Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Colitis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 973 records · Page 54Linked to original sources
PubMed2003

A new flavonoid derivative, dosmalfate, attenuates the development of dextran sulphate sodium-induced colitis in mice.

In this study, we have evaluated the efficacy of dosmalfate, a new flavonoid derivative compound, for the prevention and treatment of experimental colitis. To induce colitis, BALB/c mice received 5% dextran sulphate sodium (DSS) in their drinking water continuously for 7 days. Colitis was quantified by a clinical damage score, colon length, weight loss, stool consistency and rectal bleeding. Inflammatory response was assessed by neutrophil infiltration, determined by histology and myeloperoxidase (MPO) activity. Interleukin (IL)-1 beta, prostaglandins (PG)E(2) and (PG)D(2) concentrations in colonic tissue, histological and histochemical analysis of the lesions were also measured. Dosmalfate (400-800 mg/kg body weight, p.o.) ameliorated severe colitis reduced the degree of inflammation through reduction of neutrophil infiltration and IL-1 beta levels. (PG)E(2) and (PG)D(2) synthesis were significantly reduced in colitis control group and treatment with dosmalfate abolished the decrease in PG synthesis in colon mucosa. We conclude that dosmalfate is protective in acute DSS-induced colitis. The beneficial effects seem to be related to a decrease of neutrophil infiltration, absence of up-regulation of IL-1 beta and increase of PG production in colon mucosa.

Administration, Oral↗
PubMed2005

Fumigaclavine C, an fungal metabolite, improves experimental colitis in mice via downregulating Th1 cytokine production and matrix metalloproteinase activity.

In the present paper, the effect of Fumigaclavine C, a fungal metabolite, on experimental colitis was examined. Fumigaclavine C, when administered intraperitoneally once a day, significantly reduced the weight loss and mortality rate of mice with experimental colitis induced by intrarectally injection of 2, 4, 6-trinitrobenzene sulfonic acid (TNBS). This compound also markedly alleviated the macroscopic and microscopic appearances of colitis. Furthermore, Fumigaclavine C, given both in vivo and in vitro, showed a marked inhibition on the expression of several inflammatory cytokines, including IL-1beta, IL-2, IL-12alpha, IFN-gamma, TNF-alpha as well as MMP-9 in sacral lymph node cells, colonic patch lymphocytes and colitis tissues from the TNBS colitis mice. Meanwhile, the compound caused a dose-dependent reduction in IL-2 and IFN-gamma from the lymphocytes at the protein level and MMP-9 activity. These results suggest that Fumigaclavine C may alleviate experimental colitis mainly via down-regulating the production of Th1 cytokines and the activity of matrix metalloproteinase.

Acremonium↗
PubMed2006

Reconstitution of Scid mice with CD4+CD25- T cells leads to rapid colitis: an improved model for pharmacologic testing.

Improved experimental colitis models are needed for evaluation of treatment strategies for IBD. Most current models either lack resemblance to IBD, are complicated to establish, or the colitis occurs slowly and inconsistently. Our aim was to characterize the course of colitis in C.B-17 Scid mice reconstituted with syngeneic CD25-depleted CD4+ cells, including the identification of useful biomarkers, and assessment of the similarities to IBD with focus on the relationship between colonic epithelial proliferation and inflammatory parameters. Groups of reconstituted and un-reconstituted mice were sacrificed weekly from week 1 to 4. Clinical signs of colitis occurred approximately 2 weeks after reconstitution. Disease onset and severity based on histopathology correlated well with the colonic weight:length ratio, fecal consistency score, presence of occult blood in feces, and fecal IL-1beta content. Loss in body weight was not apparent until colitis was well established and exhibited lower coefficient of correlation to the histologic score. Early colonic histopathology was dominated by epithelial hyperproliferation, loss of mucus and mild lymphoid infiltration. Epithelial hyperproliferation was paralleled by increased fecal soluble tumor necrosis factor receptor II content. Cytokines in colonic tissue homogenates exhibited a Th1-like profile. We conclude that adoptive transfer of CD4+CD25- T cells results in colitis resembling IBD with a rapid onset and limited variability between individuals. Purification of CD4+CD25- T cells is a simple procedure, and does not require flow-cytometric sorting. Fecal consistency score and colonic weight:length ratio are readily measurable and consistent disease parameters. This model is thus highly suitable for pharmacological testing of intervention strategies.

