Pancreatic hepatoid carcinoma: a case report
Case Report

Pancreatic hepatoid carcinoma: a case report

Fenfang Wang1, Xiaoyuan Han2, Qihuan Wu3

1Department of Medical Oncology, The Affiliated Xiangshan Hospital of Wenzhou Medial University, Xiangshan, China; 2Department of Center for cancer prevention and treatment, The Affiliated Xiangshan Hospital of Wenzhou Medial University, Xiangshan, China; 3Department of Hepatology, The Affiliated Xiangshan Hospital of Wenzhou Medial University, Xiangshan, China

Contributions: (I) Conception and design: F Wang; (II) Administrative support: None; (III) Provision of study materials or patients: F Wang; (IV) Collection and assembly of data: X Han; (V) Data analysis and interpretation: Q Wu; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

Correspondence to: Qihuan Wu, BS. Department of Hepatology, The Affiliated Xiangshan Hospital of Wenzhou Medial University, 291 Donggu Road, Dandong Street Ningbo, Xiangshan 315700, China. Email: 18868638750@163.com.

Background: Pancreatic hepatoid carcinoma (PHC) is an extremely uncommon neoplasm of pancreas that resembles hepatocellular carcinoma (HCC). The morphological and immunohistochemical features of PHC are similar to those of HCC. The lack of specificity on clinical features of PHC makes it easy to be ignored in clinical diagnosis. And there is currently no standardized treatment for PHC.

Case Description: We presented a case of PHC with specific clinical examinations and treatments. The patient reported that he suffered from a history of chronic viral hepatitis B, laboratory tests showed elevated serum alpha-fetoprotein (AFP) levels. No significant liver mass was found on imaging, the contrast-enhanced abdominal computed tomography revealed a slightly nodular low-density shadow in the head of the pancreas. The patient received neoadjuvant chemotherapy combined with programmed cell death protein 1 (PD-1) antibody and he underwent radical resection of pancreatic cancer. The post-operative histopathological examination of the resection specimen revealed a diagnosis of poorly differentiated PHC. Half a month after the surgery, this patient’s serum AFP dropped to within the normal range. The patient recovered without complications, and regular reexaminations showed no signs of tumor recurrence and metastasis.

Conclusions: We analyzed the previous PHC-related literature to enhance the understanding of PHC and persistently improve PHC treatment strategies for clinicians.

Keywords: Case report; pancreatic hepatoid carcinoma (PHC); hepatocellular carcinoma (HCC); alpha-fetoprotein (AFP); pancreas

Received: 16 September 2024; Accepted: 27 February 2025; Published online: 13 May 2025.

doi: 10.21037/acr-24-195

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Key findings

• Pancreatic hepatoid carcinoma (PHC) is an extremely uncommon neoplasm of pancreas that resembles hepatocellular carcinoma (HCC). PHC can also present as elevated alpha-fetoprotein (AFP) and be misdiagnosed as liver cancer.

What is known and what is new?

• There are many patients infected with hepatitis B or C virus infection in China, so AFP is usually acted as a routine tumor marker in health examinations. Also, AFP has been employed in clinical practice for a long time as a tumor marker for HCC.

• Elevation of serum AFP may be a clue to diagnose PHC, however, PHC lacks specific clinical manifestations and imaging features and is difficult to diagnose before surgery. Most patients need to be confirmed by postoperative pathology.

What is the implication, and what should change now?

• The lack of specificity on clinical features of PHC makes it easy to be ignored in clinical diagnosis. When AFP is elevated, it is not limited to the diagnosis of HCC, but to the possibility of hepatoid adenocarcinoma.

Introduction

Pancreatic hepatoid carcinoma (PHC) is a primary extrahepatic carcinoma of non-germ cell origin and remains an extremely rare form of neoplasm. Its morphological and immunohistochemical features are similar to those of hepatocellular carcinoma (HCC) (1,2). Ishikura et al. reported the first hepatoid adenocarcinoma (HAC) in the stomach (3). Since then, HAC has been reported in multiple organs, such as the stomach, ovary, colon, esophagus, gallbladder, uterus, lung, kidney, and urinary bladder (3-6). PHC primarily found in the tail of the pancreas, which is characterized by a low incidence rate, high malignancy, strong invasiveness, early propensity for lymphatic and distant metastasis, rapid disease progression, and poor prognosis. The lack of specificity on clinical features of PHC makes it easy to be ignored in clinical diagnosis. However, most PHC patients have exhibited elevated alpha-fetoprotein (AFP) levels, which serve as a diagnostic clue. Apart from that, the definitive PHC diagnosis requires pathological examination. There is currently no standardized treatment for PHC, radical surgical resection is still the preferred treatment. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-24-195/rc).

