Diagnostic Radiology
•
The Cathartic Colon: Pathological Findings and Radiological/Pathological Correlation 1
•
Frank P. Urso, M.D., May J. Urso, M.D., and Chlu H. Lee, M.D. Cathartic colon has been described radiologically, but the pathological characteristics have not been reported. The authors describe a case in which radiological/pathological correlation was possible, with emphasis on the pathology of the colon. The disease simulates chronic ulcerative colitis radiological. ly and pathologically. INDEX TERMS:
Cathartics. Colitis, ulcerative. Colon, abnormalities
Radiology 116: 557-559, September 1975
•
•
1943, Heilbrun first called attention to chronic laxative abuse as a cause of severe abnormalities of the terminal ileum and colon (1). In the subsequent 30 years the radiological similarity between the purged colon and chronic ulcerative colitis has been described well (1-7), but we still have little knowledge of the underlying pathology. The exact clinical significance remains obscure, and the entity has remained in the realm of the radiologist (1, 2). The rare opportunity to obtain a precise pathological description and radiological correlation in a case of cathartic colon prompted this communication.
I
N
CASE REPORT A 42-year-old white woman was admitted for recurrent urinary tract infection with occasional blood-streaked stools. Physical examination was unremarkable, and laboratory values were normal except for an albumin level of 2.4 g/100 ml. A barium-enema study revealed reflux into the terminal ileum, a shortened colon, lack of haustrations, and an abnormal terminal ileum and colonic mucosa, as well as a 5-cm filling defect in the sigmoid. The radiological impression was long-standing ulcerative colitis and carcinoma (Fig. 1). Sigmoidoscopy revealed edema and punctate ulcerations. The biopsy sample was interpreted as chronic ulcerative colitis. At laparotomy, the small bowel was normal except for a dilated and atonic distal ileum. The colon was dilated, atonic, and foreshortened, and haustrations were absent. The operative impression was chronic ulcerative colitis and carcinoma. A subtotal colectomy was performed. The distribution of the disease process in the resected colon and the absence of characteristic features of chronic ulcerative colitis led to a detailed medical history. The patient had constipation rather than diarrhea, and there was nothing to suggest ulcerative colitis. She was unduly concerned about her bowel movements and admitted taking two tablets of Dulcolax daily for 4 years. Her husband disclosed that she had been taking laxatives habitually for at least 18 years. A previous barium-enema study performed 11 years earlier was normal, but plain abdominal films taken 6 years earlier revealed a dilated, air-filled cecum and loss of haustral markings. Unexplained hypokalemia and hypoalbuminemia had been noted on previous admissions.
approximately 130 cm) were removed. The colon (especially the cecum) was dilated, atonic, and lacking in mucosal haustrations. The serosa showed no evidence of inflammation. The ileal mucosa was swollen and the lumen dilated. The ileal wall was 0.4 cm thick, the colonic wall 0.6 cm. The colonic mucosa was smooth, thinned and atrophic. Multiple punctate superficial ulcerations 2-3 mm in diameter were distributed randomly throughout the colon. The ileocecal valve was distorted and incompetent and the colon foreshortened. Minute submucosal retention cysts were present. The sigmoid contained one pedunculated polyp measuring 5 cm and 2 identical but smaller polyps (0.5 cm) (Fig. 2). The predominant histopathological changes were confined to the mucosa and submucosa (Fig. 3). The mucosa and the lamina propria were infiltrated by mononuclear cells, chiefly plasma cells, lymphocytes, and eosinophils. Severe mucosal atrophy was characterized by areas where a single layer of tall columnar epithelium cells replaced the normal glandular pattern. The colonic glands contained less intracellular and intraluminal mucus than normal. Exuberant crypt abscesses, as seen in active ulcerative colitis, were not present. Superficial ulcerations disrupted the muscularis mucosae focally; it was mixed with fibrous tissue, with strikingly disorganized proliferation and hypertrophy. In some areas the muscularis was replaced by fibrosis, though not enough to produce narrowing or strictures. Transmural inflammation characteristic of Crohn's disease and exuberant granulation tissue (pseudopolyps) of chronic ulcerative colitis were absent. Buried cystic colonic glands were mixed with muscularis mucosae and fibrous tissue haphazardly, producing the appearance of colitis cystica profunda. Increased submucosal fat was present focally. Disorderly proliferation of submucosal nerve fibers was seen, with an apparent decrease in neurons in both Meissner's and Auerbach's plexuses. A prominent mononuclear infiltrate was observed in some perineural spaces. The polyps were characterized by haphazardly arranged fibrous tissue containing colonic glands and inflammatory cells.
