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Capsule endoscopy features of human immunodeficiency virus and geographical diseases
Gastrointest Endoscopy Clin N Am 14 (2004) 169 – 177
Capsule endoscopy features of human immunodeficiency virus and geographical diseases John P. Cello, MD Department of Medicine and Surgery, University of California, San Francisco General Hospital, 3D-GI Unit, 1001 Potrero Ave., San Francisco, CA 94110, USA
In the 1860s a golden spike was driven near Ogden, Utah, marking the completion of the American transcontinental railroad bridging East and West Coasts. This seminal event in American history opened up a new era of exploration and discovery, leading to a whole new appreciation of the continent. Capsule enteroscopy has now effectively bridged the void in the gastrointestinal (GI) tract between the maximum depth of insertion of the push enteroscope and the proximal advancement of the colonoscope. Just as multiple new disease entities and new manifestations of established ones were made at the time of the wide spread availability of endoscopy, so too newer diseases and newer manifestations of well-described diseases are now possible with the advent of capsule enteroscopy. Small bowel manifestations of classical diseases were largely described based on information gained at surgery, autopsy, or contrast radiography. Because so few patients with small bowel diseases are definitely visualized, one’s understanding of these diseases is based on the most glaring complications of far-advanced disease. Capsule enteroscopy enables us to visualize and describe earlier and atypical manifestations of these diseases (Figs. 1 –7). HIV and AIDS is clearly a global problem infecting probably 100 million individuals around the globe. Even the recently described GI manifestations of AIDS needs to be extended and amplified now in the era of capsule enteroscopy. In addition to the enteric manifestations of HIV disease, now readily available for observational diagnosis by capsule endoscopy, certain diseases unique to particular regions of the globe are being discovered by capsule enteroscopy (see E-mail address: [email protected] 1052-5157/04/$ – see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.giec.2003.10.008
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Fig. 1. Patient with tuberculosis. (See also Color Plate 53).
Figs. 2, 5 and 6). In approaching patients who undergo capsule enteroscopy one must be aware that new disease entities will invariably be described, and previously unreported enteric manifestations of well-established disease entities will be forthcoming.
HIV and AIDS HIV clearly is enterotrophic with special affinity for mononuclear cells in the lamina propria. Acute HIV infection without depletion of the helper cell population to less than 150 to 200 cells per cubic millimeter is not associated with
Fig. 2. A 49-year-old man suffering from weight loss, recurrent abdominal pain and diarrhea, and polypoid lesions in duodenum with thickened mucosa and linear erosions. This lesion was proven to be a lymphoma of the small bowel. (See also Color Plate 54). (From Rossini FP, Pennazio M. Neoplastic diseases. In: Halpern M, Jacob H, editors. Atlas of capsule endoscopy. Norcross (GA): Given Imaging; 2002. p. 47 – 62; with permission.)
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Fig. 3. NSAID-induced small bowel stricture. (See also Color Plate 55). (From Cave DR. Iatorgenic diseases. In: Halpern M, Jacob H, editors. Atlas of capsule endoscopy. Norcross (GA): Given Imaging; 2002. p. 63 – 80; with permission.)
distinguishing endoscopic appearances in the small bowel [1]. Acute HIV ulcerations of the small bowel, such as that described in the esophagus with acute HIV infection, have not been described in the small bowel. The principal manifestations of HIV disease in the gut are those associated with the emergence of opportunistic infections and malignancies. It is widely assumed, though not completely documented, that the previously acquired resident flora of the GI tract, including suppressed potential pathogens, blossom with the withdrawal of normal immune surveillance. Thus, patients previously exposed to potential pathogens may remain asymptomatic for years until and unless the CD4 cells drop below 150 to 200 per cubic millimeter [1]. In some instances newly acquired
Fig. 4. NSAID-induced small bowel stricture. (See also Color Plate 56). (From Cave DR. Iatrogenic diseases. In: Halpern M, Jacob H, editors. Atlas of Capsule endoscopy. Norcross (GA): Given Imaging; 2002. p. 63 – 80; with permission.)
