Heterochronic gastric adenosquamous carcinoma combined with colonic adenoma: A case report

Abstract

BACKGROUND

Metachronous gastric cancer usually refers to a tumor that occurs in the stomach more than half a year after esophageal cancer surgery, and metastasis of primary esophageal cancer should be excluded. There are few reports of metachronous gastric adenosquamous carcinoma with signet ring cell carcinoma combined with early tubular adenoma of the colon after esophageal cancer surgery, which has a high degree of malignancy. This is also the reason for the poor treatment results.

CASE SUMMARY

A 54-year-old male patient was admitted to the hospital with “dysphagia obstruction”. Seven years ago, the patient was diagnosed with well-differentiated squamous cell carcinoma in the middle esophagus (T4N1M0 stage) and left gastric lymph node metastasis. In the final resection of the esophageal cancer, no residual cancer tissue was found in the esophageal and gastric stump. The patient’s medical history 7 years ago (preoperative gastroscopy and other examinations) revealed no gastric tumor. Combined with the patient’s history, the diagnosis of recurrent esophageal cancer was made on this admission. The final pathological results were surprising: Metachronous gastric adenosquamous carcinoma with signet ring cell carcinoma combined with early tubular adenoma of the colon. Considering the high malignancy of the tumor, the complexity of the second operation, and many complications, the patient received chemotherapy.

CONCLUSION

He had a history of esophageal cancer resection. Gastroenteroscopy should be performed simultaneously to avoid missed diagnosis and misdiagnosis.

Key Words: Heterochronic tumor; Gastric adenosquamous carcinoma; Colonic adenoma; Esophageal cancer; Signet ring cell carcinoma; Case report

Core Tip: The common type of gastric cancer is adenocarcinoma, but the pathological type of gastric adenosquamous carcinoma is rare, so metachronous gastric adenosquamous carcinoma with signet ring cell carcinoma is even rarer. The metachronous tumors after esophageal cancer surgery are mostly found in the stomach, head and neck, but those occurring in the stomach and distal colon at the same time are rare.

INTRODUCTION

Metachronous gastric cancer is usually a malignant tumor that occurs in the stomach after esophageal squamous cell carcinoma resection[1,2]. The usual pathological type of gastric cancer is adenocarcinoma, while gastric adenosquamous carcinoma (GAC) accounts for < 1% of gastric cancers[3], accompanied by signet ring cell carcinoma (SRCC), and neoplastic lesions with early tubular adenoma of the colon (ETAC) are rarely reported. To date, the relationship between postoperative esophageal cancer and metachronous tumors is unclear. The occurrence of metachronous tumors is often closely related to normal physiological and structural changes in the digestive tract after esophageal cancer surgery, Helicobacter pylori infection, smoking, alcoholism, and other factors[2,4]. However, the patient had only a history of resection of esophageal cancer. Our case report aims to improve our understanding of metachronous tumors after esophageal cancer surgery.

CASE PRESENTATION

Chief complaints

A 54-year-old male patient was admitted to the hospital for swallowing obstruction half a month ago.

History of present illness

A 54-year-old male patient was admitted to the hospital for swallowing obstruction half a month ago and there was no abdominal pain or bloating. The patient did not receive medical treatment, his symptoms were not relieved, and he was admitted to our hospital for medical treatment.

History of past illness

The patient had a history of esophageal cancer resection.

Personal and family history

The patient had a history of esophageal cancer resection and no adverse living habits. There was no family history of malignant tumors.

Physical examination

Physical examination showed that there were no abnormalities in the superficial lymph nodes of the whole body. The old surgical scar was approximately 15 cm in the chest and no abnormal signs, such as an abdominal mass, were observed.

