| Abstract|| |
Lymphoid polyposis is a lymphoid hyperplasia of the gastrointestinal tract that usually presents as multiple small polyps in the colon during childhood. This should be differentiated from other neoplastic or familial polyposis of the intestine. Pseudomembranous colitis (PMC) is commonly associated with Clostridium difficile infection (CDI) but can be a consequence of other disease processes. We report a case of benign lymphoid polyposis of the colon with pseudomembranous colitis in a 4-month child.
Keywords: Childhood, colitis, lymphoid, polyposis, pseudomembranous
|How to cite this article:|
Swami SY, D'Costa G F, Baste B D, Narhire V V, Vinay N C. Lymphoid polyposis with pseudomembranous colitis in a 4-month child: A rare coexistence. Ann Trop Med Public Health 2017;10:453-6
|How to cite this URL:|
Swami SY, D'Costa G F, Baste B D, Narhire V V, Vinay N C. Lymphoid polyposis with pseudomembranous colitis in a 4-month child: A rare coexistence. Ann Trop Med Public Health [serial online] 2017 [cited 2020 Sep 19];10:453-6. Available from: http://www.atmph.org/text.asp?2017/10/2/453/208727
| Introduction|| |
Lymphoid polyposis is a part of the spectrum of lymphoid hyperplasia of the gastrointestinal tract. Lymphoid hyperplasia of the intestines is a benign reactive process also known as pseudolymphoma, lympho-nodular hyperplasia (LNH), or terminal lymphoid ileitis. It occurs in all age groups but is best described in children., LNH is not always benign and may be associated with intussusception or even fatal colonic torsion.,
Lymphoid polyposis usually presents as multiple small polyps in the colon during childhood. This should be differentiated from other neoplastic or familial polyposis of the intestine.
The earliest description of Pseudomembranous colitis (PMC) was in 1893 when a young woman died following gastric surgery. PMC is rare in the pediatric age group. PMC is currently believed to be caused almost exclusively by toxins produced byClostridium difficile.
| Case Report|| |
A 4-month-old female child came with complaint of intestinal obstruction including abdominal pain, distention, vomiting, and constipation. Radiologic diagnosis was intussusception with the target sign. She had undergone exploratory laparotomy with resection of terminal ileum, appendix with caecum, and right ascending colon.
On gross examination, right hemicolectomy specimen showed numerous small sessile polyps that were diffusely scattered throughout the segment, the largest measuring 2 cm × 3 cm in diameter with adjacent ulceration [Figure 1].
|Figure 1: Gross (cut section): Sessile polypoid growth with adjacent ulcerated area|
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The polyps consisted of mature lymphoid tissue with numerous germinal centers that were located mostly in the lamina propria and submucosa [Figure 2].
|Figure 2: Multiple polyps showing primary and secondary lymphoid follicle in the lamina propria and submucosa. [HandE: 40X]|
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Pseudomembranes were observed in right-sided colon with hyperplastic lymphoid polyps. Histologically “volcano” lesions were observed in biopsy specimen showing superficially damaged crypts distended by a mucopurulent exudate that formed an eruption reminiscent of a volcano. These exudates coalesced to form pseudomembranes composed of fibrinous material with mixed inflammatory cells [Figure 3].
|Figure 3: Pseudomembranous volcano-like eruptions composed of fibrinous material with mixed inflammatory cells. [HandE: 10X and 40X]|
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| Discussion|| |
Lymphoid aggregates are normally found throughout the small and large intestine. Known as LNH, these aggregates are observed especially in young children and are not associated with clinical symptoms being considered physiologic. In children presenting with gastrointestinal symptoms (i.e., recurrent abdominal pain), the number and size of the lymphoid follicles are increased. In accordance with previous published works, LNH was defined as a cluster of more than 10 extruding lymphoid nodules, whereas a lymphoid nodule was defined as an extruding lymphoid follicle with a diameter of 2 mm or more. Intestinal LNH has also been associated with viral and bacterial infection and immune deficiency status.
There are no definitions or valid criteria for when normal lymphoid tissue becomes hyperplastic, or for when hyperplasia becomes pathologic.
The dividing line between physiologic nodules and hyperplasia is thus ill defined. Lymphoid hyperplasia may be discovered incidentally, at colonoscopy or in patients undergoing colectomy, especially in the last few centimeters of the terminal ileum. However, cases that are symptomatic due to intussusception or prolapse are well documented.,
Lymphoid hyperplasia occurs mainly in the rectum and in the ileocecal region. Eighty percent of lymphoid polyps are sessile and solitary, the remainder are pedunculated and/or multiple (numbering 2-6).
Reactive hyperplasia of Peyer's patches and other mucosa-associated lymphoid tissue acts as the leading edge of the intussusception. Intussusception is the most common cause of intestinal obstruction in children younger than 2 years of age.
The pathology of lymphoid hyperplasia is quite characteristic, consisting of prominent lymphoid follicles with active germinal centers located in the mucosa and submucosa. The most important differential diagnosis is with lymphomatous polyposis. The presence of highly reactive germinal centers, numerous cell types, prominent vascularity, and polyclonality as determined immunohistochemically are the most important features in the differential diagnosis with lymphoma. Lymphoid hyperplasia may be differentiated from follicular lymphoma presenting as lymphomatous polyposis by Bcl-2 immunostaining of follicular germinal centers.