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J.P. Cello / Gastrointest Endoscopy Clin N Am 14 (2004) 169–177
Fig. 5. Submucosal nodular lesions of small bowel in Kaposi’s sarcoma. (See also Color Plate 57). (From Rossini FP, Pennazio M. Neoplastic diseases. In: Halpern M, Jacob H, editors. Atlas of capsule endoscopy. Norcross (GA): Given Imaging; 2002. p. 47 – 62; with permission.)
infections such as that seen with waterborne cryptospordiosis develop de novo in the context of severely immunocompromised patients.
Cytomegalovirus Cytomegalovirus (CMV) is one of the most prevalent herpes viruses, which may remain latent in patients who are infected and only manifest clinical illness decades after primary infection. The clinical and enteric diseases associated with CMV occur with reactivation of the virus once immunosuppression reaches a profoundly low level. CMV is a systemic infection and as such can be associated with retinitis, pneumonitis, and hepatitis. The most dramatic illnesses associated with CMV in the immunocompromised patients occur in the gastrointestinal tract [2].
Fig. 6. Patient with cryptosporidiosis of the small bowel. (See also Color Plate 58).
J.P. Cello / Gastrointest Endoscopy Clin N Am 14 (2004) 169–177
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Fig. 7. Villous atrophy. Note AVM at 6 o’clock. (See also Color Plate 59). (From Gay G, Fassler I, Florent C, Delvaux M. malabsorption. In: Halpern M, Jacob H, editors. Atlas of capsule endoscopy. Norcross (GA): Given Imaging; 2002. p. 83 – 101; with permission.)
In patients with severe immunocompromise, particularly those with CD4 counts less than 100, cytomegalovirus may manifest itself anywhere in the gastrointestinal tract from mouth to anus [3]. Early CMV lesions appear as vasculitic lesions of the gut manifested as submucosal hemorrhages and shallow erosions or ulcers. With more extensive disease, larger ulcerations may be seen having a ‘‘geographic’’ or markedly irregular boarder. These ulcers are large but shallow and nonetheless can be associated with moderate bleeding. There are rare instances wherein CMV can produce an inflammatory mass or (viroma). This mass may have all the gross characteristics of a neoplasm.
Cryptosporidiosis The most common opportunistic infection of the gastrointestinal tract in patients with severe immunodeficiency is cryptosporidiosis [4]. This infection, caused by Cryptosporidium parvum, is usually transmitted through contaminated water as evidenced by a notorious outbreak of cryptosporidiosis in Milwaukee, Wisconsin [5– 7]. C parvum is a common sporozoan and can be transmitted in a person-to-person or even animal to person. The overall prevalence of cryptosporidiosis among patients with AIDS is anywhere between 5% to 15%, most of these patients having CD4 counts less than 100 to 150 per mm [3]. The infection can occur following the ingestion of as few as 10 oocysts. There is only a minimal inflammatory reaction associated with the intracellular migration of the parasite into the brush border and apical cell surface of these epithelia cells. In most instances, the enteroscopic images are unimpressive except for mild to moderate mucosal edema. The extracellular parasite lives on the brush boarder of the enterocytes and may produce a ‘‘frosted’’ appearance to the mucosa (see Fig. 6). Although the infection is found throughout the gastrointestinal tract, there may be disproportionate disease in the terminal ileum in some patients. The
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intestinal transit in patients with cryptosporidiosis may be exceedingly rapid and the bowel seems to have a wet appearance with an excessive amount of intraluminal fluid.
Mycobacterium avium complex Atypical myocobacteria are ubiquitous in nature, yet are only associated with significant disease in moderately to severely immunocompromised individuals. Infection occurs in anywhere from 15% to 30% of patients with AIDS. Once again the illness rarely becomes clinically manifested until the CD4 count drops below 100 per mm3. Clinical manifestations of mycobacterium avium complex (MAC) include fevers, chills, weight loss, anorexia, and small bowel watery diarrhea. In addition, patients often have impressive hepatosplenomegaly and adenopathy. MAC is a systemic illness with a predilection to infect macrophages and other mononuclear cells [8– 10]. The mononuclear cells within the lamina propria of the gut are commonly severely infected with MAC, which produces a gross appearance of markedly thickened valvulae of the small bowel. The mucosal folds may be so markedly thickened as to give the appearance of luminal obstruction. In some instances, one may actually see intramucosal miliaria-like whitish papules on the surface in patients infected with MAC. On occasions, patients with MAC may actually ulcerate the mucosa producing shallow ulcerations.
