Incomplete Reversal of Barrett's Esophagus

Does ablation of non-dysplastic Barrett's esophagus make sense?

According to one recent study and another ten-year old study, squamous islands, created during the incomplete ablation of Barrett's esophagus, may still be genomically unstable and prone to carcinogenesis.

The creation of squamous islands (i.e., islands of normal esophageal cells in the sea of Barrett's esophagus cells) can occur as a result of prolonged PPI therapy. The simplest hypothesis is that normal squamous cells grow over or grow out from under the Barrett's cells once conditions in the esophagus return to normal due to acid suppression. The potential creation of squamous islands is promoted as one of the successes of PPI therapy.

However, a study way back in 1999 found that these squamous islands possess abnormal biomarkers (e.g., Ki-67, p53 abnormalities) that suggest genomic instability and continued risk for cancer progression. I am not aware of any follow up studies showing that such squamous islands progress to cancer at higher rates than other tissue, and suspect the implications of this finding are not fully understood yet.

Interestingly, the recent study cited above showed that incomplete photodynamic abaltion produces similar results -- abnormal biomarkers, including Ki-67, cyclooxygenase-2 (COX-2), and p53 staining.

The moral of the story is that if you get photodynamic therapy, don't be one of the 30%-50% of people whose doctors do it wrong... The more serious moral of the study, is that it might not be a good idea to get photodynamic ablation unless you already have dysplasia.

I just don't know whether the 1999 finding is a good enough reason to stop PPI therapy. I guess I have some faith that, since this has been known for 10 years, somebody would have noticed if those "lucky" people with squamous islands were dropping dead faster than those without. Perhaps the abnormal biomarkers are just a temporary sign of genomic instability in the good sense -- i.e., caused by the reversion to neo-epithelial cells -- and not a genomic instability that leads to cancer?

In any case, I suspect that eating and supplementing in a manner that promotes genomic stability should help. Vitamin D seems to be one powerful weapon in this fight. There are others that I will discuss in future posts.

Image from here.