Case presentation

A 43-year-old man was transferred to our hospital with a history of painless jaundice. Meanwhile, the patient reported that he suffered from a history of chronic viral hepatitis B but did not receive any antiviral therapy. Physical examination showed obviously yellow stained skin and sclera but soft abdomen without tenderness, distension or masses and normal bowel sounds. Laboratory tests showed elevated serum AFP levels to 2,682 ng/mL (normal limit, 0–7 ng/mL). The levels of other tumor markers [carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9), carbohydrate antigen 125 (CA125), and prostatic antigens] were all within their normal limits. Liver function tests showed elevated transaminases [alanine aminotransferase (ALT) 197 U/L and aspartate aminotransferase (AST) 1,156 U/L], alkaline phosphatase (417 U/L), gamma-GT (1,027 U/L), total bilirubin (48.3 µmol/L), direct bilirubin (18.3 µmol/L), and indirect bilirubin (30.0 µmol/L). Markers for hepatitis B virus serology were positive. Hepatitis B virus (HBV) viral load was 1.59×104 IU/mL.

The results of imaging examinations are shown in Figure 1. Magnetic resonance cholangiopancreatography (MRCP) and magnetic endoscopic resonance imaging showed that unenhanced axial T2W and T1W images showed an irregular soft tissue mass of pancreatic head (encircled), moderate T2 signal hyperintensity and T1 signal slightly hypointensity. MRCP image showed abrupt stenosis of the common bile duct with dilatation and dilated common bile duct secondary to a soft tissue mass (encircled). Gadolinium-enhanced T1W image in the arterial phase, venous phase and delayed phase showed a hypovascular mass located in the pancreatic head (encircled). The main pancreatic duct was truncated and the distal pancreatic duct was dilated, involving the lower common bile duct. There was a mass measured 2.3 cm × 2.0 cm close to the duodenum and adjacent to the superior mesenteric vein. A few subfoci formed in the superior mesenteric vein and main portal vein, and multiple enlarged lymph nodes were around the pancreas and the abdominal aorta. Endoscopic retrograde cholangiopancreatography showed stenosis of the pancreatic segment of the common bile duct and dilation of the upper common bile duct. The patient underwent pancreatic duct stent implantation under general anesthesia and pathology of endoscopic ultrasound-guided fine-needle aspiration/fine-needle biopsy (EUS-FNA/FNB) of the mass in pancreas indicated a diagnosis of poorly differentiated carcinoma. Immunohistochemically, the tumor cells were positive for MSH2, MSH6, MLH1, PMS2, CK7, CK19, P53, CDX2, DPC4, Her2, and Ki-67, EBER, CK20 were negative.

Figure 1 MRCP and magnetic endoscopic resonance imaging. Unenhanced axial T2W (A) and T1W (B) images showed an irregular soft tissue mass of pancreatic head (encircled), moderate T2 signal hyperintensity and T1 signal slightly hypointensity. MRCP image (C) showed abrupt stenosis of the common bile duct (red arrow) with dilatation and dilated common bile duct (yellow arrow) secondary to a soft tissue mass (encircled). Gadolinium-enhanced T1W image in the arterial phase (D), venous phase (E) and delayed phase (F) showed a hypovascular mass located in the pancreatic head (encircled). MRCP, magnetic resonance cholangiopancreatography; T1W, T1-weighted; T2W, T2-weighted.

The patient received neoadjuvant chemotherapy combined with PD-1 antibody before surgical procedure. After 8 cycles of modified folinic acid, fluorouracil, irinotecan, and oxaliplatin (FOLFIRINOX) and 6 cycles of sintilimab, he underwent radical resection of pancreatic cancer on October 13, 2022. The post-operative histopathological examination of the resection specimen revealed a diagnosis of poorly differentiated PHC. The surgically removed mass measured 5.3 cm × 3.5 cm with perineural invasion present, but no lymph node invasion or necrosis was identified. Surgical to achieve an R0 resection. Figure 2 depicts the polygonal tumor cells with round nuclei, evident central nucleolus, abundant cytoplasm and enlarged prominent nuclei. The excision margins were free of neoplasia and no metastasis was in 16 specimen lymph nodes (pathological stage ypT4N0M0). According to the morphology of the postoperative specimen, it does not match the common pancreatic ductal adenocarcinoma. Immunohistochemically, the tumor cells were positive for MSH2, MSH6, MLH1, PMS2, CK7, CK19, P53, glypican-3 (GPC3), spalt like transcription factor 4 (SALL4), AFP, and DPC4, Her2 (1+), EBER was negative.

