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PubMed1989

Hepatoportal arteriovenous fistula: morphologic features studied after orthotopic liver transplantation.

A 51-year-old woman underwent orthotopic liver transplantation because of a small-duct primary sclerosing cholangitis associated with chronic ulcerative colitis and a hepatoportal arteriovenous fistula. Arteriograms before liver transplantation and specimen arteriograms revealed a convolution of arteries in the right hepatic lobe which communicated with a massively dilated and partly thrombosed portal vein branch. The lesion was probably the result of a previous liver biopsy. Microscopic examination of the fistula and of specimens taken at a distance from the fistula showed prominent intimal fibroplasia of portal vein branches. The vascular changes were so severe that hepatic artery and portal vein branches closely resembled each other on routine sections. We are unaware of such a finding in other conditions and therefore believe that recognition of the described vascular abnormalities in liver biopsy specimens should lead pathologists to comment that an arterioportal fistula might be present.

Angiography↗
PubMed1987

[Colitis caused by cytomegalovirus in acquired immunodeficiency syndrome. Report of 2 cases of autopsy].

Two autopsy cases of CMV colitis in AIDS are reported. Intestinal manifestations lasted 2 and 5 months in each case and included: diarrhea and abdominal colic pain. The causes of death were: disseminated CMV infection in case 1 and miliary tuberculosis in case 2. In case 1 small ulcers were apparent in the ileum and the cecum. Microscopic foci of necrosis were also observed. Case showed: sigmoid dilatation with mucosal hemorrhages, small acute ulcers and submucosal fibrosis in the transverse portion of the colon. In both cases cytomegalic inclusion bodies within the endothelial cells of the capillaries at the bottom and the margin of the ulcers were observed. We compare our findings with those in other recently published cases.

Acquired Immunodeficiency Syndrome↗
PubMed1990

A grading system for lymphocytic plasmacytic colitis in dogs.

Colonic mucosal samples were obtained every 4 weeks for 13 months from 6 clinically normal dogs and from 47 dogs with a clinical diagnosis of chronic inflammatory bowel disease. All samples were graded on a scale of 0-5, based upon the quantity of lymphocytes and plasma cells in the lamina propria, epithelial changes, and the presence of ulcers and erosions. A grade of less than or equal to 2.0 was considered normal and was assigned to 77 of 78 samples from clinically normal dogs and 28 of 48 samples from dogs with diarrhea. A transient increase in cellularity was noted in 1 sample from 1 control dog. Nineteen dogs with clinical disease had obvious histologic abnormalities. The grading scheme described provides the pathologist with an objective criterion for the microscopic evaluation of colonic mucosal samples obtained by endoscopic techniques and offers clinicians a method of assessing the dog's progress and response to therapy.

Animals↗
PubMed1999

Aminoguanidine has both an anti-inflammatory effect on experimental colitis and a proliferative effect on colonic mucosal cells.

BACKGROUND: The aim of this study was to assess the effect of aminoguanidine (AG) on developed colitis and cell proliferation. METHODS: Colitis was induced by means of trinitrobenzene sulphonic acid (TNB) in male Wistar rats weighing about 250 g. Seven days after induction of TNB colitis the rats were divided into two groups at random, and one group was orally treated with 1.5 micromol/kg AG each day. We assessed the effect of AG by measuring the mucosal damage, the ulcer area, myeloperoxidase (MPO) activity, inducible nitric oxide synthase (iNOs) activity, and nitrogen oxide in serum 7 days after the beginning of treatment. RESULTS: AG significantly ameliorated the macroscopic damage score (AG versus control, 5.25 +/- 0.80 versus 7.50 +/- 0.50), the microscopic damage score (5.88 +/- 1.13 versus 9.25 +/- 0.31), ulcer area (0.57 +/- 0.14 versus 1.24 +/- 0.17 cm2), decreased MPO activity (51.5 +/- 9.4 versus 192.2 +/- 60 units/g tissue), and nitrogen oxide in serum (27.2 +/- 1.4 versus 32.3 +/- 1.8 microM) but did not decrease iNOs activity (8732 +/- 435 versus 8672 +/- 357 cpm/g tissue). Moreover, AG accelerated T84 cell proliferation in a dose-dependent manner. CONCLUSIONS: These results suggest that AG ameliorates TNB colitis not only by its anti-inflammatory effect but also by accelerating the proliferation of colonic mucosal cells. AG, accordingly, might well be a useful new medicine to ameliorate inflammatory bowel disease.