Although several cases of histologically benign lymphoid intestinal polyposis have been reported to accompany lymphomas or leukemia's, lymphoid polyposis remains as a benign entity. Therefore, it is important to recognize this entity for the differential diagnosis of polypoid lesions of the bowel. Clinically, these patients have intermittent abdominal pain, diarrhea, constipation, rectal bleeding, and intestinal obstruction.
The clinical significance of lymphoid hyperplasia lies in the possibility of these nodules serving as a nidus for prolapse and intussusception and in the association with immunosuppressive states. Local excision is curative; occasionally, spontaneous remission has been noted.
PMC is rare in the pediatric age group. PMC is diagnosed by assessing the patient on three levels: clinical evaluation, stool assays for enteric pathogens, and visualization of the colonic mucosa. Pseudomembranes may occur throughout the colon but are most frequent in the left colon. Unlike ulcerative colitis, which extends proximally from the rectum, PMC can be patchy and the rectum may be spared.
PMC is commonly associated with hospitalization and prior antibiotic exposure and is currently believed to be caused almost exclusively by toxins produced by C. difficile. The clinical spectrum of this disease may range from a mild, nonspecific diarrhea to severe colitis with toxic megacolon, perforation, and death.
Histologic findings include epithelial necrosis, distended goblet cells, infiltration of the lamina propria with leukocytes, and plaques consisting of inflammatory cells, fibrin, and mucin. Diffuse pseudomembranes are more common in C. difficile PMC, whereas ischemic colitis is associated with hyalinized lamina propria, atrophic crypts, hemorrhage, and full-thickness mucosal necrosis. Even when there are no gross pseudomembranes, histologic examination of biopsies may show an inflammatory exudate, which erupts from the surface epithelium in a “summit” or “volcano” lesion, often near or overlying normal-appearing mucosa. Crohn's disease and ulcerative colitis rarely exhibit these summit-like lesions and the mucosa is more inflamed and necrotic.
The intussusception in this case was supposed to have developed from altered bowel motility caused by extensive bowel edema associated with right-side PMC attributable to C. difficile infection, even though the use of antibiotics was not explicitly stated.
We may conclude that the lead point is the swollen hyperplastic lymphoid tissues from the inflammatory reaction to PMC, even if the causal relation between PMC and intussusception could not be sufficiently clarified.
| Conclusion|| |
The clinical significance of lymphoid polyposis lies in the possibility of these polyps serving as a nidus for prolapse and intussusceptions and in the association with PMC. We report this case due to its rarity and rare coexistence of double pathology. Local excision is curative; occasionally, spontaneous remission has been noted.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Doo HC, Jeong KS, Kwi WP, Je GC. Colorectal lymphoid polyposis in a child. Seoul J Med 1994;35:213-6.
Colon AR, DiPalma JS, Leftridge CA. Intestinal lymphonodular hyperplasia of childhood: patterns of presentation. J Clin Gastroenterol 1991;13:163-6.
Cooper HS. Intestinal neoplasms In: Sternberg SS,Diagnostic surgical pathology. Vol. 2, 3rd ed. Philadelphia: Lippincott Williams and Wilkins; 1999. p. 1424.
Vestergaard H, Westergaard T, Wohlfahrt J, Pipper C, Melbye M. Association between intussusception and tonsil disease in childhood. Epidemiology 2008;19:71-4.
Coulibaly B, Piercecchi-Marti MD, Bartoli C, Liprandi A, Sanvoisin A, Leonetti G. Benign lymphoid polyposis: two diffuse cases leading to fatal intestinal ischemia in children. Pediatr Int 2009;51:428-31.
Finney JMT. Gastroenterostomy for cicatrizing ulcer of the pylorus. Bull Johns Hopkins Hosp 1983;45:53-5.
Viscidi RP, Bartlett JG. Antibiotic-associated pseudo-membranous colitis in children. Pediatrics 1981;67:381-6.
Brook I. Pseudomembranous colitis in children. J Gastroenterol Hepatol 2005;20:182-6.
Riddell RH, Petras RE, Williams GT, Sobin LH. Lymphoproliferative disorders of the intestinesTumors of the intestines.Washington, DC: Armed Forces Institute of Pathology. 2003;395-430.In: Riddell RH, Petras RE, Williams GT, Sobin LH,editors .Atlas of Tumor Pathology; 3rd series, fascicle 32
Robbins Cotran. Pathologic Basis of Disease 9th778.
Andrejak M, Lafon B, Decocq G, Chetaille E, Dupas JL, Ducroix JP, et al
. Antibiotic-associated pseudomembranous colitis: retrospective study of 48 cases diagnosed by colonoscopy (in French). Thérapie 1996;51:81-6.
McFarland LV. Clostridium difficile
-associated disease.In: Surawicz Owen RL.Gastrointestinal and hepatic infections. hiladelphia: Saunders 1995;153-75.
Cleary RK. >Clostridium difficile
-associated diarrhea and colitis: clinical manifestations, diagnosis, and treatment. Dis Colon Rectum 1998;41:1435-49.
Surawicz CM, McFarland LV. Pseudomembranous colitis: causes and cures. Digestion 1999;60:91-100.
Sunil Y Swami
Bhagwanbaba Chowk, Gitta Road, Shepwadi, Ambajogai, Maharashtra
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2], [Figure 3]