Special stains can distinguish hepatic necrosis with regenerative nodules from cirrhosis

Ferrell, Linda D.; Greenberg, Mathew S.

doi:10.1111/j.1478-3231.2007.01466.x

Cited by 17 publications

(27 citation statements)

References 1 publication

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“…These include characteristic apposition of the portal vein, the arteriole, and the bile duct, which is not usually present in scarred central veins with arteriolar ingrowth, as well as a distinctive, dense pattern of portal fibrosis and elastin deposition typically not seen in scarred central zones. 37 Cognizance of the potential diagnostic pitfalls imposed by portal tract mimicry of scarred central zones, as well as the distinctive architectural features of normal portal tracts, can thus help differentiate portal tracts from aberrant central zones in chronic venous outflow obstruction, thereby minimizing misinterpretation and diagnostic errors.…”

Section: Discussionmentioning

confidence: 99%

Aberrant Centrizonal Features in Chronic Hepatic Venous Outflow Obstruction

Krings

Can

Ferrell

2014

American Journal of Surgical Pathology

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Chronic hepatic venous outflow obstruction is characterized by centrizonal scarring but may also display features that can lead to portal tract mimicry and misdiagnosis as biliary disease, especially given elevated cholestatic liver profiles in these patients. However, these histopathologic features have not been systematically described. We graded the numbers of centrizonal arterioles, ductules, keratin 7+ hepatocytes, CD34+ microvessels, and capillarized sinusoids in 61 cases of chronic venous outflow obstruction and assessed changes in metabolic zonation by glutamine synthetase staining. Centrizonal arterioles and ductules were present in 82.0% and 72.1% of cases, respectively, and correlated with fibrosis. Centrizonal CD34+ microvessels and sinusoidal capillarization were closely associated and present in 25 (92.6%) and 26 (96.3%) of 27 cases, respectively. Centrizonal capillarized sinusoids and microvessels, which were present in all cases with advanced fibrosis, were demonstrated in 90% and 80% of the cases without significant fibrosis, respectively. The results suggest that capillarization and/or microvessel formation precede and may contribute to centrizonal scarring, whereas arterialization likely reflects vascular remodeling associated with progressive fibrosis. Centrizonal ductules were often immature, being either keratin 7+/keratin 19- (36.4%) or keratin 7-/keratin 19- (10.0%). Centrizonal keratin 7+ intermediate-phenotype hepatocytes were present in 25 (92.5%) of 27 cases. Lastly, 22 (91.7%) of 24 cases showed loss of metabolic zonation, with reversed zonation in 2 (8.3%) cases. Together, the findings indicate that vascular and lobular reorganization in chronic venous outflow obstruction may result in mimicry of central zones as portal tracts. Recognition of these changes is essential to prevent misdiagnosis of this condition as biliary tract disease.

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Section: Discussionmentioning

confidence: 99%

Aberrant Centrizonal Features in Chronic Hepatic Venous Outflow Obstruction

Krings

Can

Ferrell

2014

American Journal of Surgical Pathology

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“…Aggressive non-alcoholic steatohepatitis shares similar histologic features with alcoholic steatohepatitis, namely abundant Mallory–Denk bodies, prominent neutrophil infiltrate around ballooned hepatocytes, central vein obliteration, pericellular fibrosis, and cholestasis. 6,7 The finding of subacute injury, which can be best identified on a well-controlled trichrome stain (though occasionally an elastic stain is needed for confirmation of these findings, as elastic fiber deposition supports early fibrosis 20,21 ), further supports consideration of a rapidly progressive or acute/subacute process. Four of six patients had an increased aspartate aminotransferase/alanine aminotransferase ratio (42:1), which has been associated with alcoholic steatohepatitis.…”

Section: Discussionmentioning

confidence: 99%

“…Trichrome and elastic stains (orcein stain or Elastic Van Gieson stain) were used to assess fibrosis and subacute hepatocellular dropout. 20,21 …”

Section: Methodsmentioning

confidence: 99%

Aggressive non-alcoholic steatohepatitis following rapid weight loss and/or malnutrition

et al. 2017

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While non-alcoholic steatohepatitis is a slowly progressive disease, patients may rarely present in acute liver failure. We describe six patients who developed severe hepatic dysfunction following rapid weight loss or malnutrition. Rapid weight loss (18 to 91 kg) occurred after Roux-en-Y gastric bypass in four patients and starvation-like dieting or hypoalbuminemia was noted in two patients. Four patients either died or received an urgent liver transplant. Pathologic findings were characterized by advanced alcoholic steatohepatitis-like features, including extensive/circumferential centrizonal pericellular fibrosis, central scar with perivenular sclerosis/veno-occlusion with superimposed hepatocellular dropout, abundant/prominent hepatocellular balloons, and numerous Mallory–Denk bodies, but there was no history of excess alcohol consumption. This study characterizes clinicopathologic features of aggressive non-alcoholic steatohepatitis following rapid weight loss or malnutrition, which should be included in the differential diagnosis with alcohol when a patient is considered for liver transplantation. The mechanism of liver injury in aggressive steatohepatitis is unknown, but rapid fat mobilization in obese patients may potentially cause oxidative stress to the liver and further study is needed to determine if there is a genetic predisposition to this form of injury and if antioxidants may protect the liver during rapid weight loss/malnutrition.

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“…A combination of stains for collagen and elastic fibers may be helpful in confirming fibrosis. Special stains have also been recommended to distinguish cirrhosis from hepatic necrosis with regenerative nodules …”

Section: Epidemiologymentioning

confidence: 99%

“…Special stains have also been recommended to distinguish cirrhosis from hepatic necrosis with regenerative nodules. (67)…”

Section: Review Article | 953mentioning

confidence: 99%

Acute Severe Autoimmune Hepatitis: Corticosteroids or Liver Transplantation?

et al. 2019

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Acute severe presentations of autoimmune hepatitis (AIH) represent a challenge for the transplant community. As a disease, it is poorly characterized, and there is a weak evidence base to guide diagnosis and treatment. Early identification of acute severe AIH is key because it determines the initiation of corticosteroids, which can be lifesaving. However, their use in this setting remains controversial. The Model for End‐Stage Liver Disease score, severity of coagulopathy, and grade of encephalopathy may be predictors of outcome with corticosteroid therapy. The optimal timing of liver transplantation (LT) can be difficult to determine and, as such, the decision to proceed to transplantation should not be delayed by protracted courses of corticosteroids. The aim of this review is to better characterize this subset of patients; to differentiate them clinically, serologically, and histologically from chronic AIH and other causes of acute liver failure; and to present the role, predictors, and optimal timings of corticosteroid therapy and LT. Although this review is specific to adults, many principles hold true for the pediatric population.

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Special stains can distinguish hepatic necrosis with regenerative nodules from cirrhosis

Abstract: We conclude that this trio of special stains can be helpful adjuncts for this diagnostic problem.

Cited by 17 publications

References 1 publication

Aberrant Centrizonal Features in Chronic Hepatic Venous Outflow Obstruction

Aberrant Centrizonal Features in Chronic Hepatic Venous Outflow Obstruction

Aggressive non-alcoholic steatohepatitis following rapid weight loss and/or malnutrition

Acute Severe Autoimmune Hepatitis: Corticosteroids or Liver Transplantation?

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