Analysis of Variance↗
PubMed1983

Ultrastructure of colonic endocrine cells in ulcerative colitis.

Endoscopic specimens of colonic mucosa from 40 ulcerative colitis patients were investigated. Specimens were taken from both sexes patients, aged 16-74 (means = 41 years). An average number of 5 biopsies was examined in each patient taken 10, 20, 40, 50 and 80 cm from rectum. Material was divided into 3 groups: 1. histologically confirmed ulcerative colitis (CU), 2. clinical diagnosis of CU in remission-histologically non specific inflammation, 3. functional disorders of the large bowel-histologically normal colonic mucosa. The latter was a control group. Biopsies were fixed in glutaraldehyde, postfixed in osmium tetroxide. Ultrastructural examination was performed on Epon sections in Tesla BS-500 electron microscope operating at 60 kV. A Lausanne classification of endocrine cells was used in the study. The most common were EC cells, followed by PP, D1 and L respectively. In the first group of patients damaged endocrine cells were more commonly observed. These destructive changes were: vacuolisation of cytoplasm, degranulation and discharge of endocrine granules into intercellular space and degradation of the entire cells.

Adolescent↗
PubMed1994

Enterotoxic activity of Klebsiella oxytoca cytotoxin in rabbit intestinal loops.

We examined the enterotoxicity of a Klebsiella oxytoca cytotoxin which is produced by K. oxytoca OK-1, a strain from a patient with antibiotic-associated hemorrhagic colitis. Injection of the cytotoxin into ligated ileal and colonic loops in rabbits caused the accumulation of fluid in the loops. The fluid was bloody in the ileal loops but not in the colonic ones. Histological examination revealed intense mucosal hemorrhage with erosion in the ileum, whereas no microscopic change was noted in the colon. The fluid accumulation was shown to be a dose-dependent response in both ileal and colonic loops. The amounts of the cytotoxin required for maximal fluid accumulation in ileal and colonic loops were 60 and 10 micrograms, respectively. Fluid accumulation was first noticeable in ileal loops 12 h and in colonic ones 5 h after the injection of these doses of the cytotoxin and then proceeded with time. When K. oxytoca OK-1, a cytotoxin-producing strain, was inoculated into the loops at doses of 1 x 10(8) and 5 x 10(9) CFU, similar fluid accumulation was observed. However, inoculation of K. oxytoca ATCC 13182, a non-cytotoxin-producing strain, at the same doses did not cause any change. These results suggest that the cytotoxin-producing strain of K. oxytoca is the causative organism of antibiotic-associated hemorrhagic colitis and that the toxin is the factor responsible for pathogenesis.

Animals↗
PubMed1995

Therapeutic effect of colloid bismuth subcitrate in experimental colitis in the rat.

Colloid bismuth subcitrate (CBS) has a protective effect on ulcerated gastric and duodenal mucosa. To investigate its effect on large intestinal mucosal injury, we used acetic acid-induced colitis in the rat. Colitis was produced in male Wistar rats by rectal instillation of 1 ml of 10% acetic acid followed immediately by 1.5 ml of NaCl 0.9% (saline) enema. 1.5 ml of saline containing 240 mg of CBS or saline alone were then administered rectally every 24 h for 5 days. Another group of animals received CBS only. On the sixth day the distal colon was examined macroscopically and histologically using a 0 (normal) to 3 (necrosis) score. Prostaglandin E2 (PGE2) was measured by RIA (ng/mg protein). CBS significantly reduced both macroscopic and microscopic scores from 2.09 to 1.25 (p < 0.02) and from 2.4 to 1.08 (p < 0.02) respectively. It also induced a significant reduction in PGE2 from 1.6 to 0.57 (p < 0.004) in the inflamed colonic mucosa. The significant protective effect of topical CBS, which is accompanied by a reduction of PGE2, indicates that CBS may have a role in the treatment of colitis.

