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CLINICAL VIGNETTE Eosinophilic GastroenteritisDaniel Cole, M.D., M.P.H.Eosinophilic syndromes have been well described in many organ systems. The lungs, skin, kidney, muscle, heart, brain, bone marrow all have associated eosinophilic infiltrative disorders. The gastroin-testinal tract is no exception and has an eosinophilic infiltrative disorder associated with it. Case ReportThe patient is a pleasant 44-year-old African American female in her usual state of excellent health until 8 weeks prior to admission to the hospital. She began to develop repeated episodes of nausea, vomiting, diarrhea and severe cramping abdominal pain, which were present most of the time. She denied any prior history of this. The symptoms were unremit-ting and the patient lost about 12 pounds. Her normal bowel pattern was one formed stool daily. Now she was having 4 to 6 watery stools per day with marked urgency. There was no rectal bleeding. There was very little smell to the stool since it was mostly water. One week before admission, she was seen in the Emergency Department (ED) and given compazine as well as hydration therapy. The patient returned to the ED the next day with the same symptoms. On both ED visits, the complete blood cell count and differen-tial showed an elevated white blood cell count (WBC) of about 12,000 with 45% eosinophilia. She was again discharged to her primary care physician. On the following day, she was admitted to the hospital for treatment of severe dehydration and evaluation of the symptom complex. The past history was unremarkable. She had no prior surgery and was not on any medication. Physical examination revealed a well-developed, well-nour-ished female complaining of abdominal pain and retching repeatedly. The vital signs were normal, as was the entire examination, except for the abdomen. This was soft with active bowel sounds but was diffusely moderately tender. There was no rebound or guarding. Reviewing her medical record revealed that, in 2004, she had a normal WBC and differential with 5% eosinophils. In May 2006, her WBC was 12,000 with 27% eosinophils. Two weeks later, the WBC was 14,000 with 45% eosinophils. To help document the presumptive diagnosis of eosinophilic gastroenteritis, an endoscopy and small bowel biopsy was done (Figures 1-2). The histology revealed large numbers of intraepithelial eosinophils but with no increase in lymphocytes. The villi appeared slightly edematous with prominent capillaries. The lamina propria was expanded by a mixed inflammatory infil-trate containing markedly increased numbers of eosinophils. The infiltrate also included scattered lymphocytes and plasma cells. The eosinophils focally infiltrated the crypt epithelium but no crypt abscesses were seen. No infectious organisms or gran-ulomas were seen. The vessels appeared normal without evidence of amyloid deposition or vasculitis.
Even before the biopsy was available the patient was started on prednisone 60 mg per day. Within 4 days, the patient was asymptomatic. DiscussionEosinophilic syndromes can affect virtually any organ of the body. Eosinophilic gastroenteritis is a well-described infiltrative disorder of the bowel usually involving the stomach and small bowel, causing a combination of diarrhea, nausea and vomiting, and cramping abdominal pain. Eosinophilic infiltrates have been seen in all areas of the intestine from esophagus to colon. Eosinophilic esophagitis is a separate entity and will not be discussed here. The case presented here is a very characteristic, almost classical presentation of the disease when it involves the small bowel. However, the actual presentation is dependent on which layer of the bowel is involved. If the disease is limited to the mucosa then most patients will present with diarrhea. If most of the small bowel is involved, the patients may even have signs and symptoms of malabsorption.1 The most common presenting symptoms were abdominal pain (100%), diarrhea (62.5%), vomiting (62.5%), and nausea (50%).2 When the muscle layer is involved the patient is more likely to present with symptoms of obstruction. This is more common with eosinophilic esophagitis but can also be seen with small bowel or gastric disease.3 Finally, serosal disease has been described as the cause of eosinophilic ascites. Generally, this will not occur in isolation but rather in conjunction with mucosal and/or muscular involvement. The etiology of eosinophilic gastroenteritis is unknown. About half of patients have an allergic history.1 Unfortunately, avoiding the allergen has no impact on the disease.4 The diagnosis can be made by a combination of laboratory and biopsy findings. Most patients will have a significant peripheral eosinophilia but this can be normal in up to 20% of patients.1 Parasitic infestation of the bowel can present in the same way and there-fore stool analysis to exclude Ancylostoma, Anisakis, Ascaris, Strongyloides, Toxicara, Trichura, Capillaria, and Trichinella needs to be done. The definitive diagnosis is with biopsy of the area involved. This has a characteristic eosinophilic infil-trate as described in this case. Most patients with eosinophilic gastroenteritis will require treatment. A small percentage of patients will remit sponta-neously.5 Treatment consists of prednisone 40 mg per day with rapid tapering after about 2 weeks. Most patients will notice a dramatic improvement of symptoms within 1 to 2 weeks. The subsequent course is quite variable. Some patients will never have recurrent problems and the steroids can be discontinued. Others may require low-dose steroids indefinitely since they relapse quickly after the steroids are stopped. Finally, some patients will require repeat treatment intermittently depending on the duration of the remission.2,3 There are no predictive signs of treatment response. Oral cromalyn has also been described as effective treatment but it does not work for all patients, as does prednisone.6 Eosinophilic gastroenteritis is an uncommon disease whose presentation is dependent on the area involved as well as the layer of wall involved. Fortunately, it is amenable to steroid therapy. REFERENCES
Submitted August 26, 2006 |
