Precancerous states of the GI tract

There are multiple different precancerous states of the GI tract. Inflammatory bowel diseases also increase the risk for cancer but are not covered here.

Colonic polyps

Several colonic polyps, especially adenomatous polyps, are precancerous.

Barrett oesophagus

Barrett oesophagus is a consequence of chronic GERD where the chronic acid exposure of the oesophageal mucosa causes intestinal metaplasia (Barrett metaplasia). On histology goblet cells can be seen in the mucosa. It occurs in up to 15% of patients with GERD.

Barrett oesophagus is a precancerous lesion which must be treated or at the very least frequently monitored. It may progress into adenocarcinoma.

Barrett oesophagus is asymptomatic and is often discovered when a patient is being evaluated endoscopically for GERD. The diagnosis is based on biopsy and histology.

All patients with Barrett oesophagus should be on PPI.

Barrett oesophagus with high-grade dysplasia is treated with mucosectomy (endoscopic resection) or endoscopic ablation, same as T1A oesophageal cancer. No dysplasia or low-grade dysplasia may be managed either with regular surveillance or endoscopic removal.

Oral leukoplakia and erythroplakia

Leukoplakia is an unbrushable white lesion, while the erythoplakias are fiery red. They are associated with increased risk of cancer and have normally no symptoms. The risk factors for leuko- and erythroplakias are smoking, chewing tobacco and excessive alcohol intake.

The risks of progression into invasive squamous cell carcinoma is 3-25% with leukoplakia, and more than 50% with erythroplakia. It’s important to distinguish them from benign oral lesions like oral candidiasis.

These precancerous lesions should be surgically removed, or alternatively, regularly surveyed. Avoiding risk factors is important to prevent recurrence or progression.

Familial adenomatous polyposis

Familial adenomatous polyposis (FAP) is an autosomal dominant and caused by the mutation of the adenomatous polyposis coli gene, APC. This disease manifests with hundreds to thousands(!!) polyps in the colon and rectum and start to appear already in the teenage years. They are actually morphologically indistinguishable from colorectal adenomas, so the only way to diagnose a patient with FAP is to count that more than 100 polyps are present.

As FAP is autosomal dominant, there is often a family history of the disease, but not always. Genetic testing is necessary for the diagnosis, which shows the characteristic germline mutation in APC.

Because FAP is associated with a 100% risk of progression to CRC by the age of 45, surgery is required in all cases. Surgery is performed at age 16 – 20, or at the time of diagnosis if later than this.

The preferred surgical procedure is restorative proctocolectomy with ileum pouch and anal anastomosis.

Atrophic gastritis

Atrophic gastritis increases the risk of gastric cancer. It is commonly asymptomatic. Autoimmune metaplastic atrophic gastritis (AMAG) may cause pernicious anaemia. Environmental metaplastic atrophic gastritis (EMAG, H. pylori associated) may cause peptic ulcers.

Treatment involves eradication of H. pylori for EMAG, B12 supplements for AMAG, and possibly regular endoscopic surveillance (although this is controversial). ‎