Symptomatic eosinophilic gastritis cured with Helicobacter pylori eradication

Eosinophilic gastroenteritis is a disorder of unknown aetiology, characterised by eosinophilic infiltration of the gastric and intestinal mucosa and peripheral eosinophilia. To date, only two cases have reported the coexistence of Helicobacter pylori gastritis and eosinophilic gastroenteritis. In none of these cases was a causal association between these two entities documented.^1,2 We present a case of eosinophilic gastritis cured with H pylori eradication therapy.

A 44 year old woman presented with a two month history of vomiting, nausea, and crampy abdominal pain. Her past medical history included idiopathic thrombocytopenic purpura, splenectomy at the age of 11 years, hyperlipidaemia, hypertension, diabetes mellitus type II, and depression. Her medication included valsartan, atenolol, nifedipine, gliclazide, metformin hydrochloride, indapamide, and venlafaxine hydrochloride. No food allergy or intolerance was reported.

She lived on a Greek island and did not smoke or drink alcohol. Physical examination revealed only mild diffuse epigastric and abdominal tenderness, and no signs of systemic vasculitis or connective tissue disease were present. Laboratory evaluation revealed a white blood cells count of 14 900 cells/mm³ (normal 4000–10 000) with an eosinophilic count of 2680 cells/mm³ (normal 0–800), and a normal platelet count (187 000/mm³) and haemoglobin level (12.8 g/dl). Serum glucose was 158 mg/dl (normal 70–105), alanine aminotransferase 38 mU/ml (normal 10–28), γ-glutamyl transferase 44 mU/ml (normal 9–30), erythrocyte sedimentation rate 29 mm, and C reactive protein 9.19 mg/l (normal 0.00–6.00). Stool studies for ova and parasites and stool cultures were negative. Thyroid function tests, serum IgE, abdominal ultrasound, and computed tomography scan were normal. No findings of extra-abdominal malignancy were evident. Colonoscopy with terminal ileoscopy was normal, as was histology of the ileum and colon. Gastroscopy showed small erosions at the corpus, the antral mucosa, and the duodenal bulb. Biopsies were taken from the gastric corpus, antrum, and from the second part of the duodenum. Gastric biopsies showed H pylori infection and dense eosinophilic infiltration (29 eosinophils per high power field) of the gastric mucosa, but biopsies from the 2nd–3rd parts of the duodenum were normal.

She was discharged with a diagnosis of eosinophilic gastritis and H pylori erosive gastritis, and was treated with esomeprazole (40 mg/day), amoxycillin (1 g/day), and clarithromycin (1 g/d) for seven days. No treatment was given for eosinophilia. There were no known reports implicating her medications in the aetiology of her symptoms and so it was decided that she should remain on her regular medical treatment. Two months after completion of the eradication therapy repeat gastroscopy was normal. Gastric biopsies showed no H pylori infection and only trivial (five eosinophils per high power field) eosinophilic infiltration. She was symptom free, with a white blood count of 3280 cells/mm³ and a normal eosinophilic count of 780 cells/mm³. No significant change in platelet count was noted.

Ours is the third reported case of the coexistence of H pylori infection and eosinophilic gastroenteritis. In contrast with the previous cases, blood and tissue eosinophilia resolved completely after successful eradication of H pylori infection.

Although no confirmed association between H pylori gastritis and eosinophilic gastroenteritis can be documented in the literature, our case shows that H pylori may play a pathogenic role in the development of blood eosinophilia and eosinophilic gastroenteritis and that H pylori eradication may be of value in treating certain cases of this rare syndrome.