Introduction
Gastric (stomach) cancer is a challenging disease worldwide. Despite the decline in gastric cancer cases over the past decades, it remains one of the most common and deadly cancers. The high death rate of gastric cancer can be attributed to the late initial diagnosis. Gastric dysplasia (the presence of abnormal cells within a tissue) is a premalignant (before cancer) lesion and the final stage in gastric carcinogenesis (cancer formation). It is a marker of an increased probability or risk of malignant change in the stomach. Its clinical importance was underestimated before its association with gastric cancer. Hence, early identification, management, and follow-up of gastric dysplasia are essential for the detection and prevention of gastric cancer.
What Are the Clinical Features and Course of Dysplasia in the Stomach?
The prevalence of gastric dysplasia is about four percent in Western countries and 20 percent in developing countries. Patients with gastric dysplasia are male and younger than gastric cancer patients. Gastric dysplasia lesions can be found anywhere in the stomach. Gastric dysplasia is low-grade (LGD; mild abnormal features) and high-grade (HGD; severe abnormal features).
Both low grade dysplasia and high grade dysplasia can progress to cancer. Hence, the risk of malignant change increases with the grade of dysplasia. However, the real risk of progression for dysplasia remains unclear. Various studies have demonstrated that patients with high grade dysplasia are at high risk of progression to carcinoma. The rate of malignant change of high grade dysplasia is about 60 to 85 percent over four years. Low grade dysplasia has a lower risk of cancer progression as compared to high grade dysplasia. Moreover, low grade dysplasia has been documented to regress in about 75 percent of cases.
What Are the Conditions That Lead to Gastric Dysplasia?
Many stomach diseases and lesions contain dysplastic contents. However, the clinically important ones are listed below.
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Atrophic Gastritis (AG): AG is a chronic inflammatory condition and thinning of the stomach lining. The main features are inflammation, atrophy (decrease in size) of gastric glands, and metaplasia (altered cell type). These changes are more commonly found in the antrum (part of the stomach). Patients with atrophic gastritis are at increased risk of cancer. However, the correct risk measurement is undetermined.
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Gastric (Peptic) Ulcers: Peptic ulcers (stomach sores) occur in the stomach lining. The incidence of cancer developing in a peptic ulcer is debated for many years. There are two essential criteria for the diagnosis: definite evidence of a pre-existing ulcer and malignant change at the edge of the ulcer. Furthermore, it is essential to remember that chronic (long-standing) ulcers and cancer may coexist in the stomach.
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Pernicious Anemia (PA): PA is a rare autoimmune disorder that causes a deficiency in vitamin B12 absorption, resulting in B12 deficiency and anemia. Gastric cancer is three to four times more common in patients with PA than in the general population. Despite being less common, pernicious anemia is a classic risk factor for gastric cancer.
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Gastric Polyps: Polypoid lesions of the stomach (masses of cells) have malignant potential. Polypoid lesions showing dysplasia (called adenomas) have a significant capacity for malignant change. Most gastric adenomas develop based on atrophic gastritis and metaplasia.
How Is the Diagnosis of Dysplasia in the Stomach Made?
Mostly, gastric dysplasia is asymptomatic and discovered incidentally during screening examinations. Hence, the two modalities for gastric cancer screening are upper endoscopy and contrast radiography.
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Endoscopic Gastric Cancer Screening: Endoscopy is a non-surgical technique used to examine the digestive tract. Gastric cancer screening is done in countries with high rates of gastric cancer. Recently, a study reported a 30 percent reduction in gastric cancer deaths via endoscopic screening. Further, various studies suggest the best cost-effective strategy for detecting early gastric cancer as endoscopy. Also, endoscopy is more sensitive (a positive case) and specific (a negative case) than barium radiographic studies.
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Barium Swallow: The barium swallow study is a contrast-enhanced radiographic study used to assess the structural characteristics of the esophagus and stomach. Barium radiography can identify malignant gastric ulcers, infiltrating lesions, and early gastric cancers. In gastric dysplasia and early gastric cancer, the response of a barium study is about 14 percent. The barium swallow is non-invasive and requires only radiographic capability and a contrast medium. Hence, it is useful despite the current wide availability of computed tomography (CT).
How Is Dysplasia in the Stomach Managed?
Factors designing management guidelines include understanding the biological process. As a result, recent molecular studies support the microscopic assessment that gastric dysplasia is a cancerous lesion. In addition, follow-up studies have also established risks and time frames for the development of gastric cancer.
High-grade dysplasia lesions require endoscopic resection (a minimally invasive surgery for removing gastric dysplasia and cancer using an endoscope) due to the potential for cancer progression and the coexistence of cancer. Hence, endoscopic resection can be curative. Furthermore, with advances in endoscopic localization and staging of cancer, endoscopic mucosal resection (EMR) can offer a non-surgical cure. EMR removes precancerous, early-stage cancer, or other abnormal lesions from the stomach. However, modern interventional endoscopic procedures are not available outside specialist centers. Hence, their treatment role and availability need to be defined.
In contrast, few guidelines regarding the management of low-grade dysplasia are available. Low-grade dysplasia has a lower risk of malignant transformation. Therefore, some investigators recommend yearly endoscopic surveillance with repeat biopsy (removal of stomach tissue) for low-grade dysplasia. Still, repeated endoscopic examination with biopsy can impose a physical, psychological, and financial burden on the patient. However, endoscopic resection is less invasive than surgery. Endoscopic treatment or surgical treatment is recommended for high-grade dysplasia. In addition, endoscopic treatment or follow-up is recommended for low-grade dysplasia. The choice of treatment depends on the size of the lesion, depth of invasion, and other factors (patient age and comorbidities).
Endoscopically unclear lesions should undergo follow-up within one year after diagnosis. In addition, endoscopic resection should be considered for patients only with endoscopically defined high-grade dysplasia. Moreover, the guidelines highlight that the absence of dysplasia during follow-up biopsies does not exclude the progression to cancer. Finally, a thorough evaluation of the entire stomach should be done, and any abnormalities biopsied.
Conclusion
The importance of gastric dysplasia is stressed because of its close association with gastric cancer development. However, despite the latest clinical data and use of upper endoscopy, challenges persist regarding diagnosis and management. Due to the significant diagnostic discrepancies between biopsy and endoscopic resection, the latter should be considered for the diagnosis and management of gastric dysplasia. Further, the frequency of the follow-up is recommended every three to 12 months during the first year.