Lymphoma The promise of improved immunocompetance has led to the wide spread belief that opportunistic infections are dramatically decreasing in patients with AIDS. The advent of highly active antiretroviral therapy (HAART) has largely lived up to that promise. It is less certain however that lymphoma, particularly B cell lymphomas, are decreased in incidence in patients with AIDS [11,12]. Small bowel lymphomas in patients with AIDS are usually large, bulky, excavating, and nonobstructing. (see Fig. 2) On occasion, these may ulcerate and present with GI tract hemorrhage. Characteristically, the lymphomas have a gross appearance of pale pink nodular tissue, often with a sizeable intramural component. In most instances, patients with lymphoma have extensive lymphadenopathy involving the para-aortic and mesenteric lymph nodes.
Nonsteroidal anti-inflammatory drug ulcerations Patients with HIV and AIDS are often subjected to relentless diurnal fevers and chills. Because of suspected or documented liver disease, many of these patients will take standard non-steroidal anti-inflammatory drugs (NSAIDs). Although most lesions from NSAIDs are found in the stomach and duodenum,
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increasingly more lesions associated with pain and occult bleeding are found throughout the small bowel. These ulcers are usually small with apthoid-like appearance. (see Fig. 3) On occasion, prolonged NSAID administration causes multiple strictures of the small bowel. (see Fig. 4) Not surprisingly, these patients may have strictures that limit the passage of capsule through the entire small bowel. Nonetheless, the information gained by capsule enteroscopy is important because it demonstrates hold up of the capsule at a single site for the duration of the recording. One must be suspicious of strictures, whether caused by long standing NSAID administration or radiation therapy or to adhesions, by noting whether the capsule remains in the same position for an exceedingly long period of time. It is particularly important to be certain that the capsule ultimately passes through the small bowel in all patients. Thus, for those patients in whom the last images viewed are still those of the small bowel, a follow up plain film of the abdomen must be taken to document passage into the colon.
Kaposi’s sarcoma Kaposi’s sarcoma is commonly found in the stomach and small bowel of patients who are severely immuno-compromised. Most patients with enteric Kaposi’s have cutaneous lesion, but the appearance of the smaller lesions in the GI tract is different from those in the skin. Most cutaneous KS lesions are dusky, violaceous papules, or nodules. In the stomach and small bowel, however, Kaposi’s sarcoma appears as bright red submucosal vascular nodules with intact overlying mucosa. (see Fig. 5) As the implants increase in size, they become more irregular and develop a central umbilicated ulceration. The most common presentation of Kaposi’s sarcoma in the GI tract is GI hemorrhage manifested by hematemesis, melena, or hematochezia. On occasion, the Kaposi’s lesions can become large and bulky producing partial or complete small bowel obstruction or intussusception. The smaller Kaposi’s lesions need to be distinguished from intramural hemorrhage caused by coagulopathy or cytomegalovirus.
Histoplasma capsulatum Histoplasmosis is an uncommonly encountered fungal infection of the gastrointestinal tract. In most instances, enteric histoplasmosis is incidental to widely disseminated disease including pulmonary and hepatic infiltration. The most common enteric appearance of histoplasmosis is irregular deep ulcerations with superimposed adjacent nodular masses [13 –15]. On occasion, the lesions of histoplasmosis may mimic those of tuberculosis or even carcinoma. The diagnosis usually can be made by biopsying sites other than the enteric system, particularly lymph node or bone marrow. Although the lesions of histoplasmosis in the GI tract may become quite large and ulcerative, they rarely present with GI tract bleeding.