Acetates↗
PubMed2004

Development of colonic neoplasia in p53 deficient mice with experimental colitis induced by dextran sulphate sodium.

BACKGROUND: Several animal models for human ulcerative colitis (UC) associated neoplasia have been reported. However, most neoplasias developed in these models have morphological and genetic characteristics different from UC associated neoplasia. AIMS: To establish a new colitis associated neoplasia model in p53 deficient mice by treatment with dextran sulphate sodium (DSS). METHODS: DSS colitis was induced in homozygous p53 deficient mice (p53(-/-)-DSS), heterozygous p53 deficient mice (p53(+/-)-DSS) and wild-type mice (p53+/+-DSS) by treatment with 4% DSS. Numbers of developed neoplasias were compared among the experimental groups, and macroscopic and microscopic features of the neoplasias were analysed. Furthermore, K-ras mutation and beta-catenin expression were assessed. RESULTS: p53(-/-)-DSS mice showed 100% incidence of neoplasias whereas the incidences in p53(+/-)-DSS and p53+/+-DSS mice were 46.2% and 13.3%, respectively. No neoplasias were observed in the control groups. The mean numbers of total neoplasias per mouse were 5.0 (p53(-/-)-DSS), 0.62 (p53(+/-)-DSS), and 0.2 (p53+/+-DSS). The number of neoplasias per mouse in the p53(-/-)-DSS group was significantly higher than that in the other DSS groups. The incidences of superficial type neoplasias were 91.7% in p53(-/-)-DSS mice, 75.0% in p53(+/-)-DSS mice, and 33.3% in p53+/+-DSS mice. The K-ras mutation was not detected in any of the neoplasias tested. Translocation of beta-catenin from the cell membrane to the cytoplasm or nucleus was observed in 19 of 23 (82.6%) neoplasias. CONCLUSIONS: The p53(-/-)-DSS mice is an excellent animal model of UC associated neoplasia because the morphological features and molecular genetics are similar to those of UC associated neoplasia. Therefore, this model will contribute to the analysis of tumorigenesis related to human UC associated neoplasia and the development of chemopreventive agents.

Animals↗
PubMed1980

Quantitation of the late effects of X-radiation on the large intestine.

A model for quantitating late effects of x-radiation on the large intestine utilizing the rectum of the Sprague-Dawley rat is reported. This model was constructed prefatory to establishing relative biological effectiveness for negative pions as a component of preclinical trials at the Clinton P. Anderson Meson Physics Facility, Los Alamos Scientific Laboratory, Los Alamos, New Mexico. The endpoint involves microscopic evaluation of the severity of the experimental lesion, compared with surgically resected bowel lesions we have studied following clinical radiation exposure of the bowel. Individual components of the overall lesion include mucosal ulceration, atypical epithelial regeneration, colitis cystica profunda, fibrosis, and vascular sclerosis. Dose response curves were established for animals receiving 1, 2, 5 and 10 fractions with groups sacrificed at both four and 12 months after completion of radiation exposures.

Adenocarcinoma↗
PubMed1997

Multiple ulcers of the ileum due to Cytomegalovirus infection in a patient who showed no evidence of an immunocompromised state.

