Gastric carcinoid tumor

Introduction to gastric carcinoid tumor Gastric carcinoid is a malignant tumor originating from gastric mucosal chromaffin cells (APUD cells). It belongs to neuroendocrine tumors. Compared with other gastric malignant tumors, gastric carcinoids have different histological, pathological and biological characteristics. Compared with gastric cancer, its degree of malignancy is relatively low. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: diarrhea

Gastric carcinoid cause

Causes:

Modlin statistics of gastric carcinoids have increased from 0.3% to 0.54% of all gastric tumors, accounting for 2 to 6% of all carcinoids. The diagnostic rate of hypergastrinemia is more obvious, possibly with acid-suppressing drugs (such as H2). Long-term use of receptor antagonists or proton pump inhibitors has been associated with low gastric acid, hypergastrinemia, and may be associated with advances in modern diagnostic techniques that have led to an increase in the rate of diagnosis of the disease. Hypertension for more than 4 months can cause intestinal chromoblast-like cells (ECL) to proliferate, which can further cause carcinogenesis of the gastric mucosa.

Pathogenesis:

Gastrin hypothesis

It has long been believed that the regulation of gastric acid secretion by parietal cells is related to the release of gastrin from gastric antrum G cells. At first, it was thought that gastrin directly caused parenchyma to secrete gastric acid. It is found that this mechanism at least includes ECL cells at the fundus. Gastrin of the antrum enters the blood circulation through various mechanisms, and then causes ECL cells to release histamine, which binds to the H2 receptor of parietal cells, activates the proton pump, and causes gastric acid secretion. However, gastrin also acts on ECL cells. It has a nutritive effect and can promote the self-replication of ECL cells, leading to the proliferation of ECL cells. Therefore, gastrin not only affects the secretion of ECL cells, but also has a nutritional effect. The gastric antrum acid can reduce the circulation of gastric secretion through negative feedback inhibition. The concentration of the sinus, gastric antrum separation, acid transfer, the result of induction of high gastrinemia, ECL cells were found to be significantly proliferated 8 weeks after surgery, on the contrary, gastric antrum resection can cause hypogastrinemia, can reduce ECL cells The amount and volume of the wall cells, the decrease in the secretion of acid from the parietal cells can reflexively increase the level of gastrin in the circulation, and thus the drug that inhibits gastric acid secretion can induce hypergastrinemia. Activation of ECL cells, causing ECL cell proliferation, once the drug treatment is stopped, gastrin levels are reduced to normal, this effect can be reversed, gastrin hypothesis that effective inhibition of gastric acid secretion eliminates gastric acid in the stomach Feedback inhibition of the cells causes hypergastrinemia, which activates ECL cells, first causing diffuse hyperplasia of ECL cells, followed by focal hyperplasia, micronodule formation, and finally carcinogenesis.

Hirth and colleagues continued to orally administer the H2 receptor antagonist BL-6341 hydrochloride for 2 years, found that the formation of hypergastrinemia was dose-dependent, and observed ECL cells from diffuse hyperplasia, focal gland Tumor-like hyperplasia to carcinogenesis, and they also proved that the drug itself has no toxic effects through toxicological tests. It is believed that its tumorigenic effect is mediated by gastrin, and Bilch feeds the feed containing H2 receptor antagonist. In rats, rats were found to have hypergastrinemia first, and they were killed and dissected to find carcinogenesis in the stomach. These animal experiments showed that hypergastrinemia is associated with the formation of gastric carcinoid.

In recent years, the results of clinical studies have verified the correctness of animal experiments, further proving that human gastric carcinoids are mainly caused by hypergastrinemia. In 1992, Japanese scholar Toshihisa studied 27 cases of multiple gastric carcinoid tumors in Japan. And analysis, pointed out that type A atrophic gastritis due to its main lesions in the fundus, corpus, wall cells, damage, so mostly low acid or a few acid-free, long-term acid-free or low acid will inevitably cause high gastrin Hypertension, which eventually leads to gastric carcinogenesis, Zollinger-Ellison syndrome is another hypergastrinemia, and the risk of developing gastric carcinoids is higher, with 10% to 15% of MEN-I eventually developing. For carcinoid, the incidence of MEN-I is similar to that of the general population. It has been reported that after gastric antrum resection, micro-nodules or carcinoids (ECL cell proliferation) disappear in this type of patient, Borch reported with argyrophilic cell knots. The level of plasma gastrin in hyperplastic anemia patients is higher than that in patients without ECL cell proliferation. The plasma gastrin level is the highest in carcinoid patients. So far, there has been no long-term application of drug-induced hypergastrin in human gastric cancer. Report.

