Dr John P Wright
Updated: 14 March 2011
The relative incidences of malignancies are constantly changing for reasons that we do not understand. These variations highlight our ignorance of the disease patterns we live with.
While gastric cancer has become increasingly rare oesophageal cancer has increased exponentially. Squamous cell cancer, a cancer that was common in our black population, is decreasing worldwide while adenocarcinoma is increasing. Unfortunately the 5 year survival is similar at about 10 to 13% although time of diagnosis and local therapeutic facilities may influence this.
Etiological factors for squamous carcinoma include local environmental factors such as alfatoxin, alcohol ingestion and smoking. These contribute to the geographic variations in high risk countries such as China and Southern Africa. Other factors such as pickled food has also been implicated. This is thought to be related to foods rich in N-nitroso compounds. Finally mother’s advice not to drink our tea at too high a temperature appears to be wise as tea consumed at 65o has been associated with an increased incidence of oesophageal cancer.
Underlying oesophageal diseases such as achalasia and previous caustic burns also predispose to squamous cell carcinoma.
When it comes to oesophageal damage little is more aggressive than the oral bisphosphonates. The advice to patients to drink fluids and stand up when taking their medication does not guarantee that the oesophagus will not be damaged. This damage related to oral bisphosphonates is such that the newer systemic bisphosphonates should replace the oral medication in most patients The reduction in the incidence of squamous cell carcinoma may be as a result of changing environmental factors but the increase in adenocarcinoma is not explained. Smoking and obesity have been implicated but oesophageal reflux disease appears to be the most important predisposing factor. As most oesophageal adenocarcinoma arises from an area of Barrett's metaplasia, the relationship between reflux and Barrett’s is crucial.
In patients with oesophageal reflux the risk of developing oesophageal cancer is increased at least 30-fold above that of the general population. Although most patients with adenocarcinoma have Barrett’s not all patients with Barrett's metaplasia will develop adenocarcinoma. In fact the incidence of adenocarcinoma in patients with Barrett’s is low IE less than 2%. .
The relationship between Barrett’s oesophagus and oesophageal adenocarcinoma has spawned surveillance programs of repeat oesophageal endoscopies and biopsies. The value of this effort is not yet clear. Patients with Barrett’s oesophagus have a 0.5% risk of adenocarcinoma. Whereas the risk associated with low grade dysplasia is unclear while the rate of cancer development in patients with high grade dysplasia is 5 to 8 percent per year. Even this high risk has to be balanced against the morbidity of total oesophagectomy, radiotherapy and chemotherapy. A further complication is the reliability of the pathological classification of Barrett’s oesophagus and the grade of dysplasia. Attempts to standardise the diagnostic criteria is an ongoing challenge.
In the end patients with Barrett’s oesophagus have an increased risk of oesophageal adenocarcinoma and a strategy is needed to handle this risk. The Practice Parameters Committee of the American College of Gastroenterology has published guide lines in this regard.
Once a diagnosis of Barrett’s oesophagus is made the first surveillance endoscopy should be performed a year later. Generally this is done annually with multiple circumferential biopsies. For patients who have had two consecutive endoscopies that show no dysplasia, surveillance endoscopy at an interval of every three years is recommended.
For patients with low-grade dysplasia yearly surveillance endoscopy is recommended.
Patients with high grade dysplasia should be treated. At present endoscopic therapy is the preferred over total oesophagectomy.