Immunosuppression in patients with Barrett's esophagus

Patients with Barrett's esophagus have a higher incidence of esophageal cancer than has the general population. Local tissue injury and exposure to carcinogens presumably play a role in malignant transformation, but the possibility of altered host immune surveillance must also be considered.

The level of immunoreactivity was investigated in six healthy control subjects; 14 patients with gastroesophageal reflux, seven with and seven without esophagitis; and nine patients with Barrett's esophagus. Parameters studied were (1) T-cell and B-cell function with mitogen-stimulated lymphocyte blastogenesis, (2) immunosuppressive properties of autologous serum, and (3) interleukin-2 production by peripheral blood mononuclear cells. Nutritional status as a possible cause for immunosuppression was assessed by measurement of serum albumin, transferrin, and prealbumin.

Patients with Barrett's esophagus had a significant suppression of all T-cell (p less than 0.01) and B-cell function (p less than 0.01) and interleukin-2 production (p less than 0.001) when they were compared to the controls. Interleukin-2 production was also reduced significantly compared to that in patients with gastroesophageal reflux with and without esophagitis (p less than 0.05). No differences were observed in serum immunosuppression or nutritional factors.

Although the immunosuppression observed in the patients with Barrett's esophagus was milder than that found in other immunocompromised states, it may be sufficient to encourage the malignant transformation of Barrett's mucosa.