Colon polyps and polyposis

Introduction to colon polyps and polyposis Mucosal protuberances that protrude from the lumen of the colon are called colon polyps and include all types of lesions that are neoplastic or non-neoplastic. Among the 2755 colonic polyps in the Zhejiang Colorectal Cancer Cooperative Group (1978), 72.3% were neobiotics and 82.7% were Shinya in the United States. The proportion in China is slightly lower, probably due to the higher proportion of data from schistosomiasis and the relatively lower neobiotics. basic knowledge The proportion of sickness: 0.2% - 0.5% Susceptible people: no special people Mode of infection: non-infectious Complications: anemia, blood in the stool, schistosomiasis, colon cancer, rectal cancer, colorectal cancer

Colon polyp and polyposis

Dietary factors (25%):

The incidence of colorectal polyps was significantly higher in long-term high-fat, high-protein, low-fiber diets, and the incidence of polyps in fresh fruits and vegetables and vitamin C was reduced.

Bile metabolism disorder: gastroduodenal ulcer gastrojejunostomy and patients after cholecystectomy, bile flow and discharge time changes, bile acid content in the large intestine increases, experiments show bile acids and bile acid metabolites deoxycholic Both acid and lithocholic acid induce the formation of adenomatous polyps or carcinogenesis in colorectal mucosa.

Genetic factors (20%):

About 10% of patients with colorectal cancer have a family history of cancer. Similarly, when some members of the family have adenomatous polyps, the likelihood of colorectal polyps is significantly higher in other members, especially familial. Polyposis has obvious family heritability. In addition, the incidence of colorectal polyps in patients with other cancers such as digestive tract cancer, breast cancer, uterine cancer and bladder cancer is also significantly increased.

Intestinal inflammatory disease (10%):

Chronic inflammatory lesions of the colonic mucosa are the main cause of inflammatory polyps, most commonly seen in chronic ulcerative colitis, Crohn's disease and amoebic dysentery, intestinal schistosomiasis and intestinal tuberculosis, etc., also seen in the anastomotic site after colon surgery .

Gene abnormalities (10%):

The occurrence of familial polyps may be related to the loss of function and lack of an allele suppressor gene called APC (adenomatous polyposis coli) in the long arm of the fifth chromosome. Under normal circumstances, the allele needs to play simultaneously. In order to inhibit the growth of the tumor, when the gene is absent or a mutation occurs, the inhibition of the tumor disappears, thereby causing colorectal adenomatous polyposis and canceration.

Pathogenesis

The distribution of polyps in the colorectal area often varies from source to source. The colon and rectum are more common in the following stages, and the colorectal is 55.4% to 76.7%, while the autopsy is only 8.9%.

Colon polyp

(1) adenoma: According to the autopsy data of the United States, adenoma can be found in 22% to 61% of the population. According to the fiber colonoscopy, there is no family history in the general population, and the personal history or asymptomatic examination is 25% to 41%. Epidemiological data show that the incidence of adenoma increases, indicating that the environment and lifestyle habits change, adenoma occurs more men than women, with increasing age, from the autopsy data, the incidence of adenoma before the age of 50 is 17%, 50 59 years old is 35%, 60-69 years old is 56%, and those over 70 years old are 63%. It is generally believed that colorectal cancer originates from adenomatous polyps, and its cancer rate is 1.4%-9.2%. The risk of developing rectal cancer.

1 pathological form:

A. Early classification: Early stages of colorectal adenoma can be divided into 4 types: a. small flat adenoma: a tubular adenomatous image, the lesion mucosa thickens, the abnormal epithelium involves the mucosal affected part, extending to the periphery without Vertically extending to the bottom, b. small recessed adenoma: the mucosal recessed area is a tubular adenoma structure, which can occupy the entire mucosal layer, c. micro adenoma: a tubular tube that can be found only under light microscopy and affects the entire gland tube Adenoma, d. "serrated" adenoma: adenoma with hypertrophic polyps and tubular adenoma two images, about 2 / 3 tumors less than 1cm.