Laboratory examinations

Blood cells, electrolytes, and liver and kidney functions were normal at admission. After admission, gastroscopy showed that the gastric mucosa was rough, erosive, brittle, and easily bled. The structure of the gland duct stained by blue light imaging disappeared and the lumen was narrow. Colonoscopy showed that the mucosa was orange-red, blood vessels were clearly visible and polyps with a diameter of approximately 0.4 cm were observed, with a smooth surface and a regular glandular duct structure (Figure 1). Hematoxylin-eosin staining of the gastric and colon lesions showed a poorly differentiated carcinoma, Helicobacter pylori (-), and ETAC in the stomach (Figure 2). Immunohistochemistry of the gastric tumor cells showed cytokeratin 7 (+), E-cadherin (+), human epidermal growth factor receptor 2 (+), Ki-67 (+), about (60%-70%) and S-100 (-). Caudal-type homeobox protein 2, cytokeratin 20, P40, CA5/6, and mucin 5AC (+) were detected in some tumor cells. The pathological diagnosis was a poorly differentiated GAC from SRCC. As there are many immunohistochemical indicators, we show only some typical images (Figure 3).

Figure 1 Gastrointestinal endoscopy performed after admission. A: Blue light imaging staining of the gastric mucosa under gastroscopy; B: Gastroscopy without blue light imaging staining; C: Colonoscopy results.

Figure 2 Hematoxylin-eosin staining of gastric and colon lesions. A: Pathological section of the stomach; B: Pathological section of the colon.

Figure 3 Results of the immunohistochemical detection of gastric tumor cells. A: Marker CA5/6; B: Marker Ki-67; C: Marker mucin 5AC.

Imaging examinations

Seven years prior, the patient’s gastrointestinal radiography revealed a hooked stomach with a smooth and soft stomach wall and slightly thick mucosal folds. No filling defects or niches were found. After admission, gastrointestinal radiography showed changes in the chest and stomach. The contrast agent slowly passed through the anastomotic stoma, and no niche was found. Enhanced chest computed tomography (CT) showed that the lower segment of the remnant stomach wall was locally layered and thickened with uneven enhancement (Figure 4).

Figure 4 Image examinations of the patient. A: Gastrointestinal radiography 7 years ago; B: Gastroenterography after this admission; C: Chest enhanced computed tomography after this admission.

FINAL DIAGNOSIS

Eventually, he was diagnosed with metachronous GAC with SRCC and metachronous ETAC.

TREATMENT

The diagnosis was confirmed by gastroscopy after admission. Considering the complexity and high risk of a second surgery, the patient chose chemotherapy. The patient received 160 mg of intravenous oxaliplatin on day 1. At the same time, capecitabine 1.5 g was taken orally three times a day for 1-14 days. Treatment was administered every three weeks. On the first day of chemotherapy, the patient vomited, and the electrolyte levels decreased. Intravenous potassium supplementation and ondansetron hydrochloride injection (8 mg intravenous drip) were administered for symptomatic treatment. On day 5, blood tests showed that electrolytes and liver and kidney functions were normal, and the patient felt that symptoms were relieved, refused to continue treatment, and was discharged automatically.

OUTCOME AND FOLLOW-UP

The patient was discharged after symptom relief from initial chemotherapy. After discharge, the patient did not return to our hospital for further treatment or outpatient follow-up. We called 5 months later and were told that the patient had died.

