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The Pathogenesis of Ulcerative Colitis; Apparent Precipitation of Acute Episodes by Standard Enemas

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Abstract

FOR many years there has been no agreement as to the pathogenesis of ulcerative colitis. In the numerous published studies on the subject the theory that infection is the cause has predominated. Bargen and Buie1 believed that a Diplococcus was the specific etiologic agent, and treated patients with a vaccine prepared from this Enterococcus. Felsen,2 among others, believed that ulcerative colitis resulted from bacillary dysentery, and reported that positive cultures were obtained from 17.7 percent of his patients. He also reported high agglutination titers from blood specimens of his patients, an observation not confirmed by others. Brown,3 on the other hand, observed that in 650 cases of proved bacillary dysentery, ulcerative colitis did not develop. In addition, Brown and Bargen4 stated that after a severe epidemic of bacillary dysentery that required hospitalization of 140 patients and resulted in 15 deaths, chronic ulcerative colitis was seen in only one patient. After World War II, during which our soldiers were stationed throughout the world and lived in many areas where amebiasis is endemic, a number of patients were seen with the typical proctoscopic and roentgenographic evidence of ulcerative colitis, but with amebas in the feces. Specific antiamebic therapy was effective in nearly 50 percent of these patients; the remainder continued to have signs and symptoms of ulcerative colitis. Other clinicians5 have observed the same relationship of ulcerative colitis to amebiasis.

The possibility remains that a specific virus or as yet unknown bacteria or other organisms may be the etiologic factor, but studies . . .


 

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