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The authors present the first case report of a 50-year-old woman with a 33-year history of severe, chronic watery diarrhea and hypokalemia secondary to chronic active microscopic enterocolitis with patterns similar to lymphocytic colitis but with acute cryptitis and terminal ileum involvement microscopically. The progressive nature of her illness resulted in multiple hospital admissions secondary to hypokalemia with subsequent chronic renal failure. High continuous doses of oral potassium supplements failed to correct the hypokalemic episodes. After subtotal colon resection, the patient made a marked clinical improvement with normal serum potassium levels without receiving potassium supplementation.

Objective To characterize the histology of AIDS-associated cryptosporidiosis and identify features that explain the clinical variability. Design A retrospective analysis of HIV-positive individuals with cryptosporidiosis who underwent endoscopy at the Johns Hopkins Hospital between 1985 and 1996. Methods The histologic features (intensity of Cryptosporidium infection, inflammation, mucosal damage, copathogens) of gastrointestinal biopsies from 37 HIV-positive individuals with cryptosporidiosis were systematically graded. These histologic features were correlated with the severity of the diarrheal illness obtained from a patient chart review. Results Histologic features associated with Cryptosporidium infection include a neutrophilic infiltrate in the stomach, villus blunting in the duodenum, cryptitis and epithelial apoptosis in the colon, and reactive epithelial changes in the stomach and duodenum. The nature and intensity of the inflammatory response varied widely; however, duodenal biopsies from a subset of patients (37%) revealed marked acute inflammation that was associated with concomitant cytomegalovirus infection. Although duodenal infection was common (93% of individuals), infection of other sites was variable (gastric cryptosporidiosis in 40% and colonic cryptosporidiosis in 74%). Widespread infection of the intestinal tract, which included both the large and small intestine, was associated with the most severe diarrheal illness. Conclusions Cryptosporidium infection produces histologic evidence of gastrointestinal mucosal injury. The inflammatory response to the infection is variable, and may be modified by copathogens such as cytomegalovirus. The clinical manifestations are influenced, in part, by the anatomic distribution of the infection, with extensive infections involving both small and large intestines producing the most severe illness.

U lcerative colitis (UC) is a chronic disease, so changes of chronicity are essential for histologic diagnosis. These chronic changes can be separated into 2 components. The first and most important component is chronic inflammation, which is mainly an increase in plasma cells (plasmacytosis) in the lamina propria. The colonic mucosa is normally in a state of chronic inflammation, so plasma cells are a normal constituent of the lamina propria, with more such cells on the right side and fewer on the left. Therefore, the determination of whether plasmacytosis is present depends on the pathologist’s knowing these normal variations and knowing the specific sites of the biopsies. Eosinophils are often also increased numerically in chronic colonic inflammation, but there is also a wide range of normal numbers of eosinophils in the lamina propria that may be geographic dependent, at least in part. In 1 study of eosinophil numbers in the lamina propria of normal left colon biopsies, there was a gradual increase from north to south along both coasts.1 The normal eosinophil counts were about 30 times higher in New Orleans than in Boston. It is likely that there is also variability in normal individual eosinophil counts as well. Thus, determination of eosinophilia in colonic lamina propria has to take these geographic and individual variations into account. The second component of chronicity is distortion. The normal colonic mucosa has uniform parallel crypts that are evenly spaced as a result of uniformity in the amount of lamina propria that separates them. The surface is flat. Destruction of the normal structures, including crypts and surface mucosa, is followed by regeneration that assumes whatever contours are available. This results in a variety of altered shapes and sizes of crypts and changes in surface contours that vary from undulating to villiform. This combination of chronic inflammation and distortion, diffusely involving some length of colon, is required in at least 1 set of biopsies sometime during the course of the disease to prove histologically that the patient has UC. In children the chronic inflammation is present, but often distortion is less evident than in adults.2,3 Furthermore, since other diseases, such as Crohn’s colitis and the microscopic colitides, including the collagenous and lymphocytic variants, have variable amounts of these two features, more proof is needed that the patient has UC. This proof comes in the form of characteristic clinical features and endoscopic findings of diffuse disease covering stretches of mucosa from rectum only to total colon, and biopsies that sample the entire areas of endoscopic disease as well as biopsies taken from proximal to the endoscopic disease to determine the extent. Full-blown Crohn’s colitis has both distortion and plasmacytosis, but the disease is patchy and intense, both histologically and endoscopically, and there is almost always evidence of small bowel involvement. Crohn’s disease (CD) also often has tiny microscopic foci of inflammation throughout the gastrointestinal (GI) tract, but these are not evidence of important structural disease. Lymphocytic and collagenous colitis have diffuse plasmacytosis, but little distortion, and the mucosa looks normal endoscopically. UC is not a static disease but is a disease that constantly changes as a result of exacerbations and remissions, some of which are treatment-induced at the clinical, endoscopic, and histologic levels. As a result, how UC appears at any given moment depends on whether the disease is in an exacerbation or a remission, and where in that exacerbation or remission it is seen. We know that with time and treatment the UC changes can resolve. The inflammation subsides and the mucosa remodels, often returning to normal. Also, at various times during its evolutions in some patients the histologic and endoscopic disease may become focal or patchy. In addition, significant rectal inflammation can heal and become endoscopically and histologically normal.4–6. In these settings the biopsy changes are no longer diagnostic and may even resemble Crohn’s colitis because of the patchy distribution and normal rectum. Similar changes are found in colectomy specimens. However, in many colectomy specimens the entire mucosa looks normal or near normal, probably because of intense medical treatment prior to resection. Finally, the chronic changes may be accompanied by active inflammation, that is, neutrophils invading crypt epithelium (cryptitis), sometimes resulting in ulcers involving parts of the crypt epithelium as well as pus filling and distending crypts (crypt abscesses). However, the changes of activity are not required for the diagnosis of UC; the chronic changes are required. From the Department of Pathology, University of Michigan, University Hospitals, Michigan, USA. Copyright © 2008 Crohn’s & Colitis Foundation of America, Inc. DOI 10.1002/ibd.20586 Published online in Wiley InterScience (www.interscience.wiley.com).

