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REVIEW

Gastrointestinal Cytomegalovirus Disease

Richard W. Goodgame

1 November 1993 | Volume 119 Issue 9 | Pages 924-935

Objective: To describe the pathogenesis of gastrointestinal cytomegalovirus (CMV) disease, the types and locations of gastrointestinal lesions, the clinical settings in which they occur, and the specific methods available to diagnose and treat the disease.

View larger version (167K): [in this window] [in a new window]   Figure 1. Endoscopic gastric mucosal biopsy specimen from an AIDS patient with severe nausea, vomiting, and epigastric pain. The gastric glands are normal except for the typical cytomegalic cell indicating cytomegalovirus infection. The cell shows a large, densely staining nucleus and abundant cytoplasm with intracytoplasmic inclusions (original magnification, x 400).

 

View larger version (113K): [in this window] [in a new window]   Figure 3. A surgical specimen from an AIDS patient who had a small-bowel resection for a perforated cytomegalovirus ulcer. Special stains for cytomegalovirus (CMV) are shown. Left. Cytomegalic cells were rare in the glandular epithelium of this patient, but they were easily identified by this in-situ DNA hybridization that stains the enlarged nucleus purple (original magnification, x 200). Center. In the same patient, many smooth muscle cells and fibroblasts stain purple, indicating the presence of CMV DNA (original magnification, x 400). Right. Immunoperoxidase stain (using a monoclonal antibody against a CMV antigen) that stains infected cells brownish-red (original magnification, x 400).

 

View larger version (76K): [in this window] [in a new window]   Figure 4. Routine histologic section from the patient described in (Figure 3). Left. The many cytomegalic cells show infection of various cell types including vascular endothelium (small arrow), fibroblasts (medium arrow), and smooth muscle cells (large arrow) (original magnification, x 200). Right. Most of the endothelial cells in the three blood vessels shown are cytomegalic. Ischemia as a result of vascular occlusion may be important in the pathogenesis of ulceration (original magnification, x 200).

 

View larger version (51K): [in this window] [in a new window]   Figure 2. Three endoscopic photographs of gastrointestinal cytomegalovirus disease causing mucosal ulceration. Left. Esophageal ulcer in a 25-year-old AIDS patient. Center. Ulcer in the gastric cardia seen by retroflexing the endoscope back toward the gastroesophageal junction. The patient was a 57-year-old man receiving corticosteroid therapy for severe chronic obstructive lung disease. Right. A yellow-based, irregular, colonic ulcer in a 54-year-old renal transplant patient.

 
Data Sources: Relevant English-language articles were identified through a MEDLINE search from 1985 to 1992. Articles referenced in the bibliographies of these articles and others were searched by hand.

Study Selection: All articles that documented the occurrence of gastrointestinal CMV infection in humans, based on the finding of typical cytomegalic cells in histologic specimens, were selected for review.

Data Extraction: Studies were grouped by content pertaining to pathogenesis, clinical setting, gastrointestinal location, diagnosis, or treatment.

Data Synthesis: Gastrointestinal CMV disease is an erosive or ulcerative process that can occur at any location in the gastrointestinal tract, from mouth to rectum. Cytomegalovirus infection of columnar epithelial cells, endothelial cells, myocytes, and fibroblasts causes tissue destruction and ulceration. Serious CMV disease most frequently occurs with immune deficiency, such as the acquired immunodeficiency syndrome, after organ transplantation, after cancer chemotherapy, and after steroid therapy. Symptoms and signs depend on which part of the gastrointestinal tract is involved. Diagnosis depends on a positive mucosal biopsy that shows the presence of CMV by histopathologic or other techniques. In patients with persistent immune deficiency, progressive intestinal disease and death are frequent. Treatment with ganciclovir or foscarnet often heals intestinal lesions.

Conclusions: Internists should be aware of the various clinical settings and locations in the gastrointestinal tract in which CMV disease occurs. Patients with immune deficiency and gastrointestinal signs and symptoms should have imaging tests and mucosal biopsies to investigate the possibility of CMV intestinal disease. Treatment with antiviral chemotherapy improves outcome in many patients.

Author and Article Information

From Baylor College of Medicine, Houston, Texas.
Requests for Reprints: Richard Goodgame, MD, Baylor College of Medicine, One Baylor Plaza, Room 525D, Houston, TX 77030.
Acknowledgments: The author thanks Dr. Robert Genta for preparing the pathology specimens for Figures 1, 3, and 4 and taking the photoµgraphs; Dr. Boris Yoffe for helping with the immunohistochemical stains shown in Figure 3; Dr. Atilla Ertan for taking the photograph in Figure 2, Right; and Drs. Linda Rabeneck, Wayne Shandera, Thomas Cate, Stephen Greenberg, and Fred Sutton for their suggestions and assistance.
Grant Support: In part by clinical research grants from the American College of Gastroenterology and the American Society for Gastrointestinal Endoscopy.

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