From symptom to diagnosis: clinical distinctions among various forms of intestinal inflammation
2004; Elsevier BV; Volume: 126; Issue: 6 Linguagem: Inglês
10.1053/j.gastro.2004.02.072
ISSN1528-0012
Autores Tópico(s)Eosinophilic Esophagitis
ResumoInflammation is the gut’s mute response to a myriad of diverse insults. Assigning a diagnosis in such cases is often straightforward, particularly when an infectious etiology can be identified. In the minority of presentations that represent new occurrences of the idiopathic inflammatory bowel diseases (IBD), making a positive diagnosis and, indeed, distinguishing between Crohn’s disease and ulcerative colitis are also routine matters. However, a casual diagnosis of IBD may result in critical errors in management in that incorrect diagnosis may result in inappropriate or even contraindicated treatment. The issue remains that no gold standard test exists for the diagnosis of IBD. For this reason, diagnosing Crohn’s disease and ulcerative colitis continues to be a more than occasional challenge to the practicing gastroenterologist. Until such time as highly specific and sensitive diagnostic tests for IBD are devised, distinguishing among various forms of intestinal inflammation of idiopathic and identifiable causes will remain a test of clinical acumen, drawing on relevant history, attentive physical examination, judicious laboratory testing, and detailed review of radiographic, endoscopic, and pathologic data.This article reviews the findings that are most helpful in distinguishing various forms of intestinal inflammation. The comments below are divided into 2 parts: first, a review of the points of history, physical examination, and laboratory data useful in correctly diagnosing patients who present with a clinical syndrome suggestive of IBD; and second, a summary of the features that help to differentiate among inflammatory conditions of the bowel, organized by clinical syndrome as presentations of ileitis, proctitis, colitis, and the difficult pouch.Presentations suggestive of IBDSymptomsWhen a patient presents with symptoms suggestive of IBD, the clinician’s task is, first, to establish whether the patient indeed has IBD or an alternative diagnosis and, second, to differentiate between Crohn’s disease and ulcerative colitis. Presenting symptoms may suggest a particular diagnosis but are not often definitive. Although acute onset of diarrhea may be seen in infectious colitides, as well as in IBD and ischemic colitis, most cases of infectious enterocolitis will not be preceded by subtle disturbances of bowel habit in the medium or long term. Detailed questioning about the timing of the onset of symptoms is also useful in placing histopathologic findings in the correct context because evidence of chronicity is an aspect of bowel histology useful in distinguishing IBD from other causes of intestinal inflammation. Increased stool frequency and decreased stool consistency are the most common presenting symptoms of ulcerative colitis and Crohn’s disease; however, altered bowel habit need not be present in either diagnosis. Patients with proctitis, in particular, may present with a complaint of constipation 5% to 10% of the time.Abdominal pain is the second most common symptom of IBD. For many patients with ileal Crohn’s disease, the predominant complaint is right lower quadrant pain, often exacerbated by eating. Other localizations of pain may be reported in rough proximity to the localization of disease. Patients with ulcerative colitis commonly report cramping prior to and relieved by a bowel movement, often localized to the left lower quadrant, reminiscent of altered defecation reported in irritable bowel syndrome. Persistent pain is an uncommon feature of ulcerative colitis except in severely active disease, when inflammation may extend to the serosa.Tenesmus is a clue to the presence of proctitis, and will be more suggestive of ulcerative colitis because of the universal involvement of the rectum, and less commonly as a presentation of Crohn’s proctitis. Particularly when tenesmus is the chief complaint, consideration should be given to sexually transmitted diseases. A history of anal receptive sexual practices should be elicited. Patients with tenesmus and hematochezia also should