mainly includes two diseases: collagenous colitis and lymphocytic colitis. The diagnosis relies on specific microscopic changes seen in colonic mucosal biopsies. Collagenous colitis was first described in 1976 by Lindstrom and the typical patient is a middle-aged or elderly woman, with the female-to-male ratio approximately 7: 1. Dear Sir, An 80-year-old Japanese woman was admitted to our hospital with a 4-month history of diarrhea and weight loss (she lost 8 kg during this period). Laboratory data were almost normal. Upper and lower endoscopic examination and radiological enteroclysis revealed no specific findings. Biopsies were taken from the colon and rectum. From seven samples, none of them showed cryptitis, crypt abscess, alternation of crypt or hyperplasia. Congo red staining was also negative. All specimens stained with the Masson trichrome method revealed thickening of the subepithelial collagen layer beneath the basal membrane, inflation of the lamina propria and epithelial lesions with intraepithelial lymphocytes ( fig. 1 ). We made a diagnosis of collagenous colitis and mesalazine therapy (1.5 g/day) was started. As the patient was elderly, we did not choose prednisolone treatment. The symptoms resolved 1 week after the procedure. Microscopic colitis is a disease defined as those entities characterized by chronic watery non-bloody diarrhea, abdominal pain, normal radiological and endoscopic appearances and microscopic abnormalities in the colon [1] . Microscopic colitis Published online: June 24, 2008

Objective: To determine the frequency of atypia and active ulcerative colitis (UC) in rectal mucosa within the anal transitional zone (ATZ). Design: Surgeons identified ATZ tissues from restorative proctocolectomy specimens for determination by surgical pathologists of specific histopathologic features in rectal mucosa of the ATZ. Setting: Surgical referral center for restorative proctocolectomy. Patients: Ninety-four patients with symptomatic UC underwent restorative proctocolectomy between January 1991 and December 1994. Interventions: Specific histopathologic features of active UC in the ATZ were evaluated by a single reviewer who did not know the clinicopathologic details of individual study patients. Main Outcome Measurements: Presence and coexistence of rectal mucosal dysplasia (high or low grade), mucosa classified as indefinite for dysplasia, and acute UC (crypt abscess or cryptitis) in the ATZ. Results: Of 94 ATZ tissue specimens, acute intracryptic inflammation was present in 60 rectal mucosa specimens (64%). In 29 (48%) of these 60 specimens, inflammation was neither widespread nor intense. Rectal mucosal dysplasia (low grade but not high grade) was present in 15 (16%) of 94 ATZs specimens. Inflammation elsewhere in the rectal mucosa accompanied dysplasia in 11 (73%) of 15 ATZ specimens. Rectal mucosa classified as indefinite for dysplasia was present in 24 (26%) of 94 ATZ specimens and coexisted with inflammation in 15 (63%) of these 24. Thus, rectal mucosal atypia was present in 39 (41%) of 94 ATZ specimens, and in 26 (67%) of these 39, abnormal rectal mucosa coexisted with acute inflammation. Conclusions: Rectal mucosa in the ATZ can exhibit active UC and/or atypia. Long-term monitoring is advisable if the ATZ is preserved during restorative proctocolectomy. (Arch Surg. 1995;130:981-983)

Introduction Bile acid malabsorption (BAM) is a common cause of chronic secretory diarrhoea via poorly characterised mechanisms. The aim of this study was to determine if histological abnormalities in colonic mucosa are linked to BAM in patients with chronic diarrhoea. Methods During a 6-year period 264 patients were investigated with SeHCAT for chronic diarrhoea and their retention values recorded (≤8% = positive result; ≥16% = negative result). Colonic biopsies and histological analysis were available in 150 (57%). The patients were categorised as: Group 1: terminal ileum Crohn9s disease, (pre or post resection) n=51. Group 2: Idiopathic BAM (including patients with diarrhoea predominant IBS) n=159. Group 3: BAM secondary to other gastrointestinal disease n=51; of which cholecystectomy (n=37), coeliac disease (n=1), chronic pancreatitis (n=1), bacterial overgrowth (n=2), diabetes (n=4) and other gastrointestinal surgeries (n=6). Group 4: terminal ileum disease plus cholecystectomy n=3. Results A histological abnormality was present in 29% (n=16/56) of the patients with positive SeHCAT, vs 23% (n=17/74) of the patients with negative SeHCAT (p=0.318, two-tailed Fisher9s exact test). Similarly, 30% (n=6/20) of the patients with equivocal SeHCAT results (8%–16% retention) had histological abnormalities. As expected, the highest prevalence of these abnormalities was noted in groups 1 and 4, the subjects with Crohn9s disease, regardless of the presence of BAM. Abnormalities were noted in descriptive terms and included colitis (n=4), chronic inflammation (n=5), cryptitis (n=4), mild non-specific inflammation (n=11), moderate non-specific inflammation (n=5), polyps (n=2), ulceration (n=6) and active inflammatory bowel disease (n=2). 30% (n=8/27) of positive SeHCAT with idiopathic BAM (group 2) had abnormalities on histology compared with 19% (n=10/52) who had negative SeHCAT in group 2, which was again a non-significant difference (p=0.397, two-tailed Fisher9s exact test). The 7% (n=2/28) of patient in group 3 with histological abnormalities also had negative SeHCAT results. Conclusion This retrospective study indicates that colonic histological abnormality is non-specific and coincidental to the presence of bile acid malabsorption in patients with chronic diarrhoea. It is unlikely to be relevant to the mechanism of diarrhoea which is probably non-inflammatory. This might be further studied in the future using faecal markers of inflammation in these patients. Competing interests None declared.