B. Classification of maturity: from pathologically divided into 3 categories:

a. tubular adenoma: also known as adenomatous polyp or polypoid adenoma, hemispherical or elliptical, smooth or lobulated surface, pink or grayish red, surface can be hyperemia, edema and erosion, polyp diameter Small from 1cm, up to 5cm, most of the clinical findings are more than 1cm, the larger ones have more pedicles, a few (15%) wide or no pedicle.

b. villous adenoma: also known as papillary adenoma, accounting for 10% to 20%, generally large volume, mostly wide base or base, more pedicle, cancer rate 30% to 40% .

c. The proportion of tubular villous adenomas is similar, but the surface of the adenoma is partially smooth, partially rough, and large in volume.

2 Adenoma size, number and anatomical distribution characteristics: from the National Polyp Research Group data in 3371 cases of endoscopic adenoma, 38% 0.5cm, 36% 0.6 ~ 1cm, 1cm is 26% 60% single hair, 40% multiple, with increasing age, multiple increases, British St Mark Hospital data: 76% <1cm, 20% for 1 ~ 2cm, > 2cm for 4%; villous adenoma 60% >2cm, 86% is mild dysplasia, 6% is severe.

3 Adenoma and Carcinogenesis: The concept of adenoma metastasis has been accepted. In this process, a series of polygenic changes are involved in epithelial cells. Multi-faceted phenomena indicate its sequence inertia. From a global perspective, when immigration to the knot In the high incidence area of rectal cancer, the prevalence of adenomas has increased, and the cancer rate is positively correlated with age and adenoma size, and is obvious in the left colon. Common adenocarcinomas and adenocarcinomas in the same period are common. Adenoma is an example of a typical neoplastic carcinoma sequence, and data from the US National Polyp Study Group confirm that adenomas reduce the incidence of cancer.

A. Molecular level study: The early change of genes from normal mucosa to adenocarcinoma is APC (adenomatous polyposis coli) gene, located at chromosome 5q, where the gene is inactivated, causing epithelial hyperplasia and developing early adenoma , followed by a series of genetic and molecular events, including DCC (18q), p53 (17q) and ras gene mutations, a large group of hereditary non-polyposis colon cancer syndrome (HNPCC) in New Zealand In the patient examination, the negative screening patients found colorectal cancer within 3.5 years. This data suggests that the incidence of cancer in patients with HNPCC is short, and there is no adenoma to adenocarcinoma sequence. Family-age I relatives are especially People with colorectal cancer before the age of 55 are more at risk.

B. Pathological changes: only a small number of adenomas are cancerous from the pathological morphology. Any adenoma with large volume, villous and severe atypical hyperplasia is susceptible, and studies at St Mark Hospital show: 1 1.3% malignant less than 1 cm, Adenoma between 1 and 2 cm is only 9.5% malignant, 46% more malignant than 2cm adenoma; 2 tubular adenoma is only 4.8% malignant, villus is 40.7%; 3 mild typical hyperplasia is 5.9% malignant, moderate and The severity is 18% and 34.5% respectively.

In sigmoidoscopy, the incidence of colon adenocarcinoma in the same period was 31%, and 8% of them were progressive adenomas or carcinomas.

C. Epidemiology: The positive correlation between the incidence of adenoma and the incidence of colorectal cancer has been confirmed by epidemiology. As the incidence of colorectal cancer increases, the discovery rate of colorectal adenoma also rises, and the knot The incidence of rectal cancer is rising rapidly, and the rate of adenoma discovery is also rapidly increasing. It is closely related to epidemiology, pathological type is related to carcinogenesis, villus is the most cancerous, tubular adenoma is less, and the former has a cancer rate of 29 %~40%, 10% of colorectal cancer specimens are from adenomas, and there are reports of 25%. In recent years, Vogelstein started with molecular genetic studies to confirm that gene mutations are related to the occurrence of colorectal cancer at the chromosome level, thus showing glandular The correlation between tumor and cancer (Fig. 2), although still about 30% directly from the flat mucosa, adenoma cancer is not the only way to develop colorectal cancer, and not all adenomas are cancerous. Regarding the development of adenomas as cancer, some people have reported 213 cases of census data, all of them are asymptomatic, the size of "polyps" are 0.2 ~ 0.5cm in diameter, and every 6 to 11 months are reviewed once for 3 to 5 Year, after follow-up 18 % of the "polyps" disappeared, 8% polyps decreased, 70% did not change, 4% increased, only 2 cases of cancer, it is believed that adenoma can exist for a long time, and growth can be very slow, adenoma cancer including glandular columnar epithelium Significantly increased rounding, nucleoli is obvious, and pathological mitosis can occur, glandular epithelial hyperplasia is pseudo-stratified, or atypical hyperplasia glandular infiltration into the submucosa, showing the relationship between atypical hyperplasia and carcinogenesis Morson found that there were many adenomas in 14.2% of the cancerous foci. After the anatomical adenomas became cancerous, there were not many invasive pedicles. The more fluffy adenomas, the more likely they were to become cancerous, up to 4.8%~29.8. %, and tubular adenomas 4% to 4.8%, the total cancerous rate of villous adenomas is significantly larger than tubular adenomas, adenomas smaller than 1.0cm in diameter, the canceration rate is estimated to be about 10%, more than 2cm, the possibility of canceration Sexuality increased significantly, and the highest reported in the literature was 50%. It was also considered to be 0% to 3% for <1cm, 2.1% to 11.1% for 1-2cm, and 8.7% to 50% for >2cm.

