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Query: UMLS:C0009324 (ulcerative colitis)
 17,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-four patients with chronic inflammatory bowel disease, 23 with ulcerative colitis, and 11 with crohn's disease, weretreated with elemental diet. thirty-one patients had been on high dose prednisonetherapy one to four weeks prior to the diet with no or insufficient response. Fifteen patients (44%) went into remission when elemental diet was introduced as the only change of treatment. Furthermore six patients (18%) went into remission when the dietary treatment was supplemented with high dose prednisone treatment (2 cases) or an increase of prednisone dose (4 cases). Remission occurred in 16 of 21 patients with disease of moderate activity, but in only 5 of 13 cases with severe disease. Remission rate was higher in patients with a limited extent of the lesion, but 8 patients with extensive colitis responded to treatment. There was no significant change of haemoglobin serum iron, transferrin, albumin, orosomucoid, or renal excretion of creatinine. However, significant decreases were observed of sedimentation rate, renal urea excretion, faecal volume and daily number of bowel movements. Colectomy was performed in 8 patients whose condition remained unchanged or aggravated during treatment. Follow-up studies of non-operated patients who went into remission showed that 6 of 13 patients with ulcerative colitis were perfectly well 7-28 months after the study, 3 patients suffered a mild recurrence after 4-24 months, and 4 patients were colectomized 5-10 months later due to severe attack. Of 8 patients with Crohn's disease 4 remained unoperated and free of symptoms 22-35 months after the study.
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PMID:Assessment of the therapeutic value of an elemental diet in chronic inflammatory bowel disease. 83 75

Simultaneous studies with 131-I-albumin and 125-I-immunoglobulin G (IgG) were made in 48 cases of chronic inflammatory bowel disease. Twenty-one had ulcerative colitis and 27 had Crohn's disease which was confirmed at laparotomy in every case. Intestinal protein loss was measured simultaneously by means of 59-Fe-iron dextran in 44 patients. All patients had abnormal intestinal protein loss. A high correlation was shown between fecal 59-Fe clearance and fractional catabolic rate of albumin, confirming the validity of 59-Fe-iron dextran as a test substance to measure intestinal protein loss. Fecal radioiodide excretion of 131-I from 131-I-albumin (A) and 125-I from 125-I-IgG (G) was significantly different in ulcerative colitis and Crohn's disease. The ratio G/A was close to unity (smaller than 1.60) in ulcerative colitis and Crohn's disease with exclusive or predominant involvement of the colon, whereas it was high in Crohn's disease of the small intestine and highest in cases with jejunal involvement. Thus, the ratio may be valuable in topographic diagnosis of chronic inflammatory bowel disease. A high ratio was found in 2 patients with Crohn's disease of the small intestine and normal radiography of the small intestine, and a low ratio was present in 7 cases of ulcerative colitis with normal radiographic findings. In all 9 patients with normal radiography, fecal 59-Fe clearance was elevated as evidence of abnormal intestinal protein loss. No correlation was present between the size of protein loss and the pathoanatomic extent of the lesions on subsequent laparotomy in 25 patients with Crohn's disease. Fecal radioiodide excretion (131-I from 131-I-albumin and 125-I from 125-I-IgG) was positively correlated with diarrhea (daily stool mass) in both ulcerative colitis and Crohn's disease. Intestinal protein loss was not.
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PMID:Fecal radioiodide excretion following intravenous injection of 131-I-albumin and 125-I-immunoglobulin G in chronic inflammatory bowel disease. An aid to topographic diagnosis. 113 26

Ferritins are iron-containing proteins found in normal tissues; they increase in concentration in many tumors and the blood of tumor-bearing individuals. We utilized a double-antibody radioimmunoassay for measurement of serum ferritin and defined the upper limit of normal as 146 ng/ml for women (mean 34 ng/ml) and 193 ng/ml for men (mean 93 ng/ml). Serum ferritin levels exceeded these limits in preoperative sera of 41% of women with mammary carcinoma (mean 199 ng/ml) and in 67% of women with locally recurrent or metastatic mammary carcinoma (mean 671 ng/ml). Individuals with hepatic inflammatory states are known to have high serum ferritin, and ferritin was increased in 43% of patients with hepatitis or cirrhosis (mean 364 ng/ml) and in 13% of patients with ulcerative colitis or gastroduodenal ulcers (mean 106 ng/ml). Measurement of serum ferritin may be useful in evaluation of patients with breast cancer and in monitoring their response to therapy.
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PMID:Measurement of serum ferritin by radioimmunoassay: results in normal individuals and patients with breast cancer. 118 3

Serum orosomucoid was compared with clinical activity, routine laboratory tests, intestinal protein loss, and albumin and IgG turnover in 22 cases of ulcerative colitis. Serum orosomucoid was well correlated with clinical activity, haemoglobin and leucocyte counts were not. A significant correlation was present between serum orosomucoid and intestinal protein loss (gastro-intestinal 59Fe-iron dextran clearance), serum albumin, fractional catabolic rates of albumin, and IgG and IgG synthesis rate. No correlation was found between serum orosomucoid and albumin synthesis rate or serum IgG. It is concluded that serum orosomucoid is a highly reliable indicator of disease activity in ulcerative colitis.
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PMID:Serum orosomucoid in ulcerative colitis: its relation to clinical activity, protein loss, and turnover of albumin and IgG. 126 38