Tu1529 Endoscopic Colon Biopsies From Patients With Chronic Clostridium Difficile Infection Have No Characteristic Histologic Abnormalities Ahren C. Rittershaus, Suntrea Hammer, Barbara J. McKenna Pathology, University of Michigan Hospitals, Ann Arbor, MI Clostridium difficile infection is a common cause of hospitaland communityacquired diarrhea, often occurring after antibiotic treatment for a separate infection. Recommended therapy for acute C. difficile colitis is 10 days of metronidazole or vancomycin. The incidence and virulence of C. difficile is increasing, as is the rate of refractory infection, which we refer to as “chronic C. difficile infection” (CCDI). The histologic findings in acute C. difficile colitis are well documented and include focal surface epithelial necrosis with a neutrophilic infiltrate early in the disease, and complete mucosal necrosis with pseudomembrane formation in the late phase (Fig. 1b). We sought to characterize the histologic findings of CCDI, a previously unstudied area.CCDI was defined as two positive stool toxin assays between 10 days and 6 months apart. In our hospital between 2000 and 2008, 792 patients met these criteria. A review of the pathology database identified 137 patients of this group who had endoscopic colon biopsies within six months after their second positive assay. Clinical history was reviewed and seventy-one patients with a known cause of colitis were eliminated from the study, including ulcerative colitis (26), Crohn disease (5), lymphocytic colitis (1) and graft-versus-host disease (39). Sixty-six patients met criteria. Biopsies were reviewed and grouped into four categories: 1) Normal (Fig. 1a), 2) Severe acute C. difficile-like changes (Fig. 1b), 3) Mild changes (focal acute cryptitis, Fig. 1c, and focal chronic changes, Fig. 1d), and 4) Other. The indication for endoscopy in 61 of 66 cases was colitis, diarrhea or hematochezia. The remaining indications were abdominal pain, iron deficiency anemia, polyps (2) and diverticulosis. Endoscopic and histologic findings are summarized in Table 1. The two cases categorized as “other” include one case of diffuse active chronic colitis without features of acute C. difficile colitis and one case of diffuse healed mucosal injury. All 7 cases with severe acute C. difficilelike changes on histology had endoscopic findings of pseudomembranous or ischemic-type colitis. This is the first study to examine the histologic changes of CCDI. We found no characteristic histologic finding or set of findings associated with CCDI. Eighty-six percent of biopsies were either normal or had only mild, non-specific changes which would likely not alert either the pathologist or gastroenterologist to the possibility of C. difficile infection. These results are somewhat unanticipated as we expected CCDI to have either changes of acute C. difficile colitis or more severe combined active and chronic changes due to ongoing mucosal injury. In summary, gastroenterologists should not be surprised when a diagnosis of “normal” is rendered by a pathologist in a patient with CCDI.

c r t e r A otherwise healthy woman presented with a 3-day history of explosive diarrhea, abdominal cramping, and right red blood per rectum. Rectal examination was notable only or trace bright red blood on the examining glove. Initial laboraory findings included hemoglobin of 10.0 g/dL and a total white lood cell count of 11.4 109/L. Stool studies were negative for Clostridium difficile and enteric pathogens. She underwent further evaluation with colonoscopy (Figure A), which revealed scattered ulcers ranging in size from 5 mm to 2 cm. In total, there were more than 20 ulcers scattered throughout the colon, except for cecal sparing. Ulcer borders were erythematous and edematous with white exudative bases, but without signs of active bleeding. The intervening mucosa between ulceration was normal. Cytomegalovirus immunostain was negative. Biopsies of the lesions showed foci of ulceration and hemorrhage within the lamina propria and scattered foci of cryptitis and crypt abscesses. Three days into her hospital course she developed new hypoxia and had apparently aspirated. A chest x-ray showed extensive infiltrates and consolidation in the left upper lobe, which was new compared with a film taken 10 days prior. She was treated for aspiration pneumonia. She was discharged to home with oxygen and instructions to complete a 10-day course of oral levofloxacin. She was readmitted 6 days later with worsened shortness of breath, intermittent hemoptysis, and acute renal failure (creatinine, 2.0 mg/dL). Unenhanced computed tomography of the chest showed extensive bilateral infiltrates in the upper lobes consistent with diffuse alveolar hemorrhage (Figure B). The patient was found to have a C-reactive protein of 253.9 mg/L and was positive for cytoplasmic anti-neutrophilic cytoplasmic antibody and equivocal for PR3. A renal biopsy demonstrated pauciimmune necrotizing and crescentic glomerulonephritis. A diagnosis of Wegener’s granulomatosis (WG) was made. Our patient underwent treatment with cyclophosphamide and systemic steroids as well as plasma exchange for 14 days. Her respiratory status and renal function improved dramatically. She had no recurrence of gastrointestinal bleeding and was eventually discharged to home. Discrete colonic ulcerations can be seen in Crohn’s disease, nonsteroidal anti-inflammatory drug ingestion, ischemia, or infectious processes (eg, amebiasis, Campylobacter or Yersinia infection.). However, in the context of new pulmonary infiltrates and renal failure, gastrointestinal involvement by vasculitis should be considered. WG, a disseminated, small-vessel necrotizing vasculitis, typically affects the kidneys and respiratory tract. In this rare case, WG initially presented with colonic ulcerations. Colonic ulcerations, typically presenting with lower gastrointestinal bleeding and diarrhea, are unusual manifestations of systemic vasculitides, but they have been described in WG.1,2 At olonoscopy, multiple ulcerations with sharp borders, no surounding inflammation, and in a nonspecific anatomic distribuion are seen.1 Characteristic histologic changes include the presnce of granulomas and vasculitis; however, these are rarely eported in mucosal biopsy material.3 In this case, biopsies of the colonic mucosa were largely nonspecific. This case illustrates that the differential for colonic ulcerations in patients with multisystemic disease should include vasculitis, specifically WG.

Background: Primary eosinophilic gastrointestinal disease (EGID) is a rare spectrum of gastrointestinal disorders that primarily affects the gastrointestinal tract. EGID causes inflammation rich in eosinophilic cells in the absence of known causes for eosinophilia. Eosinophilic colitis (EC) represents the least frequent manifestation of EGID and it is unknown whether it represents an independent group of diseases. Methods: The pathology database of the Calgary Health Region was used to identify all cases of EGID and EC. The medical records of all seven patients diagnosed with EC in the Calgary Health Region from 1996-2008 were retrospectively reviewed and the diagnosis was again confirmed by an expert pathologist. Results: The median age of presentation was 42 years. Four patients (57.1%) were females and three (42.9%) were males. Abdominal pain was present in six patients (85.7%), nonbloody diarrhea in four patients (57.1%), bloody diarrhea in two (28.6%) and two patients (28.6%) had more than 10% significant weight loss. Four patients (57.1%) reported a history of drug allergies indicating a predisposition towards allergic diseases but in none of the patients a distinct allergy causing EC was identified. Two patients (28.6%) were on non steroidal anti-inflammatory drugs at diagnosis. One patient (14.3%) was found to have additional peripheral eosinophilia. On histology, all patients had eosinophilic infiltrate in the Lamina propria, two (28.6%) had additional Muscularis propria infiltrate, and four patients (57.1%) had cryptitis. Conclusion: EC is a rare medical condition with different patterns of presentations. A high index of suspicion is needed to diagnose this disease. Pathology plays a crucial rule in diagnosis and colonic biopsies are important to rule out EC for the indication diarrhea.

