Hepatoid Adenocarcinoma of the Stomach: A Challenging Diagnostic and Therapeutic Disease through a Case Report and Review of the Literature

Najla Fakhruddin,1,2,* Hisham F. Bahmad,3 Tarek Aridi,4 Yara Yammine,4 Rami Mahfouz,1 Fouad Boulos,1 Ahmad Awada,5 and Fadi Farhat6,7,*

Author information

1Department of Pathology and Laboratory Medicine, American University of Beirut Medical Center, Beirut, Lebanon

2Department of Pathology, Hammoud Hospital University Medical Center, Saida, Lebanon

3Faculty of Medicine, Department of Anatomy, Cell Biology and Physiological Sciences, American University of Beirut, Beirut, Lebanon

4Faculty of Medicine, American University of Beirut, Beirut, Lebanon

5Medical Oncology Clinic, Jules Bordet Institute, Université Libre de Bruxelles, Brussels, Belgium

6Faculty of Medical Science, Department of Hematology-Oncology, Saint Joseph University, Beirut, Lebanon

7Department of Hematology-Oncology, Hammoud Hospital University Medical Center, Saida, Lebanon

Edited by: Arun Chaudhury, GIM Foundation, United States

Reviewed by: Madhukar Reddy Kasarla, Parkway Surgical and Cardiovascular Hospital, United States; Kiran Kumar Panuganti, Texas Health Resources Foundation, United States; Sumit Fogla, William Beaumont Hospital, United States; Sudheer Reddy Koyagura, Northwest Medical Center, United States; Sunil Kumar, Neshoba County General Hospital and Nursing Home, United States

*Correspondence: Najla Fakhruddin, bl.ude.bua@12fn

Fadi Farhat, moc.liamg@cinilc.idafrd

Specialty section: This article was submitted to Gastroenterology, a section of the journal Frontiers in Medicine.


Hepatoid adenocarcinoma of the stomach (HAS) is a rare aggressive tumor with hepatocellular differentiation. HAS often produces alpha fetoprotein (AFP) and metastasizes to the lymph nodes and the liver. Molecular studies revealed Her2 amplification and overexpression, association with p53 mutations, but no association with KRAS mutations. EGFR and BRAF mutations have not yet been evaluated in hepatoid carcinoma of the stomach so far. Hereby, we present a case of a 41-year-old female patient with HAS with high AFP level and liver metastases. Molecular analysis revealed Her2 overexpression by immunohistochemistry (IHC), but no EGFR, KRAS, or BRAF mutations were detected. The patient underwent chemotherapy type DCX (docetaxel, cisplatinum, and capecitabine) every 3 weeks with partial response after two cycles, maintained for eight cycles, and then was on maintenance therapy with trastuzumab for 7 months before relapsing and dying 18 months from the day of diagnosis. Conclusively, HAS may be misdiagnosed as hepatocellular carcinoma; therefore, it should be considered in the differential diagnosis of multiple hepatic nodules with high AFP and no history of hepatitis, liver fibrosis or cirrhosis.

Keywords: hepatoid adenocarcinoma, stomach, alpha fetoprotein, liver metastasis, case report