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J.P. Cello / Gastrointest Endoscopy Clin N Am 14 (2004) 169–177
Tuberculosis Mycobacterium tuberculosis and M bovis have a predilection for the small bowel particularly the terminal ileum. Although most of these patients have strongly suspected or documented pulmonary tuberculosis, less patients will have seemingly primary intestinal tuberculosis [16,17]. Most of these patients present with obstruction-like symptoms or with fistulization. On occasion patients with intestinal tuberculosis may present with recurrent significant GI tract blood loss. The ulcers seen with tuberculosis of the small bowel are characteristically shallow with an extensive irregular ‘‘geographic’’ borders (see Fig. 1). These ulcers are usually no larger than 1 to 2 cm in length and tend to be disproportionately transverse rather than the longitudinal ulcerations associated with Crohn’s disease. In those patients with occult small bowel bleeding, tuberculous ulcers of the small bowel may be noted only on a few images. Care must be taken therefore to carefully examine the enteroscopy images frame by frame looking for discreet ulcerations of the small bowel.
Tropical sprue Patients with sprue usually present with weight loss and watery diarrhea [18 –20]. The small bowel malabsorption produces a large bulky fowl smelling stool in these patients. Enteroscopy for these patients usually reveals scalloping of the valvulae, mucosal edema, or flattened atrophic folds (see Fig. 7). The lesions in sprue are nonspecific and can be seen in other conditions such as MAC, hypoalbuminemia or allergic enteropathy.
References [1] Kearney DJ, Steuerwald M, Koch J, Cello JP. A prospective study of endoscopy in HIVassociated diarrhea. Am J Gastroenterol 1999;94:596 – 602. [2] Meiselman MS, Cello JP, Margaretten W. Cytomegalovirus colitis: report of the clinical, endoscopic, and pathologic findings in two patients with the acquired immune deficiency syndrome. Gastroenterology 1985;88:171 – 5. [3] Goodgame RW. Gastrointestinal cytomegalovirus disease. Ann Intern Med 1993;119:924 – 35. [4] Cello JP. Gastrointestinal manifestations of HIV infection. Inf Dis Clin N Am 1998;2:387 – 96. [5] Aragon TJ, Novotny S, Enanoria W, Vugia DJ, Khalakdina A, Katz MH. Endemic cryptosporidiosis and exposure to municipal tap water in persons with acquired immunodeficiency syndrome (AIDS): a case-control study. Public Health 2003;3:2 – 12. [6] Chalasani N, Wilcox CM, Hunter HT, et al. Endoscopic features of gastroduodenal cryptococcosis in AIDS. Gastrointest Endosc 1997;45:315 – 7. [7] Greenberg PD, Cello JP. Diagnosis of Cryptosporidum Parvum in patients with severe diarrhea and AIDS. Dig Dis Sci 1996;41:2286 – 90. [8] Cappell MS, Philogence C. The endoscopic appearance of severe intestinal Mycobacterium avium complex infection as a coarsely granular mucosa due to massive infiltration and expansion of intestinal villi without mucosal exudation. J Clin Gastro 1995;21:323 – 6. [9] Jacobson MA, Hopewell PC, Yajko DM, et al. Natural history of disseminated Mycobacterium avium, complex infection in AIDS. J Infect Dis 1991;164:994 – 8.
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[10] Poorman JC, Katon RM. Small bowel involvement by Mycobacterium avium complex in a patient with AIDS: endoscopic, histologic, and radiographic similarities to Whipple’s disease. Gastrointest Endosc 1994;40:753 – 9. [11] Kaplan LD. AIDS-associated lymphomas. AIDS Clin Rev 1991;181 – 95. [12] Levine AM. AIDS-associated malignant lymphoma. Med Clin N Am 1992;76:253 – 68. [13] Gumbs MA, Girishkumar H, Yousuf A, Levy L, Patel M, Narasimha V. Histoplasmosis of the small bowel in patients with AIDS. Postgrad Med J 2000;76(896):367 – 9. [14] Hung CC, Wong JM, Hsueh PR, Hsieh SM, Chen MY. Intestinal obstruction and peritonitis resulting from gastrointestinal histoplasmosis in an AIDS patient. J Formos Med Assoc 1998; 97(8):577 – 80. [15] Forsmark CE, Wilcox CM, Darragh TM, Cello JP. Disseminated histoplasmosis in AIDS: an unusual case of esophageal involvement and gastrointestinal bleeding. Gastrointestinal Endoscopy 1990;36:604 – 5. [16] Wang HS, Chen WS, Su WJ, Lin JK, Lin TC, Jiang JK. The changing pattern of intestinal tuberculosis: 30 years’ experience. Int J Tuberc Lung Dis 1998;2(7):569 – 74. [17] Horvath KD, Whelan RL. Intestinal tuberculosis: return of an old disease. Am J Gastroenterol 1998;93(5):692 – 6. [18] Oxtentenko AS, Grisolano SW, Murray JA, Burgart LJ, Dierkhising RA, Alexander JA. The insensitivity of endoscopic markers in celiac disease. Am J Gastroenterol 2002;97(4):933 – 8. [19] Tursi A, Brandimarte G, Giorgetti GM, Gigliobianco A. Endoscopic features of celiac disease in adults and their correlation with age, histological damage, and clinical form of the disease. Endoscopy 2002;34:787 – 92. [20] Brocchi E, Tomassetti P, Misitano B, et al. Endoscopic markers in adult coeliac disease. Dig Liver Dis 2002;34(3):177 – 82.