be queried about symptoms of prolapse. Rectal prolapse may result in distal rectal inflammation reminiscent of ulcerative proctitis. Patients may not distinguish between passage of purulent exudate, suggestive of inflammation, and mucus, common in irritable bowel syndrome. The presence of blood with mucus, however, is suggestive of ulcerative colitis or a variety of infectious colitides. In general, the presence of gross blood in the stool favors ulcerative colitis over Crohn’s disease, and, the more pronounced the presence of blood, the stronger the association.History provides useful clues to differentiate organic from functional causes of altered bowel habit and abdominal pain. Alternating diarrhea and constipation more strongly suggests irritable bowel syndrome than IBD, whereas nocturnal diarrhea is rarely noted in functional disorders of the bowel. Careful elicitation of systemic symptoms such as fever or weight loss is useful, particularly in children, in whom more typical symptoms may be lacking, as is careful questioning about symptoms of any of the classic skin, eye, or joint manifestations of IBD. If not specifically queried, many patients fail to mention episodes of perianal abscess or anal fissure that may have occurred as isolated events years before the diagnosis of IBD was manifest—an unrecognized clue to the subsequent diagnosis. Functional symptoms may present a challenge even after a diagnosis of IBD has been firmly established. Lingering abdominal pain and loose, frequent or urgent stools may sometimes persist long after effective treatment has brought inflammation under control, potentially confounding accurate assessment of response to medications. It is worthwhile to seek the objective data of endoscopy and histology or biologic markers of inflammation in such seemingly refractory cases.Risk factorsMedication exposures are an important part of the history in a presentation of suspected IBD. Nonsteroidal anti-inflammatory drugs may trigger a new presentation of IBD or may themselves be a cause of a variety of conditions mimicking IBD. Exposure to antibiotics may suggest Clostridium difficile colitis and should be sought in every patient. Travel history and exposure to contacts with enteric illnesses or to unprocessed foods or water will warrant careful exclusion of infectious etiologies, including stool assay for Giardia or cryptococcal antigen. Risk factors for HIV may suggest the need for rigorous evaluation for opportunistic causes of diarrhea or dysentery.Smoking and history of prior appendectomy may be additional clues in suspected IBD. Numerous studies have robustly reproduced the observation that ulcerative colitis is a disease of exsmokers and nonsmokers, whereas Crohn’s disease is more prevalent among smokers.1Bridger S Lee J.C Bjarnason I Jones J.E Macpherson A.J In siblings with similar genetic susceptibility for inflammatory bowel disease, smokers tend to develop Crohn’s disease and non-smokers develop ulcerative colitis.Gut. 2002; 51: 21-25Crossref PubMed Scopus (82) Google Scholar Accordingly, one might more strongly suspect ulcerative colitis than Crohn’s disease in someone who has recently quit smoking. Prior appendectomy has been shown to reduce the risk of developing ulcerative colitis2Andersson R.E Olaison G Tysk C Ekbom A Appendectomy and protection against ulcerative colitis.N Engl J Med. 2001; 344: 808-814Crossref PubMed Scopus (158) Google Scholar and, conversely, may increase the risk for Crohn’s disease.3Andersson R.E Olaison G Tysk C Ekbom A Appendectomy is followed by increased risk of Crohn’s disease.Gastroenterology. 2003; 124: 40-46Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar Epidemiologic associations such as these, although consistent in observational studies, may have little discriminatory value in diagnosing the individual patient.A family history of IBD may also suggest this diagnosis. The heritable tendency for IBD appears to be greatest in those with first-degree relatives,4Freeman H.J Familial Crohn’s disease in single or multiple first-degree relatives.J Clin Gastroenterol. 2002; 35: 9-13Crossref PubMed Scopus (26) Google Scholar in Crohn’s disease more than in ulcerative colitis,5Halfvarson J Bodin L Tysk C Lindberg E Jarnerot G Inflammatory bowel disease in a Swedish twin cohort a long-term follow-up of concordance and clinical characteristics.Gastroenterology. 