How to treat esophageal carcinoid tumor?

       Esophageal carcinoid tumor originates from the neuroectoderm and mainly occurs in the digestive tract, accounting for 0.87% of the malignant tumors in the digestive tract, which is a tumor of Apudoma peptide-producing hormone tumor, also known as silver pheochromocytoma or chromophobe tumor.  It is a low-grade malignant neuroendocrine tumor that belongs to the diffuse neuroendocrine system. Its general pathological manifestation is polypoid or nodular ulcerated type, with size of 0.7-12 cm, clear tumor margin, tough, grayish white. The nodular ulcerated type often indicates that the carcinoid tumor is in the middle to late stage. Microscopically, the tumor cells have a consistent morphology and the cell boundaries are mostly clear. The tumor cells are arranged in strips, solid sheets, and partly in glandular ducts or vesicles, but there is no obvious lumen. The nuclei were round or oval, with dense chromatin, few nucleoli and few nuclear divisions. Immunohistochemical examination of the tumor cytoplasm may show positive for neurospecific enolase (NSE), chromogranin and 5-hydroxytryptamine. The tumor cells are aggregated and surrounded by unequal amounts of connective tissue, with abundant blood sinuses in the interstitium. Since the silver cells are mostly found in the middle and lower esophageal mucosa, esophageal carcinoid tumors are more likely to be found in the middle and lower esophagus.  Clinical diagnosis: The biopsy rate of esophageal carcinoid tumor is low, and pathological biopsy is mostly reported as poorly differentiated adenocarcinoma or small cell carcinoma.  1.Barium esophagogram may show destruction of esophageal mucosa, irregular filling defect, soft tissue shadow outside the esophagus, esophageal stricture, stiffness of the wall, or smooth muscle tumor-like changes.  2.Endoscopy This is the first choice method to diagnose the disease, which can determine the location, size and invasion depth of the tumor. The boundary of the tumor is clear under the endoscope, and the edge is raised, which can be located in the upper, middle or lower part of the esophagus.  3.Growth inhibitor receptor scintigraphy Some reports use growth inhibitor receptor scintigraphy to diagnose carcinoid tumor, because there are growth inhibitor high affinity sites in carcinoid tissues, using radioisotope labeling growth inhibitor analogs oxytocin can make localized diagnosis for 80%-90% of carcinoid tumor lesions, and can also show liver and extra-abdominal metastases.  Clinical manifestations: Esophageal carcinoid tumors are mostly seen in males, with the age of onset ranging from 26 to 77 years old, averaging 54 years old. The main symptom is discomfort or choking pain behind the sternum when swallowing, and serious swallowing obstruction is rare. The clinical characteristic of esophageal carcinoid tumor that distinguishes it from other esophageal malignancies is that it can be combined with carcinoid syndrome, especially when combined with liver metastasis. Because carcinoid tumor is a tumor that produces small molecule peptides or amine hormones, secretes 5-hydroxytryptamine, histamine, kinin and other bioactive substances, patients may have clinical manifestations of carcinoid syndrome such as facial flushing, diarrhea, shortness of breath and edema. concentration increases and causes symptoms.  Clinically, patients with carcinoid syndrome such as facial flushing, diarrhea, shortness of breath, edema, etc., along with choking pain when swallowing or discomfort behind the sternum, should think of the possibility of this disease. Esophageal endoscopy and histopathological examination can clarify the diagnosis.  Treatment: The treatment of esophageal carcinoid tumor should be based on surgical resection, and the correctness of surgical treatment is related to the patient’s survival quality and survival period, and the removal of primary tumor and metastatic tumor can lead to long-term survival. Radiotherapy and chemotherapy are not effective for carcinoid tumor. Carcinoid syndrome can be effectively controlled with 5-HT3 inhibitors (α-methyldopa) and 5-HT3 blockers (dimethyl ergometrine).