2. Other

Although a large body of evidence supports the role of gastrin in promoting carcinogenesis in ECL cells, there are other hypotheses that Axelson found in a study of rats that portal-cavity shunts are in the absence of hypergastrinemia. It can cause ECL cell proliferation, and it can cause hypergastrin in patients with portal-cavity shunt. OEL cell proliferation is more significant than that of omeprazole alone. In addition to the secretion of ECL, there are also ECL cell trophic factors. Berendt reported 3 cases of multi-center gastric carcinoid, positive for pro-silver reaction, and secreted serotonin and substance P. This staining is typical of small intestinal EC cells and small intestinal carcinoids. The authors believe that tumors are derived from endocrine cells of small intestinal metaplasia, rather than proliferating ECL cells. Some scholars believe that carcinoids themselves can produce gastrin releasing factor or gastrin, rather than relying on gastric acid deficiency or Zollinger-Ellison syndrome. The resulting high gastrinemia, Solcia reviewed 44 cases of gastric fundoid carcinoids, no association between carcinogenesis and Helicobacter pylori infection.

Gastric carcinoma prevention

1. Pay attention to food diversification, mainly plant food, which should account for more than 2/3 of each meal. Plant-based diet should contain fresh vegetables, fruits, beans and whole grains.

2. Control weight, avoid overweight or too light, limit the weight gain to less than 5kg after adulthood, overweight or obesity may lead to increased risk of endometrial cancer, kidney cancer, and intestinal cancer.

3. Do not eat charred food, grilled fish, barbecue should avoid burning charred. Fish, meat and bacon that are grilled directly on the fire can only be eaten occasionally. It is best to cook, steam, and fry food.

4. Eat more starchy foods, eat 600-800g of various cereals, beans, and plant roots every day. The less processing, the better. To limit the intake of refined sugar. Starch in food has the effect of preventing colon cancer and rectal cancer. High-fiber diet may prevent the occurrence of colon cancer, rectal cancer, breast cancer and pancreatic cancer.

Gastric carcinoma complications Complications, diarrhea

Although gastric cancer often secretes serotonin (5-HT) precursor serotonin (5-HTP), histamine and various peptide hormones, it affects 5-HT and other blood vessels due to lack of dopamine decarboxylase in gastric tissue. Active substance synthesis, so there are fewer carcinoid syndromes in gastric carcinoids. If there is a carcinoid syndrome, it is often variability, and it is often found in patients with liver metastases. It is characterized by diarrhea and redness.

Gastric carcinoma symptoms Common symptoms Abdominal pain, nausea, nausea, polyp, upper abdominal pain, malignant anemia, bloody nodules, hyperparathyroidism, carcinoid syndrome

The clinical manifestations of gastric carcinoids are similar to those of gastric cancer. They are generally not characterized. Upper abdominal pain is the most common symptom, followed by hematemesis, melena, weight loss, anemia, nausea and vomiting. The clinical manifestations of gastric carcinoids are variable, and Often accompanied by other digestive tract diseases, endocrine diseases and autoimmune diseases, and can be associated with chronic atrophic gastritis, peptic ulcer, stomach cancer, hypothyroidism, diabetes, esophageal cancer, prostate cancer, Crohn's disease and brain Vascular arteriovenous malformation and other diseases coexist. Gough et al retrospectively analyzed the clinical symptoms of 36 cases of gastric carcinoid, of which 72% had anemia (58% of pernicious anemia), 69% had abdominal pain, and 11% had carcinoid syndrome. Among them, chronic atrophic gastritis accounted for 67%, thyroid function was 39%, diabetes accounted for 19%, Addison disease accounted for 6%, hyperparathyroidism accounted for 6%, and a few patients did not have any clinical symptoms, only in surgery Unexpectedly discovered during or after endoscopy.

Hakan et al. classify gastric carcinoids into four types:

1. Type I: with type A chronic gastritis, is a common type, accounting for about 65%, the tumor mainly occurs in the fundus, gastric mucosa, type A chronic atrophic gastritis or pernicious anemia with gastric antrum G cells Hyperplasia and hypergastrinemia, most of the lesions are multiple polypoid lesions less than 1.0cm in diameter, the tumor grows slowly, lymphatic or hematogenous metastasis rarely occurs, the malignancy is low, and the 5-year survival rate after treatment is 95%. the above.

2. Type II: Also known as sporadic hair style, it is the most widely reported type, accounting for 21%. Tumors occur in the small sinus mucosa of the antrum. There is little chronic atrophic gastritis and high gastrinemia. It is a single-shot isolated nodule with a diameter greater than 2.0cm. The excretion of histamine in the urine increases, the endocrine symptoms are obvious, and there are many metastasis in the advanced stage. The lymphatic metastasis is 55%-80%, and the blood metastasis is 20%-30%. Higher.

3. Type III: is associated with type I Zollinger-Ellison syndrome type, this type may have chromosome 11q13 site loss, mostly occurs in the fundus mucosa, chronic atrophic gastritis is often mild, hypergastrinemia is obvious, Malignancy and prognosis are between type I and type II.

4. Type IV: for other rare endocrine tumor types in the stomach, such as G cell tumor, neuroendocrine carcinoma, endocrine and secretory mixed tumor, etc., cancer tissue containing only a small amount of endocrine cells is not included in this type, the malignant degree of such tumors Low, slow development, but the corresponding symptoms caused by various hormones secreted by tumor tissue are obvious. Domestic and foreign scholars hold the same opinion on Type I and Type II in the above classification, and the understanding of other types is not uniform, and there are also domestic scholars. Gastric carcinoids are classified into three types, and gastric cancers with Zollinger-Ellison syndrome or multiple endocrine adenoma type I syndrome are classified as type III, but regardless of the type of view, it is considered that Gastric cancer induced by nephremia is a benign or low-grade tumor, often manifested as multiple small tumors, while other types of gastric cancers have higher malignancy, often accompanied by metastases, lymph nodes, liver and bones. It is a common transfer site.