DISCUSSION Since Heilbrun's initial radiological description in 1943, surprisingly few cases of cathartic colon have been reported in the literature; anatomical descriptions of the colon have been rare (8), and there have been no illustrations of the pathological changes. Operative descriptions are few and vague (7). In the largest series reported, containing 27 cases, no surgical specimens were studied (6). All patients had a history of many years of habitual laxative abuse, commonly more than 15 years (4). Previous cases have all been associated with aloin, podophyllum, extract of cascara, senna, castor oil, jalap, colocynth, phenolphthalein, or elaterin, all of which are classified as irritant laxatives (9). The mechanism of action is not thoroughly understood; however. it has been attributed to irritation of the small and large bowel mucosa and stimulation of nerve endings (9). In addition to nonprescription laxatives. Dulcolax (blsacodylf was also used in this instance; it is classified as a stimulant laxative which has an irritant action pre-
PATHOLOGICAL FINDINGS At colectomy, 20 cm of ileum and 45 cm of colon (normal,
1 From the Department of Pathology, Akron City Hospital, Akron, Ohio (F. P. U., Chairman; Director of Clinical Laboratories; C. H. L., Chief Resident), and the Department of Radiology, Case Western Reserve University, Cleveland, Ohio (M. J. U., Senior Instructor). Revised version acceptedfor publication in February 1975. 2 bis (p-acetoxyphenyl)-2-pyridylmethane. sjh
557
I
Fig. 1. A. Admission plain film ot the abdomen shows three enteric-coated Dulcolax capsules. Marked shortening of the colon and loss of haustrations are evident. B. Barium-enema study demonstrates a severely affected colon with loss of Iiaustrations, marked shortening, and questionable pseudopolyposis. Note the incompetent ileocecal valve and involvement of the terminal ileum, interpreted as "backwash ileitis." No strictures are present, and involvement is most severe on the right side. An obvious sigmoid mass is present. C. Note the relatively normal rectum, which remains distensible. The large filling defect (arrow) was interpreted as carcinoma. Fig. 2. Resected terminal ileum and colon, showing marked shortening and dilatation, loss of haustral folds, an extremely smooth, flat, atrophic mucosa, and punctate ulcerations. Note the large inflammatory polyp and the absence of significant thickening of the ileum and colonic wall. The ileocecal valve is distorted. Fig. 3. Photomicrograph shows predominantly mucosal and submucosal involvement, with mucosal atrophy alternating with heapedup colonic glands. Fibrosis involves the muscularis mucosae and submucosa. Submucosal lymphoid aggregates, a mononuclear cell infiltrate, and fat can be seen. (20 X)
Vol. 116
559
THE CATHARTIC COLON
dominantly on the colonic mucosa and acts on parasympathetic nerve endings, stimulating peristalsis. An occasional case of Dulcolax abuse resulting in a cathartic colon has been reported (10). Bulk and emollient laxatives have not been incriminated. Clinically, the paradox of a barium enema suggesting chronic ulcerative colitis in the presence of constipation should raise the suspicion of chronic laxative abuse, often seen in white women with early and severe involvement of the cecum (1-8). Although a characteristic history may substantiate the diagnosis. the personality of some patients makes an accurate history difficult; questioning a close relative may confirm the suspicion and prevent unnecessary surgery. Despite severe radiological changes, most patients are asymptomatic except for chronic constipation and dependency on laxatives. Since surgical specimens are usually not available, the pathology of the disease has not been fully appreciated, so that diagnosis by biopsy remains unreliable. Only a reference to melanosis coli was found in the pathology literature (11). The extensive fibrosis of Crohn' s disease is absent in cathartic colon (12, 13). The pathological findings, particularly the superficial mucosal ulceration, resemble those of chronic ulcerative colitis; however, strictures, marked ulceration, crypt abscesses, and pseudopolyposis are lacking (11). The most striking feature in our patient was mucosal atrophy, which