Pathology of the gastric cardia

Adenocarcinomas of the cardia and distal esophagus have increased in incidence more rapidly than any other type of human cancer in recent years. Whereas the sequence of events leading to esophageal adenocarcinoma (esophagitis, Barrett's esophagus, dysplasia, and carcinoma) has been well described, that of cardiac adenocarcinoma has yet to be defined. We have examined 100 consecutive biopsies of the gastroesophageal (GE) junction in patients with symptoms of GERD, in order to answer the following questions: (1) What is the spectrum of cardiac pathology? (2) Can "carditis" due to GERD be histologically distinguished from carditis due to Helicobacter pylori (HP) infection? (3) Is intestinal metaplasia of the cardia more frequently related to GERD, or to HP infection? (4) What types of esophageal and gastric pathology coexist with carditis? Out of the 100 GE junction biopsies only 63 contained cardiac mucosa and all showed carditis. Carditis was related to HP in 8 cases. Distinguishing histologic features of non-HP carditis included the predominance of reactive epithelial changes over inflammatory changes, a villiform surface and a tendency of the inflammatory infiltrate to decrease with increasing distance from the squamo-columnar junction. Pancreatic metaplasia was seen in 9 cases (14%), none associated with HP. Intestinal metaplasia (IM) was seen in 15 cases (24%) and associated with HP in only 2. Non-HP carditis, with or without IM, was associated with normal or reactive esophageal squamous and distal gastric mucosa in the majority of cases. We conclude that, in our patient population, carditis and cardiac IM is primarily due to GERD and propose that the sequence of events leading to cardiac carcinoma is similar to that of esophageal adenocarcinoma.