barium column, dilatation of isolated proximal jejunal segments, and increased width of the mucosal folds (Fig. 2). Acute abdominal pain and hematemesis occurred immediately following small bowel and gastric biopsies on May 26 (Figs. 3 and 4). The hemorrhage was treated, but he died of cardiac arrest the same day. Postmortem examination demonstrated classic polyarteritis nodosa involving primarily the medium-sized vessels of the mesentery, liver, and heart with well-advanced, typical fibrinoid necrosis of the muscular arteries. The microscopic sections ofthe stomach showed heavy round cell infiltrate in the mucosa, primarily of plasma cells. Eosinophils were not prominent. The small bowel showed decreased size and thickening of the villi with a slight increase in plasma cell infiltrate in the mucosa .
Polyarteritis Nodosa "Mimicking" Eosinophilic Gastroenteritis 1 Andrew J. Nicks, M.D. and Felix Hughes, M.D.2
This case of a 71-year-old man with persistent eosinophilia (33-54%), intermittent abdominal pain, and transient pulmonary infiltrates illustrates how polyarteritis nodosa may mimiceosinophilic gastroenteritis. The radiographic manifestations andclinical findings of bothare similar. INDEX TERMS: Eosinophilia.Gastrointestinal tract. Periarteritis, Stomach, inflammation
Radiology 116:53-54, July 1975
Polyarteritis nodosa can present with a roentgenographic, laboratory, and clinical picture similar to eosinophilic gastroenteritis.
The roentgenologic appearance of eosinophilic gastroenteritis, has been described as a diffuse gastric, pyloric, and small bowel abnormality. Gastric involvement is usually restricted to the antral area, evidenced by irregular narrowing, enlargement of mucosal folds, "cobblestone pattern," polypoid filling defects, and pyloric obstruction. Small bowel abnormality may include regular nodular contour defects, "sawtoothed" pattern, effaced volvulae, and luminal narrowing and widening of bowel segments if the mesentery is involved. In malabsorption, the barium column may be somewhat segmented and flocculated (3, 9, 10). Treatment of eosinophilic gastroenteritis is conservative and consists of systemic steroid therapy. The roentgen signs may disappear within a few months after initiation of treatment (12, 14). In polyarteritis nodosa, the roentgen changes are caused
A 71-year-old Filipino man was first seen at Letterman Army Medical Center in November 1968 with anemia and an eosinophilia of 43 % which has persisted between 33 and 54 % ; platelets 800,OOO/mm3 ; and hematocrit 29-35 %. Radiologic evaluation revealed four separate pulmonary infiltrates from Jan. 1970 to May 1971, Three weeks prior to admission on 12 May 1971, dysphagia and diffuse abdominal pain developed. Upper gastrointestinal (Gl) series was negative. Laboratory data: hematocrit 24 %; platelets, 430,OOO/mm 3 ; white blood cells, 2,900/mm3 with a differential of 46 % neutrophils, 17 % lymphocytes, and 36 % eosinophils. Bone marrow aspirate was consistent with sideroblastic anemia with a high normal number of eosinophils. Twenty-four hours after admission, abdominal pain subsided, but recurred three days later and again subsided within 24 hours. An upper GI series on May 19 showed delayed gastric emptying and irregular gastric contour with a "cobblestone appearance" to the mucosa (Fig. 1). Small bowel examination revealed segmentation of the
Air contrast view of stomach. Note cobblestone appearance of mucosa.
One-hour follow-up film shows dilatation of proximal small bowel and flocculation of barium.
1 From the Department of Radiology (A. J. N., Resident), Letterman Army Medical Center, Presidio of San Francisco, Calif. 94129. Accepted for publication in February 1975. The opinions or assertations contained herein are the private views of the authors and are not to be construed as official, nor as reflecting the views of the Department of the Army or the Department of Defense. 2 Virginia Beach Hospital, Virginia Beach, Va. vb
NICKS AND FELIX HUGHES
Since the roentgenographic and clinical findings of the two conditions may appear similar, the radiologist should be familiar with the spectrum of both. REFERENCES
Fig. 3. Gastric biopsy. Note heavy round cell infiltrate, primarily plasma cells and focal lymphoid aggregates. Eosinophils are not prominent.
Fig. 4. Small bowel biopsy. Villi are reduced in size and focally thickened. Note increase in plasma cells in lamina propria. by ischemia and inflammation and may be similar to changes seen in eosinophilic gastroenteritis. This is especially true in the presence of malabsorption which occurs in both entities (4, 11, 18). Peripheral eosinophilia and pulmonary infiltrates may be present in both diseases. Numerous reports (1, 2, 6-8, 13, 15, 17, 19-22, 24) describing GI complications of polyarteritis nodosa have appeared in the medical literature. Some complications may present life-endangering abdominal emergencies, e.g., GI hemorrhage, perforation, and infarction. Other complications include small intestinal obstruction, peritonitis, pancreatitis, superior mesenteric artery thrombosis, and ulcerative enterocolitis. Maiolo et al. (16) have shown that early diagnosis and subsequent, properly timed, selective surgery have increased survival in patients with polyarteritis nodosa. If the diagnosis of eosinophilic gastroenteritis is mistakenly made, the potentially correctable lesions of polyarteritis nodosa may be masked if steroid treatment is begun. In addition, the complications of peroral gastric and jejunal biopsy may be increased.
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