Hepatocellular adenoma with malignant transformation in a patient with neonatal portal vein thrombosis

Arrivé, Lionel; Zucman‐Rossi, Jessica; Balladur, Pierre; Wendum, Dominique

doi:10.1002/hep.28590

Cited by 10 publications

(7 citation statements)

References 7 publications

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“…Progression into hepatocellular carcinoma occurs in about 10% of adenomas. 224 Ultrasonographic features of hepatic adenomas are nonspecific and triple phase computed tomography scanning or magnetic resonance imaging can distinguish them from haemangiomas, fibronodular hyperplasia and hepatocellular carcinomas in the vast majority of patients.…”

Section: Recommendationmentioning

confidence: 99%

EASL Clinical Practice Guidelines: Drug-induced liver injury

Andrade¹,

Aithal²,

Bjõrnsson³

et al. 2019

Journal of Hepatology

754

394

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Idiosyncratic (unpredictable) drug-induced liver injury is one of the most challenging liver disorders faced by hepatologists, because of the myriad of drugs used in clinical practice, available herbs and dietary supplements with hepatotoxic potential, the ability of the condition to present with a variety of clinical and pathological phenotypes and the current absence of specific biomarkers. This makes the diagnosis of drug-induced liver injury an uncertain process, requiring a high degree of awareness of the condition and the careful exclusion of alternative aetiologies of liver disease. Idiosyncratic hepatotoxicity can be severe, leading to a particularly serious variety of acute liver failure for which no effective therapy has yet been developed. These Clinical Practice Guidelines summarize the available evidence on risk factors, diagnosis, management and risk minimization strategies for drug-induced liver jury.

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Section: Recommendationmentioning

confidence: 99%

EASL Clinical Practice Guidelines: Drug-induced liver injury

Andrade¹,

Aithal²,

Bjõrnsson³

et al. 2019

Journal of Hepatology

754

394

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“…Rarely, H‐HCA may progress to HCC, and the latter should especially be suspected in cases of non‐steatotic H‐HCA, myxoid H‐HCA, 64 and VLD‐associated H‐HCA 27,65 …”

Section: Hca Classificationmentioning

confidence: 99%

“…Rarely, H-HCA may progress to HCC, and the latter should especially be suspected in cases of nonsteatotic H-HCA, myxoid H-HCA, 64 and VLDassociated H-HCA. 27,65 The pathogenesis of malignant transformation is unknown, but as yet there is no evidence for involvement of the b-catenin pathway. GS expression can be moderately increased in H-HCA, but the significance of this finding is currently uncertain.…”

Section: H -H C Amentioning

confidence: 99%

“…85 Specific clinical contexts and/or liver diseases, such as GSD 36 and VLD, 27,28 seem to be associated with a higher risk of malignant transformation of HCA, not only for b-HCA/b-IHCA 86 but also for H-HCA in VLD. 64,65 Even though 50 mm is commonly considered to be the threshold, a few cases of malignant transformation have been reported in lesions smaller than 50 mm, 76,87 both in men and in women.…”

Section: A L I G N a N T T R A N S F O R M A T I O Nmentioning

confidence: 99%

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Hepatocellular adenoma: what we know, what we do not know, and why it matters

et al. 2022

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Hepatocellular adenoma: what we know, what we do not know, and why it mattersIn the last two decades there has been significant progress in research on and diagnosis of hepatocellular adenoma (HCA), resulting in the establishment of a molecular and immunohistological HCA classification. This review aims to fine-tune the current expertise in order to enhance the histopathological diagnostic possibilities, by refining issues that are already known, addressing diagnostic difficulties, and identifying still unknown aspects of HCA. We discuss novel methods to identify HCA subtypes, in particular the sonic hedgehog HCAs and the interpretation of glutamine synthetase patterns for the recognition of b-cateninmutated HCAs. The major complications of HCAs, i.e. bleeding and malignant transformation, are considered, including the dilemmas of atypical and borderline lesions. HCAs in different clinical and geographical settings, e.g. pregnancy, cirrhosis and non-western countries, are also discussed. The natural history of the different HCA subtypes in relation to age, sex and risk factors is a feature that is still insufficiently investigated. This is also true for the risks of clinical bleeding and malignant transformation in association with HCA subtypes. As HCA is a relatively rare tumour, a multicentre and multidisciplinary approach across geographical boundaries will be the appropriate method to establish prospective programmes with which to identify, classify and manage HCAs, focusing on several aspects, e.g. aetiology, underlying liver disease, complications, regression, and growth. Updating what we know and identifying and addressing what we do not know matters for optimal patient management.

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“…Importantly, regression of some hepatocellular nodules has been reported after closure of the shunt [50]. By contrast, HCA may also progress into HCC, particularly in cases of b-HCA and H-HCA without steatosis [10,51,52]. Finally, de novo HCC have been also described.…”

Section: Congenital Porto-systemic Shunts (Cpss)mentioning

confidence: 99%