Figure 2 Hematoxylin and eosin microscopic image of a cytologic slide obtained by scraping of the fresh surgical specimen, showing polygonal tumor cells with round nuclei, evident central nucleolus, abundant cytoplasm and enlarged prominent nuclei (hematoxylin and eosin, 20×).

Half a month after the surgery, this patient’s serum AFP dropped to within the normal range (1.3 ng/mL). Later, he accepted 4 cycles of mFFX and 3 cycles of sintilimab. The patient recovered without complications, and regular reexaminations including tumor markers test like AFP, CEA, CA19-9 showed no signs of tumor recurrence and metastasis.

Ethical considerations

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

There are many patients infected with hepatitis B or C virus infection in China, so AFP is usually acted as a routine tumor marker in health examinations. Also, AFP has been employed in clinical practice for a long time as a tumor marker for HCC. The patient in the study had a history of hepatitis B and his AFP found elevated during monitoring, the high levels of AFP originally raised the question that whether a tumor or another condition was causing the expression of AFP. However, no significant liver mass was found on imaging. Finally, the pathology of EUS-FNA/FNB indicated poorly differentiated carcinoma of the pancreas. Primary PHC is rare and is difficult to be identified by imaging, especially regarding metastatic hepatocellular carcinoma, pancreatic ductal adenocarcinoma, and pancreatic acinar cell carcinoma. Its diagnosis needs to rely on typical histological features with confirmatory immunohistochemical staining. Hepatocellular carcinoma metastatic to the pancreas is really infrequent, with only 4 cases reported in the literature (7,8). Pancreatic ductal adenocarcinoma is a tumor with poor blood supply, imaging features of low-density nodule or mass, lesion enhancement scan is mild to moderate enhancement. Pancreatic ductal adenocarcinoma can involve blood vessels, early lymph node and blood metastasis, and expansion of main pancreatic duct and common bile duct, which is called “double duct sign”. Pancreatic acinar cell carcinoma magnetic resonance imaging (MRI) usually shows large solid masses with clear boundaries, mostly circular, with obvious restriction of intratumor diffusion-weighted imaging (DWI), common cystic degeneration and necrosis, clear capsular sexual interface, lack of blood supply, mild progressive enhancement in enhanced scans, easy to involve surrounding tissues, and liver and lymph node metastasis.

The pathogenesis of PHC is not completely understood currently. There are three theories having been proposed.

  • Stem cell theory: this theory is more logical since both pancreas and liver cells are derived from the foregut endoderm. Normally, the genes that control hepatocyte differentiation in pancreatic stem cells are suppressed, and can be activated during the process of carcinogenesis, thus expressing the hepatocyte phenotype (9).
  • Ectopic liver tissue theory: ectopic liver tissue may be present in the pancreas. Heterotopic liver tissue has been reported to be associated with an increased risk of developing HCC (10). However, ectopic hepatic tissue has not been demonstrated in the PHC so far (11-14).
  • Transdifferentiation theory: pancreatic stem cells usually act as inhibitors of hepatocyte differentiation genes. As animal models have shown that these genes can be activated after exposure to carcinogens (10). This kind of pathogenesis theory may help explain the existence of mixed PHC.

PHC exists as either pure or combined type. It can combine with other tumor components, such as neuroendocrine tumor and ductal adenocarcinoma (15). The microscopic histological structure consists of a typical adenocarcinoma area and a hepatoid differentiation area. The morphological characteristics of hepatoid differentiation regions are similar to HCC, including the presence of cells with abundant eosinophilic cytoplasm and centrally located nuclei in the sheet-like or trabecular portions (16). Immunohistochemically, AFP, hepatocyte, GPC3, and Arg1 should be at least partially or fully expressed; CK7 and CK19 are often positive; CK18 and CK20 would likely be positive; and SALL4 is positive or negative in tumor cells (15,17). In our case, the tumor cells were positive for CK7, CK19, P53, GPC3, SALL4, AFP, and DPC4. And in pancreatic ductal adenocarcinoma, the tumor cells were positive for CK7, CK8, CK18, CK19, CEA, CA19-9, CA125, DUPAN2, MUC1, and SALL4, AFP, DPC4 are often negative.