is not common in ulcerative colitis. Colonic biopsy in the absence of an accurate history poses a difficult diagnostic problem because similar histological changes are described in the "burned-out" phase of chronic ulcerative colitis. Some reports have stated that shortening of the colon is not a prominent feature (~ 4, 7). In our case. shortening was marked throughout and was appreciated both radiologically and pathologically. Few reports have indicated that some shortening may occur in the hepatic flexure (5, 6). Absence of marked fibrosis accounts for continued distensibility of the colon and rectum and reversibility of radiological changes following cessation of laxative use (1, 2, 4, 5, 8). The inconstant narrowing can be attributed to spasms and to the marked hypertrophic muscularis mucosae, similar to that described in chronic ulcerative colitis (14). Many of the changes described may represent a nonspecific response to injury, and the individual histopathological changes also occur in other forms of colitis. Smith demonstrated that the laxative senna resulted in injury to the myenteric plexus in mice and concluded that this was a direct toxic effect (13). The cecum is universally affected radiologically and is the most severely diseased structure pathologically. The extensive alterations in the cecum and ileocecal valve exist to a lesser degree in the terminal ileum, contrary to the findings in Crohn's disease. Slit-like ulcerations deep in the wall of the colon and transmural inflammation are not present (14-20), and fistulas and perianal disease have not been reported in this disorder. The polyps described are classified as inflammatory and are not considered neoplastic or premalignant; rather, they are the result of longstanding inflammation. (It should be stressed that these polyps are histologically distinct and are not adenomatous; they may arise from foci of colitis cystica profunda.) Unlike ulcerative colitis, the rectum in our patient was normal on radiological examination 13 years ago and is now only minimally involved. Hypokalemia and hypoalbuminemia both occur in catharticinduced factitious diarrhea (10). Albumin loss has been dem-
Diagnostic Radiology
onstrated in the gastrointestinal tract. Small-bowel biopsy has not shown significant changes (10). The changes in our patient's colon were severe, and we conclude that albumin loss most likely occurred through the colonic mucosa. Cathartic colon should be considered as another cause of protein-losing enteropathy. Approximately 10% of inflammatory bowel disease is presently unclassifiabJe pathologically (21). Radiology remains the primary method of diagnosis of cathartic colon, a~hough confirmation by biopsy is possible. Since the rectum is usually minimally involved, rectal biopsy may not be representative. Extreme mucosal atrophy should alert the pathologist to consider laxative abuse. ACKNOWLEDGMENT: We wish to thank Ms. Jane Pringle for her help with the manuscript. Department of Pathology Akron City Hospital 525 E. Market St. Akron, Ohio 44309
REFERENCES 1. Heilbrun N: Roentgen evidence suggesting enterocolitis associated with prolonged cathartic abuse. Radiology 41:486-491, Nov 1943 2. Sieisenger MH, Fordtran JS: Gastrointestinal Disease. Philadelphia, Saunders, 1973, pp 1528-1531 3. Margulis AR, Burhenne HJ, ad: Alimentary Tract Roentgenology. St. Louis, Mo., Mosby, 2d Ed, 1973, pp 763-766 4. Heilbrun N, Bernstein C: Roentgen abnormalities of the large and small intestine associated with prolonged cathartic ingestion. Radiology 65:549-556, Oct 1955 5. Jewell FC, Kline JR: The purged colon. Radiolqgy 62:368370, Mar 1954 6. Plum GE, Weber HM, Sauer WG: Prolonged cathartic abuse resulting in roentgen evidence suggestive of enterocolitis. Am J Roentgenol 83:919-925, May 1960 7. Ziter FMH Jr: Cathartic colon. New York J Med 67:546549, 15 Feb 1967 8. Lemaitre G, L'Hermine C, Decoulx M, et a\: Aspect radiologique des colites chroniques par abus de laxatifs: propos de quatre observations. J Beige Radiol 53:339-345, Sep-Oct 1970 (Fre) 9. Goodman LS, Gilman A, ed: The Pharmacological Basis of Therapeutics. New York, Macmillan, 4th Ed. 1970, pp 1020-1030 10. Heizer WD, Warshaw AL, Waldmann TA, et al: Protein-losing gastroenteropathy and malabsorption associated with factitious diarrhea. Ann Intern Med 68:839-852, Apr 1968 11. Horn RC Jr: Alimentary tract. [lnJ Anderson WAD, ad: Pathology. 