liver biopsy is important to exclude other variants of alcoholic liver disease. (Hepatology Communications 2017;1:1070–1084)

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Prediction of histologic alcoholic hepatitis based on clinical presentation limits the need for liver biopsy

Roth

Saberi

Macklin

et al. 2017

Hepatology Communications

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“…The benefit of this policy is to avoid inclusion of subjects with conditions that mimic clinical AH while lacking alcoholic steatohepatitis. Examples are alcoholic cirrhosis with sepsis, or alcoholic foamy cell hepatitis [26,27]. Furthermore, immunohistochemistry data, in conjunction with laboratory and clinical data, can provide important diagnostic and prognostic information including risk for infection and mortality [28–30].…”

Section: Controversies In Designing Ah Trialsmentioning

confidence: 99%

Controversies in clinical trials for alcoholic hepatitis

Lieber

Rice

Lucey

et al. 2018

Journal of Hepatology

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Alcoholic hepatitis (AH) is the most severe form of alcoholic liver disease, contributing to significant morbidity and mortality. Yet, the only available therapies that improve survival are corticosteroids and liver transplantation, with no new drugs successfully developed for decades. This article briefly describes the current state of affairs in AH therapy and examines the practical and ethical challenges of conducting controlled trials in patients with severe AH. While prednisolone is considered standard of care in severe AH, this recommendation remains controversial given the marginal benefits and questionable long-term safety of steroids. Placebo-controlled trials without steroids may be necessary and ethically justified in certain populations with AH who have not been adequately investigated. Ultimately, we suggest that the field will advance with the development of a plausible animal model of true AH, a consensus on a composite clinical endpoint that does not rely solely on mortality, as well as the adoption of the NIAAA Alcoholic Hepatitis Consortia recommendations regarding standard definitions and when to request a liver biopsy prior to study entry.

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Clinical Presentation and Gene Expression of Acute Alcohol‐Induced Microvesicular Steatosis Mimicking Alcoholic Hepatitis

et al. 2021

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Acute alcoholic microvesicular steatosis (MIC) may complicate heavy alcohol intake and present as alcoholic hepatitis (AH) syndrome. However, detailed clinical, biological, and histologic data associated with MIC are scarce. We compared the clinical presentation, histologic features, and hepatic transcriptomic of patients presenting with AH due to either MIC or severe alcoholic steatohepatitis (ASH). In this case‐control study, patients who drank heavily (>100 g/day) with the AH syndrome were included either in the MIC group (>50% severe microvesicular steatosis, no inflammation) or in the severe ASH group (polynuclear neutrophil infiltration, macrosteatosis, ballooned hepatocytes). All patients received standard supportive care plus steroids for those with severe ASH and were followed up for 3 months. Whole‐liver transcriptome profiling was performed on liver snap‐frozen biopsies. Compared to ASH (n = 24, mean age 49.3 years), patients in the MIC group (n = 12, mean age 49.1 years) had a higher reported alcohol intake (P < 0.01), lower Model for End‐Stage Liver Disease score (P < 0.05), lower hepatic venous pressure gradient (P < 0.01), higher alanine aminotransferase (P < 0.02) and gamma‐glutamyltransferase (P < 0.001), higher triglycerides (P < 0.001) and total cholesterol (P < 0.002), but similar bilirubin levels (P = 0.54). At histology, patients with MIC had a lower fibrotic stage compared to those with ASH (P < 0.001). A higher density of megamitochondria was seen in MIC compared to ASH (P < 0.05). During follow‐up, death or transplantation occurred in 4/12 (33%) patients with MIC and 7/24 (29%) patients with severe ASH. Differential hepatic gene expression in MIC compared to ASH included down‐regulation of genes related to inflammation and fibrosis and up‐regulation of genes involved in lipid metabolism and mitochondrial function. Conclusion: MIC is an acute, noninflammatory, potentially severe alcoholic liver injury mimicking ASH, is associated with a lower fibrosis stage, and has a distinct gene expression profile.

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Alcoholic foamy degeneration and alcoholic fatty liver with jaundice: Often overlooked causes of jaundice and hepatic decompensation that can mimic alcoholic hepatitis

Cited by 13 publications

References 12 publications

Prediction of histologic alcoholic hepatitis based on clinical presentation limits the need for liver biopsy

Prediction of histologic alcoholic hepatitis based on clinical presentation limits the need for liver biopsy

Controversies in clinical trials for alcoholic hepatitis

Clinical Presentation and Gene Expression of Acute Alcohol‐Induced Microvesicular Steatosis Mimicking Alcoholic Hepatitis

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