To date, only 41 cases of PHC have been reported in the literature, the clinical presentation of the 41 cases is summarized in Table 1 (18). The ages of patients ranged from 21 to 83 years, most of them were male (27 males/14 females). The clinical features of PHC lack specificity, 13 patients were either asymptomatic or suffered from unspecific abdominal pain. The sizes of tumors ranged from 1 to 12 cm, with a median size of 6 cm. The mass was located in the pancreatic tail in 18 of 39 patients (18,19). There is currently no standardized treatment for PHC due to the tumor rarity and the lack of evidence-based data. The literature has reported that 85% of patients received surgical treatment, radical surgical resection is still the preferred treatment (17). The effects of adjuvant therapy after the surgery resection, advocated because of the metastatic potential of the tumor, are still unclear (14,20). PHC is highly aggressive and has a poor prognosis. The literature has reported that the overall survival rates at 1 and 5 years were 71% and 40%, respectively, with a median survival of 13 months (21).

Table 1

Clinical presentations of PHC in the literature

No. First author Sex Age (years) Tumor size (cm) Serum AFP levels (ng/mL) Location Symptom Treatment Outcome
1 Hruban F 53 1 10 Tail of the pancreas Polyarthritis and tender subcutaneous nodules Chemotherapy and radiotherapy Died 11 weeks after admission to the hospital
2 Gardiner F 61 1×1×1 Elevated Head of the pancreas Painless jaundice and fatigue Surgery N/A
3 Tanno F 65 6×5 16,170 Body and tail of the pancreas Epigastric, back pain, anorexia, and weight loss Did not undergo the operation Died 6 months after diagnosis
4 Yano M 57 9×7×5 177.6 Head of the pancreas Epigastric pain, vomiting and fever Surgery Died 80 days later
5 Paner M 57 6×4×3.5 Elevated Tail of the pancreas Nausea, emesis, diarrhea, and weight loss Surgery Died 8.5 years later
6 Paner M 28 8×8×6 Elevated Diffuse Severe abdominal and back pain Debulking of the tumor plus chemotherapy Died 14 months after the initial hospitalization
7 Lam F 64 7×4×4 Elevated Tail of the pancreas Hypoglycemia and recurrent nocturnal sweating Surgery and chemotherapy Died 22 months after initial presentation
8 Cuilliere M 70 3 2.4 Body of the pancreas Asymptomatic Surgery Patient is alive and well 12 months after surgery
9 Hughes M 51 6×5.5×5.5 Normal Tail of the pancreas Asymptomatic Surgery Alive
10 Matsueda F 49 Not available 623 The whole pancreas Weight loss Surgery and chemotherapy Alive 48 months after the initial diagnosis
11 Shih M 32 7 Normal Tail of the pancreas Asymptomatic Surgery Alive
12 Oh M 21 3×3×3 Elevated Head of the pancreas Asymptomatic Surgery Seven months after the surgery, the patient is healthy without evidence of recurrence
13 Cardona M 58 3.3×2.5×2.5 Normal Body of the pancreas Back and flank pain Surgery The patient is currently alive and without evidence of disease 15 months postoperatively
14 Hameed F 41 4.5×4×3 2714 Head of the pancreas Gastro-esophageal reflux and jaundice Surgery and chemotherapy Died 26 months later
15 Kubota M 56 6.3×6.2 N/A Tail of the pancreas Diabetes Surgery The patient is currently doing well without any signs of recurrence 3 years after surgery
16 Zhang F 37 9 Elevated Widespread Upper abdominal pain, anorexia, and emaciation Surgery Died
17 Liu M 80 5×5×6 Normal Head of the pancreas Nausea, emesis, diarrhea, and weight loss Surgery Alive
18 Jung M 46 8×9 262.49 Head of the pancreas Dyspepsia Surgery The patient was healthy and had no evidence of recurrence at 4 months after the surgery
19 Petrelli F 37 11 N/A Body of the pancreas Epigastric abdominal mass Treatment with sorafenib Died 1 year after diagnosis
20 Kai F 79 7×5 Elevated Tail of the pancreas Arthralgia Surgery Died 2 months after surgery
21 Kelly F 53 N/A 148 Body and tail of the pancreas Severe epigastric pain Surgery and chemotherapy The patient is currently doing well without any signs of recurrence 22 months after surgery
22 Huang M 52 1.6×1.5×1.0 N/A Head of the pancreas Obstructive jaundice Surgery and treatment with sunitinib 4 months after the recurrence and metastasis were identified
23 Majumder M 60 5.8×6.0 Normal Head of the pancreas Left upper quadrant pain, jaundice and nausea Chemotherapy Died 3 months later