68-year-old woman presented with abdominal pain and vomiting. After initial conservative therapy, laparotomy showed multiple ulcers of the ileum, one of which had perforated and adhered to the uterus. The affected segment of the ileum was resected. Numerous cytomegalic cells, corresponding to endothelia and macrophages, with intranuclear inclusion bodies, were found in microscopic sections of the ulcerated lesions. These findings were consistent with cytomegalic vasculitis and enteritis. Cytomegalovirus infections of the alimentary tract have been reported mainly in severely immunocompromised patients or those with predisposing disorders such as ulcerative colitis; their prognosis is usually poor. In our patient, there was no obvious immunocompromised state or other gastrointestinal disorders. The postoperative course has been uneventful for 2 years after surgery. The prognosis of Cytomegalovirus-associated lesions in the alimentary tract may be quite good in the immunocompetent patient.

Aged↗
PubMed1985

Differentiation between Crohn's disease and other inflammatory conditions by electron microscopy.

The authors previously have demonstrated axonal necrosis of autonomic nerves in the surgically resected ilea of patients with Crohn's disease both in grossly normal ileal resection margins and in diseased areas. The present study of ileal stomal biopsies was carried out to obviate the possibility that the observed axonal damage might be related to the prolonged surgical manipulations required for ileal resection. The authors present studies of biopsies of ileal stomas and of small bowel from patients with Crohn's disease and various control disorders, including ulcerative colitis. Stomal biopsies were fixed immediately after they were obtained. Widespread, severe axonal necrosis of autonomic nerves was present in all Crohn's disease specimens, regardless of the patient's clinical status or the gross or routine microscopic evaluation of the same specimen. Controls either had no necrosis or displayed a minor degree of focal necrosis involving single axons. The authors conclude that Crohn's disease is accompanied by a severe and extensive necrosis of gut axons, and that such electron microscopic findings may serve to differentiate Crohn's disease from other inflammatory disorders.

Adult↗
PubMed1974

Clinical and pathological observations on the experimental passage of swine dysentery.

The length of incubation for 36 eight and 12 week old swine in eight experimental passages averaged 11 days and ranged from five to 24 days. The duration of diarrhea for 24 of these swine averaged 6.4 days and ranged from two to 19 days. The consistent macroscopic lesion was a colitis and, subsequently, a typhlitis. In the swine euthanized on the first day of diarrhea, the colitis was most intense in the coils near the apex of the colon and, frequently, these swine had a hyperemia of the fundus of the stomach. The amount of visible blood in the colon varied. Organisms identified microscopically and ultrastructurally as spirochetes were observed commonly in the feces and the mucosal glands of the colon of swine with a diarrhea, but not in the adjacent mesenteric lymph nodes. These spirochetes which were the most numerous on the first day of diarrhea, could not be isolated and propagated in vitro. Swine which recovered naturally or were medicated at the height of a diarrhea, developed a resistance to swine dysentery. Colon from infected swine remained infectious when stored at -77 degrees C for nine months but not when stored at -16 degrees C. Feces from infected swine were not infectious after lyophilization and storage at -12 degrees C.

Animals↗
PubMed1988

Cecocolitis in immunodeficient mice associated with an enteroinvasive lactose negative E. coli.

Infection with an atypical (lactose-negative) E. coli was associated with increased mortality rates in a colony of triple immune deficient N:NIH(S) III mice. Affected mice were lethargic and exhibited perianal fecal staining. Slight-to-moderate thickening of the wall of the cecum and colon was found on necropsy examination. Microscopic examination revealed segmental hyperplasia of the cecal and colonic mucosa with clusters of gram negative bacteria on the surface and within the cytoplasm of mucosal epithelial cells. Scattered foci of epithelial invasion and hyperplasia were observed in the colons of C57B1/6N-nunu mice after per os inoculation with the atypical E. coli. Immunocompetant mice housed in the same room as the N:NIH(S) III's remained healthy and exhibited no gross or microscopic lesions in spite of infection.

Animals↗
PubMed2000

Enhancement of immune tolerance via induction of NK1.1 positive liver-associated-lymphocytes under immunosuppressive conditions.