81. Louis, Mo., Mosby, 6th Ed, 1971, pp 88 and 1133-1135 12. Jones FA: Cathartic colon. Proc R Soc Med 60:503-504, May 1967 13. Smith B: Effect of irritant purgatives on the myenteric plexus in man and the mouse. Gut 9:139-143, Apr 1968 14. Goulston SJM, McGovern VJ: The nature of benign strictures in ulcerative colitis. N Engl J Med 281:290-295, 7 Aug 1969 15. Mottet NK: Histopathologic Spectrum of Regional Enteritis and Ulcerative Colitis. Philadelphia, Saunders, 1971, pp 63-154 16. Crohn BB, Berg AA: Right-sided (regional) colitis. JAMA 110:32-37, 1 Jan 1938 17. Lockhart-Mummery HE, Morson BC: Crohn's disease (regional enteritis) of the large intestine and its distinction from ulcerative colitis. Gut 1:87-105, Jun 1960 18. LOCkhart-Mummery HE, Morson BC: Crohn's disease of the large intestine. Gut 5:493-509, Dec 1964 19. McGovern VJ, Goulston SJM: Crohn's disease of the colon. Gut 9: 164-176, Apr 1968 20. McGovern VJ: The differential diagnosis of colitis. Pathol Ann 4:127-158, 1969 21. Price AB, Morson BC: Inflammatory band disease (the surgical pathology of Crohn's disease and ulcerative colitis). Hum Pathol 6:7-29, Jan 1975
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•
The Cathartic Colon: Pathological Findings and Radiological/Pathological Correlation 1
•
Frank P. Urso, M.D., May J. Urso, M.D., and Chlu H. Lee, M.D. Cathartic colon has been described radiologically, but the pathological characteristics have not been reported. The authors describe a case in which radiological/pathological correlation was possible, with emphasis on the pathology of the colon. The disease simulates chronic ulcerative colitis radiological. ly and pathologically. INDEX TERMS:
Cathartics. Colitis, ulcerative. Colon, abnormalities
Radiology 116: 557-559, September 1975
•
•
1943, Heilbrun first called attention to chronic laxative abuse as a cause of severe abnormalities of the terminal ileum and colon (1). In the subsequent 30 years the radiological similarity between the purged colon and chronic ulcerative colitis has been described well (1-7), but we still have little knowledge of the underlying pathology. The exact clinical significance remains obscure, and the entity has remained in the realm of the radiologist (1, 2). The rare opportunity to obtain a precise pathological description and radiological correlation in a case of cathartic colon prompted this communication.
I
N
CASE REPORT A 42-year-old white woman was admitted for recurrent urinary tract infection with occasional blood-streaked stools. Physical examination was unremarkable, and laboratory values were normal except for an albumin level of 2.4 g/100 ml. A barium-enema study revealed reflux into the terminal ileum, a shortened colon, lack of haustrations, and an abnormal terminal ileum and colonic mucosa, as well as a 5-cm filling defect in the sigmoid. The radiological impression was long-standing ulcerative colitis and carcinoma (Fig. 1). Sigmoidoscopy revealed edema and punctate ulcerations. The biopsy sample was interpreted as chronic ulcerative colitis. At laparotomy, the small bowel was normal except for a dilated and atonic distal ileum. The colon was dilated, atonic, and foreshortened, and haustrations were absent. The operative impression was chronic ulcerative colitis and carcinoma. A subtotal colectomy was performed. The distribution of the disease process in the resected colon and the absence of characteristic features of chronic ulcerative colitis led to a detailed medical history. The patient had constipation rather than diarrhea, and there was nothing to suggest ulcerative colitis. She was unduly concerned about her bowel movements and admitted taking two tablets of Dulcolax daily for 4 years. Her husband disclosed that she had been taking laxatives habitually for at least 18 years. A previous barium-enema study performed 11 years earlier was normal, but plain abdominal films taken 6 years earlier revealed a dilated, air-filled cecum and loss of haustral markings. Unexplained hypokalemia and hypoalbuminemia had been noted on previous admissions.
