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PubMed1999

Validation of a pharmacokinetic model of colon-specific drug delivery and the therapeutic effects of chitosan capsules containing 5-aminosalicylic acid on 2,4,6-trinitrobenzenesulphonic acid-induced colitis in rats.

A pharmacokinetic model of colon-specific drug delivery developed in a previous study has been validated by use of 5-aminosalicylic acid (5-ASA) as a model anti-inflammatory drug. The simulation curves obtained from the pharmacokinetic model were in good agreement with experimental data obtained after oral administration of 5-ASA-containing chitosan capsules. The concentrations of 5-ASA in the large intestinal mucosa after drug administration were higher than after administration of the drug in carmellose suspension. We then attempted colon-specific delivery of an anti-ulcerative colitis drug, in chitosan capsules, to accelerate healing of 2,4,6-trinitrobenzenesulphonic acid sodium salt (TNBS)-induced colitis in rats. To confirm this therapeutic model, salazosulphapyridine (SASP), a commercially available 5-ASA prodrug, was used as positive control. Colonic injury and inflammation were assessed by measuring myeloperoxidase activity and visual assessment (damage score), respectively. Because SASP is effective against TNBS-induced colitis in rats, use of the SASP-sensitive TNBS-induced colitis model validated the therapeutic effects of 5-ASA-containing chitosan capsules, which were significantly better than those of a suspension of the drug in carmellose. These findings suggest that our pharmacokinetic model of colon-specific drug delivery can accurately evaluate this colon-specific delivery system and that 5-ASA-containing chitosan capsules are more effective than other 5-ASA formulations for treatment of TNBS-induced colitis in rats.

Administration, Oral↗
PubMed1994

[Effect of mesalazine microgranules on experimental colitis].

Mesalazine microgranules are an ethylcellulose-coated formulation from which mesalazine is released throughout the intestinal tract and are expected to be effective for idiopathic inflammatory bowel disease, ulcerative colitis and Crohn's disease. Mesalazine microgranules were administered orally to investigate the distribution of mesalazine throughout the intestinal tract in rats. Mesalazine microgranules distributed sufficient amounts of mesalazine and its metabolite, N-acetyl-mesalazine, to the intestinal tissues, while pure mesalazine delivered lower amounts of both. In acetic acid-induced colitis in rats, mesalazine microgranules administered orally reduced the damage score significantly (P < 0.05) at a dose of 50 mg/kg as assessed by macroscopic observation and at 100 mg/kg as assessed by histological evaluation. The number of ulcers in carrageenan-induced colitis in guinea pigs was inhibited at doses of 50, 100, 200 mg/kg, p.o. The colonic wet weight of rats in 2,4,6-trinitrobenzenesulfonic acid (TNB)-induced colitis was reduced significantly (P < 0.05) at a dose of 50 mg/kg, p.o. Mesalazine microgranules showed the ability to distribute mesalazine efficiently throughout the intestinal tract and showed effectiveness against acetic acid-, carrageenan- and TNB-induced colitis. These studies strongly suggest that mesalazine microgranules are effective for idiopathic inflammatory bowel disease.

Aminosalicylic Acids↗
PubMed2005

Milk whey culture with Propionibacterium freudenreichii ET-3 is effective on the colitis induced by 2,4,6-trinitrobenzene sulfonic acid in rats.

This study aimed to evaluate whether milk whey culture with Propinibacterium freudenreichii ET-3 (milk whey culture), which has been reported to have Bifidogenic activity, is effective on the colitis induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) in rats. For the induction of colitis, the colon was clamped and 0.1 M TNBS in 35% ethanol was injected into the luminal side of the clamped portion under pentobarbital anesthesia. From the next day of colitis induction, milk whey culture was administered orally at doses of 1 and 3 g/kg, twice a day for 9 days. On the 10th day, rats were sacrificed and ulcer size was measured. Milk whey culture significantly accelerated the healing of the colitis in a dose-dependent manner, but culture medium did not. To clarify the active substance, the effects of propionic acid and acetic acid contained in milk whey culture was tested. Sodium propionate significantly accelerated the healing of TNBS-induced colitis, but sodium acetate did not. The above results show that milk whey culture may become a useful prebiotic for the therapy of inflammatory bowel disease and that propionic acid may be one of the active substances contained in milk whey culture.

