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PubMed1992

[Radiologic assessment of extent of ulcerative colitis in acute phase].

One of the major reference points for both prognosis and treatment of ulcerative colitis is the assessment of its extent. Plain abdominal radiographs were performed on 97 patients previously diagnosed, by means of rectoscopy and histobiopsy, as having acute ulcerative colitis. Within the following 36 hours they underwent either full colonoscopy or colectomy. The extent of colitis was evaluated by means of double-blind radiography. The results were then statistically compared with those obtained from endoscopy or from direct study of surgical colonic specimens. There was agreement between the final X-ray results and the actual extent of ulcerative colitis in 78 of 97 patients (80.4%, r = 0.86). The highest agreement was observed in those patients whose lesions were localized in the rectosigma (81%) and in those with fully extended colitis (90%). The most useful radiological findings in predicting the extent of colic lesions were irregular mucosal profile and thickening of colic wall. The presence of these two signs, together with the flattening or swelling of interhaustral folds and the impossible visualization of the right colon, are invariably suggestive of fully extended colitis. On the contrary, no abnormal findings were present on plain abdominal films in 74% of proctosigmoiditis cases. Plain abdominal radiography seems to be useful for the initial evaluation of acute ulcerative colitis. It allows the early discrimination between diffuse and localized forms, and makes it possible to postpone more invasive and dangerous investigations to a remissive phase of the disease.

Acute Disease↗
PubMed1979

Malignant potential of chronic ulcerative colitis. Preliminary report.

Prior studies confirm the increased incidence of carcinoma of the colon in chronic ulcerative colitis. The authors reviewed clinical and histologic data retrospectively in 23 patients with colon carcinoma and chronic ulcerative colitis. Twenty-two of these patients had dysplasia of colonic epithelium remote from the cancer. The authors prospectively reviewed clinical data and rectal and colonoscopic biopsy specimens on 36 patients with chronic ulcerative colitis, 12 with Crohn's colitis, and 12 with miscellaneous disorders. Eight patients with chronic ulcerative colitis had dysplasia; 6 have had colectomy, and 2 of these had carcinoma. No patient without chronic ulcerative colitis had dysplasia. Patients with chronic ulcerative colitis should have periodic rectal and colonoscopic biopsies, and those with moderate to marked dysplasia require colectomy because of the increased risk of colon carcinoma.

Adolescent↗
PubMed1976

Antibiotic-associated pseudomembranous colitis.

This review defines the entity pseudomembranous colitis and briefly outlines the supposed etiologic causes of pseudomembranous colitis including antibiotics. The incidence, mortality rate, and natural history of antibiotic-related pseudomembranous colitis is contrasted with other forms and causes of pseudomembranous colitis. The clinical spectrum of antibiotic-related pseudomembranous colitis, ranging from a nonbloody, watery diarrheal state to a life-threatening condition mimicking an acute surgical abdomen, is reviewed. The classic proctoscopic and pathologic findings, as well as common problems encountered in interpretation, are discussed. A complete review of the spectrum of radiographic findings is presented from the nonspecific to the quite characteristic radiographic findings, including both plain film and contrast studies of the colon. These findings are contrasted with the X-ray features of other inflammatory and ischemic colitides and a differential diagnosis is discussed. A section dealing with the treatment of antibiotic-associated pseudomembranous colitis will be included. This section will review the various modes of therapy that have been employed. Finally, a brief section will speculate on the possible etiologic role that antibiotics play in pseudomembranous colitis, including the alteration of the bacterial flora and possible effect on bile salt metabolism.

Administration, Oral↗
PubMed1979

Chronic immune colitis in rabbits.

