Helicobacter pylori was the common thread in two disorders —one benign and the other not.

Ms. L, a 90-year-old African American, presented with sudden onset of hematemesis. Mucosal and conjunctival pallor were present. Vital signs were temperature 98°F, pulse 90 beats per minute, respiratory rate 14 breaths per minute, and BP 110/70 mm Hg supine and 90/60 mm Hg standing. Hemoglobin and hematocrit were 8.6 g/dL and 25%, respectively.

Evaluation and management

Following volume resuscitation with crystalloids and packed RBCs, the patient underwent an upper GI series with barium contrast. Visible on the stomach was a large ulcer on the lesser curvature and a deformed antrum (Figure 1). Upper GI endoscopy with multiple biopsies of the ulcer site and deformed antrum revealed mucosal disruption and severe chronic gastritis, respectively (Figure 2). Special stains for Helicobacter pylori and a urease test were negative. However, results of an assay for immunoglobulin (Ig) G antibody to H. pylori were strongly positive, indicating the presence of a chronic, long-standing infection.

Continue Reading

Under medical management comprising quadruple therapy for H. pylori (omeprazole [Prilosec], clarithromycin [Biaxin], amoxicillin, bismuth), the benign lesser curvature ulcer healed completely in four weeks, but the antral deformity became more prominent (Figure 3). This further raised our suspicion for a coexistent gastric cancer, despite the fact that earlier biopsies had proven negative.

Ruling out other possibilities

Repeat endoscopy and multiple biopsies from the remaining lesion confirmed undifferentiated gastric carcinoma (Figure 4). To exclude mucosa-associated lymphoid tissue (MALT) B-cell lymphoma, we ordered special immunoperoxidase studies, all of which were negative. Two other findings argued against MALT B-cell lymphoma: (1) the absence on abdominal CT of metastasis in the liver or the mesenteric lymph nodes, frequently present in patients with MALT B-cell lymphoma, and (2) lack of regression following a course of treatment for H. pylori infection.

p>After learning of her diagnosis, the patient declined surgery. She lived for 18 months before succumbing to cancer cachexia and liver metastases, which developed three months before her death.


About 2% of patients with gastric ulcer may have coexisting gastric cancer, but follow-up studies have not confirmed increased long-term risk of gastric cancer in gastric ulcer patients.1 Infection with H. pylori is now recognized as an important cause in gastric and duodenal ulcers as well as gastric cancer.2,3 Interestingly, patients with duodenal ulcers have a decreased risk of gastric cancer, whereas those with gastric ulcer have an increased risk.4 This clinical paradox was recently unmasked in a large cohort of the hospitalized patients in Uppsala, Sweden.5

To determine whether our patient had indeed suffered from H. pylori infection, we again personally reviewed all biopsies and special stains, but we were unable to reach a definitive conclusion. Because the IgG antibody for H. pylori was positive, the patient was treated with quadruple therapy that resulted in healing of the gastric ulcer but no improvement in subclinical gastric outlet obstruction due to cancer. This end result, the negative immunologic studies of the biopsies, and the absence of liver metastases at the time of diagnosis confirmed that this patient indeed had gastric carcinoma rather than MALT-associated B-cell gastric lymphoma.The regression of lymphoma following a course of treatment for H. pylori infection6 did not happen in our patient.

Approximately 1% of patients infected with H. pylori eventually develop gastric carcinoma, and for this reason, the International Agency of Research on Cancer classified H. pylori as a group I carcinogen in humans. Therefore, early diagnosis and eradication of H. pylori infection are important factors in reducing the late complications of gastric carcinoma and MALT-associated gastric lymphoma.


In an elderly patient such as ours with previous history or serologic evidence of H. pylori infection, benign gastric ulcer and malignant gastric cancer may coexist. Underlying presenting symptoms may be due to one or both disease entities. Careful documentation of both diagnoses is essential to render appropriate treatment. Ultimate prognoses remain unfavorable.


Dr. Ansari is a staff member in the Department of Medicine at Fairview Southdale Hospital in Edina, Minn., where Dr. Berntson is a staff pathologist.



1. Correa P, Schmidt BA. The relationship between gastric cancer frequency and the ratio of gastric to duodenal ulcer. Aliment Pharmacol Ther. 1995;9 Suppl 2:13-19.

2. Taylor DN, Blaser MJ. The epidemiology of Helicobacter pylori infection. Epidemiol Rev. 1991;13:42-59.

3. Blaser MJ, Chyou PH, Nomura A. Age at the establishment of Helicobacter pylori infection and gastric carcinoma, gastric ulcer, and duodenal ulcer risk. Cancer Res. 1995;55:562-565.

4. Hansson LE, Nyren O, Hsing AW, et al. The risk of stomach cancer in patients with gastric or duodenal ulcer disease. N Engl J Med. 1996;335:242-249.

5. Parsonnet J. Helicobacter pylori in the stomach—a paradox unmasked. N Engl J Med. 1996;335:278-280.

6. Carlson SJ, Yokoo H, Vanagunas A. Progression of gastritis to monoclonal B-cell lymphoma with resolution and recurrence following eradication of Helicobacter pylori. JAMA. 1996;275:937-939.