Introduction Lymphogranuloma venereum (LGV) is a recognised cause of proctitis which can be difficult to distinguish clinically and histologically from inflammatory bowel disease (IBD). The condition was first described in 2004, following an outbreak in The Netherlands. Lymphogranuloma venereum (LGV) proctitis is caused by L1, L2 and L3 serovars of CT and has evaded detection in recent decades in developed countries. Aim We describe a case series of LGV proctitis seen among HIV-positive men who have sex with men (MSM) who underwent endoscopy and biopsy and were diagnosed provisionally with IBD. Methods A retrospective study was performed in an inner London hospital. Clinical data were collated from confirmed or suspected cases of LGV proctitis where endoscopy and biopsy had been performed as part of the investigation of clinical symptoms. LGV was confirmed by the detection of LGV-specific DNA from rectal swab specimens, with supportive evidence from Chlamydia serology. Stored histological specimens from rectal biopsies were analysed retrospectively for LGV-specific DNA with the use of molecular techniques. Results All 12 cases were in HIV positive homosexual men, median age 41.5 years (range 27–55). In all twelve cases of LGV proctitis rectal biopsies had been obtained. All patients were symptomatic at the time of endoscopy and endoscopic features of proctitis were present in 10 of 12 cases. Mucosal ulceration, cryptitis, crypt abscesses and granulomas were common histological findings but crypt distortion, where seen, was usually mild: in most cases these findings were attributed initially to IBD. All cases were reviewed in gastroenterology or colorectal surgical clinics, where provisional diagnosis of IBD or non-specific proctitis were made. Eight patients were commenced on courses of metronidazole or 5-aminosalicylates. Two patients were given courses of prednisolone. Extraction of LGV-specific DNA from rectal biopsy specimens enabled confirmation of three cases of suspected LGV. Conclusion During the recent epidemic of LGV proctitis among UK MSM, it has become apparent that the clinical, endoscopic and histological features of the infection may closely resemble IBD and this may obscure the diagnosis. Relevant clinicians and pathologists should be alerted to the current epidemiology and clinical features of LGV in the UK.

Segmental colitis associated with diverticular disease (SCAD) is a colonic inflammatory disorder with localized non-granulomatous inflammation at sigmoid colon, and associated with colonic diverticulosis. SCAD is an apparently uncommon disorder in Western. We experienced a rare case of SCAD in a 46-year-old woman who visited the hospital due to abdominal discomfort. Colonoscopic examination showed multiple sigmoid diverticula in association with a segment length colitis. Colonoscopic biopsies of the sigmoid colon demonstrated cryptitis and crypt abscess along with chronic inflammatory cells infiltration. The biopsies of the rectum was histologically normal. The patient was given the diagnosis of SCAD and treated with oral mesalamine. This is the first case of SCAD reported in Korea.

2 4-year-old girl had a history of an acute onset of severe generalized colicky abdominal pain, fever, oral ulcer, loody diarrhea, and melena for 7 days. An examination showed ever, and generalized abdominal tenderness without organoegaly. Her blood tests showed a white blood cell count of 6,400/mL3, a hemoglobin level of 11.8 mg/dL, a hematocrit evel of 34.2%, a platelet count of 122,000/mm3, a neutrophil evel of 80%, an albumin level 2.6, a sedimentation rate of 11 m/h, and a C-reactive protein level of 6.5 mg/dL. A stool ulture, Clostridium difficile toxin, and parasites were negative. A agnetic resonance image of the abdomen showed significant owel-wall thickening in the duodenum and jejunum with dematous changes and sloughing of the mucosa (Figure A). A outine upper endoscopy revealed marked hyperemia, friability, nd edema with focal exudates in duodenum (Figure B). olonoscopy and ileoscopy were normal. The histologic findngs showed mild esophagitis, normal gastric mucosa, crypt bscess formation and cryptitis, fibrinopurulent exudates, an ncrease in mixed primarily neutrophilic inflammatory infilrates, and diffuse submucosal hemorrhage of the duodenum Figure C). The patient responded well with methylpredisolone within 1 week. Eighteen days after her onset of the llness a group of petechial rash appeared on her buttocks and he posterior aspect of her legs and progressed to significant urpura. Henoch-Schonlein purpura (HSP) was diagnosed.

Inflammation occurring in a defunctionalized portion of bowel, following either ileostomy or colostomy, has long been recognized by endoscopists. However, little has been written about this entity, particularly the histopathologic changes. Glotzer et al in 1981 described 10 cases, and coined the term “diversion colitis”. We studied 21 patients without previous history of inflammatory bowel disease who, for reasons including perforated diverticulitis, carcinoma, or trauma, had loop colostomies or Hartmann's procedure performed. Many of these patients became symptomatic with complaints related to the defunctionalized bowel, including rectal discomfort, pain, discharge, and bleeding. Nineteen patients had endoscopic examinations, which revealed a variety of findings including mucous plugs, friability, petechia, erythema, ulcers, exudate, and nodules or polyps. All except one case had tissue from the excluded portions of bowel available for pathologic examination. Most displayed nonspecific changes with mild-to-moderate lymphoplasmacytic infiltrates in the lamina propria, mild architectural alterations of the crypts, and slight decrease in crypt numbers. Ulceration, cryptitis, and crypt abscesses simulating ulcerative colitis were uncommon findings and were observed almost exclusively in more severe cases. Granulomas were observed in two cases, raising the possibility of Crohn's disease.