D. Carcinogenesis time: Adenoma carcinogenesis is a long-term chronic process, at least 5 years, an average of 10 to 15 years, which is also consistent with the slow growth of benign adenoma.

E. Number of adenomas and carcinogenesis: 1846 cases of adenomas from St Mark Hospital in the United Kingdom showed that 29.7% of single adenomas, 51.7% to 76.9% of 2 to 5, and 80% of cancers of 6 to 48.

Domestic reports of cancerous adenomas originated from multiple adenomas accounted for 71.4%.

Clinically, most of the adenomas are less than 2cm in size. When considering the treatment, there is no need to emphasize the canceration problem too much. For adenomas with carcinoma in situ, local resection can be followed up regularly, without having to expand the operation. Patients with adenomas were followed up regularly after resection, paying attention to the occurrence of new adenomas.

(2) Juvenile polyps and polyposis: juvenile polyps (also known as congenital polyps, retention polyps or juvenile adenomas, common in young children, but also in adults, mostly under 10 years old, more than 70% Single hair, but can also be multiple (generally 3 or 4), 60% occurred within 10cm from the rectum of the anus. In the two adult censuses in Haining County, Zhejiang, the juvenile polyps accounted for 6.2% to 7.2% of all polyps. It has a round spherical shape, and the pedicle surface is smooth and pink, the surface is smashed, and the oozing exudate is covered. The cut surface can be seen in different sizes of the sacral cyst, filled with mucus, and the gland tube is scattered under the microscope. It is expanded into a sac, lined with a flat epithelium, with exfoliated epithelium and inflammatory cells inside. The interstitial is rich and there is a lot of inflammation and congestion.

Juvenile polyposis coli (JPC), multiple polyp tissue morphology with a single juvenile polyp, but familial, single is mostly benign, no malignant tendency, multiple, can occur in the gastrointestinal tract Segment, up to 25-40 or more, familial juvenile gastric polyposis limited to the stomach, or familial colonic juvenile polypoma limited to the colon, also from the stomach to the colon called familial extensive juvenile gastrointestinal Familial genereralized juvenile polyposis (FGJP), an autosomal dominant hereditary disease, and may be associated with parenteral malformations. Although the morphology of juvenile polyps is benign, it is also a malignant opportunity due to multiple and simultaneous adenomas. Large, the treatment is the removal of polyps, and the family members should start regular screening after 10 years of age.

(3) Inflammatory polyps: inflammatory polyps: non-neoplastic, with ulcers and degeneration, including Crohn's disease or ulcerative colitis, inflammatory polyps can be classified into two categories: more than one or a single Polyps consist of inflammatory interstitial or granulation tissue and hyperplastic epithelium; 2 associated with mucosal inflammatory diseases, also known as pseudopolyps, such as ulcerative colitis, Crohn's disease, schistosomiasis granuloma, etc. Performance can also occur in the inflammatory polyps at the anastomotic site of the intestinal surgery or at the edge of the ulcer.

There is a positive correlation between ulcerative colitis and colorectal cancer. Pathological changes can be seen in the proliferation of epithelium and cancer. Combined with experimental studies, this inflammatory lesion has a promoting effect on colorectal cancer.

The schistosomiasis polyps are caused by eggs, and the glands are destroyed with epithelial hyperplasia or atrophy. The latter is also called ovum nodules. The cut surface is grayish yellow. If it is accompanied by calcification, it is indurated. The schistosomiasis polyps need Different from the ovum of the tubular adenoma, regardless of the number of eggs, it depends on whether the background is adenoma, the adenoma tissue is the latter, and the schistosomiasis polyps are closely related to the occurrence of colorectal cancer.