2003; 124: 1767-1773Abstract Full Text Full Text PDF PubMed Scopus (161) Google Scholar and in families of Ashkenazi (Eastern European) Jewish heritage.6Yang H McElree C Roth M.P Shanahan F Targan S.R Rotter J.I Familial empirical risks for inflammatory bowel disease differences between Jews and non-Jews.Gut. 1993; 34: 517-524Crossref PubMed Google Scholar Although of interest for completeness, the predictive value of these historic points cannot be high because approximately 80% of patients have no family history, whereas the majority of patients with a family history of IBD who present with complaints of altered bowel habit will have other underlying conditions, irritable bowel syndrome being highly prevalent in the population.Physical findingsPhysical findings in Crohn’s disease and ulcerative colitis may overlap considerably. Fever is more often seen in Crohn’s disease than in ulcerative colitis, in which fever is more often an indication of severe inflammation. Clubbing of the fingernails is more common in Crohn’s disease than in ulcerative colitis and is indicative of chronically active disease.7Perry P.M Evans G.A Davids J.D Regional ileitis, ulcerative colitis and clubbed colitis.Gastroenterologica. 1972; 107: 272-282Google Scholar, 8Fielding J.F Cooke W.T Finger clubbing and regional enteritis.Gut. 1971; 12: 442-444Crossref PubMed Google Scholar At the extremes of age, gastrointestinal symptoms may be overshadowed by systemic findings, such as growth failure, failure to thrive, unexplained weight loss or fever.Although bleeding is far less prominent in Crohn’s disease than in ulcerative colitis, patients with the latter diagnosis may occasionally present solely with a finding of fecal occult blood.9Sakata T Niwa Y Goto H Hirooka Y Hayakawa T Ohmiya N Kobayashi S Asymptomatic inflammatory bowel disease with special reference to ulcerative colitis in apparently healthy persons.Am J Gastroenterol. 2001; 96: 735-739Crossref PubMed Google Scholar, 10Howarth G.F Robinson M.H Jenkins D Hardcastle J.D Logan R.F High prevalence of undetected ulcerative colitis data from the Nottingham fecal occult blood screening trial.Am J Gastroenterol. 2002; 97: 690-694Crossref PubMed Google Scholar When queried, most such patients will admit to some visible rectal bleeding or diarrhea, and fewer than 1 in 5 such patients are completely asymptomatic. The prognosis in these individuals is excellent because most continue to have minimal symptoms, and less than one quarter of these patients will require treatment for symptoms.10Howarth G.F Robinson M.H Jenkins D Hardcastle J.D Logan R.F High prevalence of undetected ulcerative colitis data from the Nottingham fecal occult blood screening trial.Am J Gastroenterol. 2002; 97: 690-694Crossref PubMed Google ScholarMucocutaneous manifestations in Crohn’s disease and ulcerative colitis may also overlap. Although mouth sores are more frequent and troublesome in Crohn’s disease, they are still common in ulcerative colitis and, indeed, in the general population.11Farquharson A Ajagbe O Brown R.S Differential diagnosis of severe recurrent oral ulceration.Dent Today. 2002; 21: 74-79PubMed Google Scholar Notably, recurrent and severe aphthous stomatitis may be a feature of human immunodeficiency virus (HIV) infection or Behçcet’s syndrome. Classic skin findings of IBD, such as erythema nodosum, pyoderma gangrenosum, and papulonecrotic skin lesions are also not pathognomonic of IBD or specific to either Crohn’s disease or ulcerative colitis. Historically, erythema nodosum has been said to be more common in Crohn’s disease than in ulcerative colitis,12Samitz M.H Cutaneous lesions of the lower extremities in the diagnosis of systemic disease.J Am Podiatry Assoc. 