BACKGROUND/AIMS: The liver was previously shown to play a critical role in oral tolerance induction. A subset of liver-associated-lymphocytes expressing NK1.1 marker (NK1.1+ LAL) have killing activities and it has been suggested that they play a role in immune modulation. FK506 is a powerful immunosuppressive agent affecting T-cell differentiation and function. The exact pathway involved in peripheral tolerance induction using this drug remains unknown. The aim of the present study was to determine the interaction between FK506 and NK1.1+ LAL in induction of peripheral immune tolerance in the experimental colitis model. METHODS: Colitis was induced in C57 mice by intracolonic instillation of trinitrobenzenesulfonic acid (TNBS). Mice received five oral doses of colonic proteins extracted from TNBS-colitis colonic wall with and without FK506 treatment. The effect of FK506 treatment on NK1.1+ LAL was tested by cell-sorting and cytotoxicity assay. Colitis was assessed by standard clinical, macroscopic and histologic scores. RESULTS: Both FK506 treatment and oral tolerance induced a significant increase in NK1.1+ LAL number and cytotoxicity function. FK506 treatment enhanced the effect of oral tolerance on amelioration of disease activity. Orally tolerized mice treated with FK506 had no mortality nor increase in body weight, and manifested significant improvement in disease macroscopic and microscopic scores. CONCLUSIONS: This study shows for the first time that immune tolerance induced by both oral administration of an antigen and by FK506 treatment may be mediated via enhancement of NK1.1+ LAL. This subset of lymphocytes may play an immunoregulatory role in immune tolerance induction.

Animals↗
PubMed2005

[Intestinal mucosa protection of muscovite n ulcerative colitis in rats].

OBJECTIVE: To examine the efficacy of Muscovite on acetic acid-induced ulcerative colitis in rats, and to research the mechanisms of intestinal mucosal protection. METHOD: Ulcerative colitis was induced in rats by intracolonic injection of 2 mL of 7% acetic acid. Rats were treated with three different doses of the Muscovite and SASP at random by intracolonic injecion, the normal saline was considered as control group. The rats were sacrificed and the colons were excised and opened longitudinally. Under a dissecting microscope, gross findings were observed and scored. MPO activity was assayed by spectrophotometry in colonic mucosa. RESULT: Gross finding showed that multiple ulcer with diameter more than 1 cm, surrounded with erosion, erythematous and edema in the proximal colon in ulcerative coltis. The colon from Muscovite treatment group were histopatholgically normal, with slight erosion, erythematous and edema. The colon in SASP group had small ulceration and severe erosion and edema. The score of gloss change were significant lower in Muscovite groups than that in normal saline group (P < 0.01). There were necrosis and exfoliation of mucosa, multiple cystic dilation of mucosa gland, and large number of and inflammation attenuated in Muscovite groups. There nerutrophils and vessel infiltration in ulcerative colitis. The ulceration disappeared were erosion in mucosa and inflammatory cell infiltrating into submucosa in SASP group. Compared with normal saline group, the pathological scale were significant decreased in Muscovite and SASP groups (P < 0.05). The MPO activity was significant increased in colitis tissue compared with normal group (P < 0.001). After administrating with Muscovite or SASP, the level of MPO were significant decreased (P < 0.01). CONCLUSION: Muscovite has the effect of mucosal protection by attenuating the inflammation of colonic mucosa and decreasing the activity of MPO.

Acetic Acid↗
PubMed1994

Non-polypoid adenoma of the large intestine.

