Phlegmonous gastritis in an ankylosing spondylitis patient treated with infliximab

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Korean J Intern Med. 2017;32(5):945-946
Publication date (electronic) : 2017 August 18
doi : https://doi.org/10.3904/kjim.2016.158
1Division of Rheumatology, Department of Internal Medicine, Gangneung Asan Hospital, University of Ulsan College of Medicine, Gangneung, Korea
2Division of Rheumatology, Department of Internal Medicine, Soonchunhyang University College of Medicine, Seoul, Korea
Correspondence to Hyun-Sook Kim, M.D. Tel: +82-2-709-3061 Fax: +82-2-709-9554 E-mail: healthyra@schmc.ac.kr
Received 2015 November 23; Revised 2016 January 6; Accepted 2016 January 13.
This article has been corrected. See Korean J Intern Med. 2017 Oct 27; 32(6): 1123.

A 51-year old man, with a 2-year history of ankylosing spondylitis (AS), was hospitalized for severe nausea and vomiting. On physical examination, his temperature was 37.5°C and his blood pressure was 138/86 mmHg. His laboratory findings were as follows: white blood cell count, 15,200/mm3 (neutrophils, 81.6%); hemoglobin, 9.4 g/dL; platelet count, 400,000/mm3; erythrocyte sedimentation rate, 74 mm/hr; and C-reactive protein, 4.00 mg/dL. He had been treated with infliximab beginning 6 months earlier and had last received it 2 weeks earlier. Abdominal computed tomography (CT) showed diffuse edematous submucosal wall thickening throughout the stomach and no specific findings in the colon (Fig. 1A and 1B). A characteristic feature of phlegmonous gastritis is the isolated thickening of the gastric wall, most marked in the submucosa. Esophagogastroduodenoscopy showed edematous, reddish mucosal change, and multiple ulcerative lesions on the greater curvature of the stomach. Diffuse ulcerative lesions on the fundus of the stomach were also detected (Fig. 1C). Phlegmonous gastritis was diagnosed based on CT and endoscopy findings. No phlegmonous gastritis pathogen was identified from cultures of blood, gastric aspirates, or tissue. The patient was treated conservatively with fluid resuscitation, a proton pump inhibitor, and broad-spectrum antibiotics including vancomycin and piperacillin/tazobactam for 3 weeks. Within a few days, the patient was afebrile and able to eat.

Figure 1.

(A, B) Computed tomography showed diffuse edematous submucosal wall thickening throughout the stomach, but no specific findings in the colon. (C) Esophagogastroduodenoscopy showed edematous, reddish mucosal changes, and multiple ulcerative lesions on the greater curvature of the stomach. Diffuse ulcerative lesions on the fundus of the stomach were also detected.

Phlegmonous gastritis is a rare, rapidly progressive, potentially fatal bacterial infection. Predisposing factors include mucosal injury, achlorhydria, and an immunocompromised state. Phlegmonous gastritis may follow a fulminating course involving early peripheral circulatory collapse or delayed gastric perforation. Sepsis and multiorgan failure are common. However, the rarity of this disease makes the diagnosis and choice of appropriate treatment difficult. Early recognition and therapy are important for survival. We report a case of phlegmonous gastritis in AS that was diagnosed early and treated successfully with broad-spectrum antibiotics.

Notes

No potential conflict of interest relevant to this article was reported.

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Figure 1.

(A, B) Computed tomography showed diffuse edematous submucosal wall thickening throughout the stomach, but no specific findings in the colon. (C) Esophagogastroduodenoscopy showed edematous, reddish mucosal changes, and multiple ulcerative lesions on the greater curvature of the stomach. Diffuse ulcerative lesions on the fundus of the stomach were also detected.