1975; 65: 556-567PubMed Google Scholar whereas pyoderma gangrenosum has been reported more often in ulcerative colitis. Again, the predictive value of these syndromes is low, and there is considerable overlap in these associations. The presence of an abdominal mass, especially in the right lower quadrant—representing ileocecal inflammation—or perianal disease (skin tags, anal fissure, perianal fistula) are among the more helpful physical findings suggestive of Crohn’s disease. Anal stenosis is another common finding in Crohn’s disease. Conversely, perianal fistulas and anal fissures are distinctly rare in ulcerative colitis. Even so, the distinction is not absolute because even healthy individuals may have uncomplicated fistula-in-ano (i.e., not traversing the internal anal sphincter) or a superficial anal fissure, whereas rectovaginal fistulas may occasionally complicate severe ulcerative colitis.Laboratory dataLaboratory data, when abnormal, may be useful in distinguishing functional disorders of the bowel from infection and IBD. However, numerous parameters, including white blood cell count, hemoglobin and hematocrit, platelet count, iron saturation, erythrocyte sedimentation rate, and C-reactive protein, may cover the full spectrum from normal to markedly abnormal in Crohn’s disease and ulcerative colitis, as well as in non-IBD causes of inflammation. Thrombocytosis, however, occurs to a greater extent in Crohn’s disease than in ulcerative colitis, unless active bleeding has occurred.Recent interest has focused on sensitive assays for leukocytes in the stool, such as fecal calprotectin13Bunn S.K Bisset W.M Main M.J Golden B.E Fecal calprotectin as a measure of disease activity in childhood inflammatory bowel disease.J Pediatr Gastroenterol Nutr. 2001; 32: 171-177Crossref PubMed Scopus (108) Google Scholar and fecal lactoferrin,14Kane S.V Sandborn W.J Rufo P.A Zholudev A Boone J Lyerly D Camilleri M Hanauer S.B Fecal lactoferrin is a sensitive and specific marker in identifying intestinal inflammation.Am J Gastroenterol. 2003; 98: 1309-1314Crossref PubMed Scopus (152) Google Scholar as a means of distinguishing between IBD and functional bowel disease. These tests are highly specific in differentiating IBD from functional bowel disorders.15Tibble J.A Sigthorsson G Foster R Forgacs I Bjarnason I Use of surrogate markers of inflammation and Rome criteria to distinguish organic from nonorganic intestinal disease.Gastroenterology. 2002; 123: 450-460Abstract Full Text Full Text PDF PubMed Scopus (184) Google Scholar They are not, however, specific across the entire differential diagnosis of IBD because these markers may be elevated in a variety of enteric infections,16Greenberg D.E Jiang Z.D Steffen R Verenker M.P DuPont H.L Markers of inflammation in bacterial diarrhea among travelers, with a focus on enteroaggregative Escherichia coli pathogenicity.J Infect Dis. 2002; 185: 944-949Crossref PubMed Scopus (55) Google Scholar with nonsteroidal anti-inflammatory drug (NSAID) use,17Tibble J.A Sigthorsson G Foster R Scott D Fagerhol M.K Roseth A Bjarnason I High prevalence of NSAID enteropathy as shown by a simple faecal test.Gut. 1999; 45: 362-366Crossref PubMed Google Scholar and with bowel neoplasm.18Tibble J Sigthorsson G Foster R Sherwood R Fagerhol M Bjarnason I Faecal calprotectin and faecal occult blood tests in the diagnosis of colorectal carcinoma and adenoma.Gut. 2001; 49: 402-408Crossref PubMed Scopus (77) Google ScholarAn essential part of any new diagnosis of IBD is to exclude infectious causes of enteritis or colitis. Symptoms lasting longer than 4 weeks are less likely to have an infectious etiology. It is common, however, for a first episode of IBD to present after documented enteric infection. Although every evaluation for suspected IBD should include stool sampling for culture and sensitivity, ova and parasites, and Clostridium difficile toxin assay, infectious agents are isolated in less than half of cases presumed to have enteric infections in even the best of clinical laboratories. The rate of identification increases somewhat with culture of colonic aspirate during colonoscopy and culture of biopsy material. Histology is helpful in identifying intestinal tuberculosis, amebiasis, and cytomegalovirus infection. Distinct features of intestinal histopathology may also suggest nonspecific infectious colitis (see below).Clinical syndromesPatients with symptoms, risk factors, or physical or laboratory findings consistent with possible IBD inevitably undergo radiographic and/or endoscopic imaging. These modalities are in many ways complementary, confirming the presence of suspected bowel inflammation and providing critical information about the anatomic