We report here on two cases wherein it is conceivable that the osteomyelitis of the temporal bone was brought on by secondary complications associated with tonsillar focal infection. The main change to the bone was non-specific osteomyelitis. Cryptitis of the tonsils or fibrosis surrounding the blood vessels (onion skin lesion) was characteristic findings in the pathological studies.

Introduction: Some patients with chronic ulcerative colitis (CUC) develop inflammatory changes of the distal ileum thought to be related to backwash of colonic contents, termed “backwash ileitis” (BI). One previous study showed a high association between BI and carcinoma in CUC (GASTROENTROLOGY 2001;120:841–847). However, in that study, strict pathologic criteria for BI were not utilized. The purpose of this study was to evaluate the risk of dysplasia and/or carcinoma in patients with CUC who have BI. Methods: Ileo-colonic resection specimens from 175 consecutive patients with CUC were evaluated for a wide variety of inflammatory changes in the distal ileum and colon, including the presence and grade of dysplasia and carcinoma. The pathologic features in the colon were compared between patients with BI versus those without BI. Follow-up information was obtained (mean, 32.8 months) to ensure the absence of features of Crohn’s disease. Results: Overall, 35 patients showed inflammatory changes of the distal ileum (M/F ratio, 16/19; mean age, 42 years). Ileal changes included villous atrophy and crypt regeneration without increased inflammation (n 3), increased neutrophilic and mononuclear inflammation in the lamina propria (n 6), patchy cryptitis, and crypt abscesses (n 22), and focal superficial surface erosions (n 4), some with pyloric metaplasia (n 2/4). Except for a higher prevalence rate of pancolitis in patients with BI (94% pancolitis vs. 45% pancolitis, P .001), there were no significant differences in the pathologic features in the colon between patients with or without BI. In general, the severity of ileal inflammatory changes paralleled the severity of colonic activity, except for 4 confirmed CUC patients, who had either subtotal or left-sided colitis in addition to inflammatory changes in the ileum. None of the patients with BI had dysplasia, although 2 had carcinoma (6%), in contrast to 14/140 (10%) control patients who had either low (N 6) or high-grade dysplasia (N 5), or carcinoma (N 3), as their most severe neoplastic lesion. These differences were not statistically significant (P .05). Conclusion: Ileal inflammatory changes in CUC are not uncommon (prevalence rate; 20%) and, in most cases, are consistent with a “backwash” etiology. The prevalence of dysplasia and/or carcinoma is not increased in CUC patients with BI. 6 Short-Term Vegetarian Diet Reduces Oxidative Stress and Increases Antioxidant Defense in Healthy Volunteers Henryk Witmanowski, Karl H. Herzig, Juliusz Przyslawski, Lidia Wadolowska, Jacek Piatek, and Jaroslaw M. Walkowiak

Acute self-limited colitis (ASLC) is a self-limiting diarrheal illness which is often caused by known infectious agents (Campylobacter, Salmonella, and Shigella), but many cases are of unknown etiology. This report describes the histopathologic features of acute self-limited colitis as related to its natural history. The extent of inflammation and regeneration varies with the duration of the disease. In the peak activity stage (within 0-4 days of onset of bloody diarrhea) there is mucosal edema, cryptitis, crypt ulcers, and abscesses. At the time of resolution (within 6-9 days of onset of bloody diarrhea), regenerative features become apparent along with residual focal neutrophilic cryptitis. In the latter stages of resolution, along with some regenerative features, occasional crypts with transmigrating lymphocytes may be present. A rectal biopsy is diagnostic only in the early stages of the disease. Later in the course, the rectal biopsy from patients with ASLC may be nondiagnostic or may be confused with Crohn's disease due to the persistence of focal cryptitis. In our experience, the presence of crypt distortion and basal plasmacytosis are the two most useful criteria to differentiate chronic ulcerative colitis from ASLC.

A retrospective study of cecal and colonic tissues from 28 squirrel monkeys ( Saimiri sciureus and Saimiri boliviensis) demonstrated enteric trichomonads within luminal Crypts. Twenty-One of 28 (75%) had trichomonads in the mucosal epithelium either in cup-like depressions or intraepithelial vacuoles. Organisms were also beneath the superficial luminal mucosal epithelium and between the basement membrane and crypt epitheial cells. Immunoperoxidase staining also identified organisms within the lamina propria and submucosa. Additional histologic changes included mucosal ulceration, multifocal cryptitis, and focal epithelial necrosis. Most areas containing trichomonads did not have an associated inflammatory response.

Acute self-limited colitis (ASLC) must be distinguished from chronic ulcerative colitis (CUC) for the proper early management of patients with the acute onset of bloody diarrhea. This study was undertaken to determine if any clinical, endoscopic, microbiologic, or histologic parameters can be used to make this distinction reliably and quickly. Forty-eight patients with ASLC, 36 patients with chronic ulcerative colitis during their first attack [CUC(F)], and 84 patients with recurrent flares of chronic ulcerative colitis [CUC(R)] were studied prospectively. The presence of fever (temperature greater than 100 degrees F), abdominal pain, or the time from onset of bloody diarrhea to presentation were not discriminatory. Overall clinical and endoscopic severity were identical among the three groups. Microbiologic studies identified an infectious agent in only 42% of patients with ASLC. Histopathologic features always distinguished patients with CUC from those with ASLC. No case of ASLC was misdiagnosed histologically as CUC or vice versa. Plasmacytosis in the lamina propria extending to the mucosal base and mucosal distortion were present in all cases of CUC(F) and CUC(R), but were absent in all cases of ASLC. The finding of focal cryptitis during the resolving phase of ASLC could be confused with similar lesions in biopsy specimens from patients with Crohn's disease and mandates clinical follow-up. Histopathology is thus the only reliable diagnostic tool for the rapid differentiation of ASLC from CUC. However, biopsy specimens are only diagnostic when obtained during the acute phase of illness; that is, usually within the first 4 days from the onset of symptoms.

