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Lawrence J. Brandt, MD, Associate Editor for Focal Points

Gastric malakoplakia

A 92-year-old woman was hospitalized because ofsyncope. Her medical history included GERD and type 2diabetes but no history or symptoms of infection, immu-nocompromise, or neoplasm. Physical examination wasunremarkable except for mild abdominal tenderness. A

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complete blood count revealed anemia. CT scan showedmoderate bilateral pleural effusions and a dilated esoph-agus. EGD revealed multiple friable polyps in the gastricbody, antrum, and pylorus associated with partial gastricoutlet obstruction (A) that was relieved by endoscopic

Volume 80, No. 5 : 2014 GASTROINTESTINAL ENDOSCOPY 903

At the Focal Point

dilation. Histology of the polyps showed the gastric lam-ina propria to be expanded by sheets of cytologicallybland histiocytes with lymphocytes, plasma cells, neutro-phils, and eosinophils (B). Histiocytes featured abundanteosinophilic cytoplasm containing round and targetoidcalcific inclusions characteristic of Michaelis-Gutmannbodies (C); this was confirmed with a von Kossa histo-chemical stain (D). The adjoining gastric mucosa showedchronic gastritis with focal intestinal metaplasia. No Heli-cobacter pylori was identified. The final diagnosis wasgastric malakoplakia causing bleeding and gastric outletobstruction.

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DISCLOSURE

All authors disclosed no financial relationships rele-vant to this article.

Xianzhong Ding, MD, PhD, Department of Pathology, TheMount Sinai Medical Center, New York, New York, USA,Andrew Oliff, MD, Joseph Rando, MD, Luthern MedicalCenter, Brooklyn, New York, USA, Noam Harpaz, MD,PhD, Department of Pathology, The Mount Sinai MedicalCenter, New York, New York, USA

http://dx.doi.org/10.1016/j.gie.2014.08.015

CommentaryMalakoplakia is a rare chronic granulomatous disease first described by von Hansemann in 1901 and reported by Michaelisand Gutmann in 1902. The term malakoplakia comes from the Greek “malakos” (soft) and “plakos” (plaque), reflecting itsusual appearance as a friable, yellow mucosal lesion. Microscopically, coliform bacteria often are located in the cytoplasm(phagolysosomes) of the lesion’s macrophages (von Hansemann bodies), and laminated intracytoplasmic inclusion bodies(Michaelis-Gutmann bodies) are considered diagnostic for this disorder. After the urinary tract, the GI tract is the secondmost common site of involvement, although many other organs may be affected including the lung, brain, adrenal glands,pancreas, and bone. Gastric involvement is very unusual, with 7 cases thus far reported. Although the pathogenesis ofmalakoplakia is unknown, infection is thought to play a role, especially because macrophage and monocyte killing ofmicro-organisms is defective. In the stomach, there does not seem to be any etiologic role for H pylori. Immunosuppression(patients at risk include those on chemosuppressive or immunosuppressive therapy, patients with AIDS, and variousimmunodeficiency states), systemic illness (eg, lupus and ulcerative colitis), neoplasia (usually found adjacent to themalakoplakia), and a genetic disorder are other postulated etiologies. Patients with GI malakoplakia usually present withfever and, because the most common GI location of malakoplakia is the colon, with abdominal pain, diarrhea, and hem-atochezia. Colonoscopy typically reveals 1 of 3 disease patterns: isolated (rectosigmoid) involvement (lesions appear asyellowish plaques that may be sessile, polypoid, and ulcerated with stricturing or fistulization), diffuse (characteristic ofimmunosuppressed patients), and focal (which may be adjacent to an adenomatous polyp or cancer). Histology revealsthe characteristic macrophages with voluminous cytoplasm that contains the classic von Hansemann bodies (intracellularorganisms) and Michaelis-Gutmann bodies (intracytoplasmic inclusion bodies concentrically laminated with iron and cal-cium). Treatment includes discontinuing or reducing immunosuppressive medications, if possible; antibiotics such astrimethoprim-sulfamethoxazole and ciprofloxacin; and cholinergic agents to reverse the defect in macrophage function.Sometimes surgical resection is needed. It never ceases to amaze me how the body protects itself from insult, whetherinfective, immunologic, inflammatory, or reactive, and how, when one form of protection is insufficient, another mecha-nism is conscripteddat least that is how I view the role of the walling-off cations in the Michaelis-Gutmann bodies. Isee this redundancy in cellular protective strategy as a physiologic equivalent of the “belt and suspenders” or “oars andsails” philosophy that sometimes gives us peace of mind in negotiating a difficult situation.

Lawrence J. Brandt, MDAssociate Editor for Focal Points

Pyobilia seen during small-bowel capsule endoscopy(with video)

An 89-year-old man presented to his local hospital withsyncope and melena. After negative results on bidirectionalGI endoscopy, he was referred to our department forconsideration of video capsule endoscopy, performedwith the PillCam SB2L (Given Imaging Ltd, Yoqneam,

Israel). The capsule was retained in a duodenal divertic-ulum, and the examination was incomplete because ofexhaustion of battery life. Nevertheless, spouting of pusfrom the ampulla of Vater was observed (A, Video 1, avail-able online at www.giejournal.org). At that point, the

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