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home - Liver - Liver Masses - Hepatic Adenomas Written by Dr Sebastian Zeki

Knows the epidemiology pathology clinical presentation and natural
history of benign tumours of the liver

Can define a programme of investigation and characterisation of
benign liver lesions including haemangioma focal modular
hyperplasia and adenoma

Demonstrates ability to make an appropriate differential diagnosis
Formulates appropriate plan of management
Recognises importance of the role of multidisciplinary team in
diagnosis and management



Understands the epidemiology risk factors pathology prevalence
and range of presentations of HCC

Knows the appropriate investigation and staging of the disease
Aware of treatment options including trans-arterial
chemoembolisation (TACE) radiofrequency ablation (RFA) local
ethanol injection

Appreciates the indications and contraindications of each and how
the most appropriate is selected Aware of surgical treatment options

Aware of role of surveillance and referral for specialist multidisciplinary management including liaison with oncology

Appreciates the indications and contraindications of each modality of
treatment and how the most appropriate is selected

Understands the process of selection of patients for liver resection or

Appreciates Involvement of multi-disciplinary team in management
decisions close liaison with surgical radiology oncology and
pathology colleagues

Hepatic Adenomas

Iso/ hypodense Centrip-etal flow Peripheral enhancement Late phase (as in non-contrast) Venous Phase Arterial phase Isodense T2- hy-perin-tense T1- hyper-intense R lobe Abdominal pain, a history of long duration of OCP use, multiple adenomas, and sub-capsular location are features associated with an increased risk of bleeding.Risk of malignant transformation 10% Inc ALP/ GGTNormal AFP Microscopically: Large plates of adenoma cells, which are typically larger than normal hepatocytes and contain glycogen and lipid.Small regular nuclei -mitoses are almost never seen.No normal hepatic architecture- septa, portal tracts, and bile ductules are absentCells arranged in normal or thickened trabeculae interspersed with prominent arteries and thin walled blood vessels and sinusoids.A few non-functional kupffer cells may be present( hence no uptake of technetium-99m labeled sulfur colloid) Macroscopic80 % solitary; Can grow to several cm; Often R lobe; 10 % pedunculated.Soft, smooth and tanned, large prominent surface blood vessels and within tumor- areas of hemor-rhage and necrosis.No fibrous capsule- so hemorrhage from adenoma can freely extend into liver. No normal hepatic architecture Contraceptive use and oestrogen therapy Can get multiple; Regress if OCP’s stoppedLargest risk in > 30 yrs using oestrogen OCPs >25mCause hepatocyte transformation via steroid receptors.Anabolic androgen use —Assoc. with17-alpha-alkylated steroids.As OCPs, multiple adenomas; regress once meds stoppedGlycogen storage diseases (GSD) —Type I (51%)and III (25%)< 20 years,M>F,multiple.Resolve after dietary therapy and correction of insulin, glucose, and glucagon levels.Pregnancy —Probably endogenous steroid relatedHigh foetal and maternal mortality Hepatic adenomas ManagementFor patients who are asymptomatic + OCPs +small adenoma —either stop OCP/ steroids or resect.Resect all symptomatic hepatic adenomas and consider resecting all non resolving adenomas.For women contemplating pregnancy —resect prior to pregnancy.Large or symptomatic adenomas during pregnancy should be resected as unpredictable, ideally in 2nd trimester (minimal maternal/ foetal risk).For symptomatic patients and those with large adenomas (>5 cm)The options include enucleation/resection/rarely liver transplantation (if resection impossible due to tumour size/location and those with adenomatosis).Mortality from elective surgical resection is <1 % and resection of some peripherally located adenomas can even be accomplished laparoscopically.For rupture/ haemorrhage- pre-op arterial coils reduces mortality. Adenomatosis >10 adenomas, not assoc with steroid meds or GSD. In men and womenAbnormal increases in Alk phos and GGT.Hemorrhage appears to be common esp if subcapsular and >4cm location.Malignant transfor-mation can occur Hepatic adenoma subclassifications:-Hepatocyte nuclear factor 1 alpha (HNF1alpha) mutation-occurs in 46% and are characterized by the presence of marked steatosis, and lack of cytologic abnormalities or inflammatory infiltrates).-Beta-catenin mutations- occur in14 % have frequent cytologic abnormalities and pseudo-glandular formation)- They are most likely to develop HCC.-Those with no mutation.- this is subdivided into: those with and without inflammatory infiltrates. Ultrasound —Non-specific findings; Color Doppler US can distinguish from FNH (see FNH)Magnetic resonance imaging —Variable characteristicsWell- demarcated due to fat or glycogen content of the hepatocytes.T1: Hyperintense (fat or glycogen) T2: Hyperintense- Gadolinium enhance-ment early, then isodense- suggests diagnosisGd-BOPTA chelate of Godobenate Dimeglumine also usefulAngiography —show peripheral enhancement as opposed to central enhancement with FNH. Rarely done.Computed tomography —Blood within the adenoma (common) makes it highly attenuating Abdominal mass 30 %;Hepatomegaly 25 %;RUQ pain; Rupture 20% mortality Pregnancy Type I (51%)and III (25%) glycogen storage diseases (GSD).< 20 years,M>F,multiple. Dietary therapy and correction of insulin, glucose, and glucagon levels. 17-alpha-alkylated steroids. oestrogen OCPs >25 months >30 years old Stop OCP Steroid receptor Associations Clinical Presentation Written by Dr Sebastian Zeki

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