Health Questions and Answers

Eosinophilic Gastroenteritis

How is the entity eosinophilic gastroenteritis defined?
Eosinophilic gastroenteritis is a rare, nonparasitic inflammatory disease of the gastrointestinal tract with various degrees of eosinophilic infiltration anywhere in the tubular intestinal tract and the biliary tree in the absence of vasculitis or significant extraintestinal tissue eosinophilia. Peripheral blood eosinophilia is present in up to 80%.

Why should one know features of this rare disease?
Although it is a rare disease, it is a treatable condition mimicking several gastrointestinal diseases. It presents most often with abdominal pain, diarrhea, nausea, vomiting, dysphagia, and gastric outlet obstruction.

What is the differential diagnosis of eosinophilic gastroenteritis?
Patients with eosinophils on intestinal biopsy or any form of inflammation with peripheral eosinophilia should be evaluated for the possibility of eosinophilic gastroenteritis. Many other diseases, however, can produce similar findings.

How is irritable bowel syndrome (IBS) differentiated from eosinophilic gastroenteritis?
Peripheral eosinophilia is absent in 20% of the patients with eosinophilic gastroenteritis, reinforcing the need to examine mucosa with biopsies. Careful review of the colonic histology can usually distinguish IBS by its lack of mucosal eosinophils.

How is gastroesophageal reflux disease (GERD) distinguished from eosinophilic gastroenteritis?
Solid food dysphagia without a history of heartburn among persons with allergic disorders should raise a red flag and suggest the diagnosis of eosinophilic esophagitis. Endoscopy is remarkable for an absence of typical esophagitis seen with GERD and the presence of subtle granularity with furrows or rings seen frequently with eosinophilic esophagitis. Deep biopsies of normal and abnormal mucosal sites in the esophagus, stomach, and duodenum are recommended. In gastroesophageal reflux esophagitis, intraepithelial eosinophils are present (<5 per high power field, but the eosinophilic cell count depends on the absolute thickness of the microscopic sample slice) and vanish usually under acid suppression therapy.

How is intestinal parasitic infestation or extraintestinal disease diagnosed?
Ancylostoma (hookworm), Anisakis, Ascaris, Capillaria, Isospora belli (immunocompromised patients), Strongyloides, Toxocara, Trichuris trichiura, and Trichinella are diagnosed by using concentration methods in several fresh stool samples (sedimentation methods, after fixation with ethyl-acetate formalin for ova and cysts, or polyvinyl alcohol fixatives for protozoan trophozoites).

How do you distinguish between allergies and eosinophilic gastroenteritis?
Allergies to food (e.g., cow’s milk, gliadin), dusts, or medications (e.g., gemfibrozil, clofazimine, gold salt, azathioprine, sulfamethoxazole, carbamazepine, l-tryptophan, enalapril) can imitate eosinophilic gastroenteritis and are often suggested as the pathogenetic mechanism in the pediatric literature. A thorough history and removal of the inciting agent can elucidate the cause.

What is eosinophilia-myalgia syndrome?
This l-tryptophan-induced syndrome is associated with cutaneous, hematologic, and visceral inflammation with infiltration of eosinophils as well as macrophages and lymphocytes. Immediate withdrawal of l-tryptophan can be lifesaving.

Describe the idiopathic hypereosinophilic syndrome.
This rare, often lethal multisystemic eosinophilic organ infiltration affects the lungs, heart, kidneys, brain, and gut, with peripheral blood eosinophilia (eosinophils above 1.5 K); persists for at least 6 months; and is associated with gastroenteritis in 14% of cases. The tyrosine kinase inhibitor imatinib offers a new therapeutic option in 90% of patients.

How is malignant bowel obstruction similar to eosinophilic gastroenteritis?
It can present with peripheral blood eosinophilia. Examples are gastric, colonic, and pancreatic tumors, further hematologic malignancies as Hodgkin’s lymphoma, mycosis fungoides, chronic myelogenous leukemia, or extraintestinal adenocarcinomas of the lung, ovary, or uterus.

What is the etiology of eosinophilic gastroenteritis? Describe the pathophysiologic background of eosinophilic gastroenteritis.
This immune-mediated disease is most likely the result of several different factors affecting the immunologic regulation (i.e., allergic, autoimmune). A single etiologic factor is not yet known.