localization of the process.IleitisAlong with numerous other conditions, Crohn’s disease of the ileum may cause right lower quadrant pain or diarrhea (Table 1). In many instances, abdominal computerized tomography (CT) or ultrasound will identify the appendix or female reproductive organs as the source of symptoms. Alternatively, abdominal CT may identify ileal thickening or lymphadenopathy or more suggestive findings of stricture or fistula. CT findings alone should never be taken as confirmation of Crohn’s disease, regardless of the presenting symptoms in that none of these findings are pathognomonic of the diagnosis.Table 1Differential Diagnosis of IleitisInfectionYersinia enterocoliticaYersinia pseudotuberculosisMycobacterium tuberculosisMycobacterium avium-intracellularecomplexTyphlitisHistoplasma capsulatumSalmonellaCryptococcosisAnisakiasisActinomycosis israeliiInflammationAppendicitisAppendiceal abscessCecal diverticulitisGynecologicPelvic inflammatory diseaseTuboovarian abscessOvarian cyst or tumorEndometriosisOvarian torsionEctopic pregnancyNeoplasmCecal or small bowel (ileal) adenocarcinomaLymphomaLymphosarcomaCarcinoid tumorMetastatic cancerDrug-relatedNonsteroidal antiinflammatory drug-related ulcer or strictureIschemic: oral contraceptives, ergotamine, digoxin, diuretics, antihypertensivesVascularIschemiaVasculitides: polyarteritis nodosa, Churg-Strauss syndrome, Takayasu’s arteritis, Wegener’s granulomatosis, lymphomatoid granulomatosis, giant cell arteritis, rheumatoid arthritis vasculitis, thromboangiitis obliteransHenoch-Schönlein purpuraSystemic lupus erythematosusBehçet’s syndromeInfiltrativeEosinophilic gastroenteritisAmyloidosisLymphoid nodular hyperplasia (normal or suggestive of IgG deficiency)Torsion of the appendiceal epiploicaIleitis associated with spondyloarthropathyBackwash ileitis arising in ulcerative colitisRadiation enteritis Open table in a new tab Excluding causes obviously related to other organ structures, a variety of other conditions may mimic Crohn’s ileitis. Lymphoid hyperplasia may be prominent in adolescents and young adults. The nodularity may occasionally be so marked as to be confused for Crohn’s disease. Although a normal finding in most cases, rarely, this may be a clue to unsuspected hypogammaglobulinemia.19Ajdukiewicz A.B Youngs G.R Bouchier I.A Nodular lymphoid hyperplasia with hypogammaglobulinaemia.Gut. 1972; 13: 589-595Crossref PubMed Google ScholarNotably, a small number of infections are capable of causing chronic ileal inflammation. These include Mycobacterium tuberculosis, Yersinia enterocolitica, Entamoeba histolytica, and actinomycosis. The latter, although quite rare, is capable of causing fistulization, which might otherwise be taken as strong evidence of Crohn’s disease.20Klaaborg K.E Kronborg O Elsen H Enterocutaenous fistulization due to Actinomyces odontolyticus.Dis Colon Rectum. 1978; 21: 374-376Crossref PubMed Google Scholar Yersinia species are currently of special interest because these have been proposed to play a causal role in Crohn’s disease as part of the so-called cold-chain hypothesis of Crohn’s disease.21Hugot J.P Alberti C Berrebi D Bingen E Czard J.P Crohn’s disease the cold chain hypothesis.Lancet. 2003; 362: 2012-2015Abstract Full Text Full Text PDF PubMed Scopus (97) Google ScholarNeoplastic processes are rare in the ileum, but those with a propensity for this site include adenocarcinoma, lymphoma, and carcinoid. Lymphoma in particular may cause mucosal thickening and ulceration strongly resembling Crohn’s disease.Medications associated with ileal inflammation include oral contraceptives,22Kilpatrick Z.M Silverman J.F Betancourt E Farman J Lawson J.P Vascular occlusion of the colon and oral contraceptives.N Engl J Med. 1968; 278: 438-440Crossref PubMed Google Scholar ergot derivatives, and digoxin. Each of these rarely may precipitate small vessel thrombosis and ischemic ileitis. The thin-walled, centrally perforated fibrotic strictures that arise in association with NSAIDs23Levi S de Lacey G Price A.B Gumpel M.J Levi A.J Bjarnason I “Diaphragm-like” strictures of the small bowel in patients treated with non-steroidal anti-inflammatory drugs.Br J Radiol. 