A chronic colitis has been induced in rabbits having many of the histological features of human ulcerative colitis. Animals were first immunised with the common enterobacterial antigen of Kunin and haemagglutinating antibodies demonstrated in high titre. An immune complex colitis was then established by the injection of soluble immune complexes following mild irritation of the rectum with dilute formalin as previously described. The rabbits developed an acute colitis within the first week but, in contrast with unsensitised rabbits, the inflammation persisted and was still present at six months as assessed by proctoscopy and rectal biopsy. Kunin-sensitised rabbits receiving intravenous saline, antigen, or antibody alone did not develop a chronic colitis. It is suggested that hypersensitivity to colonic bacterial antigens may be one mechanism whereby an acute colitis becomes chronic.

Animals↗
PubMed1975

Colonic epithelial cells and polymorphonuclear leukocytes in ulcerative colitis. An electron-microscopic study.

The following study cinfirms previously reported electron-microscopic findings in ulcerative colitis and agrees with the nonspecific nature of those findings. The study extends these observations in regard to relationship of PMN leukocytes, eosinophil leukocytes, and mast cells to colonic epithelial cells. Strong, though not conclusive, data that PMN and eosinophil leukocytes extensively invade epithelial cells in ulcerative colitis is presented. This finding also is not specific to ulcerative colitis and was found with much less frequency in Crohn's disease of the colon and in salmonella colitis. The presence of intravascular degranulation of PMN leukocytes in ulcerative colitis is confirmed. This study adds additional support to the concept that the major abnormality in ulcerative colitis resides within the colonic epithelial cell.

Animals↗
PubMed1992

Systemic tumor necrosis factor-alpha production in experimental colitis.

Tumor necrosis factor-alpha (TNF) is a cytokine released by mononuclear cells in response to inflammation and sepsis. Since the biological effects of TNF are consistent with the systemic and intestinal features of ulcerative colitis, the role of TNF was examined in a rabbit model of chronic colitis. Peripheral blood mononuclear cells were isolated, stimulated with lipopolysaccharide, and cultured supernatants assayed for TNF levels using a cytotoxic assay on mouse fibrosarcoma L929 cells. Basal levels of TNF production by mononuclear cells from 13 normal rabbits (124.3 units/ml +/- 27.1 units/ml, mean +/- SE) were not different from nine rabbits with colitis (83.6 units/ml +/- 24.4 units/ml, P > 0.05). Treatment with lipopolysaccharide (100 micrograms/ml) induced increased TNF production by mononuclear cells isolated from both normals (672.0 units/ml +/- 197.5 units/ml, P < 0.05) and rabbits with colitis (1114.0 units/ml +/- 489.6 units/ml, P < 0.05). However, at all lipopolysaccharide concentrations stimulated TNF levels were comparable in experimental and control groups (P > 0.05). In light of the role of leukotrienes in inflammation, a separate group of rabbits with colitis was investigated following treatment with an oral leukotriene B4 receptor antagonist. Serum TNF levels in 15 control rabbits (32.5 units/ml +/- 7.6 units/ml, mean +/- SE) were not significantly different from rabbits with colitis receiving either leukotriene B4 receptor antagonist (35.7 units/ml +/- 9.2 units/ml, N = 13) or vehicle alone (50.3 units/ml +/- 10.2 units/ml, N = 14) (ANOVA, P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Sequential histologic evaluations in collagenous colitis. Correlations with disease behavior and sampling strategy.

To evaluate the histologic manifestations of collagenous colitis and correlate histologic changes with disease behavior, 14 patients who had undergone sequential evaluations during 33 +/- 6 months of follow-up were studied. Two hundred twelve tissue specimens from all anatomic regions of the colon (mean, 15 +/- 3 samples per patient) were interpretated independently under code by two pathologists. Eight patients (57%) had histologic resolution after 14 +/- 4 months of empiric therapy and in only one of these (12%) did symptoms persist. Four patients (29%) had sequential histologic examinations from the same anatomic region that varied from classical collagenous colitis to inflamed mucosa without a thickened collagen band to normal mucosa. Eight patients (57%) had varying histologic findings from different anatomic regions during the same examination that ranged from classical collagenous colitis to increased inflammation with resolution of the collagen band to normal mucosa. Normal mucosa was found mainly in specimens from the rectosigmoid, and proctosigmoidoscopic examinations alone would have missed the diagnosis of collagenous colitis in 40% of cases. Pathologic interpretations were concordant in 171 of 212 instances (81%). We conclude that histologic resolution of collagenous colitis can occur and it is associated with loss of symptoms. The histologic features of collagenous colitis are distinctive, but they may be patchy and inconsistently sampled. Rectosigmoid biopsies underestimate the diagnosis.