Adoptive Transfer↗
PubMed2004

Overt ischemic colitis after endovascular repair of aortoiliac aneurysms.

OBJECTIVE: Controversy exists as to the cause of ischemic colitis complicating endovascular aneurysm repair. Occlusion of the hypogastric arteries (HAs) during endovascular repair of aortoiliac aneurysms (AIAs) results in a significant incidence of buttock claudication, and has been suggested as a causative factor in the development of postprocedural colonic ischemia, in addition to factors such as systemic hypotension, embolization of atheromatous debris, and interruption of inferior mesenteric artery inflow. To analyze the relationship between perioperative HA occlusion and postoperative ischemic colitis, we reviewed our experience over 2 years with Food and Drug Administration-approved endovascular graft devices for treatment of AIAs. METHODS: Elective repair of AIAs with bifurcated endovascular grafts was performed in 233 patients over a 2-year period. These included 184 AneuRx grafts, 17 Ancure grafts, and 32 Excluder grafts. During the experience, 44 patients (18.9%) underwent unilateral perioperative HA occlusion (28 right, 16 left) during the course of endovascular AIA repair, and 1 patient (0.4%) underwent bilateral HA occlusion. RESULTS: In 4 patients (1.7%) signs and symptoms of ischemic colitis developed 2.0 +/- 1.4 days postoperatively. In all patients the diagnosis was confirmed at sigmoidoscopy, and initial treatment included bowel rest, hydration, and intravenous antibiotic agents. Three patients with bilateral patent HAs required colonic resection 14.7 +/- 9.7 days after the initial diagnosis, and 2 of these 3 patients died in the postoperative period. Pathologic findings confirmed the presence of atheroemboli in the colonic vasculature in all 3 patients who underwent colonic resection. The fourth patient had undergone multiple manipulations of the left HA in an unsuccessful attempt to preserve patency of this vessel during AIA repair. This patient recovered completely with nonoperative management. Perioperative unilateral HA occlusion was not associated with a significantly higher incidence of postoperative ischemic colitis. CONCLUSION: Perioperative HA occlusion during aortoiliac open or endovascular surgery may contribute to development of the rare but potentially lethal complication of ischemic colitis. However, our extensive experience suggests that embolization of atheromatous debris to the HA tissue beds during endovascular manipulations, rather than proximal HA occlusion, is the primary cause of clinically significant ischemic colitis after endovascular aneurysm repair.

Aged↗
PubMed2005

Adoptive transfer of NK 1.1+ lymphocytes in immune-mediated colitis: a pro-inflammatory or a tolerizing subgroup of cells?

UNLABELLED: T lymphocytes expressing NK1.1 marker (NKT) have been suggested to play crucial roles in immune modulation. AIM: To determine the role of NK1.1+ cells in induction and maintenance of pro-inflammatory and/or tolerizing responses. METHODS: Colitis was induced in C57/B6 donor mice by intracolonic instillation of trinitrobenzenesulfonic acid (TNBS). Donor mice received five oral doses of colonic proteins extracted from TNBS-colitis colonic wall. Depletion of NK1.1+ lymphocytes was performed before lymphocyte harvesting. Splenocytes were harvested and separated into T-cell subpopulations, and transplanted into recipient mice before intracolonic instillation of TNBS. Standard clinical, macroscopic, and microscopic scores, and intracellular staining, flow cytometry, and cytotoxicity assays were performed. RESULTS: The adoptive transfer of CD4+ and NK1.1+ cells harvested from tolerized mice markedly ameliorated the colitis in recipient mice. In contrast, the adoptive transfer of CD8+ and double negative lymphocytes failed to transfer the tolerance. Recipients of splenocytes from tolerized mice exhibited an increase in CD4+ IL4+/CD4+ IFNgamma+ ratio. In contrast, recipients of splenocytes from NK1.1-depleted-tolerized mice exhibited severe colitis with a significant decrease of the CD4+ IL4+/CD4+ IFNgamma+ ratio. However adoptive transfer of splenocytes from non-tolerized NKT-depleted mice led to an alleviation of colitis with a relative increase of the CD4+ IL4+/CD4+ IFNgamma+ ratio. CONCLUSIONS: NK1.1+ lymphocytes play a critical role in immune regulation. They may be accountable for an alteration of the inflammatory response and the CD4+ IL4+/CD4+ IFNgamma ratio immune-mediated colitis and in peripheral tolerance induction.