Capsule endoscopy features of human immunodeficiency virus and geographical diseases John P. Cello, MD Department of Medicine and Surgery, University of California, San Francisco General Hospital, 3D-GI Unit, 1001 Potrero Ave., San Francisco, CA 94110, USA
In the 1860s a golden spike was driven near Ogden, Utah, marking the completion of the American transcontinental railroad bridging East and West Coasts. This seminal event in American history opened up a new era of exploration and discovery, leading to a whole new appreciation of the continent. Capsule enteroscopy has now effectively bridged the void in the gastrointestinal (GI) tract between the maximum depth of insertion of the push enteroscope and the proximal advancement of the colonoscope. Just as multiple new disease entities and new manifestations of established ones were made at the time of the wide spread availability of endoscopy, so too newer diseases and newer manifestations of well-described diseases are now possible with the advent of capsule enteroscopy. Small bowel manifestations of classical diseases were largely described based on information gained at surgery, autopsy, or contrast radiography. Because so few patients with small bowel diseases are definitely visualized, one’s understanding of these diseases is based on the most glaring complications of far-advanced disease. Capsule enteroscopy enables us to visualize and describe earlier and atypical manifestations of these diseases (Figs. 1 –7). HIV and AIDS is clearly a global problem infecting probably 100 million individuals around the globe. Even the recently described GI manifestations of AIDS needs to be extended and amplified now in the era of capsule enteroscopy. In addition to the enteric manifestations of HIV disease, now readily available for observational diagnosis by capsule endoscopy, certain diseases unique to particular regions of the globe are being discovered by capsule enteroscopy (see E-mail address: [email protected] 1052-5157/04/$ – see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.giec.2003.10.008
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J.P. Cello / Gastrointest Endoscopy Clin N Am 14 (2004) 169–177
Fig. 1. Patient with tuberculosis. (See also Color Plate 53).
Figs. 2, 5 and 6). In approaching patients who undergo capsule enteroscopy one must be aware that new disease entities will invariably be described, and previously unreported enteric manifestations of well-established disease entities will be forthcoming.
HIV and AIDS HIV clearly is enterotrophic with special affinity for mononuclear cells in the lamina propria. Acute HIV infection without depletion of the helper cell population to less than 150 to 200 cells per cubic millimeter is not associated with
Fig. 2. A 49-year-old man suffering from weight loss, recurrent abdominal pain and diarrhea, and polypoid lesions in duodenum with thickened mucosa and linear erosions. This lesion was proven to be a lymphoma of the small bowel. (See also Color Plate 54). (From Rossini FP, Pennazio M. Neoplastic diseases. In: Halpern M, Jacob H, editors. Atlas of capsule endoscopy. Norcross (GA): Given Imaging; 2002. p. 47 – 62; with permission.)