Acetic Acid↗
PubMed1991

[A case-control study of ulcerative colitis].

In order to evaluate the epidemiological characteristics of ulcerative colitis, we conducted a matched case-control study of ulcerative colitis. Fifty patients with ulcerative colitis diagnosed at three hospitals in Kyoto, Osaka and Hyogo Prefectures in Japan during 1984 and 1987 were interviewed about their habitual and pre-illness diets, personal habits, past histories and family histories. The results were compared to those for fifty healthy controls who were matched for sex and age (+/- 2 years) and participated in health-screening examinations in Kyoto or Osaka during the same period. Frequent intake of rice (4 or more bowls a day), bread (3 or more times a week), and green tea (7 or more cups a day) significantly increased the relative risk of ulcerative colitis. However, a past history of appendectomy was negatively correlated with the disease. There were no relationships between ulcerative colitis and consumption of animal foods and tobacco.

Adolescent↗
PubMed2003

Medical management of ulcerative colitis.

Patients with ulcerative colitis have no increased mortality compared to population controls and the disease can be cured be colectomy. This review concentrates on the medical management of ulcerative colitis including the management of active colitis, acute severe colitis and first presentation of colitis, maintenance of remission and long-term complications.

Acute Disease↗
PubMed2004

Probable ischemic colitis caused by pseudoephedrine with tramadol as a possible contributing factor.

OBJECTIVE: To report a case of acute self-limiting ischemic colitis in a patient who was self-medicating with a proprietary over-the-counter oral decongestant containing pseudoephedrine. CASE SUMMARY: A 46-year-old white man developed clinical, endoscopic, and histologic features of acute ischemic colitis after taking a proprietary oral decongestant containing pseudoephedrine 240 mg/day for one week. The total daily dose was at the upper limit of recommended doses for pseudoephedrine (as a single drug or in combination products). The patient was also taking tramadol 150 mg/day for chronic back pain. He made a complete recovery. There were no other explanations for the episode of ischemic colitis. DISCUSSION: An objective causality assessment based on the Naranjo probability scale revealed pseudoephedrine to be a probable cause of ischemic colitis in our patient. Pseudoephedrine occasionally causes vascular insufficiency due to intense vasoconstriction, even at standard doses. Although our patient was not taking an excessive dose of pseudoephedrine, it is possible that the concurrent use of pseudoephedrine and tramadol may have increased adrenergic vasoconstriction, predisposing to ischemic colitis. CONCLUSIONS: Prolonged or intensive use of medications containing pseudoephedrine should be avoided, and the package information should contain advice that the medication should be ceased if abdominal pain or other ischemic symptoms occur.

Analgesics, Opioid↗
PubMed2005

Cyclosporine for severe ulcerative colitis.

OBJECTIVE: To evaluate evidence for the use of cyclosporine in treating patients with severe ulcerative colitis. DATA SOURCES: A literature search was performed using MEDLINE, EMBASE, Cochrane Database, and ISI Web of Knowledge (1966-November 2005) with the search terms cyclosporine, cyclosporin A, CsA, ulcerative colitis, UC, inflammatory bowel disease, IBD, steroid-refractory, and immunosuppression. Additional papers were located by hand-searching relevant references. Only human studies in adults and literature published in English were included. DATA SYNTHESIS: Intravenous cyclosporine has been evaluated for the treatment of severe ulcerative colitis in 4 randomized, controlled trials, as well as in many open-label and retrospective studies. Studies that evaluated cyclosporine for severe ulcerative colitis were reviewed. All 4 controlled trials showed an initial positive clinical response as defined by the Crohn's Activity Index when intravenous cyclosporine 4 mg/kg/day was administered as monotherapy or combined with intravenous corticosteroids. One of the 4 trials indicated that high-dose cyclosporine (4 mg/kg/day) has no additional clinical benefit over the low-dose (2 mg/kg/day) and that the lower dose may improve safety related to dose-dependent adverse effects. CONCLUSIONS: There is evidence to support the use of intravenous cyclosporine for patients with severe ulcerative colitis who are refractory to corticosteroid therapy. Because most of the adverse effects associated with cyclosporine are dose dependent, therapy should be initiated with the lower 2 mg/kg/day dose. Subsequent doses should be adjusted based on cyclosporine blood concentrations of 150-250 ng/mL. Cyclosporine should be used only to induce remission and serve as a "bridge" to azathioprine or 6-mercaptopurine maintenance therapy. At this time, there are insufficient data to support the long-term use of cyclosporine monotherapy for avoidance of surgery or maintenance of remission.