Adult↗
PubMed1992

Oxygen radicals in ulcerative colitis.

This article reviews the pathophysiologic concept that superoxide and hydrogen peroxide, generated by activated leukocytes, together with low-molecular-weight chelate iron derived from fecal sources and from denatured hemoglobin, amplify the inflammatory response and subsequent mucosal damage in patients with active episodes of ulcerative colitis. The putative pathogenic mechanisms reviewed are as follows: (1) Dietary iron is concentrated in fecal material owing to normally limited iron absorption. (2) Mucosal bleeding, characteristic of ulcerative colitis, as well as supplemental oral iron therapy for chronic anemia, further conspire to maintain or elevate mucosal iron concentration in colitis. (3) Fenton chemistry, driven especially by leukocyte-generated superoxide and hydrogen peroxide, leads to formation of hydroxyl radicals. (4) The resultant oxidative stress leads to the extension and propagation of crypt abscesses, either through direct membrane disruption by lipid peroxidation or through generation of secondary toxic oxidants such as chloramines. (5) Chemotactic products of lipid peroxidation, including 4-hydroxynonenal, provide positive feedback to accelerate this inflammatory/oxidative process, leading to acute exacerbations of the disease. (6) Other oxidized products, such as oxidized tryptophan metabolites, created by free radical mechanisms in or near the mucosa, may act as carcinogens or tumor promotors that contribute to the exceedingly high incidence of colon carcinoma in patients suffering from chronic ulcerative colitis. In this way, self-sustaining cycles of oxidant formation may amplify flare-ups of inflammation and mucosal injury in ulcerative colitis. This concept, if proved correct by subsequent research, would provide a rationale for several novel clinical approaches to the management of ulcerative colitis, including use of SOD mimetics, iron chelators, and chain-breaking antioxidants.

Antioxidants↗
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↗
PubMed1992

Childhood exposure to environmental tobacco smoke and the risk of ulcerative colitis.

Previous reports have suggested that there may be a protective effect of active cigarette smoking on the risk of ulcerative colitis. Because passive smoking may also have other health consequences, the authors examined the effect of exposure to environmental tobacco smoke during childhood on adult risk of ulcerative colitis in a case-control study of 172 cases drawn in 1986-1987 from the rosters of North Carolina chapters of the Crohn's & Colitis Foundation of America and 131 peer-nominated neighborhood controls. Active smokers were less likely to develop ulcerative colitis than were nonexposed nonsmokers (odds ratio = 0.53, 95% confidence interval 0.24-1.14). The risk was also decreased in passive smokers, i.e., those whose parents had smoked (odds ratio = 0.50, 95% confidence interval 0.25-1.00). Risk estimates were not related to sex, education, age at onset of symptoms, or year of onset of symptoms. Both active smoking in adulthood and passive childhood exposure to environmental tobacco smoke appear to decrease the risk of ulcerative colitis. The results indicate that childhood passive smoke exposures can influence adult susceptibility to ulcerative colitis.

Adult↗
PubMed1976

The extra-intestinal complications of Crohn's disease and ulcerative colitis: a study of 700 patients.