1990; 63: 186-189Crossref PubMed Google Scholar should not be confused for the more robustly fibrotic or inflammatory strictures of Crohn’s disease. NSAIDs may also cause scattered ulcers in the small bowel and the colon. Finally, numerous vasculi-tides that are primary to the intestine or that occur secondary to systemic vasculitis may imitate the endoscopic appearance of Crohn’s ileitis. Findings of vasculitis elsewhere, such as in skin, kidneys, or other organs, should clarify the diagnosis, as should histologic findings consistent with ischemia and perivascular inflammation.Among these conditions, 2 deserve special mention. In Henoch-Schöonlein purpura, gastrointestinal bleeding and crampy or continuous right lower quadrant pain are common presentations. The endoscopic findings may be dramatic, with marked mucosal congestion, submucosal hemorrhage, and ulceration, consistent with ischemia. Classic IgA deposition in purpuric skin lesions, kidney, or bowel will confirm the diagnosis.The ileitis associated with spondyloarthropathies is also of interest and may have considerable overlap with bona fide Crohn’s ileitis.24Mielants H Veys E.M The gut in the spondyloarthropathies.JRheumatol. 1990; 17: 7-10PubMed Google Scholar Ankylosing spondylitis may be seen in patients with either Crohn’s disease (6%) or ulcerative colitis (2.6%) and is strongly associated with being HLA-B27 positive.25Palm O Moum B Ongre A Gran J.T Prevalence of ankylosing spondylitis and other spondyloarthropathies among patients with inflammatory bowel disease a population study (the IBSEN study).J Rheumatol. 2002; 29: 511-515PubMed Google Scholar Peripheral arthropathy has long been known to be associated with colonic inflammation, whether as a reactive arthropathy after infectious colitis or in IBD. By contrast, terminal ileal inflammation is highly prevalent among patients with spondyloarthropathies. In most cases, however, the inflammation is subclinical and most often escapes detection unless colonoscopy is warranted by symptoms. Findings include shallow ulceration and acute and chronic inflammation.Eosinophilic gastroenteritis is a rare inflammatory condition of the gastrointestinal tract that most typically presents with abdominal pain, often with associated diarrhea. The inflammatory infiltrate consists predominantly of eosinophils, with involvement of the submucosa or serosa or the full thickness of the bowel.26Talley N.J Shorter R.G Phillips S.F Zinsmeister A.R Eosinophilic gastroenteritis a clinicopathological study of patients with disease of the mucosa, muscle layer, and subserosal tissues.Gut. 1990; 31: 54-58Crossref PubMed Google ScholarProctitisThe differential diagnosis of inflammation limited to the rectum is brief (Table 2). In addition to ulcerative proctitis, proctitis may also occasionally be the presentation of Crohn’s disease. Clues to Crohn’s proctitis include prominent anal complications, such as fistula, fissure, skin tags, or anal stricture. A variety of sexually transmitted diseases may also manifest as proctitis, including herpes simplex, gonorrhea, chlamydia, lymphogranuloma venereum, and syphilis. Injury by blunt or chemical trauma may also be confused for IBD. Rectal prolapse should be suspected when findings are confined to the distal-most few centimeters of the rectum. The focal lesion of a solitary rectal ulcer may lead one to an erroneous diagnosis of Crohn’s proctitis. The anterior location of the lesion, as well as the predominance of fibrosis and muscular hypertrophy on biopsy, will help redirect the clinician to the correct diagnosis.Table 2Differential Diagnosis of ProctitisProlapseSolitary rectal ulcerTraumaChemical injuryInfectionHerpes simplex type IINeisseria gonorrhoeaeSyphilis (Treponema pallidum)Lymphogranuloma venereumChlamydia trachomatisWhipworm infestationUlcerative proctitisCrohn’s proctitis Open table in a new tab ColitisThe causes of colitis are legion (Table 3). Numerous infectious agents may cause a transient colitis, but the clinical course of most enteric infections is usually complete within 2 weeks of onset. Nevertheless, some episodes may last longer than 6 weeks. When a causative agent is not identified, the issue of sorting out a first presentation of IBD from an acute self-limited colitis arises. Such a distinction relies strongly on histologic rather than endoscopic