approximately 130 cm) were removed. The colon (especially the cecum) was dilated, atonic, and lacking in mucosal haustrations. The serosa showed no evidence of inflammation. The ileal mucosa was swollen and the lumen dilated. The ileal wall was 0.4 cm thick, the colonic wall 0.6 cm. The colonic mucosa was smooth, thinned and atrophic. Multiple punctate superficial ulcerations 2-3 mm in diameter were distributed randomly throughout the colon. The ileocecal valve was distorted and incompetent and the colon foreshortened. Minute submucosal retention cysts were present. The sigmoid contained one pedunculated polyp measuring 5 cm and 2 identical but smaller polyps (0.5 cm) (Fig. 2). The predominant histopathological changes were confined to the mucosa and submucosa (Fig. 3). The mucosa and the lamina propria were infiltrated by mononuclear cells, chiefly plasma cells, lymphocytes, and eosinophils. Severe mucosal atrophy was characterized by areas where a single layer of tall columnar epithelium cells replaced the normal glandular pattern. The colonic glands contained less intracellular and intraluminal mucus than normal. Exuberant crypt abscesses, as seen in active ulcerative colitis, were not present. Superficial ulcerations disrupted the muscularis mucosae focally; it was mixed with fibrous tissue, with strikingly disorganized proliferation and hypertrophy. In some areas the muscularis was replaced by fibrosis, though not enough to produce narrowing or strictures. Transmural inflammation characteristic of Crohn's disease and exuberant granulation tissue (pseudopolyps) of chronic ulcerative colitis were absent. Buried cystic colonic glands were mixed with muscularis mucosae and fibrous tissue haphazardly, producing the appearance of colitis cystica profunda. Increased submucosal fat was present focally. Disorderly proliferation of submucosal nerve fibers was seen, with an apparent decrease in neurons in both Meissner's and Auerbach's plexuses. A prominent mononuclear infiltrate was observed in some perineural spaces. The polyps were characterized by haphazardly arranged fibrous tissue containing colonic glands and inflammatory cells.
DISCUSSION Since Heilbrun's initial radiological description in 1943, surprisingly few cases of cathartic colon have been reported in the literature; anatomical descriptions of the colon have been rare (8), and there have been no illustrations of the pathological changes. Operative descriptions are few and vague (7). In the largest series reported, containing 27 cases, no surgical specimens were studied (6). All patients had a history of many years of habitual laxative abuse, commonly more than 15 years (4). Previous cases have all been associated with aloin, podophyllum, extract of cascara, senna, castor oil, jalap, colocynth, phenolphthalein, or elaterin, all of which are classified as irritant laxatives (9). The mechanism of action is not thoroughly understood; however. it has been attributed to irritation of the small and large bowel mucosa and stimulation of nerve endings (9). In addition to nonprescription laxatives. Dulcolax (blsacodylf was also used in this instance; it is classified as a stimulant laxative which has an irritant action pre-
PATHOLOGICAL FINDINGS At colectomy, 20 cm of ileum and 45 cm of colon (normal,
1 From the Department of Pathology, Akron City Hospital, Akron, Ohio (F. P. U., Chairman; Director of Clinical Laboratories; C. H. L., Chief Resident), and the Department of Radiology, Case Western Reserve University, Cleveland, Ohio (M. J. U., Senior Instructor). Revised version acceptedfor publication in February 1975. 2 bis (p-acetoxyphenyl)-2-pyridylmethane. sjh
557
I