J.P. Cello / Gastrointest Endoscopy Clin N Am 14 (2004) 169–177
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Fig. 3. NSAID-induced small bowel stricture. (See also Color Plate 55). (From Cave DR. Iatorgenic diseases. In: Halpern M, Jacob H, editors. Atlas of capsule endoscopy. Norcross (GA): Given Imaging; 2002. p. 63 – 80; with permission.)
distinguishing endoscopic appearances in the small bowel [1]. Acute HIV ulcerations of the small bowel, such as that described in the esophagus with acute HIV infection, have not been described in the small bowel. The principal manifestations of HIV disease in the gut are those associated with the emergence of opportunistic infections and malignancies. It is widely assumed, though not completely documented, that the previously acquired resident flora of the GI tract, including suppressed potential pathogens, blossom with the withdrawal of normal immune surveillance. Thus, patients previously exposed to potential pathogens may remain asymptomatic for years until and unless the CD4 cells drop below 150 to 200 per cubic millimeter [1]. In some instances newly acquired
Fig. 4. NSAID-induced small bowel stricture. (See also Color Plate 56). (From Cave DR. Iatrogenic diseases. In: Halpern M, Jacob H, editors. Atlas of Capsule endoscopy. Norcross (GA): Given Imaging; 2002. p. 63 – 80; with permission.)
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Fig. 5. Submucosal nodular lesions of small bowel in Kaposi’s sarcoma. (See also Color Plate 57). (From Rossini FP, Pennazio M. Neoplastic diseases. In: Halpern M, Jacob H, editors. Atlas of capsule endoscopy. Norcross (GA): Given Imaging; 2002. p. 47 – 62; with permission.)
infections such as that seen with waterborne cryptospordiosis develop de novo in the context of severely immunocompromised patients.
Cytomegalovirus Cytomegalovirus (CMV) is one of the most prevalent herpes viruses, which may remain latent in patients who are infected and only manifest clinical illness decades after primary infection. The clinical and enteric diseases associated with CMV occur with reactivation of the virus once immunosuppression reaches a profoundly low level. CMV is a systemic infection and as such can be associated with retinitis, pneumonitis, and hepatitis. The most dramatic illnesses associated with CMV in the immunocompromised patients occur in the gastrointestinal tract [2].
Fig. 6. Patient with cryptosporidiosis of the small bowel. (See also Color Plate 58).
J.P. Cello / Gastrointest Endoscopy Clin N Am 14 (2004) 169–177
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Fig. 7. Villous atrophy. Note AVM at 6 o’clock. (See also Color Plate 59). (From Gay G, Fassler I, Florent C, Delvaux M. malabsorption. In: Halpern M, Jacob H, editors. Atlas of capsule endoscopy. Norcross (GA): Given Imaging; 2002. p. 83 – 101; with permission.)
In patients with severe immunocompromise, particularly those with CD4 counts less than 100, cytomegalovirus may manifest itself anywhere in the gastrointestinal tract from mouth to anus [3]. Early CMV lesions appear as vasculitic lesions of the gut manifested as submucosal hemorrhages and shallow erosions or ulcers. With more extensive disease, larger ulcerations may be seen having a ‘‘geographic’’ or markedly irregular boarder. These ulcers are large but shallow and nonetheless can be associated with moderate bleeding. There are rare instances wherein CMV can produce an inflammatory mass or (viroma). This mass may have all the gross characteristics of a neoplasm.
Cryptosporidiosis The most common opportunistic infection of the gastrointestinal tract in patients with severe immunodeficiency is cryptosporidiosis [4]. This infection, caused by Cryptosporidium parvum, is usually transmitted through contaminated water as evidenced by a notorious outbreak of cryptosporidiosis in Milwaukee, Wisconsin [5– 7]. C parvum is a common sporozoan and can be transmitted in a person-to-person or even animal to person. The overall prevalence of cryptosporidiosis among patients with AIDS is anywhere between 5% to 15%, most of these patients having CD4 counts less than 100 to 150 per mm [3]. The infection can occur following the ingestion of as few as 10 oocysts. There is only a minimal inflammatory reaction associated with the intracellular migration of the parasite into the brush border and apical cell surface of these epithelia cells. In most instances, the enteroscopic images are unimpressive except for mild to moderate mucosal edema. The extracellular parasite lives on the brush boarder of the enterocytes and may produce a ‘‘frosted’’ appearance to the mucosa (see Fig. 6). Although the infection is found throughout the gastrointestinal tract, there may be disproportionate disease in the terminal ileum in some patients. The
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intestinal transit in patients with cryptosporidiosis may be exceedingly rapid and the bowel seems to have a wet appearance with an excessive amount of intraluminal fluid.