In order to find non-polypoid (flat) adenomas in the large intestine, one hundred and twenty-six consecutively resected large bowels were stained with methylene blue or haematoxylin and examined using a stereoscopic microscope with special attention to pit pattern abnormalities. The primary diseases were classified into familial adenomatous polyposis (FAP) in 9 cases, multiple adenomas in 2 cases, colorectal cancers in 90 cases, Crohn's disease in 5 cases, ulcerative colitis in 2 cases, constipation in 9 cases, diverticular disease in 3 cases and others in 6 cases, respectively. Thirty-five flat adenomas were detected in 14 colons (14/126 = 11%). Twenty-one flat adenomas were found in 9 non-FAP cases (7 colons removed for cancer and 2 for multiple adenomas) and the remaining 14 flat adenomas were found in 5 FAP colons. No flat adenomas were found in any of the 25 colons removed for non-neoplastic disease. Nine flat adenomas (26%) had a depressed shape. The mean age of the non-FAP cases was 57 years and that of the FAP cases was 29 years (P < 0.005). The mean size of non-FAP flat adenomas was 6.1 mm and that of FAP flat adenomas was 3.1 mm (P < 0.005). Non-FAP flat adenomas were more frequently right-sided than those in FAP. Epithelial dysplasia was graded as mild in 31 (89%) and moderate in 4 (11%), respectively. Moderate dysplasia was found in non-FAP cases exclusively. These results suggest that flat adenomas may be heterogeneous. The significance of these lesions is discussed.

Adenoma↗
PubMed1979

Pathological observation on experimental swine dysentery.

Experimental swine dysentery caused by 4 cultured strains (S73/2, DJ183, DJ70 and DK762) of Treponema hyodysenteriae was studied pathologically. The distribution and quantity of treponemes were examined on tissue sections stained by the Warthin-Starry method. Of the organs the colon contained the largest number of treponemes and the cecum and rectum the second largest number. Histopathological lesions were restricted to the large intestine. They ranged from mild catarrhal colitis in the mild case to desquamative, hemorrhagic colitis in the severest case. The severity of lesion was closely associated with the quantity of treponemes present. There was no difference in quality of the lesion between any two of the strains used in this study. Electron microscope revealed a large number of free treponemes present in the intestinal lumen and crypts. Treponemes were seen more frequently in the cytoplasm of goblet cells than in that of intestinal epithelial cells. They were also observed in desquamated degenerative epithelia. A small number of them were found in intact epithelia. Morphologically, the treponeme had a granular protoplasmic cylinder at the center which was surrounded by a thin envelope. Between the cylinder and the envelope there were axial fibrils.

Animals↗
PubMed2002

Dietary polyunsaturated fatty acids improve histological and biochemical alterations in rats with experimental ulcerative colitis.

The aim of the present study was to determine whether dietary intake of monounsaturated (MUFA) and/or polyunsaturated fatty acids (PUFA) of the (n- 3) and (n-6) series could improve intestinal damage and reduce inflammation in experimental ulcerative colitis (UC). Rats were treated with 80 mg/kg body of 2,4,6-trinitrobenzenesulfonic acid and fed for 1 or 2 wk diets enriched in olive oil (OO), fish oil (FO), or purified pig brain phospholipids (BPL), as sources of monounsaturated and PUFA of the (n-3) and (n-3) + (n-6) series. Evaluation of macroscopic and microscopic colonic damage was assessed. Ultrastructural and histologic changes were analyzed as well as plasma and colonic mucosa fatty acid profiles and some biochemical markers of injury and inflammation [alkaline phosphatase (AP), mieloperoxidase (MPO), prostaglandin E(2) (PGE(2)) and leukotriene B(4)]. Fatty acid profiles of both plasma and mucosa mostly reflected the dietary fatty acid composition. Plasma MUFA proportions were higher in UC animals fed the OO diet compared with FO or BPL groups 1 and 2 wk and (n-3) long chain PUFA (LC-PUFA) were higher in the FO than in the OO and BPL groups. At 1 wk, UC led to lower MUFA mucosa levels and (n-3)LC-PUFA were higher in the FO group compared with the OO and BPL groups. Rats with UC fed FO at 1 wk showed significantly less macroscopic and microscopic colonic damage. They also have lower AP and MPO activities and PGE(2) levels compared with the OO and BPL groups and showed enhanced histological repair, less necrotic areas within the mucosa, and more goblet cells with mature mucin granules. These results suggest that the use of balanced diets containing (n-3) LC-PUFA could ameliorate the inflammation and mucosal damage in UC.

Alkaline Phosphatase↗