Colitis, Ulcerative↗
PubMed1998

Collagenous colitis in a patient with Addison's disease: a case report.

Diarrhea is a non-specific symptom which may be associated with Addison's disease and several causes had been demonstrated in the aetiology. We describe a patient with Addison's disease who was suffering from chronic diarrhea for three months. She was diagnosed as having collagenous colitis and successfully treated with Sulphasalazine, 2 g/day. Collagenous colitis is an uncommon cause of chronic diarrhea and the association of collagenous colitis with Addison's disease has not previously been described. We think that collagenous colitis may play a role in the aetiology of diarrhea in patients with Addison's disease and therefore we suggest a full colonoscopic examination in other patients with Addison's disease and diarrhea to determine the incidence of collagenous colitis in the aetiology of diarrhea.

Addison Disease↗
PubMed2000

Serum eosinophil cationic protein in active and quiescent ulcerative colitis.

Inflammatory bowel disorders are characterized by an accumulation of eosinophilic granulocytes, mast cells, lymphocytes and neutrophilic granulocytes in the intestinal mucosa. The aim of this study was to examine the concentration of eosinophilic granulocytes in the blood of patients during active ulcerative colitis in comparison with patients during remission and apparently healthy control subjects. Besides counting, the activity grade of eosinophilic granulocytes has been studied by estimation of their degranulation product eosinophil cationic protein. Subjects with active ulcerative colitis could be distinguished from patients with quiescent ulcerative colitis by establishment of the eosinophil cationic protein concentration, neutrophilic granulocyte count, erythrocyte sedimentation rate, C-reactive protein and albumin concentration. After two weeks of corticosteroid treatment, serum eosinophil cationic protein concentrations and eosinophil counts in blood were significantly decreased. A decrease in blood eosinophil count was accompanied by a decrease in eosinophil cationic protein concentrations in serum in most subjects with ulcerative colitis. After twelve weeks of corticosteroid administration, serum albumin concentrations were significantly increased, whereas serum concentrations of C-reactive protein were significantly decreased. During treatment with corticosteroids, serum eosinophil cationic protein concentrations and blood eosinophil counts are appropriate laboratory markers to detect the effect of medication in the course of ulcerative colitis.

Adrenal Cortex Hormones↗
PubMed2003

[Immunonutrition in experimental colitis: beneficial effects of omega-3 fatty acids].

BACKGROUND: Recent data have given emphasis to the benefits of immunonutrition with omega-3 fatty acids (n-3 FA) in various clinical situations. This work presents the results of parenteral administration of different lipid emulsions in experimental acute colitis and reviews the pertinent literature. METHODS: Seventy-four adult male Wistar rats were randomized in six groups that had 10% acetic acid-induced colitis (except CS). During 7 days, control groups CS (without colitis) and CC (with colitis) received physiological solution and the others received specific lipid emulsion by a central venous catheter (0.5 mL/h). The n-3/n-6 FA ratio and lipidic compositions were: group L--1:7.7 (LCT, n = 12), M--1:7.0 (MCT and LCT, n = 12), LW-3--1:4.5 (LCT plus FO, n = 12) and MW-3--1:3.0 (MCT and LCT plus FO, n = 13). Rats were evaluated to assess abdominal and intestinal alterations, macrophage cellularity and colonic concentrations of LTB4, LTC4, PGE2 and TXB2. RESULTS: N-3 FA treated rats (LW-3 and MW-3) presented less inflammatory abdominal alterations than CC rats. Mucosal ulcer formation in MW-3 group was the only comparable to CS group. Only CS, M and MW-3 rats presented smaller cellularity than CC group. Comparing to CC group, there were found smaller averages of LTB4 in CS, LW-3 and MW-3 groups, of PGE2 in CS, M and MW-3 groups, and of TXB2 in CS and MW-3 groups. LTC4 averages were not different. CONCLUSIONS: 1) LCT-containing lipid emulsion with low n-3/n-6 ratio do not modify inflammatory colitis derived manifestations; 2) the association of MCT/LCT-containing lipid emulsion with fish oil with high n-3/n-6 ratio impels great beneficial impact, attenuating morphological and inflammatory consequences and decreasing colonic concentrations of proinflammatory mediators.

