Stomach cancer primary prevention
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Parminder Dhingra, M.D. [2] Mohammed Abdelwahed M.D[3]
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Overview
Effective measures for the primary prevention of stomach cancer include smoking cessation, eradication of Helicobacter pylori infection, and having a balanced diet rich in fruits and vegetables. In areas of low gastric cancer incidence, screening for gastric cancer with upper endoscopy should be reserved for specific high-risk subgroups. Individuals at increased risk for gastric cancer include; gastric adenomas, pernicious anemia, gastric intestinal metaplasia, familial adenomatous polyposis, Lynch syndrome, Peutz-Jeghers syndrome, Juvenile polyposis syndrome.
Primary prevention
Lifestyle modifications
- Dietary modification is an important approach to control gastric cancer. There is a link between physical inactivity and obesity to many types of cancer.
- Diet with low consumption of red meat, high in fruits and vegetables may have a protective effect against many cancers.
- The World Health Assembly adopted the WHO Global Strategy on Diet, Physical Activity, and Health, in May 2004 to reduce deaths and diseases.
H.pylori eradication
- The incidence of metachronous gastric cancer following the endoscopic resection of a gastric neoplasm is known to be reduced by the eradication of H. pylori infection.
Recommended first-line therapies for H pylori infection:
| Regimen | Drug dose | Dosing frequency | Duration(days) | FDA approval |
|---|---|---|---|---|
| Clarithromycin triple | PPI (standard or double dose)
Clarithromycin (500mg) Amoxicillin (1gm) or Metronidazole (500mg TID) |
BID | 14 days | YES† |
| Bismuth Quadruple | PPI (standard dose)
Bismuth subcitrate (120-300mg)or Subsalicylate (300mg) Tetracyclin (500mg) Metronidazole (250-500mg) |
BID
QID QID TID to QID (500mg) |
10-14 days | NO‡ |
| Concomitant | PPI (standard dose)
Clarithromycin (500mg) Amoxicillin (1gm) Nitroimidazole (500mg)c |
BID | 10 -14 days | NO |
| Sequential | PPI (standard dose) + Amoxicillin (1gm)
PPI, Clarithromycin (500mg) + Nitroimidazole (500mg) |
BID
BID |
5-7 days
5-7 days |
NO |
| Hybrid | PPI (standard) + Amoxicillin (1gm)
PPI, Amoxicillin, Clarithromycin (500mg), Nitroimidazole (500mg) |
BID
BID |
7 days
7 days |
NO |
| Levofloxacin triple | PPI (standard dose)
Levofloxacin (500mg) Amoxicillin (1gm) |
BID
QID BID |
10-14 days | NO |
| Levofloxacin sequential | PPI (standard or double dose) + Amoxicillin (1 gm)
PPI, Amoxicillin, Levofloxacin (500mg QD), Nitroimidazole (500mg) |
BID
BID |
5-7 days | NO |
| LOAD | Levofloxacin (250mg)
PPI (double dose) Nitazoxanide (500mg)c Doxycycline (100mg) |
QD
QD BID QD |
7-10 days | NO |
| †: Several PPI, Clarithromycin, and Amoxicillin combinations have achieved FDA approval, PPI, Clarithromycin, Metronidazole are not an FDA approved treatment regimen.
‡: PPI, Bismuth, Tetracycline, and metronidazole prescribed separately are not an FDA approved treatment regimen.
c: Metronidazole or Tinidazole[1] | ||||
After the failure of first-line therapy, such patients should be considered for referral for salvage treatment.
| Salvage therapies for Helicobacter pylori infection | ||||
|---|---|---|---|---|
| Regimen | Drugs(doses) | Dosing frequency | Duration(days) | FDA approval |
| Bismuth quadruple |
|
BID
QID QID TID or QID |
14 | NO |
| Levofloxacin triple |
|
BID
QD BID |
14 | NO |
| Concomitant |
|
BID
BID BID BID or TID |
10-14 | NO |
| Rifabutin triple |
|
BID
QD BID |
10 | NO |
| High-dose dual |
|
TID or QID
TID or QID |
14 | NO |
- Whenever H. pylori infection is identified and treated, testing to prove eradication should be performed using:
- A urea breath test
- Fecal antigen test
- Biopsy-based testing at least 4 weeks after the completion of antibiotic therapy and after PPI therapy has been withheld for 1–2 weeks.
Screening
In countries with a high incidence of gastric cancer such as east Asia countries, universal screening is recommended. [17-19]
In Japan, population-based screening for gastric cancer is recommended for individuals older than 50 years with conventional double-contrast barium radiograph with photofluorography every year or upper endoscopy every two to three years [20,33,34].
Screening interval is recommended to be every two years but may be widened to a three-year rather than a two-year interval without significant effect [38-40].