Lymphocytic colitis, previously termed "microscopic colitis", is a clinicopathologic syndrome of watery diarrhea, grossly normal colonoscopy, and mucosal inflammatory changes. Since lymphocytic colitis is a new, incompletely characterized entity, a histopathologic study was performed to compare lymphocytic colitis (n = 16), collagenous colitis (n = 17), idiopathic inflammatory bowel disease (n = 16), acute colitis (n = 16), and histologically normal colon (n = 12). The study was a blinded semiquantitative analysis of histologic features in the surface epithelium, lamina propria, and crypts. The most distinctive feature of lymphocytic colitis was increased intraepithelial lymphocytes, particularly in the surface epithelium (P = .0001 v idiopathic inflammatory bowel disease, acute colitis, and normal colon). Other prominent features of lymphocytic colitis included surface epithelial damage (P less than .005 v idiopathic inflammatory bowel disease and normal colon), increased lamina propria chronic inflammation (P less than .01 v normal), and minimal crypt distortion or active cryptitis. There were striking similarities between lymphocytic colitis and collagenous colitis, but subepithelial collagen thickening was seen only in collagenous colitis. Idiopathic inflammatory bowel disease showed prominent crypt distortion and greater active inflammation, in addition to minimal intraepithelial lymphocytes. Acute colitis occasionally demonstrated prominent surface epithelial damage, but was otherwise dissimilar from lymphocytic colitis. We reached the following conclusions: (1) the entity "microscopic colitis" shows characteristic histopathology including prominent lymphocytic infiltration of epithelium, and thus, a more appropriate designation is lymphocytic colitis; (2) although lymphocytic colitis closely resembles collagenous colitis, each entity is distinct on biopsy; and (3) lymphocytic colitis is readily distinguishable from idiopathic inflammatory bowel disease, acute forms of colitis, and normal colorectum.

The clinical and pathologic findings in 11 patients with pneumatosis cystoides intestinalis (PCI) are described. Symptoms were variable but localized to the gastrointestinal tract. Only one patient had obstructive airway disease. Although gas cysts of varying sizes were present in the colonic wall in all cases, distinctive changes were also observed in the mucosa. Architectural disturbances were seen in 11 of 13 specimens, and changes mimicking those of inflammatory bowel disease, including cryptitis, crypt abscesses, chronic inflammation, and granulomas, were present. In addition, crypt dilation and partial crypt rupture, with formation of intramucosal cysts, were seen in association with clusters of small gas cysts in the lamina propria. The transgression of gas cysts through the muscularis mucosae and the presence of larger giant cell-lined cysts in the submucosa suggested entry of gas generated in the colonic lumen or within inflamed crypts from the mucosal aspect. Other postulated pathogeneses of PCI are discussed.

The histopathologic features of collagenous colitis were studied in 14 women and one man. All but one patient presented with chronic watery diarrhea; 10 had a history of thyroid disease or unspecified arthritis. All 15 patients showed characteristic thickening of the subepithelial collagen layer (SCL) in colorectal biopsy specimens, but in the distal colorectum the thickening was sometimes absent or borderline. Patchy or diffuse injury to the surface epithelium was seen in all cases and was independent of SCL thickening. The injured surface epithelium was infiltrated by lymphocytes and variably by eosinophils and neutrophils, causing it to resemble the surface epithelial injury seen in the small intestine in celiac disease. Crypts were commonly infiltrated by lymphocytes but without associated epithelial injury. The lamina propria in all patients was expanded by lymphocytes, plasma cells, and eosinophils. Neutrophilic cryptitis was seen in seven patients but was usually sparse. Watery diarrhea abated in eight patients treated with corticosteroids or sulfasalazine and was often paralleled by restoration of surface epithelium, reduction in surface epithelial lymphocytes, diminished SCL thickening, and reduced lamina propria eosinophils. Therapy did not consistently alter other inflammatory changes. The possible role of autoimmunity in collagenous colitis should be investigated because of the following circumstantial evidence: the over-whelming female predominance; the frequent presence of possible immunologically mediated disorders such as thyroid and joint disease; the resemblance of surface epithelial changes to those in celiac disease; and the response to corticosteroids.

Ulcerative colitis in children has not been reported previouslyin Bangladesh. This case report is of a 7 year old girl whopresented with frequent passage of slimy stool mixed with bloodfor 4 months. She also had fever, weight loss, abdominal painand urgency at defecation. Barium enema showed pancolitiswith multiple pseudopolyps and collar button appearance.Colonoscopy revealed a friable and granular mucosa withdiffuse ulceration and multiple pseudopolyps. There was bloodyexudate and the lumen was narrow. Histopathology findingsshowed necrosed tissue probably representing a base of ulcerand inflammatory cell infiltrate in the lamina propria. Thecrypt architecture was distorted with cryptitis and goblet celldepletion. There was no granuloma. She was diagnosed as acase of ulcerative colitis & treated with Sulfasalazine and oralcorticosteroid. Her response to treatment was very well andnow she is on regular follow up.DOI: 10.3329/jbcps.v28i2.5372J Bangladesh Coll Phys Surg 2010; 28: 117-120

Summary A group of 124 patients with ulcerative colitis, who had colon surgery, an autopsy, or both, was studied. Review of clinical data and of proctoscopic, roentgenologic, and histopathologic findings revealed frequent lack -of correlation between them. A segment of bowel, although normal grossly by inspection or x-ray examination, may reveal disease when examined microscopically. Ulceration and pseudopolyp formation were the most constant histologic features. Cryptitis could not account for the mechanism of the ulcerative process. Other features observed in a large proportion of cases were granuloma formation, giant cells, and tissue eosinophilia. Their possible relation to the presence of a hyperimmune mechanism in the bowel wall is discussed. Vascular thrombosis, lymphatic dilation, and perivascular infiltrates were present frequently. Similar features are associated with hypersensitive states in the experimental animal. Acute vasculitis was present in only 1 case; it does not seem to play a role in the mechanism of ulceration in ulcerative colitis. Endothelial desquamation, observed in 3 cases, could not account for either thrombosis or ulceration. No information was obtained concerning the role of changes of the homogenous ground substance or of the number and activity of mast cells—both requiring special techniques and special studies. No suggestion could be found in our material of defective cellular regeneration. Adenomas and carcinomas were present in 26 and 19 per cent of the cases, respectively.