Benign lymphoid polyps, which are caused by submucosal lymphoid tissue hyperplasia, are common in the rectum. They may be discomfort after enlargement. Lipoma is occasionally seen in the ileocecal area, which is caused by submucosal fat hyperplasia.

(4) metaplastic (hyperplastic polyps): for the smaller semi-circular protruding mucosa surface like dew-like, no pedicle, more than the autopsy or resection of the intestine specimens found, often seen in the census At the time, the microscopic examination is different from the local mucosa, the lesion hypertrophy protrudes the mucosal surface, the glandular hyperplasia, the lumen is dilated, the goblet cells are reduced, the cytoplasm is red stained, and the epithelial cells are different in height, so the inner edge of the gland lumen is jagged. It resembles the absorption epithelium of the small intestinal mucosa, and most of the metaplastic polyps are self-limiting.

(5) mucosal hypertrophy (mucosal hyperplasia): mucosal small protrusions, ie, mucous membrane polyps, less than 0.5 cm at the endoscopy, the normal mucosa is uplifted by the submucosal tissue, accounting for 18% of the excised small polyps, no Clinical significance.

2. Colorectal polyposis

The difference between colorectal polyposis and colorectal polyps is the number of polyps or adenomas. According to Morson's standard, more than 100 people are polyp (adenoma) diseases, including neobiological and abiotic, but in polyposis, Tumor characteristics such as malignant transformation often occur in non-neoplastic animals.

(1) Familial adenomatous polyposis (FAP): is an autosomal dominant hereditary disease. The colorectal is often filled with polypoid adenoma. If not treated in time, about 3/4 cancer is changed before the age of 35. Almost all of them develop cancer after the age of 50. Because of the absence of polyps in infancy, the disease is not a congenital disease, but it is definitely related to family inheritance. Both men and women can inherit, but there is no genetic discovery, that is, only those with this disease. Passed to the next generation, recent research shows that the disease is related to the deletion and mutation of APC gene on the long arm of chromosome 5. Recently, 3 cases of APC gene loss were found in peripheral blood lymphocytes of a family, one of which has Found in the FAP syndrome, 2 cases of colonic multiple adenomas have been found by fiberoptic colonoscopy.

A small number of patients have no obvious family history (10% to 20%), but they can be found in the next generation. They are thought to be caused by mutations in the gene, but they may also be due to incomplete family investigations, so they are called non-familial polyposis.

In 1980, Blair first discovered that patients with Gardner syndrome had congenital hypertrophy of the rectinal pigment epithelium (CHRPE). The fundus lesions were clear flat lesions with deep boundary of the retina, and there were many translucent halos around. Bara et al reported that the combined rate of CHRPE and FAP was 87%, and the family may be associated with CHRPE 50%. The change of CHRPE was the flat bordered pigmented lesion in the deep retina of the fundus. The FAP follow-up of the Chinese in 1993. In the examination, 8 cases of fundus were examined, and CHRPE was seen in 8 cases. In 8 cases of double eyes, 43 lesions were classified into 4 types:

1 pigment type: there are translucent halo around, pigment dark color, brownish yellow to dark brown, lesions are round or elliptical and irregular, the size is 0.1 ~ 1mm.

2 Depigmentation type: there is halo around, the surrounding color is clearer than the surrounding fundus, showing the change of depigmentation, and the rest are the same pigment type.

3 mixed type: no halo around, pigmented and depigmented lesions mixed.

4 plaque type: no halo or halo around, lesions appear plaque or spotted, small volume.

(2) Gardner syndrome: Gardner and Richard first reported in 1953, Gardner syndrome is a hereditary disease, less common than familial polyposis, its clinical features are in addition to colorectal polyps, but also concurrently Each case:

1 adenoma: multiple adenomas in the colorectal, gastric and small intestine can also be seen, adenoma can occur later than 30 to 40 years old.

2 osteosarcoma: benign osteoma or exostosis, more common in craniofacial bones, especially above the mandible.

3 skin soft tissue tumors: often multiple, located in the skin or subcutaneous, such as epidermoid cysts, fibroids, neurofibroma, especially in the scars of abdominal surgery, in addition to abdominal surgery can be seen in the mesenteric fibroids.

