Haematologica 2002; 87:(01)ELT01
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Acute necrotizing gastritis by Escherichia coli in a severely neutropenic patient

Carmen Martínez-Chamorro, Elena Martínez*, Juan José Gil-Fernández, Antonio Escudero, Agustín Acevedo°, José Mª Fernández-Rañada
Hematology, Radiology* and Pathology° Departments; Clínica Ruber, C/ Juan Bravo, 49, 28006 Madrid, Spain.


Correspondence: Carmen Martínez-Chamorro, C/ General Oraá, 3-1º, 28006- Madrid, Spain. Phone: +34.1. 4111917. Fax: +34.1.4111853. E-Mail: m-chamorro@navegalia.com
Acute necrotizing gastritis is an extremely severe and uncommon condition in the antibiotic era. We report a case of acute necrotizing gastritis caused by Escherichia coli in a patient with severe acquired aplastic anemia, successfully managed with conservative therapy. Biopsy and culture of gastric mucosa established the diagnosis. A 59-year-old man with an unremarkable past medical history was diagnosed of severe aplastic anemia. He was treated with immunosuppressive therapy consisting of antithymocyte globulin (ATG) 20 mg/kg/day for 8 days and cyclosporine A (CyA) 5 mg/Kg/day. Methylprednisolone 1 mg/kg/day and omeprazole 40 mg/day were administered to prevent serum sickness and gastric toxicity, respectively. He did not receive any antimicrobial prophylaxis other than oral nystatin. On the 5th day of therapy, the patient developed severe non-irradiated, non-colicky, epigastric pain, hiccups, nausea and vomiting. Examination disclosed upper abdominal tenderness without signs of peritonitis. Serum amylase value was normal. Abdominal radiography was unremarkable. Computed tomography revealed marked thickening of the gastric walls with involvement of adjacent fat tissue (
Figure 1). ATG, CyA and corticoids were withdrawn, and morphine was added to relieve abdominal pain. On the 7th day, the patient showed intense vomiting yielding abundant fetid hematic material and his temperature rose to 38.6°C. Upper gastrointestinal endoscopy showed an extremely narrowed gastric lumen with diffuse involvement of the stomach walls and pyloric stenosis; resembling an infiltrative process. Gastric biopsy samples were taken for pathological examination and culture. The patient was treated with nasogastric tube drainage, empirical antimicrobial therapy with meropenem and amikacin and total parenteral nutrition. Gastric mucosa cultures yielded isolates of Escherichia coli and pathologic examination of biopsy specimens revealed extensive necrosis and a large amount of bacteria in gastric mucosa, but no neoplastic infiltration (Figure 2). The patient's clinical condition progressively improved and allowed satisfactory oral tolerance three weeks later. Immunosuppressive therapy with CyA and G-CSF was reintroduced. The patient was discharged with a partial response in granulocyte count and transfusion-dependent platelet and red blood cell counts. Acute necrotizing gastritis is a variant of phlegmonous gastritis1 and occurs secondary to an over-whelming necrobiotic infection.2 Since 1945, fewer than 50 cases of phlegmonous gastritis have been described.3,4 In spite of neutropenia leading to a significant propensity to infection, to our knowledge, acute necrotizing gastritis associated with neutropenia has not been reported in English literature. Besides, pre-operative diagnosis has been sparsely made. The pathogenesis is unclear, although described predisposing factors are mucosal injury, achlorhydria, immunocompromised states, upper respiratory and bucco-pharyngeal infections.5 Most cases have been caused by hemolytic streptococci (70%), but pneumococci, staphylococci, Proteus, Haemophilus influenzae, Escherichia coli and Clostridia have been also reported.6 In contrast to other reported cases, we did not observe infiltration of neutrophils or focal abscesses in the gastric wall, as inflammatory response to infection is limited in neutropenia. No distant infective focus was identified and blood cultures were negative. We hypothesized that omeprazole-induced hypochlorhydria, which might have altered gastric bacterial flora, neutropenia and immunosuppressive treatment, and gastric mucosal injury due to corticosteroids and thrombocytopenia might have facilitated the development of acute necrotizing gastritis. We conclude that acute necrotizing gastritis should be included in the differential diagnosis of acute epigastralgia in immunocompromised patients. Early diagnosis by endoscopy with biopsy and culture and prompt treatment with antibiotics and supportive measures are important in managing this life-threatening infection, especially in pancytopenic patients.

Key Words: necrotizing gastritis, Escherichia coli, neutropenia.

References

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