Fig. 1. A. Admission plain film ot the abdomen shows three enteric-coated Dulcolax capsules. Marked shortening of the colon and loss of haustrations are evident. B. Barium-enema study demonstrates a severely affected colon with loss of Iiaustrations, marked shortening, and questionable pseudopolyposis. Note the incompetent ileocecal valve and involvement of the terminal ileum, interpreted as "backwash ileitis." No strictures are present, and involvement is most severe on the right side. An obvious sigmoid mass is present. C. Note the relatively normal rectum, which remains distensible. The large filling defect (arrow) was interpreted as carcinoma. Fig. 2. Resected terminal ileum and colon, showing marked shortening and dilatation, loss of haustral folds, an extremely smooth, flat, atrophic mucosa, and punctate ulcerations. Note the large inflammatory polyp and the absence of significant thickening of the ileum and colonic wall. The ileocecal valve is distorted. Fig. 3. Photomicrograph shows predominantly mucosal and submucosal involvement, with mucosal atrophy alternating with heapedup colonic glands. Fibrosis involves the muscularis mucosae and submucosa. Submucosal lymphoid aggregates, a mononuclear cell infiltrate, and fat can be seen. (20 X)
Vol. 116
559
THE CATHARTIC COLON
dominantly on the colonic mucosa and acts on parasympathetic nerve endings, stimulating peristalsis. An occasional case of Dulcolax abuse resulting in a cathartic colon has been reported (10). Bulk and emollient laxatives have not been incriminated. Clinically, the paradox of a barium enema suggesting chronic ulcerative colitis in the presence of constipation should raise the suspicion of chronic laxative abuse, often seen in white women with early and severe involvement of the cecum (1-8). Although a characteristic history may substantiate the diagnosis. the personality of some patients makes an accurate history difficult; questioning a close relative may confirm the suspicion and prevent unnecessary surgery. Despite severe radiological changes, most patients are asymptomatic except for chronic constipation and dependency on laxatives. Since surgical specimens are usually not available, the pathology of the disease has not been fully appreciated, so that diagnosis by biopsy remains unreliable. Only a reference to melanosis coli was found in the pathology literature (11). The extensive fibrosis of Crohn' s disease is absent in cathartic colon (12, 13). The pathological findings, particularly the superficial mucosal ulceration, resemble those of chronic ulcerative colitis; however, strictures, marked ulceration, crypt abscesses, and pseudopolyposis are lacking (11). The most striking feature in our patient was mucosal atrophy, which is not common in ulcerative colitis. Colonic biopsy in the absence of an accurate history poses a difficult diagnostic problem because similar histological changes are described in the "burned-out" phase of chronic ulcerative colitis. Some reports have stated that shortening of the colon is not a prominent feature (~ 4, 7). In our case. shortening was marked throughout and was appreciated both radiologically and pathologically. Few reports have indicated that some shortening may occur in the hepatic flexure (5, 6). Absence of marked fibrosis accounts for continued distensibility of the colon and rectum and reversibility of radiological changes following cessation of laxative use (1, 2, 4, 5, 8). The inconstant narrowing can be attributed to spasms and to the marked hypertrophic muscularis mucosae, similar to that described in chronic ulcerative colitis (14). Many of the changes described may represent a nonspecific response to injury, and the individual histopathological changes also occur in other forms of colitis. Smith demonstrated that the laxative senna resulted in injury to the myenteric plexus in mice and concluded that this was a direct toxic effect (13). The cecum is universally affected radiologically and is the most severely diseased structure pathologically. The extensive alterations in the cecum and ileocecal valve exist to a lesser degree in the terminal ileum, contrary to the findings in Crohn's disease. Slit-like ulcerations deep in the wall of the colon and transmural inflammation are not present (14-20), and fistulas and perianal