(3) Black spot polyposis (Pentz-Jeghers syndrome): Black spot polyposis is a rare familial disease, also known as Peutz-Jeghers syndrome. Peutz first described the disease in 1921, and Jeghets et al. The system summary is named as a hamartoma, which can occur in any part of the gastrointestinal tract. Although it is considered to be non-neoplastic but cancerous, the disease is characterized by oral mucosa, lips, perioral, perianal and two-finger soles. Spotted hyperpigmentation with multiple polyps in the gastrointestinal tract is a dominant genetic disease. Both males and females can carry this genetic factor. 30% to 35% of patients have a positive family history, and polyps can be distributed from the stomach to the rectum. Any part of the jejunum and ileum is the most common, followed by the duodenum, about 1/3 of cases involving the colorectal, 1/4 involving the stomach, patients often with ovarian tumors, testicular Sertoli cell tumor, cervical cancer, Breast cancer, pancreatic cancer, etc.

Pathologically, the polyp consists of normal mucosal glands, similar to tubular adenomas, including the mucosal muscle layer extending into the gland between the ducts, so the intermedullary interstitial is seen, and smooth muscle fibers are pathological features.

(4) Cronkhit Canada syndrome: first reported by Cronkyr and Canada in 1955, coexisting skin pigmentation spots and juvenile polyps, pigment distribution on the palmar side of the finger and back of the hand, nail atrophy, change of juvenile polypoma with ectoderm The former has a typical lamina propria, the inflammatory cells are filled in the enlarged and displaced glandular cavity, and the medium form, there is not enough evidence to suggest the possibility of suffering from malignant tumors of the digestive tract.

Colon polyp and polyposis prevention

The basic principle of familial adenomatous polyposis treatment is to remove the diseased intestine before the polyp is cancerous, and conduct a census and follow-up of its family members. Careful registration of the family tree is very important for the discovery of high-risk groups. For children in the family, it begins in adolescence. After the colorectal examination, the sigmoidoscopy should be performed once a year or so until the age of 40. If there is no polyp in the colorectal, there will be less chance of polyps, but it is worth noting that there are very few Patients will develop polyposis after the age of 60. In addition, the upper digestive tract should be regularly examined, especially around the ampulla of the duodenum, to exclude the possibility of polyps around the duodenum and ampulla.

In recent years, many authors have found that patients with no clinical symptoms have an accuracy of 100% by detecting mutations in the APC gene. This method avoids the pain of regular colonoscopy and is an early finding for patients with familial adenomatous polyposis. A new way is provided.

Colon polyp and polyposis complications Complications anemia, blood septicemia, colon cancer, rectal cancer, colorectal cancer

1. Anemia: Because the surface of the polyp is erosive, ulcer or inflammation, causing intestinal bleeding, the patient can express brown, black stool or blood in the stool. Some patients have multiple bleedings and the hemoglobin drops to 5g, which is the main reason for the treatment.

2. Malignant transformation: schistosomiasis, inflammatory polyps formed by Crohn's disease and familial polyposis are related to colon cancer variability. According to Weedon, the incidence of colorectal cancer in Crohn is 20 times higher than that in the control group, in the epidemic area of schistosomiasis. The incidence of colorectal cancer is also high. In 1882 Cripps described the malignant transformation of familial polyps. After Hauser's research and literature review, the malignant tendency of polyposis was basically confirmed.

Symptoms of colon polyp and polyposis Common symptoms Defecation frequency abnormal blood in the stool, transverse colon polyps, acute mucus, constipation, abdominal distension, abdominal pain, colon polyps, exhaust disorder

About half of the polyps have no clinical symptoms, are often found by census or autopsy, or are discovered when complications occur. The symptoms are summarized as follows:

1. Intestinal irritation: diarrhea or increased frequency of bowel movements. In severe cases, water and electrolyte imbalance may occur. If there is infection, mucus and blood may be seen.

2. Blood in the stool: It can be used for different degrees of blood in the stool. For example, blood in the lower part of the rectum can be seen in the stool. Blood in the high polyp is often mixed with blood or blood clots in the stool. The amount of bleeding can be directly blood or blood clots. Blood and so on.

3. Intussusception or intestinal obstruction: caused by polyps themselves, and even visible polyps out of the anus, often seen in children, can fall off or retract themselves.

