A 61-year-old man was referred for evaluation because of iron-deficiency anemia.
Six months ago, he developed pain, swelling, and stiffness of both hands and the right knee. His symptoms did not improve with analgesics or nonsteroidal anti-inflammatory drugs (NSAIDs). Three months ago, he was diagnosed with rheumatoid arthritis. He began methotrexate and had dramatic improvement in joint symptoms. One month later, he was diagnosed with iron-deficiency anemia. He was begun on oral iron supplementation and recently was referred for gastrointestinal evaluation.
The review of systems was negative for fever, night sweats, or weight loss. There was no dysphagia, dyspepsia, nausea, vomiting, abdominal pain, hematemesis, melena, or hematochezia. There was no alteration in frequency or consistency of bowel movements.
The patient works in a funeral home performing various tasks, including embalming. He does not smoke, use illegal drugs, or drink excessive amounts of alcohol. His father has hypertension, and his mother has rheumatoid arthritis.
There was no other history of serious medical illness, hospitalizations, or surgery. Medications included methotrexate 15 mg taken orally every week, famotidine 20 mg daily, and ferrous gluconate 300 mg twice daily. The famotidine had been prescribed by the referring physician for unclear reasons.
The physical examination showed normal vital signs. The patient weighed 201 lb; body mass index was 28. All systems were examined and found to be normal.
Important laboratory studies at the time of referral revealed the following: hemoglobin, 11.7 g/dL; mean corpuscular volume, 75; white blood cell count, 9,900 cells/mcL; and platelets, 248,000 cells/mcL. Electrolytes and routine serum chemistries were normal. Serum iron was 38 mcg/dL; total iron-binding capacity was 307 mcg/dL; ferritin was 8 mcg/dL; antinuclear antibody was negative; thyroid-stimulating hormone level was 0.6 mU/L; antithyroglobulin antibody was <20 IU/mL; and serum gastrin level was 399 pcg/mL. He was positive for anti-Helicobacter pylori antibodies and negative for antiparietal cell antibodies.
The patient had a normal colonoscopy. He also underwent upper gastrointestinal endoscopy. The body of the esophagus was normal but a polypoid mass protruded up from the gastric cardia at the gastroesophageal junction (Figure 1). The retroflexed view from the stomach confirmed that the lesion originated from the gastric side of the gastroesophageal junction (Figure 2). The lesion was 3 cm long and was erythematous, nodular, friable, and oozing blood. Adjacent mucosa (arrow in Figure 2) appeared erythematous, nodular, and irregular. There were at least 6 other polypoid masses originating from the gastric mucosa in both the gastric corpus (Figures 3 to 5) and antrum (Figures 6 and 7). The masses varied in size from 0.5 cm to 3.0 cm, and all were covered with an abnormal mucosa that appeared erythematous and irregular. The gastric mucosa between the lesions did not have the usual smooth uniform texture -- it was irregular in contour and inhomogeneous color (Figures 8 and 9). Some of the gastric folds in the corpus appeared thick (Figure 10).
The mass in Figure 1 actually originated from the gastric cardia. The arrow points to the adjacent mucosa, which is abnormal-appearing.
1. What is a reasonable differential diagnosis for the endoscopic findings shown in Figures 1 through 10?
Cite this: A Man With Rheumatoid Arthritis and Iron-Deficiency Anemia - Medscape - Sep 27, 2007.