disease have not been reported in this disorder. The polyps described are classified as inflammatory and are not considered neoplastic or premalignant; rather, they are the result of longstanding inflammation. (It should be stressed that these polyps are histologically distinct and are not adenomatous; they may arise from foci of colitis cystica profunda.) Unlike ulcerative colitis, the rectum in our patient was normal on radiological examination 13 years ago and is now only minimally involved. Hypokalemia and hypoalbuminemia both occur in catharticinduced factitious diarrhea (10). Albumin loss has been dem-
Diagnostic Radiology
onstrated in the gastrointestinal tract. Small-bowel biopsy has not shown significant changes (10). The changes in our patient's colon were severe, and we conclude that albumin loss most likely occurred through the colonic mucosa. Cathartic colon should be considered as another cause of protein-losing enteropathy. Approximately 10% of inflammatory bowel disease is presently unclassifiabJe pathologically (21). Radiology remains the primary method of diagnosis of cathartic colon, a~hough confirmation by biopsy is possible. Since the rectum is usually minimally involved, rectal biopsy may not be representative. Extreme mucosal atrophy should alert the pathologist to consider laxative abuse. ACKNOWLEDGMENT: We wish to thank Ms. Jane Pringle for her help with the manuscript. Department of Pathology Akron City Hospital 525 E. Market St. Akron, Ohio 44309
REFERENCES 1. Heilbrun N: Roentgen evidence suggesting enterocolitis associated with prolonged cathartic abuse. Radiology 41:486-491, Nov 1943 2. Sieisenger MH, Fordtran JS: Gastrointestinal Disease. Philadelphia, Saunders, 1973, pp 1528-1531 3. Margulis AR, Burhenne HJ, ad: Alimentary Tract Roentgenology. St. Louis, Mo., Mosby, 2d Ed, 1973, pp 763-766 4. Heilbrun N, Bernstein C: Roentgen abnormalities of the large and small intestine associated with prolonged cathartic ingestion. Radiology 65:549-556, Oct 1955 5. Jewell FC, Kline JR: The purged colon. Radiolqgy 62:368370, Mar 1954 6. Plum GE, Weber HM, Sauer WG: Prolonged cathartic abuse resulting in roentgen evidence suggestive of enterocolitis. Am J Roentgenol 83:919-925, May 1960 7. Ziter FMH Jr: Cathartic colon. New York J Med 67:546549, 15 Feb 1967 8. Lemaitre G, L'Hermine C, Decoulx M, et a\: Aspect radiologique des colites chroniques par abus de laxatifs: propos de quatre observations. J Beige Radiol 53:339-345, Sep-Oct 1970 (Fre) 9. Goodman LS, Gilman A, ed: The Pharmacological Basis of Therapeutics. New York, Macmillan, 4th Ed. 1970, pp 1020-1030 10. Heizer WD, Warshaw AL, Waldmann TA, et al: Protein-losing gastroenteropathy and malabsorption associated with factitious diarrhea. Ann Intern Med 68:839-852, Apr 1968 11. Horn RC Jr: Alimentary tract. [lnJ Anderson WAD, ad: Pathology. 81. Louis, Mo., Mosby, 6th Ed, 1971, pp 88 and 1133-1135 12. Jones FA: Cathartic colon. Proc R Soc Med 60:503-504, May 1967 13. Smith B: Effect of irritant purgatives on the myenteric plexus in man and the mouse. Gut 9:139-143, Apr 1968 14. Goulston SJM, McGovern VJ: The nature of benign strictures in ulcerative colitis. N Engl J Med 281:290-295, 7 Aug 1969 15. Mottet NK: Histopathologic Spectrum of Regional Enteritis and Ulcerative Colitis. Philadelphia, Saunders, 1971, pp 63-154 16. Crohn BB, Berg AA: Right-sided (regional) colitis. JAMA 110:32-37, 1 Jan 1938 17. Lockhart-Mummery HE, Morson BC: Crohn's disease (regional enteritis) of the large intestine and its distinction from ulcerative colitis. Gut 1:87-105, Jun 1960 18. LOCkhart-Mummery HE, Morson BC: Crohn's disease of the large intestine. Gut 5:493-509, Dec 1964 19. McGovern VJ, Goulston SJM: Crohn's disease of the colon. Gut 9: 164-176, Apr 1968 20. McGovern VJ: The differential diagnosis of colitis. Pathol Ann 4:127-158, 1969 21. Price AB, Morson BC: Inflammatory band disease (the surgical pathology of Crohn's disease and ulcerative colitis). Hum Pathol 6:7-29, Jan 1975
a