Animals↗
PubMed2003

Ethanol-induced colitis prevents oral tolerance induction in mice.

The gut mucosa is a major site of contact with antigens from food and microbiota. Usually, these daily contacts with natural antigens do not result in inflammatory reactions; instead they result in a state of systemic hyporesponsiveness named oral tolerance. Inflammatory bowel diseases (IBD) are associated with the breakdown of the immunoregulatory mechanisms that maintain oral tolerance. Several animal models of IBD/colitis are available. In mice, these include targeted disruptions of the genes encoding cytokines, T cell subsets or signaling proteins. Colitis can also be induced by intrarectal administration of chemical substances such as 2,4,6-trinitrobenzene sulfonic acid in 50% ethanol. We report here a novel model of colitis induced by intrarectal administration of 50% ethanol alone. Ethanol-treated mice develop an inflammatory reaction in the colon characterized by an intense inflammatory infiltrate in the mucosa and submucosa of the large intestine. They also present up-regulation of both interferon gamma (IFN-gamma) and interleukin-4 (IL-4) production by cecal lymph node and splenic cells. These results suggest a mixed type of inflammation as the substrate of the colitis. Interestingly, cells from mesenteric lymph nodes of ethanol-treated mice present an increase in IFN-gamma production and a decrease in IL-4 production indicating that the cytokine balance is altered throughout the gut mucosa. Moreover, induction of oral tolerance to ovalbumin is abolished in these animals, strongly suggesting that ethanol-induced colitis interferes with immunoregulatory mechanisms in the intestinal mucosa. This novel model of colitis resembles human IBD. It is easy to reproduce and may help us to understand the mechanisms involved in IBD pathogenesis.

Administration, Rectal↗
PubMed1980

Studies on blood coagulation in ulcerative colitis and Crohn's disease.

An investigation was made on 23 aspects of coagulation in 14 cases of ulcerative colitis, 5 cases of Crohn's disease and 3 cases of related diseases using a classification of increased and decreased coagulability. Of the 14 cases of ulcerative colitis, 10 were total colitis and 4 were left-sided colitis; 12 were on the active stage and 2 were in a state of remission. Treatment at the time of the investigation included prednisolone and/or Salazopyrin. In these cases, increased fibrinogen content, increased Factor VIII and Factor IX activity, increased platelet count, accelerated platelet aggregation rate and platelet retention rate were found. This hypercoagulability is thought to contribute to the clinical picture of these diseases and may prove useful as an index for determining the severity and prognosis of such cases and for deciding the indication for surgery. Furthermore, in cases where there is a marked increase in coagulability, combined anticoagulant therapy is thought necessary to improve the course of both ulcerative colitis and Crohn's disease.

Adolescent↗
PubMed2005

How important is onset of action in ulcerative colitis therapy?