The records of a series of 700 patients with inflammatory bowel disease, 498 with Crohn's disease and 202 with ulcerative colitis, have been analyzed to determine the relative incidence and characteristic features of their extra-intestinal manifestations. The group with Crohn's disease included 62 with colitis, 223 with ileocolitis, and 213 with regional enteritis. A consideration of the clinical patterns and an understanding of their pathophysiology suggested a subdivision into two main groups: one "colitis related" and one related to the pathophysiology of the small nonspecific third group. Group A, colitis related, comprises joint, skin, mouth, and eye disease. The complications might be immunologically determined, were closely associated with active inflammation, and often responded to medical or surgical treatment of the underlying bowel disease. They occurred in 36% of the entire series of patients: joints were involved in 23%, skin in 15%, and mouth and eye each in 4%. Pyoderma gangrenosum was observed most often in ulcerative colitis and erythema nodosum most often in granulomatous colitis. The incidence of Group A complications was higher in disease involving the colon (42%) than in disease restricted exclusively to the small bowel (23%). There were interrelationships among the various members of Group A, with multiple manifestations occurring in a third of affected patients. Group B, related to small bowel pathophysiology, includes malabsorption, gallstones, kidney stones, and non-calculous hydronephrosis and hydroureter. Disorders in this group were generally related to the severity of the disease in the small bowel and tended to persist even in the absence of active inflammation. In contrast to Group A, this group occurred most frequently in small bowel disease, and least in colonic disease. Malabsorption was virtually confined to the patients with small bowel disease (10% incidence), while gallstones and renal stones were also both more frequent in Crohn's disease (11% and 9% respectively), the latter usually in association with small bowel resection or ileostomy. Group C, found in a small percentage of patients, consists of nonspecific complications, including osteoporosis (3%), liver disease (5%), peptic ulcer (10%), and amyloidosis (1%).

Amyloidosis↗
PubMed1976

Anergy to dinitrochlorobenzene and depression of T-lymphocytes in Crohn's disease and ulcerative colitis.

Skin reactivity to dinitrochlorobenzene (DNCB) and levels of circulating T-lymphocytes were measured in 15 patients with ulcerative colitis, 15 patients with Crohn's disease, and 12 normal control subjects. Diminished reactivity to DNCB was demonstrated in 87% of patients with Crohn's disease (P less than 0-001) and in 53% with ulcerative colitis (P less than 0-02), as compared with only 8-5% of controls; anergy was more frequent in Crohn's disease than in ulcerative colitis (P less than 0-05). Levels of circulating T-lymphoctes were also depressed in both Crohn's disease and ulcerative colitis (P less than 0-001) as compared with controls, with the values lower in Crohn's disease than in ulcerative colitis (P less than 0-02). There were no correlations of DNCB response with extent, duration, or severity of disease nor with T-cell levels within any patient group. These data provide further support for the concept that there is impairment of cell-mediated immunity among many patients with chronic inflammatory bowel disease, including both Crohn's disease and ulcerative colitis.

Colitis, Ulcerative↗
PubMed1992

DNA aneuploidy in Crohn's disease and ulcerative colitis: results of a comparative flow cytometric study.

DNA ploidy and S-phase fractions were assessed by flow cytometry in colonic biopsy specimens from 28 patients with ulcerative colitis and 51 with Crohn's disease. Whereas only diploid DNA histograms were found in Crohn's disease and control subjects, three patients with ulcerative colitis exhibited DNA aneuploidy. In one case, aneuploidy was associated with low grade dysplasia. S-phase fractions were higher in ulcerative colitis (mean (SD) 17.8 (7.7)%) than in Crohn's disease (13.1 (4.6)%) or control subjects (14.2 (4.6)%), but did not correlate with either disease activity or duration in any group. In this study, aneuploidy was associated exclusively with ulcerative colitis, even in the absence of dysplasia. In view of the epidemiological differences in malignant colonic transformation between ulcerative colitis and Crohn's disease, this study suggests that flow cytometry may help to identify individuals with an increased cancer risk in ulcerative colitis.

Aneuploidy↗
PubMed1992

Indomethacin worsens and a leukotriene biosynthesis inhibitor accelerates mucosal healing in rat colitis.