Hereditary cancer prevention
Screening
In areas of low gastric cancer incidence, screening for gastric cancer with upper endoscopy should be reserved for specific high-risk subgroups
Individuals at increased risk for gastric cancer include those with the following:
- Gastric adenomas
- Pernicious anemia
- Gastric intestinal metaplasia
- Familial adenomatous polyposis
- Lynch syndrome
- Peutz-Jeghers syndrome
- Juvenile polyposis syndrome
Prevention
- Asymptomatic patients with a family history of HDGC and CDH1 mutations have a high probability of developing signet ring cell adenocarcinoma of the stomach. Prophylactic total gastrectomy is recommended for patients with family history of HDGC and CDH1 mutations.[2]
- For patients with a CDH1 mutation but who are not from an HDGC family, we recommend individualized evaluation at an experienced center before prophylactic total gastrectomy is offered.[3]
- Prophylactic gastrectomy is often advised between age 20 and 30.
- Some suggest timing total gastrectomy in CDH1 mutation carriers at an age that is five years younger than the youngest family member who developed gastric cancer.[4]
- Older patients are less likely to benefit from a prophylactic gastrectomy than younger patients because of a shorter life-expectancy and a higher perioperative risk.
- patients who are older than 75 years should not undergo such a procedure, as their mortality from the procedure outweighs their mortality from gastric cancer.
- Decisions should be individualized based upon their comorbidities and the age of gastric cancer onset in their respective kindred.[5]
Gatric polyps
- Polypectomy should be performed for all known neoplastic polyps and for all polyps ≥1 cm in diameter, as biopsies alone cannot exclude foci of high-grade dysplasia or early gastric cancer.
- In patients with multiple polyps, the largest polyp should be excised and representative biopsies obtained from the remaining polyps.
- Fundic gland polyps are associated with a low risk of progression to cancer.
- Small proximal gastric polyps should be biopsied in patients with FAP to confirm their histology.
- Large or irregular appearing polyps should be biopsied or resected completely to assess for dysplasia.
- Low-grade dysplasia is common in fundic gland polyps, but surgery should be reserved for high-grade dysplasia or cancer.
- Antral polyps are usually adenomas and should be completely resected endoscopically if possible.
Hyperplastic polyps
- Hyperplastic polyps occur in association with H. pylori-related atrophic gastritis.
- Surveillance with upper endoscopy should be performed based on the risk factors for gastric cancer one year after initial resection of adenomatous gastric polyps.
- In individuals at high risk for gastric cancer, surveillance is continued long life.
Juvenile polyposis syndrome
- Screening the upper gastrointestinal tract with upper endoscopy starting at the age of 12 years.
- If polyps are detected, upper endoscopy should be repeated annually.
- In the absence of upper gastrointestinal tract polyps, upper endoscopy can be performed every two to three years.
Lynch syndrome
- Individuals with a germline mutation in the DNA mismatch repair MMR or EPCAM genes have a definitive diagnosis of Lynch syndrome and should undergo screening for Lynch syndrome associated cancers.
- Extent of screening in these individuals can be individualized based on their personal and family cancer history and evidence of microsatellite instability on tumor testing.
- Individuals at risk for Lynch syndrome include:
- Individuals in families meeting Amsterdam I or II criteria or revised Bethesda guidelines
- Endometrial cancer prior to age 50 years
- First-degree relative of those with known MMR/EPCAM gene mutation
- Individuals with >5 percent chance of an MMR gene mutation
References
- ↑ "www.nature.com" (PDF).
- ↑ Keller G, Vogelsang H, Becker I, Hutter J, Ott K, Candidus S; et al. (1999). "Diffuse type gastric and lobular breast carcinoma in a familial gastric cancer patient with an E-cadherin germline mutation". Am J Pathol. 155 (2): 337–42. doi:10.1016/S0002-9440(10)65129-2. PMC 1866861. PMID 10433926.
- ↑ Pharoah PD, Guilford P, Caldas C, International Gastric Cancer Linkage Consortium (2001). "Incidence of gastric cancer and breast cancer in CDH1 (E-cadherin) mutation carriers from hereditary diffuse gastric cancer families". Gastroenterology. 121 (6): 1348–53. PMID 11729114.
- ↑ Norton JA, Ham CM, Van Dam J, Jeffrey RB, Longacre TA, Huntsman DG; et al. (2007). "CDH1 truncating mutations in the E-cadherin gene: an indication for total gastrectomy to treat hereditary diffuse gastric cancer". Ann Surg. 245 (6): 873–9. doi:10.1097/01.sla.0000254370.29893.e4. PMC 1876967. PMID 17522512.
- ↑ Chun YS, Lindor NM, Smyrk TC, Petersen BT, Burgart LJ, Guilford PJ; et al. (2001). "Germline E-cadherin gene mutations: is prophylactic total gastrectomy indicated?". Cancer. 92 (1): 181–7. PMID 11443625.