4. Signs: Abdominal examination can touch the mass with tenderness, most of them are nested intestinal fistula, bowel sounds hyperthyroidism, etc., may also have no obvious abdominal signs, black spot polyposis can be seen in oral mucosa, lips, perioral, perianal and two fingers Spotted pigmentation on the sole of the foot.

Although adenoma may have bleeding or a small amount of bleeding, it can often be asymptomatic. Regular fecal occult blood test (FOB) can be found to be positive. Further fiber colonoscopy or X-ray angiography can be used to diagnose adenoma in occult blood stage. However, not adenomas may occur or a small amount of occult blood, 1/3 to 1/2 adenomas have no bleeding, and sequential screening and high-risk factors combined with high-risk factors can make up for the lack of FOB screening.

Examination of colon polyps and polyposis

1. Histopathological examination

The pathological diagnosis of polyp biopsy or resection specimens is essential for determining further treatment options. Clinicians must pay attention to the following points: 1 Materials: The villus components of different parts of the same adenoma are distributed differently, and the degree of hyperplasia of different parts is different. Carcinogenesis may be central and focal, so biopsy specimens taken from different parts may have different pathological diagnosis. Multiple or multiple materials should be taken. It is best to remove all polyps for examination. Marking and localization of 2 specimens: The specimen should be correctly fixed and marked in time so that the pathologist can identify the head, base and margin of the specimen. When the adenoma is associated with epithelial hyperplasia or carcinogenesis, different diagnoses can be made due to differences in pathologist experience.

2. Fecal occult blood test (FOBT)

The total polyps detection rate is low. In recent years, some new FOB detection methods have been developed. Zheng Shu et al reported in 1991 using reverse indirect hemagglutination fecal occult blood test (RPHA-FOBT) and computer risk assessment. Colorectal cancer screening, found that RPHA method sensitivity and specificity are higher, the method has a certain detection rate of colorectal polyps (21.1%), polyps size and bleeding closely related, polyps bleeding >1cm diameter detected The rate of 43.5% increased the positive rate of FOB in adenomas with a large malignant tendency. The positive rate of RPHA-FOB in tubular, tubular villous and villous adenomas was 17.8%, 30.0%, 45.5%, and the cause of adenomas <1cm. No bleeding and false negative FOBT, which can be found by fiberoptic colonoscopy.

3. Tumor marker detection

For example, monoclonal antibody and immunohistochemical techniques are used to determine tumor-associated antigens such as MC3, CA19-9, CEA, and CA50 in tumor tissues; DNA content in tumor tissues or DNA ploidy levels are determined by flow cytometry or microspectrophotometry. Etc., the abnormalities of these indicators are considered to be related to carcinogenesis. Some indicators appear before morphological changes, and can be used for early canceration, cancer progression and early recurrence monitoring. However, the current adenoma test is still mainly in the research stage, and the clinical is extensive. The prospects for application remain to be seen.

4. Rectal examination

It is the simplest and most reliable method to check the lower intestine within 7~8cm from the anus. Touching the induration is a reliable indicator of malignant transformation of polyps, but if the polyp is higher, the rectal examination often cannot be touched.

5. Sigmoidoscopy

It is the most important method for examining low colorectal polyps, and it is often used to supplement the length of the rectal enema.

6. Barium enema angiography

It is not easy to detect small polyps. It is difficult to display polyps in the lower part, especially in the lower rectum. Double contrast gas angiography can improve the detection rate of polyps, and can reduce the misdiagnosis caused by air bubbles in the intestinal cavity. Patients with sigmoid colonoscopy found polyps >0.5cm Further need for barium enema and fiberoptic colonoscopy for the proximal colon, often associated with colonic lesions, the sensitivity of single-contrast barium enema to proximal intestinal polyps is lower than double contrast, so the gland is found in sigmoidoscopy Patients with tumors should be further examined. First, a fiberoptic colonoscopy is used. If the complete colon cannot be examined, a double contrast barium enema test is used.