Adoptive Transfer↗
PubMed2004

Contrasting roles for CXCR2 during experimental colitis.

Neutrophil recruitment into the colon is believed to play a crucial pathogenic role in the progression of clinical and experimental inflammatory bowel diseases (IBDs). The chemokine receptor CXCR2 is highly expressed on neutrophils, and promotes neutrophil recruitment in several inflammatory diseases. The present study determined the biological role of CXCR2 during trinitrobenzene sulfonic acid (TNBS)-induced colitis in the rat by assessing effects of CXCR2 antibody neutralization on neutrophil accumulation during the early (8 h) and late phase (day 7) of TNBS-induced colitis. CXCR2 expression was elevated (>3-fold above control) within 8 h and remained elevated to day 7 of colitis induction, in parallel with significant increases in neutrophil infiltration. Treatment of colitic rats with a single dose of CXCR2 neutralizing antibody significantly reduced colonic neutrophil accumulation during the early (8 h) phase of TNBS-induced colitis. However, chronic administration of CXCR2 antibody did not reduce colonic neutrophil accumulation during the late phase (day 7) of TNBS-induced colitis. In summary, the present findings suggest a functional role for CXCR2 in initiating neutrophil recruitment during the early phase of TNBS-induced acute colitis, and demonstrate that: early colonic neutrophil accumulation is CXCR2 dependent and the late phase colonic neutrophil accumulation is CXCR2 independent.

Animals↗
PubMed2003

Development of colitis in signal transducers and activators of transcription 6-deficient T-cell receptor alpha-deficient mice: a potential role of signal transducers and activators of transcription 6-independent interleukin-4 signaling for the generation of Th2-biased pathological CD4+ betabetaT cells.

Forbidden CD4(+)betabeta T cells, which produce interleukin (IL)-4 predominantly, are a pathological subset in the development of colitis in T-cell receptor alpha chain (TCRalpha)-deficient mice. Stimulation of naive CD4(+) T cells with IL-4 induces Th2 development via the activation of signal transducers and activators of transcription (STAT) 6. In the present study, we had found that IL-4 enhanced the expression of STAT6 in CD4(+)betabeta T cells isolated from TCRalpha(-/-) mice with colitis, suggesting that the IL-4 signal in the CD4(+)betabeta T cells is mediated by STAT6. To further investigate the role of STAT6 in the development of colitis induced by TCRalpha deficiency, we generated double-deficient mice by crossing TCRalpha(-/-) mice and STAT6(-/-) mice. Surprisingly, STAT6 deficiency did not result in decreased severity of colitis in TCRalpha(-/-) mice. STAT6-deficient CD4(+)betabeta T cells produced IL-4 and intraperitoneal injection of anti-IL-4 monoclonal antibody in the nondiseased TCRalpha(-/-) and STAT6 double-deficient mice prevented the colitis formation, thus indicating that the cells differentiated into the Th2 phenotype have the ability to mediate the development of the colitis in the absence of STAT6.

Animals↗
PubMed1979

Bowel wall thickness as a differentiating feature between ulcerative colitis and Crohn's disease of the colon.

