Hepatocellular adenoma is a relatively rare benign clinical tumor of the liver, with an incidence of about 1 in 10,000 women. 1, etiology The occurrence may be due to: (1) long-term oral contraceptive pills may cause hepatocyte necrosis, prompting hepatocyte hyperplasia leading to the occurrence of HCA; (2) secondary to cirrhosis or other operations, such as syphilis, viruses, venous congestion caused by compensatory hepatocyte nodular hyperplasia; (3) from the embryonic development of isolated liver embryonic cell masses disconnected from normal tissue structure; (4) some metabolic diseases (4) Some metabolic diseases, extensive liver damage and vasodilatation caused by drugs may cause the development of HCA, such as glycogen metabolic disease, Fanconi anemia, Hurler disease, severe mixed immunodeficiency disease, diabetes mellitus, galactosemia and drugs such as corticosteroids, danazol and carbamazepine. 2.Diagnosis Early tumor is small, patient has no history of hepatitis cirrhosis, symptoms and signs are non-specific, laboratory examination of methemoglobin is normal, diagnosis mainly relies on ultrasound, CT and so on. (1) Ultrasound examination: It can be seen that the lesions have clear boundaries, rich blood supply, uneven echogenicity in the tumor, and acoustic corona around the tumor, in which small HCAs are mostly hypoechoic with uniform distribution, while large HCA lesions have rich speckled and striped blood flow signals, showing “color ball sign”. Pulsed Doppler can measure the continuous low-velocity venous spectrum and low-velocity low-resistance arterial spectrum. In the early stage of ultrasonography, the arterial phase can be seen as a thick trophoblastic artery branching into the tumor with tortuous travel under the envelope, and later it shows uniform and rapid hyperenhancement. (2) CT: The typical presentation on plain scan is isointense or slightly hypointense shadow, with clear boundary and lower density hemorrhagic necrosis area within the tumor, and high density shadow when fresh bleeding is combined. Enhanced scan shows significant enhancement in the arterial phase, slightly dense or isointense shadow in the portal phase, and isointense in the delayed phase. (3) MRI: Typical T1 and T2-weighted images show mixed heterogeneous iso- or high-signal shadows, large HCA signal heterogeneity, and fibrous tissue proliferation around the lesion to form an envelope. If combined with glycogen accumulation disease T1 and T2-weighted images show high signal. Subacute hemorrhagic foci show significant high signal in MRIT1 and T2-weighted images. Since HCA has a tendency to become malignant and is prone to rupture and bleeding, it should be treated by surgery early after diagnosis. However, some scholars believe that those with a diameter of less than 5 cm or normal AFP can be followed up, while those with a diameter of more than 5 cm or elevated AFP should be operated promptly. For multiple HCA that cannot be completely removed surgically, hepatic artery ligation or hepatic artery embolization is feasible, and for those with liver insufficiency or cancerous tendency, liver transplantation is feasible. If HCA ruptures and bleeds, there are many complications and high mortality, so selective hepatic artery embolization should be preferred. Those with a history of oral contraceptives and small tumors can be observed for tumor changes after discontinuing contraceptives.