DISCUSSION

Although current research shows that metachronous gastric cancer is increasing, the total incidence of gastric cancer for esophageal replacement is between 1.5% and 8.6%[1,5], and gastric cancer is common as a pathological type of adenocarcinoma. However, this pathological type of GAC is rare[1,3], so it is even rarer for metachronous GAC with SRCC combined with ETAC. Generally, the necessary condition for diagnosing adenosquamous carcinoma is that the proportion of squamous cell carcinoma reaches 25%. The pH value of the growth environment of human squamous cells is higher than that of the stomach. According to the hypothesis of adenosquamous carcinoma, including squamous cell heterotopia and adenometaplasia, it is a long-term process[6], and a small number of squamous cells die because they are not adapted to the gastric acid environment, making it difficult to detect the components of squamous cell carcinoma and the pathological types are rare. The relationship between postoperative esophageal cancer, metachronous gastric cancer, and colon adenoma remains unclear. However, related literature suggests that changes in the structure of the digestive system after esophageal cancer surgery are the basis for metachronous tumors[7]. However, our patients did not have risk factors such as smoking, drinking, and Helicobacter pylori infection[2,4]. Preoperative and intraoperative examination of esophageal cancer did not suggest gastric neoplastic lesions, and the canceration of ETAC is usually approximately 5 years after its discovery[8], indicating that the gastrointestinal metachronous tumor is a new tumor after esophageal cancer, which provides evidence for the gastrointestinal metachronous tumor after esophageal cancer surgery[7]. Usually, after esophageal cancer surgery, it is necessary to remove part of the stomach and create a tube to replace the esophagus. This changes the physiological structure of the stomach and digestive tract and decreases gastric acid secretion, leading to a weakening of sterilization. At the same time, intestinal juice and bile reflux occur, leading to damage to the gastric protective barrier. Long-term negative stimulation by bacteria may promote glandular metaplasia and squamous cell heterotopia, leading to GAC[1,5]. SRCC is a unique type of adenocarcinoma[9]. Insufficient gastric acid can’t destroy bacteria, causing bacteria to enter the intestinal tract, affecting intestinal flora, damaging the lower digestive tract, and promoting intestinal tumors[7]. To date, there are no detailed research reports on the relationship between postoperative esophageal cancer and metachronous GAC, SRCC, or ETAC. Therefore, more research is needed to clarify the relationship between these factors.

Imaging revealed that the contrast agent slowly passed through the digestive tract when our patient underwent gastrointestinal radiography. Chest-enhanced CT showed that the stomach wall was thickened, and the thickened stomach wall showed uneven enhancement. Combined with the literature[10], it is indicated that we should pay attention to the occurrence of metachronous gastric cancer when these imaging features appear because metachronous gastric cancer is asymptomatic in the early stage and is mostly found in the middle and late stages. Complications such as esophageal stricture, tumor recurrence, and metastasis can occur after esophageal cancer surgery, and the recurrence time of the tumor is different[11,12]. Esophageal cancer is asymptomatic or atypical in the early stages[11], and most patients do not know enough about the tumor. Therefore, follow-up is helpful in determining the patient’s condition in time, providing useful suggestions in time, and identifying and treating early. At the same time, postoperative follow-up can help to understand the quality of life of patients, which is beneficial for evaluating surgical effect[13]. Therefore, a gastroscopy must be performed every year after esophageal cancer surgery, which lasts more than 10 years[1]. Metachronous gastric cancer and colon adenoma can be treated surgically, but complications such as esophageal cancer can occur again after surgery, complicating the operation[1,5]. This patient had poorly differentiated adenosquamous carcinoma with a high degree of malignancy, and most complications of surgical treatment were eventually treated with chemotherapy. However, in recent years, endoscopic treatment of early metachronous gastric cancer has been favored[5], but it must be confirmed by large sample data to improve the prognosis.

CONCLUSION

After esophageal cancer surgery, the tumor can recur, which may also cause metachronous GAC and SRCC, and at the same time, it can be complicated by intestinal adenoma. Our literature search reveals that the latter is uncommon. Chest CT, gastrointestinal radiography, and other imaging examinations are often used to examine typical lesions that are not sufficient to diagnose early metachronous tumors of the digestive tract. Therefore, it is best to use a gastroscope as a reexamination method after esophageal cancer surgery and, at the same time, colonoscopy should be reexamined to avoid missed diagnosis. Combined with previous case reports, factors such as Helicobacter pylori infection and drinking can promote the occurrence of postoperative metachronous tumors. However, this patient only had factors of change in digestive tract structure. Therefore, we speculate that the latter may promote the occurrence of metachronous gastrointestinal tumors. However, the relationship between the occurrence and development of metachronous tumors and esophageal cancer and its treatment remains unclear and more research is needed to confirm this.

ACKNOWLEDGEMENTS

We thank all authors who helped with this research.