A review of 100 cases of ischiorectal and pararectal abscess showed that 44 already had fistular formation upon entering the clinic and 23 had had one or more incomplete operations. The origin and pathology of pararectal inflammatory disease is traced from the relatively simple acute cryptitis to the complex picture of ischiorectal abscess and fistula. Three factors appear to complicate the picture; (1) delay on the part of the patient; (2) delay on the part of the doctor and (3) incomplete therapy. The principal sources of infection of the ischiorectal space other than that outlined, are tuberculosis, pilonidal cyst with abscess, perforated rectal diverticulitis, trauma and malignancy. The entire excision of the fistular tract with widely open drainage is advocated as the desired form of treatment. Bacteriophage therapy as an adjunct to surgery is suggested.

The original histopathologic description of chronic graft-versus-host disease (CGVHD) of the gastrointestinal (GI) tract was from autopsy series. There is little information on the evaluation of living patients with CGVHD and GI symptoms. We reviewed data on 40 consecutive patients with CGVHD and persistent GI symptoms who underwent endoscopic examinations. The diagnosis of CGVHD in these 40 patients was made on the basis of clinical criteria and confirmed by histology of other involved organs in 70%. Patients had progressive (in 19 patients, or 48%), quiescent (in 11, or 27%) or de novo–type (in 10, or 25%) onset of their CGVHD. Four groups were defined based on the following histologic criteria: (1) consistent with acute GI GVHD if there was marked apoptosis with or without cryptitis, (2) suggestive of acute GI GVHD if there was scattered apoptosis with or without cryptitis, (3) suggestive of chronic GI GVHD if there were at least 2 histologic indicators of chronicity such as fibrosis and significant crypt distortion, and (4) no histologic evidence of GVHD. Results of microbiologic, radiologic, and malabsorption studies, if performed, were also retrieved. Median time from diagnosis of CGVHD to GI endoscopy was 4.5 months (0-109 months). The major GI symptoms at the time of endoscopy were diarrhea, abdominal pain/cramping, nausea/vomiting, weight loss, dysphagia, and early satiety. The endoscopic examination was nonspecific for the diagnosis of GI GVHD except for diffuse mucosal sloughing. Based on the histologic criteria in 22 patients with biopsies, 13 cases (59%) were considered to have acute GI GVHD, and 3 cases (14%) were felt to show possible chronic GI GVHD; changes of both acute and chronic GVHD were seen in 6 (27%) cases. GI dysmotility was diagnosed in 7 (18%) patients, including 2 of the patients who had histologic changes suggestive of chronic GVHD. Other causes of the GI symptoms included infection, drug side effect, and malabsorption. In conclusion, GI involvement by acute GVHD appears to be a major cause of persistent GI symptoms in patients with chronic GVHD. An isolated form of chronic GI GVHD confirmed by histology is an uncommon phenomenon in the actual clinical setting. © 2003 American Society for Blood and Marrow Transplantation Biology of Blood and Marrow Transplantation 9:46-51 (2003)

Campylobacter fetus subspecies have recently been recognized as an important cause of diarrheal illness in humans. We report a case of culture positive C. fetus colitis with colonoscopic findings of segmental mucosal edema, loss of normal vascular pattern with ulceration, and patchy involvement of mucosa. These colonoscopic findings were similar to those seen in granulomatous colitis. However, these findings may be difficult to distinguish from a number of other colonic mucosal diseases such as antibiotic-associated colitis, amebiasis, shigellosis, salmonellosis, invasive E. coli colitis, and ischemic colitis. On histopathologic examination of the mucosa, acute and chronic colitis with crypt abscess formation, mucosal atrophy, and mucous depletion was found which suggested the diagnosis of chronic ulcerative colitis. Cryptitis and crypt abscess are not specific to chronic ulcerative colitis alone and can be seen in many nongranulomatous inflammations of the colonic mucosa. Therapy with erythromycin led to prompt clinical improvement, clearance of the pathogen, and normalization of the colon by repeat examination 11 days after the initiation of the therapy.

A case of acute colitis due to antihypertensive therapy with methyldopa is reported . The colonic biopsies showed heavy infiltrates of eosinophils with crypt abscesses, cryptitis and vascular cuffing. Cessation of methyldopa therapy relieved the colitis with recurrence after restarting methyldopa on two separate occasions.

Fistula-in-ano in infants is thought to begin with a cryptitis that proceeds to a perianal abscess. Of 52 patients in 15 years, 51 were male, 45 were under 12 months, 7 had multiple tracts, and 2 recurred in 6 years; all of which points to a developmental anomaly. We believe the anomaly to be a markedly irregular thickened dentate line that harbors from 3 to 13 deep (3 to 10 mm) abnormal crypts (AC), which foster cryptitis. There have been no recurrences since we started doing cryptotomies on these AC in addition to the fistulotomy. The cause may be a defect in the dorsal portion of the cloacal membrane which fuses with the hindgut during the seventh week.

The whipworm (Trichuris trichiura) is an occasional finding in anorectal disease. All cases of anorectal discharge should include a test for ova and parasites. Trichuris infestations can be eliminated by the use of mebendazole (Vermox), a specific drug which has almost no side effects. It should be remembered that structural diseases of the anorectum, occurring during an infection such as fissure, fistula, and abscess, may persist after the infection has been cured and usually must be treated surgically.

