Ulcerative and granulomatous colitis

Abstract

Inflammatory bowel disease includes several pathologic entities, although the term generally implies either nonspecific ulcerative or granulomatous colitis or ileocolitis. Before these two conditions are discussed, four etiologically specific abnormalities sometimes confused with ulcerative colitis require comment. lschemic colitis is often believed to be ulcerative colitis clinically, radiologically, and endoscopically. In an extensive form the grossly hemorrhagic and partly necrotic mucosa is distinctive (fig. 1A). The colon is grossly thickened, particularly the submucosa, as pointed out by Morson [1] (fig. 1B). The thumbprint appearance seen radiologically is not as evident pathologically. Microscopically, necrosis and ulceration of the mucosa are present, with submucosal hemorrhage, necrosis, and subsequently fibrosis. Leukocytes are increased in the mucosa and submucosa, but their numbers are fewer than in genuine inflammation. Small arteries and arterioles in the submucosa are abnormally thickened, narrowed, and locally nearly occluded by sclerosis. Veins may contain thrombi. The appearance at the time of biopsy or autopsy is usually that of a healing infarct [2] (fig. 1C). There is an analogy in that healing myocardial infarcts were once called chronic myocarditis. Proximal to a colonic stenosis, usually due to carcinoma, instances of “ulcerative colitis” have been reported [3]. The only such cases I have personally observed have had the gross and microscopic lesions of ischemic colitis. Schwartz [4] demonstrated that experimental intermittent obstruction of the rabbit colon by a balloon produced at first temporary and then persistent vasospasm, a precursor of ischemic degeneration and necrosis. Pseudomembranous colitis may also be confused with ulcerative colitis. There are patches or sheets of inflammatory exudate attached to the surface of a mucosa whose superficial half is locally necrotic (figs. 4 1D and 1E). Gram staining may show myriads of staphylococci in one specific subtype of pseudomembranous colitis [5], but more often the etiology is uncertain. After clindamycin or lincomycin therapy, the pseudomembranes are histologically distinguished by having narrow bases and mushroom-shaped spreading surfaces [6, 7]. Amebic colitis is probably the most important disease to distinguish from ulcerative colitis. Many examinations of stool or rectal scrapings may fail to demonstrate amebae, and the patient may undergo a colectomy for fulminant colitis (fig. iF). Only after histologic examination are the liquefactive type of inflammatory reaction and flask shaped ulcers recognized, and when amebae are found in the exudate, the correct diagnosis is made [8, 9]. Amebic colitis occasionally is associated with pseudopolyps or toxic megacolon, features usually attributed to ulcerative colitis. Balantidial colitis has been confused clinically and radiologically with ulcerative colitis, and treated by colectomy. Microscopically some crypts are dilated and contain leukocytes, but the process involves the entire crypt length and is not confined to the base as in ulcerative colitis (fig. 1G). The relatively large balantidium parasites are found in the crypts. This is said to be the rarest human parasitic colitis [10].