High Risk for Gastric Cancer in Patients With Gastric Lesions

Medscape Medical News > Oncology
High Risk for Gastric Cancer in Patients With Gastric Lesions

Liam Davenport
July 30, 2015



Patients with precancerous gastric lesions face an increased risk of developing gastric cancer that increases dramatically with increasing severity of the lesion, say Swedish scientists. The findings underscore the importance of patient surveillance, they add.

The study was published online July 27 in the BMJ.

Patients with minor changes in intestinal mucosa had a 1.8-fold risk of developing gastric cancer during the next 20 years vs those with healthy tissue. The risk rose to almost 11-fold risk in patients with dysplasia.

The findings confirm the validity of Correa's cascade, a widely accepted pathologic progression to gastric cancer that is thought to be initiated by Helicobacter pylori infection, say the authors. The cascade leads from normal mucosa to dysplasia via minor mucosal change, gastritis, atrophic gastritis, and intestinal metaplasia.

"Our results in a low risk Western patient population show that all stages of Correa's cascade predict an incidence of gastric cancer above that of the general population," they note.

Study Details

To determine the incidence of gastric cancer among patients with gastric precancerous lesions, the researchers conducted a population-based cohort study using data on 405,211 patients from Swedish national registers who had undergone gastric biopsies between 1979 and 2011.

Excluding the first 2 years of follow-up, the team identified 1599 cases of gastric cancer diagnosed during an average follow-up period of approximately 10 years.

They calculated that the annual crude incidence of gastric cancer was 20 x 10−5 for those in the normal mucosa group, 42 x 10−5 for patients with minor changes, 59 x 10−5 for those with gastritis, 100 x 10−5 for patients with atrophic gastritis, 129 x 10−5 for the intestinal metaplasia group, and 263 x 10−5 for those with dysplasia.

This translated into standardized incidence ratios compared with the general Swedish population of 1.0, 1.5, 1.8, 2.8, 3.4, and 6.5, respectively.

It was determined that the 20-year risk of developing gastric cancer was approximately as follows:

1 in 256 for patients with a normal mucosa;

1 in 85 for those with gastritis;

1 in 50 for patients with atrophic gastritis;

1 in 39 for those with intestinal metaplasia; and

1 in 19 for dysplasia.

On Cox regression analysis, the risk for gastric cancer increased monotonically with progression along Correa's cascade, ranging from a hazard ratio compared with normal mucosa of 1.8 for minor mucosal change to 10.9 for dysplasia.

Highlights Need for Surveillance

Senior author Weimin Ye, MD, PhD, Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden, discussed the findings with Medscape Medical News.

He described the study as a "first step" in characterizing the risks faced by patients with gastric precancerous lesions, but one that nevertheless confirms the validity of Correa's cascade.

Although more work, including cost-benefit analyses, would be needed to develop surveillance strategies from the results, Dr Ye believes the results the importance of closely following patients with more severe lesions.

"The problem is...[that] clinical guidelines already recommend that even atrophic gastritis patients be followed up every year or every 2 years, [but] very few [doctors] really follow this," he said.

Although noting that the decision is often taken out of doctors' hands, owing to the limitations of their healthcare system, he added: "I think this study reemphasizes that this is really important, but the problem here is also that I think we need more risk markers to try to further stratify patients."

For Dr We and colleagues, the next steps will be to incorporate such markers alongside precancerous lesion stage to develop a more complete picture of a patient's likelihood of developing gastric cancer.

One such marker involves use of genome analysis to determine the H pylori subtype with which a patient is infected, and another involves tumor mutation profiling.

Dr We concluded: "The other way is a more traditional approach, for example, family history, smoking, something like that.... But I think the most important thing is first two approaches."

This study was supported by the Swedish Research Council and Cancerfonden. Coauthor Huan Song was partly supported by a scholarship from the China Scholarship Council. Coauthor Isabella Guncha Ekheden is partly supported by a scholarship from the Karolinska Institutet MD/PhD programme. The funders had no role in the conduct of this research. The other authors have disclosed no relevant financial relationships.

BMJ. Published online July 27, 2015. Abstract