24 Steen F 61 5.3×3.5 4.9 Tail of the pancreas Asymptomatic Surgery He is currently doing well without any signs of recurrence 5 years after surgery
25 Xin F 33 2×1.4×1.8 300 Head of the pancreas Asymptomatic Surgery Up till now, the patient has survived 46 months since the initial diagnosis
26 Vanoli F 57 3.5×3×3 Elevated Head of the pancreas Jaundice Surgery and chemotherapy The patient is currently doing well without any signs of recurrence 10 months after surgery
27 Antonini M 59 6×5 Normal Body of the pancreas Weight loss and abdominal discomfort Sorafenib Died 4 months later
28 Soofi M 69 5.9 Elevated Body and tail of the pancreas Atypical chest pain Surgery No evidence of recurrence 4 months after surgery
29 Veerankutty M 47 3.1×2.9×2.6 NA Tail of the pancreas Asymptomatic Surgery No evidence of recurrence 8 months after surgery
30 Kuo M 67 2×2 Normal Tail of the pancreas Asymptomatic Surgery No evidence of recurrence 6 months after surgery
31 Williams M 71 5 0.6 Head of the pancreas Abdominal pain Surgery and chemotherapy N/A
32 Chang M 61 1.3 N/A Tail of the pancreas Asymptomatic Surgery The patient has no evidence of disease 6 months following resection
33 Akimoto M 59 5.0×3.5 Normal Body of the pancreas Asymptomatic Surgery The patient has no evidence of disease 12 months following resection
34 Stamatova M 78 12 Normal Head of the pancreas Asymptomatic Surgery The patient suddenly died of acute coronary artery disease 2 months after surgery
35 Pellini Ferreira M 43 9 Normal Tail of the pancreas Jaundice, epigastric pain, and watery diarrhea Chemotherapy The patient has no evidence of disease 16 months
36 Ma M 75 7.8 1,897.7 Tail of the pancreas Weight loss Neoadjuvant chemotherapy and surgery The patient has a progression-free survival of 13 months after diagnosis
37 Yang M 72 12.0×10.5×4.5 N/A Tail of the pancreas Severe back pain Surgery The patient died a month after surgery because of bilateral pulmonary emboli confirmed on autopsy
38 Yang M 83 2.7×2.5×1.5 N/A Body of the pancreas Abdominal pain Surgery The patient was alive with no evidence of disease at follow-up of 8 years and 11 months
39 Yang M 54 10.0×9.0×9.0 8,338 Body and tail of the pancreas Asymptomatic Surgery Died of disease at 29 months after initial diagnosis
40 Zeng M 36 7×7 475.6 The whole pancreas Progressive jaundice, weight loss and epigastric palpable mass Surgery Died of disease at 4 months after initial diagnosis
41 He F 44 12×15×10 77,481.0 Tail of the pancreas Dull pain in the left upper abdomen and aggravated with vomiting Surgery and treated with the PD-1 inhibitor and transcatheter arterial chemoembolization The patient was alive with no evidence of disease at follow-up of 8 years and 11 months

AFP, alpha-fetoprotein; F, female; M, male; N/A, not available; PD-1, programmed cell death protein 1; PHC, pancreatic hepatoid carcinoma.

Conclusions

PHC is an extremely rare form of neoplasm, which has morphological and immunohistochemical features similar to those of HCC. Elevation of serum AFP may be a clue to diagnose PHC, however, PHC lacks specific clinical manifestations and imaging features and is difficult to diagnose before surgery. Most patients need to be confirmed by postoperative pathology. Currently, radical surgical resection combined with chemotherapy/neoadjuvant chemotherapy remains the first-line treatment choice. Surgical excision for PHC patients may be associated with long-term good outcomes, but further studies and longer follow-ups are needed to correctly assess prognostic features.

Acknowledgments

The authors wish to thank the patient and his family members for participating in this study.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-24-195/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-24-195/prf

Funding: This study was supported by the Xiangshan country Science and Technology Project (No. 2023C6013).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-24-195/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration (as revised in 2013). Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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doi: 10.21037/acr-24-195
Cite this article as: Wang F, Han X, Wu Q. Pancreatic hepatoid carcinoma: a case report. AME Case Rep 2025;9:75.

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