7. Fiber colonoscopy

It is the most accurate and reliable method for diagnosing colorectal polyps. More than 90% of the skilled technicians can reach the ileocecal area. It can estimate the carcinogenesis of polyps. It is reported that tubular adenomas and villous glands can be found by endoscopic smearing of dyes. In recent years, there have been many reports on the examination of fiberoptic colonoscopy in foreign countries. It has been reported that 10% to 25% of people over 40 years old have endoscopically found asymptomatic polyps, and found a large number of polyps in the 60cm sigmoidoscope. Outside the scope, a colonoscopy should be performed on any polyp patients found in sigmoidoscopy, or in patients with recurrence after polypectomy, in order to detect concurrent cancer or concurrent polyps in time, and about half of the polyps and cancers are discouraged. Enema missed diagnosis, because of the response to colorectal cancer before the colonoscopy of the entire colon to promote the discovery of simultaneous tumors, reducing the incidence of early metachronous cancer and adenoma cancer, currently there are people who have advocated adenoma resection Patients should have long-term, periodic fiberoptic colonoscopy, but some people disagree that the risk of dying from cancer in a single small adenoma is very low. .

8. Colon ultrasound

It is a method of continuous transabdominal ultrasound of the colon in the colon after retrograde perfusion. The method is sensitive, economical, reliable, and has no side effects. The report can examine the segments of the colorectal and detect most polyps and cancer. It has been reported that the sensitivity of polyps of >0.7 cm is 91%, and there is no false positive.

Diagnosis and differential diagnosis of colon polyp and polyposis

Diagnostic criteria

1. Diagnosis of high-risk population

The high-risk group does not have clinical symptoms. The asymptomatic stage can be applied to the sequential screening program. The FOB combined with the high-risk factor AD value is used as the primary screening. This program is proved to be simpler and easier to implement, which is more than 40 years old. , 1 fecal occult blood immunoassay (RPHA-FOB) positive; 2I grade relatives colorectal cancer history; 3 I have a history of cancer and polyps, a history of adenoma; 4 of the 6 symptoms of this item have 2 or more positive As a number of positive, including: mucus bloody stool, chronic constipation history, chronic diarrhea, history of appendicitis, history of obvious trauma and history of gallbladder disease, any of the four items are considered as high-risk groups for fiberoptic colonoscopy, The Optimization Plan was validated. In 1993, 1722 cases of polypectomy were performed in Haining City as a 60cm fiber colonoscopy, and 9 cases of colorectal cancer were diagnosed (5 cases of Dukes A and 4 cases of Dukes B). 138 adenomas and 58 polyps, indicating the feasibility of the program.

2. Diagnostic steps and synchronized adenoma

Further diagnosis can be made from screening high-risk groups. Gastrointestinal double angiography and fiberoptic colonoscopy can be used to confirm the histopathology. At the endoscopy, it is found that the tumor is less than 1cm and removed for pathological examination; for example, >1cm If the difficulty of removal is taken, the tissue biopsy is taken for pathological diagnosis. This segment of colon adenoma has reported that 31% of the proximal segment has synchronous adenoma, 8% of which are >1cm or villous moderate or severe dysplasia, so only The diagnosis of sigmoid colonoscopy is easy to cause misdiagnosis. Adenoma is found in 60cm colonoscopy, and 42% can have synchronous adenoma in the proximal segment. If the distal end of the screening has adenoma of <1cm, the proximal segment exists >1cm. Or villous adenomas are not present at the same time, less than 1%.

3. Follow-up after resection

According to the long-term follow-up of St Mark Hospital, in small (<1cm) tubular adenomas with mild or moderate dysplasia, the risk of subsequent colorectal cancer is not higher than in the general population, so regular colonoscopy of this type of patients Can be designed for a longer follow-up interval.

Fiber endoscopy is clearly easier to diagnose than sputum X-ray examination, not only for diagnosis but also for treatment, but the diagnosis is still confirmed by pathological examination.

Differential diagnosis

1. Identification of hyperplastic polyps

The shape and structure of hyperplastic polyps are similar to those of tubular adenomas or microadenomas. If not carefully analyzed, misdiagnosis may occur, and the three may be identified from the following characteristics.

About 20% of hyperplastic polyps have focal tubular adenoma components, especially at the bottom of polyps, with 1/3 of villous adenomas, and focal hyperplastic polyps can also be found. These mixed forms should be diagnosed as tubular. Adenoma or villous adenoma for proper clinical treatment.

2. Identification of polyp syndrome

Polyposis refers to multiple polyps or polyposis in the intestine, and lesions appear in specific tissues of the intestine at the same time or in succession, including Garder combined with Turcot syndrome, Cronkhite-Canada syndrome and Pertz-Jeghers syndrome. Common clinical features.

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