The colonic wall thickness was assessed from the plain abdominal radiograph and double contrast barium enema in 33 patients with ulcerative colitis, 28 with Crohn's colitis and 20 with neoplasia. The maximum wall thickness in the control group with neoplasia measured in non-diseased colon, was 2 mm. Accurate measurement was possible from only 34% of the plain films, owing to inadequate gas in the lumen. Measurement was possible in 84% of barium enemas, mainly in the descending colon. The maximum wall thickness associated with ulcerative colitis was 5 mm. In 50% of Crohn's colitis the wall thickness was above 5 mm. Estimation of the wall thickness was a slightly less sensitive index of the presence of colitis than the mucosal changes on double contrast enema. Distinction between the types of colitis was usually possible from the mucosal lesions. Where these could be similar, such as with confluent shallow ulceration, the tendency of Crohn's disease to be associated with a wall thickness in excess of 5 mm was valuable diagnostically.

Barium Sulfate↗
PubMed2002

Beneficial effect of a novel non-steroidal anti-inflammatory agent with basic character and antioxidant properties on experimental colitis in rats.

Ulcerative colitis is a chronic disorder of unknown etiology. Conservative treatment remains empirical, even today. The aim of this study was to test the efficacy of a novel non-steroidal anti-inflammatory agent [5-(2-hydroxy-ethylamino)-1-cyclohexyl-2-pentanone] (compound A), with basic character and antioxidant properties on an experimental model of ulcerative colitis in rats. The effect of this compound was compared with that of methylprednisolone on the histological abnormalities and serum levels of tumor necrosis factor-alpha (TNF-alpha) in experimental colitis produced by 2,4,6-trinitrobenzenesulfonic acid (TNB). A total number of 24 rats were randomly assigned to one of four groups of six rats each. Group 1: colitis without treatment (disease control), group 2: normal animals (control), group 3: induction of experimental colitis treated with methylprednisolone (5.3 x 10(-3) mmol/kg i.v. every day for 7 days) and group 4: induction of experimental colitis plus administration of compound A (0.6 mmol/kg i.v. every day for 7 days). The administration of compound A resulted in a statistically significant reduction of the extent of tissue damage and of certain histological features (edema, inflammatory infiltration) (P<0.05). Compound A also resulted in a statistically significant reduction of the levels of serum TNF-alpha, compared to those of controls (P<0.005). The beneficial effect of this compound was probably due to the combination, on a single molecule, of anti-inflammatory and antioxidant properties as well as to its basic character. The reduction of the serum TNF-alpha levels could be one of the possible mechanism(s) of action of the compound. Further studies are necessary to establish the direct mechanism of action(s) of the drug and to evaluate its long-term efficacy and safety.

Animals↗
PubMed2002

Delineation of the protective action of zinc sulfate on ulcerative colitis in rats.

The protective action of zinc compounds in Crohn's disease-like inflammatory bowel disease in animals has been shown. A similar action of zinc sulfate on ulcerative colitis has not been defined. The present study aimed to delineate the protective action of zinc sulfate and the pathogenic mechanisms of 2,4-dinitrobenzene sulfonic acid (DNBS)-induced ulcerative colitis in rats. Zinc sulfate at different concentrations was given either orally (p.o.) or rectally (p.r.) to rats at 42, 48, 66 and 72 h following the induction of colonic inflammation by DNBS. Rats were killed 96 h after instillation of DNBS rectally to assess the severity of colonic damage, myeloperoxidase and xanthine oxidase activities. The involvement of mast cell degranulation and histamine release in the pathogenesis of DNBS-induced colitis was determined by using a mast cell stabilizer (ketotifen) and histamine receptor blockers (terfenadine and ranitidine). DNBS given rectally produced inflammation and ulceration in rats with a pathology resembling ulcerative colitis. Myeloperoxidase activity but not xanthine oxidase activity was sharply increased by this agent. Intrarectal administration of zinc solution and parenteral injection of histamine blockers significantly reduced tissue damage and myeloperoxidase but not xanthine oxidase activity. Ketotifen, a mast cell stabilizer, also significantly decreased mucosal injury and myeloperoxidase activity in the colon. In conclusion, mast cell degranulation followed by histamine release plays an important role in the pathogenesis of DNBS-induced ulcerative colitis. Zinc given rectally has a therapeutic effect against this colitis model, perhaps through the reduction of inflammation and inhibition of the above pathogenic mechanisms.