Why does eosinophilic gastroenteritis have so many different clinical faces?
The anatomic location of the affected organs and the depth of the inflammatory infiltration of the intestinal wall layers and of the surrounding visceral structures determine the clinical manifestation. Examples include:

  • Mucosal eosinophilic infiltration without muscular involvement
  • Inflammation of the intestinal muscle layer (muscularis propria)
  • Subserosal/serosal inflammation (present in 10%)

What symptoms and signs suggest a probable diagnosis of eosinophilic gastroenteritis?
Dependent on the involved anatomic structures, eosinophilic gastroenteritis presents as dyspepsia, dysphagia/chest pain, gastric outlet obstruction, duodenal obstruction, gastroduodenal ulcer disease, diarrhea, malabsorption syndrome, protein-losing enteropathy, intestinal blood loss, enteritis syndrome, obstruction of the small or large intestine, intestinal perforation, peritoneal disease with ascites, biliary obstruction, periampullary tumor, or pancreatitis. Peripheral eosinophilia is present in most (80%) but not all patients with eosinophilic gastroenteritis.

What are possible x-ray features of eosinophilic gastroenteritis?
Gastric retention, small intestinal hypomotility, or obstruction can be demonstrated by barium studies. Double contrast barium enema or enteroclysis can show mucosal thickening with a cobble-stoned or saw-tooth silhouette, nodular filling defects, or coarse folds in the small intestine. It can mimic regional enteritis (Crohn’s disease). Eosinophilic esophagitis presents with circumferential rings or feline esophagus. Muscle layer disease presents with stiffened and narrowed tubular gut structures, complicated by obstruction of the esophagus, gastric outlet, duodenum, jejunum, ileum, or colon. Computer tomography or MRI imaging can reveal duodenal, jejuno-ileal, or colonic wall thickening, inflammatory tumors, or ascites.

What should one exclude in patients with suspected eosinophilic gastroenteritis?

  • Drug-induced: aspirin, gold therapy, gemfibrozil, clofazimine, l-tryptophan, enalapril
  • Intestinal parasites
  • Inflammatory bowel disease or collagenous colitis
  • Collagen-vascular disease: PAN, SLE, systemic sclerosis, dermatomyositis, Churg-Strauss syndrome
  • Malignant infiltration
  • Lymphoma: Sezary T-cell and intestinal lymphomas, chronic myelogenous leukemia, Hodgkin’s disease.

How should one treat eosinophilic gastroenteritis?
Traditionally, glucocorticoid therapy is recommended. Oral prednisone 0.5 mg/kg/day for a period of 2 weeks will induce remission in 90% of patients, irrespective of the affected gut layer. Most patients do not require maintenance therapy; however, a small number will require 2-3 months of corticosteroid therapy for symptoms to resolve. Severe disease should be treated with parenteral methylprednisolone (bolus of 125 mg followed by 0.5 mg/kg/day b.i.d.). Even in severe duodenal obstruction, a parenteral glucocorticoid therapeutic trial is recommended before surgery is considered.
Recurrences occur in up to 40% and can be treated with repeat short courses of prednisone. Topical corticosteroids have been reported to be effective. Cases of eosinophilic esophagitis have clinically and histologically responded to fluticasone propionate MDI that are swallowed NOT inhaled. One report documented effectiveness of nonenteric coated budesonide (formula of water soluble tablets produced for rectal enema dissolutions) in gastric transmural eosinophilic gastroenteritis with ascites.
Nonglucocorticoid immune-modulatory therapies may be an alternative in the future:

  • Montelukast: a leukotriene1-receptor antagonist
  • Suplatast tosilate: a leukotriene inhibitor (not available in the US)
  • Cromoglycate sodium: a mast cell stabilizer
  • Ketotifen: a mast cell stabilizer

Elemental diet was used for a period of 1-3 months with some success in pediatric patients. In suspected food allergy a trial elimination diet can rarely elucidate the individual pathogenesis and resolve the disease in a few patients. Symptomatic treatment includes adequate pain relief, loperamide for diarrhea, and supplementation of deficiencies acquired by malabsorption.

References

WEBSITES
http://www.vhjoe.com
http://www.dave1.mgh.harvard.edu/

BIBLIOGRAPHY

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