Mycobacterium avium complex Atypical myocobacteria are ubiquitous in nature, yet are only associated with significant disease in moderately to severely immunocompromised individuals. Infection occurs in anywhere from 15% to 30% of patients with AIDS. Once again the illness rarely becomes clinically manifested until the CD4 count drops below 100 per mm3. Clinical manifestations of mycobacterium avium complex (MAC) include fevers, chills, weight loss, anorexia, and small bowel watery diarrhea. In addition, patients often have impressive hepatosplenomegaly and adenopathy. MAC is a systemic illness with a predilection to infect macrophages and other mononuclear cells [8– 10]. The mononuclear cells within the lamina propria of the gut are commonly severely infected with MAC, which produces a gross appearance of markedly thickened valvulae of the small bowel. The mucosal folds may be so markedly thickened as to give the appearance of luminal obstruction. In some instances, one may actually see intramucosal miliaria-like whitish papules on the surface in patients infected with MAC. On occasions, patients with MAC may actually ulcerate the mucosa producing shallow ulcerations.
Lymphoma The promise of improved immunocompetance has led to the wide spread belief that opportunistic infections are dramatically decreasing in patients with AIDS. The advent of highly active antiretroviral therapy (HAART) has largely lived up to that promise. It is less certain however that lymphoma, particularly B cell lymphomas, are decreased in incidence in patients with AIDS [11,12]. Small bowel lymphomas in patients with AIDS are usually large, bulky, excavating, and nonobstructing. (see Fig. 2) On occasion, these may ulcerate and present with GI tract hemorrhage. Characteristically, the lymphomas have a gross appearance of pale pink nodular tissue, often with a sizeable intramural component. In most instances, patients with lymphoma have extensive lymphadenopathy involving the para-aortic and mesenteric lymph nodes.
Nonsteroidal anti-inflammatory drug ulcerations Patients with HIV and AIDS are often subjected to relentless diurnal fevers and chills. Because of suspected or documented liver disease, many of these patients will take standard non-steroidal anti-inflammatory drugs (NSAIDs). Although most lesions from NSAIDs are found in the stomach and duodenum,
J.P. Cello / Gastrointest Endoscopy Clin N Am 14 (2004) 169–177
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increasingly more lesions associated with pain and occult bleeding are found throughout the small bowel. These ulcers are usually small with apthoid-like appearance. (see Fig. 3) On occasion, prolonged NSAID administration causes multiple strictures of the small bowel. (see Fig. 4) Not surprisingly, these patients may have strictures that limit the passage of capsule through the entire small bowel. Nonetheless, the information gained by capsule enteroscopy is important because it demonstrates hold up of the capsule at a single site for the duration of the recording. One must be suspicious of strictures, whether caused by long standing NSAID administration or radiation therapy or to adhesions, by noting whether the capsule remains in the same position for an exceedingly long period of time. It is particularly important to be certain that the capsule ultimately passes through the small bowel in all patients. Thus, for those patients in whom the last images viewed are still those of the small bowel, a follow up plain film of the abdomen must be taken to document passage into the colon.
Kaposi’s sarcoma Kaposi’s sarcoma is commonly found in the stomach and small bowel of patients who are severely immuno-compromised. Most patients with enteric Kaposi’s have cutaneous lesion, but the appearance of the smaller lesions in the GI tract is different from those in the skin. Most cutaneous KS lesions are dusky, violaceous papules, or nodules. In the stomach and small bowel, however, Kaposi’s sarcoma appears as bright red submucosal vascular nodules with intact overlying mucosa. (see Fig. 5) As the implants increase in size, they become more irregular and develop a central umbilicated ulceration. The most common presentation of Kaposi’s sarcoma in the GI tract is GI hemorrhage manifested by hematemesis, melena, or hematochezia. On occasion, the Kaposi’s lesions can become large and bulky producing partial or complete small bowel obstruction or intussusception. The smaller Kaposi’s lesions need to be distinguished from intramural hemorrhage caused by coagulopathy or cytomegalovirus.