The implication of leukotrienes as mediators of inflammation and recent evidence that prostaglandin analogues provide a beneficial effect during experimental colitis led to the speculation that (i) leukotrienes may be injurious and (ii) prostaglandins may be protective to colonic mucosa. Using a 2% acetic acid induced rat colitis model, we administered specific cyclooxygenase (indomethacin) and leukotriene biosynthesis inhibitors (MK-886) to examine the effect of endogenous prostaglandins and leukotrienes on colonic macroscopic injury, mucosal inflammation as measured by myeloperoxidase activity, net in vivo intestinal fluid absorption, and colonic PGE2 and LTB4 levels as measured by in vivo rectal dialysis. Indomethacin treatment prior to induction of colitis reduced endogenous mucosal PGE2 levels and exacerbated macroscopic ulceration and net fluid absorption. Addition of the exogenous PGE1 analogue misoprostol to the indomethacin-exacerbated colitis completely healed colonic macroscopic ulceration and inflammation but only partially improved fluid absorptive injury. The specific leukotriene biosynthesis inhibitor MK-886 administered prior to induction of colitis healed macroscopic ulceration and inflammation but not fluid absorptive injury. This mucosal reparative effect of MK-886 occurred at a dose that reduced colonic LTB4 synthesis while concomitantly enhancing PGE2 levels. Combining MK-886 with misoprostol treatment improved not only macroscopic ulceration and inflammation but also provided a synergistic effect that maintained net colonic fluid absorption at noncolitic control levels. These studies suggest that, during the induction of experimental colitis, endogenous prostaglandins play a pivotal role in providing a mucosal healing effect, and that leukotriene biosynthesis inhibitor may manifest part of its beneficial effect by shifting arachidonic acid metabolism towards production of prostaglandins.

Acetates↗
PubMed1977

The leucocyte chemotactic function in patients with ulcerative colitis.

The intermittent course of ulcerative colitis could hypothetically be be caused by fluctuations of the patients' natural systems of resistance. To evaluate this hypothesis the chemotactic function of leucocytes in ulcerative colitis patients has been investigated. The patient group comprised 59 patients, 24 men and 35 women. All activity stages were represented. The control group comprised 25 normal subjects, 10 men and 15 women. The chemotactic reaction was investigated in a double chamber with a cellulose-ester-micropore filter with a pore size of 3 mum as a diaphragm in which the migration takes place. The variable applied was the ratio between the number of cells 50 mum down in the filter and at the surface, calculated as a chemotactic Index. Casein was used as chemotactic agents. The corrected chemotactic was defined as the difference between stimulated and unstimulated Chemotactic Index. The chemotactic as well as the corrected chemotactic response of leucocytes from ulcerative colitis patients was significantly lower than in control subjects. The subgroup, active ulcerative colitis,showed the lowest corrected Chemotactic Index, whereas the unstimulated Control Index was significantly higher than in normal subjects. The results did not correlate with treatment. The investigation has shown that leucocytes in active ulcerative colitis cases have a high spontaneous mobility, whereas their chemotactic function after stimulation is significantly subnormal. Further investigation is needed to demonstrate whether this phenomenon plays a major role in the pathogenesis of ulcerative colitis.

Adolescent↗
PubMed1992

Do technetium-99m hexamethylpropylene amine oxime-labeled leukocytes truly reflect the mucosal inflammation in patients with ulcerative colitis?

Twenty-five patients with ulcerative colitis and nine controls with macroscopically non-inflamed colon were investigated with technetium-99m hexamethylpropylene amine oxime-labeled leukocyte scintigraphy and colonoscopy with biopsies. The interval between leukocyte scintigraphy and colonoscopy was < or = 14 days in all patients with ulcerative colitis and < or = 30 days in eight of nine controls. Scintigrams were obtained at approximately 45 min and 4 h after injection of labeled leukocytes. One nuclear physician, one internist, and one pathologist graded blindly and independently of each other the degree of active inflammation in seven different colonic segments for each patient, using 4-grade scales for scans and macroscopically and histologically viewed inflammation, respectively. A positive correlation between endoscopic and histologic grading of all colonic segments and scan gradings for all subjects and for ulcerative colitis patients separately was found (all, p < 0.001). By means of kappa statistics, the inter-observer agreement between scintigraphic grading at 45 min and endoscopy was, for all subjects, 0.32 (95% confidence interval (CI), 0.20-0.44; p < 0.001) and, for patients with ulcerative colitis, 0.19 (CI, 0.07-0.31; p < 0.001). When 17 patients who had complete colonoscopies were divided into those with total, extensive, or distal colitis, leukocyte scintigraphy underestimated the extension of active inflammation. A simple scintigraphic scoring system reflects the colonic inflammation viewed endoscopically and histologically in patients with ulcerative colitis but underestimates the presence of active inflammation in individual colonic segments.