Some patients with chronic idiopathic diarrhea have an apparent nonspecific inflammation of colonic mucosa, even though their colons appear normal by barium enema and colonoscopy. This has been referred to as microscopic colitis. However, the significance of this finding is unclear, because the ability of pathologists to accurately distinguish mild degrees of abnormality has not been established. Furthermore, even if the mucosa of these patients is nonspecifically inflamed, it is not known whether this is associated with deranged colonic function that could contribute to the development of chronic diarrhea. To assess these questions, we first examined colonic biopsy specimens in a blinded fashion, comparing biopsy results from patients with microscopic colitis with biopsy specimens from subjects in two control groups. This analysis revealed that colonic mucosa from six patients with microscopic colitis was in fact abnormal. For example, their mucosa contained an excess of both neutrophiles and round cells in the lamina propria, cryptitis, and reactive changes. These and other differences were statistically significant. Second, colonic absorption, measured by the steady state nonabsorbable marker perfusion method, was severely depressed in the patients. For example, mean water absorption rate was 159 ml/h in normal subjects and was reduced to only 26 ml/h in six patients with microscopic colitis. Results of net and unidirectional electrolyte fluxes and of electrical potential difference suggested that colonic fluid absorption was abnormal because of reduced active and passive sodium and chloride absorption and because of reduced Cl/HCO3 exchange. Small intestinal fluid and electrolyte absorption was abnormally reduced in two of the six patients, suggesting the possibility of coexistent small intestinal involvement in some of these patients. We conclude that nonspecific inflammation of colonic mucosa is associated with a severe reduction of colonic fluid absorption, and that the latter probably contributes to the development of chronic diarrhea.

Histologic and bacteriologic evaluations of tonsils removed at surgery from ten patients with a diagnosis of recurrent tonsillitis were performed. The bacteriology was complex, with an average of 6.3 aerobic bacteria and 3.3 anaerobic bacteria isolated from each patient. Histologic sections revealed chronic cryptitis, with intact tonsillar architecture. These findings provide a possible explanation for the failure of commonly used antibiotic regimens to eradicate recurrent infection from this site.

Inflammatory processes within this transitional zone cannot be separated from one another and often occur together. The source of the infection will usually be found in the crypts of Morgagni, originating in the dorsal crypts and spreading to the adjacent papillae. The area of involvement appears erythematous and edematous, and pus occasionally exudes from the crypts. An association exists between cryptitis and the development of anal fissures, and between anal fissures and hemorrhoidal diseases. The anal canal is for the most part also involved in the inflammatory process. One encounters an anitis, which because of an increased secretion produces a perianitis and perpetuates a perianal eczema (Plate VII/1 and 2). Hypertrophy of the papillae then develops (Plate VII/3–6). These changes have also been described with gonorrhea and lues, which can be diagnosed microscopically using a smear or darkfield examination.

The basic principles of plastic surgery for sliding skin graft have been employed routinely in and about the anal canal. In 2,072 patients operated upon by the authors the infected fissure and crypt-bearing hemorrhoidal tissue was excised and the defect closed primarily with a broad-based sliding skin graft. Any associated disease—hemorrhoids, cryptitis, etc.—was also removed, employing the closed technic.

To the Editor.— The recent publication by Green et al1of two cases of acquired immunodeficiency syndrome (AIDS), in which the presenting features mimicked Crohn's disease, prompts us to report a similar case. Report of a Case.— A 46-year-old homosexual Frenchman, with multiple sexual partners, was admitted to the hospital because of diarrhea and fever. Stool examination revealedGardia lamblia, Endolimax nana, andPseudolimax butchilii, but noSalmonella, Shigella, and Campylobacter. Colonoscopy showed disseminated superficial linear or irregular ulcerations predominantly in the left colon. Pathological study of distal ileal and colonic biopsy specimens showed a mild inflammatory infiltration of the lamina propria by plasma cells, polymorphs and macrophages, rare signs of cryptitis, and colonic erosions. Neither ileal villous atrophy nor pathogens were observed. (A basophil body at the basal area of an enterocyte could have been a Coccidia, ofIsospora bellitype, but this finding was not confirmed by

The large role in anal disease which is played by the crypts of Morgagni is generally recognized. According to Rankin, Bargen and Buie, 1 infection of these structures is the underlying factor not only of cryptitis, anal fissure, periproctitic abscess and anal fistula but also of hemorrhoids. Our own microscopic studies 2 of more than four hundred proctologic specimens demonstrated that the crypts of Morgagni were not by themselves responsible for the frequency of anal infection but that infection originated as a rule in preformed tubules which we called anal ducts. They were found to open into the crypts, affording a ready path for infective organisms from the intestinal lumen into the wall of the anal canal. While the pathogenic significance of the anal ducts was thus established, the question presented itself whether these structures have a definite function or whether they represent a vestigial organ. We hoped to obtain

In a study of 700 children with anorectal complaints, anal stenosis, redundant rectal mucosa, fissures, fistula in ano, cryptitis, colitis, and polyps were diagnosed in all but 20%. In this 20%, two thirds of whom were seen for constipation, no organic cause for the complaint could be found. An anorectal examination should be a part of every physical examination of the newborn, infant, and child. Careful examination of the distal bowel is indicated in all instances of gastrointestinal complaints. All too often, many of these infants and children are treated for intestinal colic, milk allergy, and emotional problems when definite pathological abnormality amenable to correct treatment was present.

To the Editor:— We were surprised and somewhat dismayed at "Non-operative Ligation Treatment of Internal Hemorrhoids" ( 204 :375, 1968). We have used Barron ligation technique since the ligator became commercially available. This is considerably longer than the 18 months mentioned in the article. In our practice of colon and rectal surgery, the patient who has only internal hemorrhoids as a cause of symptoms is a distinct rarity. Anal ulceration, fistula, hypertrophied papillae, and cryptitis frequently coexist with internal hemorrhoids in symptomatic individuals. Hemorrhoids which traverse the anal canal and are distal to the pectinate line are far more likely to cause symptoms than are pure internal hemorrhoids. The article states that hemorrhoidectomy is "extremely unpleasant" for the patient. However, it is our experience that nine out of ten patients undergoing anorectal surgery make some variation of the statement, "If I'd known that this was all there was to it, I

This well-organized volume, based on 450 consultations carried out by the author at the Hopital des Enfants-Malades in Paris, discusses the anorectal anatomy of the child, the technique and indications for endoscopy, and the relative frequency of anorectal disorders in children. Separate chapters cover vascular disorders (angiomas and hemorrhoids), ulcerations, cryptitis, venereal infections, fissures, rectal infections, mucous prolapse, encopresis, constipation, polyps, and malignant tumors. The illustrations are very good, and the therapy recommended is sensible. Each chapter is headed by a brief summary of its contents, and there is an excellent bibliography of the world literature. This book would be a valuable addition to the library of any physician doing endoscopy or anorectal surgery in children, and would be of interest to the general pediatrician.