Histoplasma capsulatum Histoplasmosis is an uncommonly encountered fungal infection of the gastrointestinal tract. In most instances, enteric histoplasmosis is incidental to widely disseminated disease including pulmonary and hepatic infiltration. The most common enteric appearance of histoplasmosis is irregular deep ulcerations with superimposed adjacent nodular masses [13 –15]. On occasion, the lesions of histoplasmosis may mimic those of tuberculosis or even carcinoma. The diagnosis usually can be made by biopsying sites other than the enteric system, particularly lymph node or bone marrow. Although the lesions of histoplasmosis in the GI tract may become quite large and ulcerative, they rarely present with GI tract bleeding.
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J.P. Cello / Gastrointest Endoscopy Clin N Am 14 (2004) 169–177
Tuberculosis Mycobacterium tuberculosis and M bovis have a predilection for the small bowel particularly the terminal ileum. Although most of these patients have strongly suspected or documented pulmonary tuberculosis, less patients will have seemingly primary intestinal tuberculosis [16,17]. Most of these patients present with obstruction-like symptoms or with fistulization. On occasion patients with intestinal tuberculosis may present with recurrent significant GI tract blood loss. The ulcers seen with tuberculosis of the small bowel are characteristically shallow with an extensive irregular ‘‘geographic’’ borders (see Fig. 1). These ulcers are usually no larger than 1 to 2 cm in length and tend to be disproportionately transverse rather than the longitudinal ulcerations associated with Crohn’s disease. In those patients with occult small bowel bleeding, tuberculous ulcers of the small bowel may be noted only on a few images. Care must be taken therefore to carefully examine the enteroscopy images frame by frame looking for discreet ulcerations of the small bowel.
Tropical sprue Patients with sprue usually present with weight loss and watery diarrhea [18 –20]. The small bowel malabsorption produces a large bulky fowl smelling stool in these patients. Enteroscopy for these patients usually reveals scalloping of the valvulae, mucosal edema, or flattened atrophic folds (see Fig. 7). The lesions in sprue are nonspecific and can be seen in other conditions such as MAC, hypoalbuminemia or allergic enteropathy.
References [1] Kearney DJ, Steuerwald M, Koch J, Cello JP. A prospective study of endoscopy in HIVassociated diarrhea. Am J Gastroenterol 1999;94:596 – 602. [2] Meiselman MS, Cello JP, Margaretten W. Cytomegalovirus colitis: report of the clinical, endoscopic, and pathologic findings in two patients with the acquired immune deficiency syndrome. Gastroenterology 1985;88:171 – 5. [3] Goodgame RW. Gastrointestinal cytomegalovirus disease. Ann Intern Med 1993;119:924 – 35. [4] Cello JP. Gastrointestinal manifestations of HIV infection. Inf Dis Clin N Am 1998;2:387 – 96. [5] Aragon TJ, Novotny S, Enanoria W, Vugia DJ, Khalakdina A, Katz MH. Endemic cryptosporidiosis and exposure to municipal tap water in persons with acquired immunodeficiency syndrome (AIDS): a case-control study. Public Health 2003;3:2 – 12. [6] Chalasani N, Wilcox CM, Hunter HT, et al. Endoscopic features of gastroduodenal cryptococcosis in AIDS. Gastrointest Endosc 1997;45:315 – 7. [7] Greenberg PD, Cello JP. Diagnosis of Cryptosporidum Parvum in patients with severe diarrhea and AIDS. Dig Dis Sci 1996;41:2286 – 90. [8] Cappell MS, Philogence C. The endoscopic appearance of severe intestinal Mycobacterium avium complex infection as a coarsely granular mucosa due to massive infiltration and expansion of intestinal villi without mucosal exudation. J Clin Gastro 1995;21:323 – 6. [9] Jacobson MA, Hopewell PC, Yajko DM, et al. Natural history of disseminated Mycobacterium avium, complex infection in AIDS. J Infect Dis 1991;164:994 – 8.
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