Pharmacotherapy is the cornerstone of management in ulcerative colitis. However, controversy remains over optimal medical strategies. Specifically, differences in the onset of action of various drug therapies are thought to influence the achievement and maintenance of remission of disease, yet this is poorly characterised. There is a wide range of recent data concerning aminosalicylates, with much debate as to the relative merits of the various formulations and delivery systems. Meta-analyses confirm the efficacy of aminosalicylates for the induction and maintenance of remission and suggest that the newer agents are comparable in efficacy to sulfasalazine. Among aminosalicylates, data from clinical trials reveal that the onset of action is earlier with balsalazide than mesalazine. Although the efficacy of the newer 5-aminosalicylate agents is no greater than that of sulfasalazine, they have better adverse effect profiles. Factors such as tolerability and adherence appear more important than onset of action in long-term maintenance. Corticosteroids have long been used in the treatment of ulcerative colitis, yet there is a paucity of data regarding this. They have a rapid onset of action but considerable systemic adverse effects. Therefore, corticosteroids are reserved for disease that fails to respond to other agents or for primary therapy in patients with severe disease, although there is no universal acceptance of a threshold at which to initiate corticosteroid treatment.Rectal preparations of both aminosalicylates and corticosteroids have been developed in an attempt to exert a more rapid and direct onset of action while minimising adverse systemic effects. In clinical trials, topical preparations of both aminosalicylates and corticosteroids are effective in inducing remission. However, patient acceptability and proximal extent of disease dictate selection of a topical agent more than concern with rate of onset.A wide range of immunomodulators have been investigated in patients with steroid-refractory ulcerative colitis. The thioguanine derivatives are the most widely used but have a limited evidence base to support this use with controlled trials providing equivocal results regarding efficacy in severe ulcerative colitis. In addition, the thioguanine derivatives have a protracted onset of action and a considerable serious adverse effect profile. Calcineurin inhibitors and methotrexate have a more rapid onset of action than the thiopurines but have even less data to support their widespread use. They are widely regarded as salvage therapy and further data are required. Regarding biological agents, infliximab revolutionised the treatment of Crohn's disease, yet results in ulcerative colitis have been disappointing. Further trials are ongoing with great anticipation for more favourable data. The practical clinical implications of any differences between the agents depend on patient satisfaction with various therapies. Noncompliance is a major concern in maintenance therapy and is probably associated with relapse. Dose administration schedules and acceptability of therapy appear to be important factors in adherence. Overall, it is not clear that onset of action has a major influence on patient adherence and addressing issues of compliance may have more direct clinical impact.

Adrenal Cortex Hormones↗
PubMed2001

Basedow's disease and chronic ulcerative colitis: a case report and review of the Japanese literature.

A case of Basedow's disease, that developed after successful treatment of ulcerative colitis with a total colectomy, is presented, along with a review of the Japanese literature on the coexistence of hyperthyroidism and ulcerative colitis. A 26-year-old man was referred to our department, complaining of general fatigue, appetite loss, and palpitation. At age 14, blood was discovered in his stool and a diagnosis of ulcerative colitis was made. Since then, he has been treated with salazosulfapyridine and prednisolone. On examination, mild exophthalmos and thyroid swelling were observed. Both serum free T3 and T4 levels were increased along with a positive TSH receptor antibody, while TSH was decreased. Scintigraphic and ultrasonographic examinations of the thyroid gland showed diffuse enlargement. Treatment with thiamazole relieved the symptoms and normalized the thyroid function. Although a high incidence of autoimmune thyroid diseases in association with ulcerative colitis has been suggested, only 6 cases of hyperthyroidism coexisting with ulcerative colitis have been reported in Japan. A common immunological process has been suggested to be implicated in the pathogenesis of this association, however, the exact mechanism remains unclear.

Adult↗
PubMed1997

[Cytomegalovirus colitis in a normal woman].

A 32-year-old woman was admitted to our hospital because of diarrhea, fever, and liver dysfunction. IgM antibody to hepatitis C antibody and hepatitis B makers were negative. Antibodies to human deficiency virus was negative. Bacterial cultures of the stool were negative. Sigmoidoscopy on the 9th hospital day showed diffuse edematous and inflated mucosa in the rectum and left-sided colon. Multiple erosions and small ulcers were also present. Polymerase chain reaction examination revealed cytomegalovirus (CMV) DNA in the biopsy specimen of the rectum and the blood on the 10th hospital day. IgG antibody titer to CMV was low, but IgM titer was high. Her physical state had improved and fever resolved without anti-CMV therapy. Second sigmoidoscopy on the 24th hospital day showed normal mucosa. One month later the patient was free from any symptoms. Immunocompromised patients such as recipients of solid organ and bone marrow transplants, patients with AIDS, and patients with malignancies frequently complicate CMV colitis, which can be a major cause of death. Thus, CMV colitis is rarely overlooked in immunocompromised patients. Only a few cases of CMV colitis are reported in adult patients with no risk for CMV infection or associated disease. CMV colitis should be concluded in the differential diagnosis of acute or subacute colitis even in immunocompetent patients.

Adult↗
PubMed2005

Sonographic findings in ischemic colitis in 58 patients.