Gastric carcinoid examination

Serum carcinoembryonic antigen (CEA) is rarely elevated in carcinoid patients. Therefore, a patient with normal CEA should consider the possibility of carcinoid, 65% of patients have elevated serum gastrin value, and the serum gastrin value is normal. About 66% of the patients had tumors >2.0 cm, suggesting that the malignancy of this carcinoid is large. A large amount of 5-HTP can be found in the urine test, and a small amount of 5-hydroxyindoleacetic acid (5-HIAA) can also be found. That is, the ratio of 5-HTP to 5-HIAA in urine increases, which is a characteristic urine test for gastric carcinoid.

X-ray inspection

X-ray examination is less valuable for the diagnosis of submucosal carcinoid, and it is effective for the detection of polypoid carcinoid. For polypoid carcinoids above 2cm, round or oval filling defects can be seen in the gastrointestinal barium meal, sometimes in the center of the shadow. There is a depression. When the ring-shaped filling defect is found, the edge is neat and sharp, the surrounding boundary is clear like a knife, and the central part is relatively regular. It should be considered as a carcinoid. Balthazar et al. classify its X-ray performance as isolated. Intramural filling and defect type, multiple gastric polypoid type, large ulcer type and polypoid type intratumoral tumor type 4.

2. Gastroscopic examination

Nakamura described the characteristics of 8 cases of gastric cancer with gastroscope visually as follows: polypoid changes, more common in the fundus, corpus, most of the protrusions without pedicle, individual pedicle, single hair, grayish white to pink, Appearance is normal mucosal coverage, smooth round submucosal mass with irregular depression erythema or ulcer is a characteristic manifestation of gastric carcinoid, where the positive rate of biopsy is high, and the gastroscopic performance of gastric malignant carcinoid is difficult. Different from gastric cancer, gastroscopic biopsy is the best tool for diagnosing carcinoid. Endoscopic mucosal biopsy can be used in patients who cannot be diagnosed by conventional biopsy. Giovannini reports that endoscopic ultrasonography can provide submucosal carcinoid before surgery. Location and infiltration around.

3. Radionuclide scanning

Radionuclide scanning has been used in the localization diagnosis of clinical carcinoids in recent years. It can detect microscopic lesions that B-ultrasound and CT can not display. The positive rate is 80%-90%. Radiolabeled somatostatin analogues can help determine The location of the tumor and the depth of invasion.

4. Other inspections

B-ultrasound, CT, and magnetic resonance imaging examination have guiding significance for the diagnosis of primary or metastatic cancer of the liver. CT can rarely detect primary gastric carcinoid, only help to determine whether there is lymph node and liver metastasis, B-guided liver Puncture or abdominal mass biopsy can help to confirm the diagnosis, while intracavitary B-ultrasound or endoscopic ultrasonography can diagnose the tumor size, tissue invasion depth, and lymph node metastasis.

Diagnosis and diagnosis of gastric carcinoid tumor

The disease is asymptomatic early, and as the disease progresses, it can show symptoms similar to ulcers, gastric polyps and adenocarcinoma, such as abdominal pain, nausea, vomiting, hematemesis, blood in the stool, and other non-specific symptoms, no specific significance for diagnosis, the diagnosis depends mainly on clinical Performance and laboratory and other auxiliary inspections.

Differential diagnosis

Poorly differentiated adenocarcinoma

Most of the pathological types of malignant gastric cancer are ulcer invasive, and the diagnosis is easily confused with poorly differentiated adenocarcinoma. Differential diagnosis requires pathological electron microscopy, argyrophilic staining and immunohistochemical staining, poorly differentiated adenocarcinoma of the stomach, and cell presentation. The nested or irregular glandular tube and papillary arrangement, the cell size is extremely inconsistent, there are more mitotic phases and necrosis, the size of gastric cancer cells is basically the same, the mitotic phase and necrosis are rare, and the poorly differentiated adenocarcinoma is negative for silver staining. Response, but there are reports in the literature that less than 10% of patients with gastric carcinoids also have a negative reaction to argyrophilic staining, so these patients need to be further identified by immunohistochemical staining.

2. Gastric neuroendocrine carcinoma

The diagnosis depends on pathological diagnosis. The tumor tissue of gastric neuroendocrine carcinoma is easy to infiltrate extensively. The tumor cells are mostly nested. The cells are small fusiform, with little cytoplasm. The morphology is like oatmeal with mitotic and necrotic, immunohistochemical staining. Neuroendocrine cells can be found to be more than 50%.

3. Carcinoid in the midgut

Urine tests showed a high concentration of 5-HIAA, while those with gastric carcinoid tumors belonging to the foregut carcinoid had the lowest 5-HIAA content in the urine.

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