Adolescent↗
PubMed1992

Chronic colitis associated with human immunodeficiency virus infection.

OBJECTIVE: A clinical and pathological description of chronic colitis associated with human immunodeficiency virus (HIV) infection. DESIGN: A retrospective case review. SETTING: Tertiary referral institution and specialist gastroenterology practice. PATIENTS: A series of six patients with human immunodeficiency virus infection and chronic colitis observed for up to four years. RESULTS: The six patients had chronic diarrhoea for longer than six months, rectal bleeding, abdominal pain and stool leukocytosis. The mucosal pattern on colonoscopy showed diffuse proctocolitis, consisting of contact bleeding, superficial ulcerations, exudates, and/or loss of vascular pattern. Colonic biopsies showed a persisting diffuse colitis characterised principally by a mixed inflammatory cell infiltrate (mononuclear cells and neutrophils) and essentially preserved crypt architecture after six to 39 months of histological follow-up. The histopathology over this time frame was not typical of ulcerative colitis or Crohn's disease, nor of the conventionally described forms of infective colitis. HIV nucleic acid was identified by insitu hybridisation in colonic biopsies from four patients. In two of three patients tested, the presence of HIV DNA was confirmed by Southern blot analysis. No other microbial agent could be demonstrated as the cause of diarrhoea. At presentation all patients had CD4+ lymphocyte counts greater than 265 x 10(6)/L and none had the acquired immunodeficiency syndrome. Four patients have gone into remission, the other two patients were not in remission at four and a half to five years after onset. CONCLUSION: We suggest that chronic colitis may represent a new entity related to infection of the colon with human immunodeficiency virus.

Acquired Immunodeficiency Syndrome↗
PubMed1975

Carcinoma and epithelial dysplasia complicating ulcerative colitis.

The pathology of 19 specimens of carcinoma complicating ulcerative colitis, resected in the University Department of Surgery of the General Infirmary at Leeds, was reviewed with particular reference to the incidence of epithelial dysplasia. The carcinomas were found to be more frequently multiple, more evenly distributed in the large bowel, and much more often of atypical macroscopic appearances and of mucoid histological type than ordinary colorectal carcinomas, but the proportion of poorly differentiated tumours complicating ulcerative colitis was not as high as previously reported. Of the patients in our series 26% are alive and well at least 5 years after surgery. Unequivocal epithelial dysplasia was demonstrated in some part of the large intestine in 15 of 19 specimens with colitis carcinoma, but was also found in 4 of 14 specimens from a "control" series of patients with longstanding total colitis but without carcinoma. Clearly, therefore, the finding of dysplasia in a rectal biopsy of a patient with colitis is not a reliable guide to the presence of a frank carcinoma elsewhere in the bowel. Whether it indicates a special predisposition to the development of a growth in the future, as might be postulated from the analogy of similar changes in other organs, cannot be determined on the data of this study. The fact that epithelial dysplasia when present in colitis is often patchy in distribution and frequently spares the rectum even in patients with definite carcinomas makes a negative rectal biopsy particularly unreliable in deciding on the absence of a tumour or the lack of predisposition to it. Multiple biopsies from different parts of the colon as well as the rectum would thus seem to be desirable if mucosal sampling is to be employed as a screening test.

Adult↗