Animals↗
PubMed2003

The adenosine A3 receptor agonist, N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide, is protective in two murine models of colitis.

This study evaluated the effects of the adenosine A(3) receptor agonist, N(6)-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (IB-MECA), in two murine models of colitis, the dextran sodium sulphate-induced colitis and the spontaneous colitis found in interleukin-10 gene deficient mice. IB-MECA was given orally twice a day at a dose of either 1 or 3 mg/kg/day. Evaluation of colon damage and inflammation was determined grossly (body weight, rectal bleeding) and biochemically (colon levels of myeloperoxidase, malondialdehyde, chemokines and cytokines). There was significantly increased inflammatory cell infiltration into the colon associated with an increase in colon levels of cytokines and chemokines; with subsequent free radical related damage in both dextran sodium sulphate-induced colitis and 10-week-old interleukin-10(-/-) mice. IB-MECA protected in both models against the colitis induced inflammatory cell infiltration and damage and attenuated the increases in colon inflammatory cytokine and chemokine levels. Thus activation of the adenosine A(3) receptor is effective in protecting against colitis.

Adenosine↗
PubMed1985

Characterization of spontaneous colitis in cotton-top tamarins (Saguinus oedipus) and its response to sulfasalazine.

Chronic colitis in the cotton-top tamarin (CTT) has been characterized by obtaining distal colonic biopsy specimens, hematocrits, serum albumins, and stools for bacteriologic and parasitic examination in nondebilitated living CTTs. The species specificity of the histologic features of colitis observed in the CTT was assessed by obtaining distal colonic biopsy specimens from 10 animals of other primate species for histologic examination. Histologic evidence of active colitis was found in 50% of adult CTTs but was absent in all non-CTT species studied. Forty-two stool samples obtained from 18 CTTs yielded only one isolate (Campylobacter). In addition to active colitis, CTT rectal mucosa also often had subtle irregularities in mucosal structure that were not present in nonrelated primate species and might represent chronic colitis. Metaplasia was not observed. The therapeutic effects of oral sulfasalazine (50 mg/kg X day) on CTT colitis were assessed in a randomized 10-wk placebo controlled crossover study. This study demonstrated significant improvement in disease activity as judged histologically (p less than 0.05) and significant increases in animal weight (p less than 0.01) and serum albumin (p less than 0.01) during sulfasalazine therapy when compared with saline control. Sulfasalazine therapy can ameliorate the effects of this disease and offers promise in maintaining experimental colonies of this endangered species for future studies.

Animals↗
PubMed1988

Fecal lactate and ulcerative colitis.

Impaired metabolism of short-chain fatty acids, as well as a modified fecal ionogram, have been reported in ulcerative colitis. Fecal water samples from 62 patients with ulcerative colitis were analyzed in the present investigation to evaluate changes in SCFAs and lactic acid in relation to activity and severity of disease. Short-chain fatty acid levels were high in quiescent and mild disease (162.6 +/- 63.6 and 147.8 +/- 63.2 mM/L, respectively), but significantly decreased in the severe form (64.7 +/- 46.9 mM/L). Lactate showed a progressive increase from mild colitis (3.0 +/- 1.8 mM/L) to severe colitis (21.4 +/- 18.6 mM/L). It thus appears that mild colitis displayed a fecal pattern characterized by normal pH and bicarbonate, slightly impaired electrolyte handling, high short-chain fatty acid values, and only moderately increased lactate. Severe colitis, on the other hand, was characterized by low fecal pH, bicarbonate, and potassium, high sodium and chloride, low short-chain fatty acid levels, and very high lactate levels. A critical lowering of intraluminal pH, which shifts bacterial metabolism from short-chain fatty acid to lactate production, may be responsible for the intraluminal pooling of lactate.

Colitis, Ulcerative↗
PubMed1997

The mechanism of altered neural function in a rat model of acute colitis.