findings. Once a diagnosis of IBD has been established, Crohn’s disease should be distinguished from ulcerative colitis.Table 3Differential Diagnosis of Colonic InflammationUlcerative colitisCrohn’s colitisIndeterminate colitisAcute self-limited colitisSegmental colitis associated with diverticular diseaseDiverticulitisInfectionsCytomegalovirusShigellaCampylobacterClostridium difficileSalmonellaAeromonas pleisioidesAmebiasisEnterohemorrhagic E. coli (EHEC)Mycobacterium tuberculosisYersinia enterocoliticaSchistosomiasisStrongyloidesIschemic colitisBehçet’s diseaseMicroscopic colitisCollagenous colitisLymphocytic colitisRadiation colitisDiversion colitisChronic granulomatous diseaseGraft-vs.-host diseaseGastrointestinal sarcoidosisEosinophilic gastroenteritisDrug-related (NSAIDs, gold, penicillamine) Open table in a new tab Acute self-limited colitisA variety of names have been given to this syndrome of colitis that is strongly suspected to be infectious in etiology, whether or not an infectious agent has been isolated. In the literature, designations of this syndrome have included the terms “acute self-limited colitis” (ASLC), “acute infectious-type colitis,” and “non-relapsing colitis.”27Kumar N.B Nostrant T.T Appelman H.D The histopathologic spectrum of acute self-limited colitis (acute infectious-type colitis).Am J Surg Pathol. 1982; 6: 523-529Crossref PubMed Google Scholar, 28Schumacher G Sandstedt B Mollby R Kollberg B Clinical and histologic features differentiating non-relapsing colitis from first attacks of inflammatory bowel disease.Scand J Gastroenterol. 1991; 26: 151-161Crossref PubMed Google Scholar When an enteric pathogen is not identified, signs and symptoms distinguish poorly between ASLC and IBD. Onset and duration of symptoms, presence of blood, fever, abdominal pain, number of bowel movements, and even endoscopic appearance do not reliably discriminate between the 2 diagnoses.In this situation, histopathology takes center stage in accurate diagnosis. Evidence-based guidelines for the histopathologic diagnosis of IBD have been developed by the British Society of Gastroenterology.29Jenkins D Balsitis M Gallivan S Dixon M.F Gilmour H.M Shepherd N.A Theodossi A Williams G.T Guidelines for the initial biopsy diagnosis of suspected chronic idiopathic inflammatory bowel disease. The British Society of Gastroenterology Initiative.J Clin Pathol. 1997; 50: 93-105Crossref PubMed Google Scholar The 2 characteristics most suggestive of chronic idiopathic IBD are (1) the presence of architectural distortion and (2) prominent increase in the cellularity of the lamina propria. However, architectural distortion requires time to develop and may not be identified in the first 6 to 8 weeks of either major form of IBD30Allison M.C Hamilton-Dutoit S.J Dhillon A.P Pounder R.E The value of rectal biopsy in distinguishing self-limited colitis from early inflammatory bowel disease.Q J Med. 1987; 65: 985-995PubMed Google Scholar—potentially longer if the inflammation is mild. Features suggesting ASLC include normal architecture, superficial (rather than basal) increase in lamina propria cellularity, intense neutrophilic infiltrate in the early phase of inflammation (without chronic inflammation as signified by basal plasmacytosis or lymphoid aggregates), mucin depletion, discontinuous inflammation, and focal cryptitis. However, the significance of each of these findings depends in large part on the timing of biopsy in relation to onset of the inflammatory process, which is in many cases difficult to know.Epithelioid granulomas, although highly suggestive of Crohn’s disease, cannot be considered diagnostic even when mycobacterial infection has been excluded. Short of finding acid-fast bacilli, histologic features that suggest tuberculosis over Crohn’s disease include the presence of a greater number of granulomas (approximately 5 vs. 1 per high-power field), granulomas with wider diameter (193 micrometer vs. 95), and confluent granulomas with caseating necrosis.31Pulimood A.B Ramakrishna B.S Kurian G Peter S Patra S Mathan V.I Mathan M.M Endoscopic mucosal biopsies are useful in distinguishing granulomatous colitis due to Crohn’s disease from tuberculosis.Gut. 1999; 45: 537-541Crossref Pu
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