OBJECTIVE: The purpose of this study was to describe the sonographic findings of 58 patients with proven ischemic colitis and to evaluate whether any of the findings are related to the presence or development of transmural necrosis. MATERIALS AND METHODS: We reviewed the histories of patients diagnosed with ischemic colitis over a period of 5.5 years. Sixty-two patients had undergone sonographic examinations. The spectrum of sonographic findings in ischemic colitis was based on the original imaging report, with an analysis of the presence of colonic abnormalities and their associated alterations. In the second part of the study, we divided the patients into two groups according to the presence or absence of transmural necrosis, and the sonographic findings of each group were compared. Ten patients had sonographic follow-up studies during their hospital stay. RESULTS: The prospective sensitivity of sonography for the characterization of colonic abnormalities was 93.5% (58/62 patients). Segmental involvement was detected in 57 of the 58 patients, with left-sided colitis in 47 (81%). The mean length of bowel involved was 19 cm, with a mean wall thickness of 7.6 mm. Colon wall stratification was preserved in 38 patients (66%). Altered pericolic fat was observed in 16 patients (28%). Absence of or barely visible color Doppler flow in the thickened bowel wall was recorded in 80% of patients. Altered pericolic fat was the only sonographic variable significantly associated with the presence of transmural necrosis (p = 0.004). Improvement as assessed on sonography was observed in all patients with a good clinical course. In patients with transmural necrosis, sonography did not show improvement. CONCLUSION: Sonography is a valuable technique for the detection of colonic abnormalities resulting from ischemic colitis. In this study, altered pericolic fat or the absence of improvement in sonographic follow-up studies were factors associated with transmural necrosis.

Aged↗
PubMed2006

Differential angiogenic regulation of experimental colitis.

Inflammatory bowel diseases (IBDs) are chronic inflammatory disorders of the intestinal tract with unknown multifactorial etiology that, among other things, result in alteration and dysfunction of the intestinal microvasculature. Clinical observations of increased colon microvascular density during IBD have been made. However, there have been no reports investigating the physiological or pathological importance of angiogenic stimulation during the development of intestinal inflammation. Here we report that the dextran sodium sulfate and CD4+CD45RBhigh T-cell transfer models of colitis stimulate angiogenesis that results in increased blood vessel density concomitant with increased histopathology, suggesting that the neovasculature contributes to tissue damage during colitis. We also show that leukocyte infiltration is an obligatory requirement for the stimulation of angiogenesis. The angiogenic response during experimental colitis was differentially regulated in that the production of various angiogenic mediators was diverse between the two models with only a small group of molecules being similarly controlled. Importantly, treatment with the anti-angiogenic agent thalidomide or ATN-161 significantly reduced angiogenic activity and associated tissue histopathology during experimental colitis. Our findings identify a direct pathological link between angiogenesis and the development of experimental colitis, representing a novel therapeutic target for IBD.

Angiogenesis Inhibitors↗
PubMed2006

Signal transducer and activator of transcription 5b promotes mucosal tolerance in pediatric Crohn's disease and murine colitis.

Growth hormone (GH) regulates anabolic metabolism via activation of the STAT5b transcription factor and reduces mucosal inflammation in colitis. Peroxisome proliferator-activated receptor (PPAR) gamma suppresses mucosal inflammation and is regulated by GH through STAT5b. We hypothesized that the GH:STAT5b axis influences susceptibility to colitis via regulation of local PPARgamma abundance. Colon biopsies from children with newly diagnosed Crohn's disease (CD) and controls were exposed to GH in short-term organ culture. Trinitrobenzene sulfonic acid (TNBS) administration was used to induce colitis in STAT5b-deficient mice and wild-type controls, with and without rosiglitazone pretreatment. GH receptor, STAT5b, PPARgamma, and nuclear factor kappaB activation and expression were determined. Epithelial cell GH receptor expression and GH-dependent STAT5b activation and PPARgamma expression were reduced in CD colon. STAT5b-deficient mice exhibited reduced basal PPARgamma nuclear abundance and developed more severe proximal colitis after TNBS administration. This was associated with a significant increase in mucosal nuclear factor kappaB activation at baseline and after TNBS administration. Rosiglitazone ameliorated colitis in wild-type mice but not STAT5b-deficient mice. GH-dependent STAT5b activation is impaired in affected CD colon and contributes to chronic mucosal inflammation via down-regulation of local PPARgamma expression. Therapeutic activation of the GH:STAT5b axis therefore represents a novel target for restoring both normal anabolic metabolism and mucosal tolerance in CD.

Animals↗