BACKGROUND & AIMS: Distal colitis induced in rats by trinitrobenzene sulfonic acid (TNBS) causes a suppression of [3H]noradrenaline release from the myenteric plexus, of inflamed distal colon, as well as in noninflamed regions of colon and ileum. The aim of this study was to explore the mechanisms underlying these neural changes in TNBS colitis. METHODS: Colitis was induced by intrarectal administration of TNBS, and the animals were killed on day 5. Inflammation was assessed by measuring myeloperoxidase (MPO) activity, and noradrenaline release was measured as 3H release from rats myenteric plexus preparations preloaded with [3H]noradrenaline. These end points were examined: (1) after administration of the locally active steroid budesonide; (2) in congenitally athymic rats; and (3) in rats treated with the interleukin 1 receptor antagonist (IL-1ra) to interleukin 1 beta. RESULTS: In colitis, both topical budesonide and systemic IL-1ra treatments attenuated the suppression of KCl-evoked 3H release from longitudinal muscle myenteric plexus in both inflamed and noninflamed segments. However, neither of these treatments altered MPO activity. A similar suppression of [3H]noradrenaline release was observed in athymic rats after TNBS, although there was a substantially greater increase in MPO activity compared with euthymic rats with colitis. CONCLUSIONS: TNBS-induced colitis alters myenteric nerve function at inflamed and noninflamed sites via a steroid-sensitive and interleukin 1-mediated process that does not require T lymphocytes.

Acute Disease↗
PubMed1999

VCAM-1 and ICAM-1 mediate leukocyte-endothelial cell adhesion in rat experimental colitis.

BACKGROUND & AIMS: The molecular mechanisms responsible for leukocyte recruitment in experimental colitis are poorly understood. The aims of this study were to measure expression of endothelial intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) and to determine their role in leukocyte recruitment in experimental colitis. METHODS: Rats with trinitrobenzene sulfonic acid (TNBS)-induced colitis and control rats were studied 1, 7, or 21 days after treatment. ICAM-1 and VCAM-1 expressions were measured by the double radiolabeled antibody technique. Leukocyte-endothelial cell interactions were determined in colonic venules by fluorescence intravital microscopy. Therapeutic effects of treatment with anti-VCAM-1 antibodies were also assessed. RESULTS: Colonic endothelial ICAM-1 was constitutively expressed and did not increase in colitic animals. In contrast, constitutive expression of VCAM-1 was low but markedly increased (6-fold) 1 and 7 days after induction of colitis. Increased colonic expression of VCAM-1 paralleled macroscopic damage score, myeloperoxidase activity, and increased leukocyte adhesion in colonic venules. The latter was significantly decreased by immunoneutralization of ICAM-1 and completely abrogated by immunoneutralization of VCAM-1. Long-term administration of anti-VCAM-1 antibody resulted in significant attenuation of colitis. CONCLUSIONS: Induction of colitis in rats by TNBS is followed by up-regulation of endothelial VCAM-1. VCAM-1 and constitutive ICAM-1 are major determinants of leukocyte recruitment to the inflamed intestine.

Animals↗
PubMed1998

Evaluation of the colorectal wall in normal subjects and patients with ulcerative colitis using an ultrasonic catheter probe.

BACKGROUND: Ulcerative colitis is usually evaluated by barium enema and colonoscopy, methods of imaging that are limited to the mucosal surface. Endoscopic ultrasonography (EUS) is the best modality for the evaluation of transmural changes in the bowel wall. We therefore evaluated the colorectal wall in normal control subjects and patients with ulcerative colitis using an ultrasonic catheter probe. METHODS: Endoscopic ultrasound with a catheter probe was performed on 36 normal control subjects (36 examinations) and 72 patients (111 examinations) with documented ulcerative colitis. RESULTS: In normal control subjects, the total wall, mucosa, submucosa, and muscularis propria were significantly thicker in the rectum than in the colon. There was no significant difference in the thickness of the colon and rectum among different age groups or between men and women. In ulcerative colitis, we classified the boundary of each layer into three patterns (smooth, irregular, and blurred) and then classified the wall into six types. In Matts grade 2 and 3 ulcerative colitis lesions, the total wall and each layer were significantly thicker than lower grade lesions and normal control subjects. For grade 1 and most of the grade 2 lesions, the boundary of each layer was smooth. In some of the grade 3 lesions, the mucosa-submucosa and submucosa-muscularis propria layer borders were abnormal. In all grade 4 cases, the mucosa-submucosa boundary was blurred. There was some correlation between the Matts grade and EUS findings except for Matts grade 3 lesions which had various EUS patterns. CONCLUSION: Endoscopic ultrasound with a catheter probe is a useful modality for the transmural assessment of the colorectal wall and, when used in conjunction with the many clinical and endoscopic parameters currently available, may contribute to the diagnosis and treatment of ulcerative colitis.

Adult↗
PubMed1998

Cytomegalovirus colitis in acquired immunodeficiency syndrome: a clinical and endoscopic study.

BACKGROUND: Cytomegalovirus colitis is an important complication of the acquired immunodeficiency syndrome (AIDS), although the clinical and colonoscopic manifestations of this disease have not been systematically characterized. METHODS: Patients with AIDS and cytomegalovirus colitis were prospectively identified at two medical centers. The diagnosis of cytomegalovirus disease was based on established endoscopic and histologic criteria. At the time of sigmoidoscopic and/or colonoscopic examination, clinical features were recorded; the location, size, and appearance of all endoscopic abnormalities were documented; and multiple biopsies of any lesions were performed. RESULTS: Fifty-six patients were studied. The majority of the patients were homosexual men with severe immunodeficiency (median CD4 lymphocyte count 15/mm3, range 1 to 294/mm3). Chronic diarrhea and abdominal pain were the most frequent clinical manifestations, seen in 45 (80%) and 28 (50%) patients, respectively. Five patients (9%) presented with lower gastrointestinal hemorrhage, three of whom had no antecedent history of diarrhea. The colonoscopic abnormalities could be categorized into three main groups: colitis associated with ulcer (39%), ulceration alone (38%), or colitis alone (20%). Subepithelial hemorrhage was a prominent endoscopic manifestation of disease. Of the 31 patients undergoing colonoscopy to the cecum, in four (13%) endoscopic evidence of disease was limited to the colon proximal to the splenic flexure. CONCLUSIONS: Cytomegalovirus colitis in AIDS appears to have variable but stereotypical clinical and colonoscopic manifestations. Distal colitis associated with ulceration is the most common colonoscopic pattern.

Acquired Immunodeficiency Syndrome↗
PubMed1999

Appendiceal orifice inflammation as a skip lesion in ulcerative colitis: an analysis in relation to medical therapy and disease extent.

BACKGROUND: Although several reports have claimed that the appendix can be involved as a skip lesion in ulcerative colitis, they do not exclude the possibility that this skip lesion occurs as a result of medical therapy. Also, little is known about the relation between the presence of appendiceal orifice inflammation and the extent of the disease. METHODS: The presence of appendiceal orifice inflammation was prospectively assessed both endoscopically and histologically in 94 patients with active ulcerative colitis, the extent of whose disease had not been beyond the hepatic flexure. To evaluate the effect of prior medical therapy on the prevalence of appendiceal orifice inflammation, all cases were divided into two groups. Group A consisted of 66 patients who had been treated before inclusion; group B was composed of 28 patients newly diagnosed at inclusion. RESULTS: Appendiceal orifice inflammation was diagnosed in 24 (26%) of 94 patients with active subtotal ulcerative colitis, with no statistical difference observed between group A (23%) and group B (32%). In all 94 patients, the frequency of appendiceal orifice inflammation decreased significantly as the extent of disease increased, i.e., 37% in proctitis (n = 49), 17% in left-sided colitis (n = 36), and 0% in extensive colitis (n = 9) (p < 0.05). CONCLUSIONS: Appendiceal orifice inflammation as a skip lesion of ulcerative colitis is not rare, is more frequently observed in patients with less extensive disease, and is not the result of patchy improvement due to medical therapy.

Adult↗