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.
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PMID:Oxygen radicals in ulcerative colitis. 135 59

We report a case of ulcerative colitis (UC) in a 15 year old female undergoing treatment for anemia with oral ferrous sulfate. We suggest that the oral ferrous sulfate initiated the typical symptoms of UC in this case. This case is the first clinical report to our knowledge supporting the 'iron-catalysed oxidant-mediated ischemic injury theory' of UC.
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PMID:A case of ulcerative colitis induced by oral ferrous sulfate. 141 40

Ulcerative colitis (UC) is a recurrent inflammation of the colon and rectum that is characterized by subepithelial hemorrhage, epithelial cell necrosis, infiltration of large numbers of phagocytic leukocytes (neutrophils, eosinophils, macrophages), and mucosal ulcerations. Recent evidence suggests that mucosal lipid peroxidation may play an important role in that pathogenesis of the inflammation-induced intestinal injury. Using hemoglobin (Hb)-catalyzed, H2O2-dependent peroxidation of phospholipid as a model of oxidative injury to membrane lipids, we assessed the ability of the anti-inflammatory drugs sulfasalazine (SAZ), olsalazine, and their metabolites, 5-aminosalicylic acid (5-ASA), N-acetyl-5-ASA, and sulfapyridine (SP) to inhibit this reaction. We found that Hb interacted with H2O2 to yield the radical and nonradical forms of ferryl Hb (Hb(V)) which were capable of initiating the peroxidation of a phospholipid. This interaction did not result in the peroxide-dependent release of iron from the hemoprotein. In addition, we demonstrated that the pharmacologically active moiety of SAZ (or olsalazine), 5-ASA, was significantly better at inhibiting the Hb-catalyzed peroxidative reaction. The concentration of 5-ASA required to inhibit lipid peroxidation by 50% (IC50) was determined to be 50 microM. Neither parent compound (SAZ, olsalazine) nor the pharmacologically inactive metabolite (SP) were effective in attenuating the lipid peroxidation at concentrations up to 100 microM. The N-acetylated derivative of 5-ASA was less effective as an inhibitor in this system possessing an IC50 of 100 microM. The mechanism by which 5-ASA inhibited lipid peroxidation appeared to be due to its ability to donate electrons to and thus scavenge the radical and nonradical forms of HB(IV).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of sulfasalazine metabolites on hemoglobin-catalyzed lipid peroxidation. 167 20

Surgical specimens from 2 patients with chronic ulcerative colitis accompanied with colon cancer were evaluated by immunoperoxidative staining using monoclonal antibodies A7 (against human colon cancer), S202 (against human gastric cancer), and anti-carcinoembryonic antigen (CEA). The three monoclonal antibodies were reactive with cancerous tissue, anti-CEA antibody and monoclonal antibody S202 reacted with dysplasia tissues, whereas monoclonal antibody A7 did not. Using high-iron diamine technique for mucosubstances (sialomucin and sulfomucin), cancer and dysplasia showed no secretory elements. Surrounding mucosa showed both sialomucin and sulfomucin secretion.
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PMID:[Two cases of ulcerative colitis with colon cancer: immunoperoxidase staining using monoclonal antibodies against gastrointestinal tumor and mucin staining]. 169 18

A new assay for the determination of faecal alpha-1-antitrypsin including a simplified extraction of native stool and nephelometric measurement was studied. Its validity was established by a comparison with standardized methods and with well-known activity parameters. Excellent correlations were found, comparing this method with radial immuno-diffusion carried out on lyophilized (R = 0.96; p less than 0.05) and native (R = 0.97; p less than 0.05) stool samples. Faecal alpha-1-antitrypsin concentrations as measured with this method were significantly (p less than 0.001) higher in patients with inflammatory bowel diseases (Crohn's disease = 40, ulcerative colitis = 15) than in 25 normal controls (0.51 +/- 0.06 mg/g vs. 0.13 +/- 0.02 mg/g; x +/- SEM). There was a significant correlation of faecal alpha-1-antitrypsin with CDAI, activity index van Hees, and with various laboratory parameters (ESR, CRP, serum alpha-1-antitrypsin, orosomucoid, albumin, iron, haematocrit, haemoglobin, leucocytes, and thrombocytes). The presented method is equivalent to standard techniques in measuring faecal alpha-1-antitrypsin concentrations. It is highly useful for clinical routine and for follow-up studies in patients with inflammatory bowel disease.
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PMID:[Initial clinical experiences with a simplified analytic method for fecal alpha-1-antitrypsin]. 177 47

Total colectomy, mucosal proctectomy and straight ileo-anal anastomosis was performed in four adult patients with chronic ulcerative colitis (three males, one female; mean age 27.4 years). During a follow-up period of one to five years, all patients were continent, had spontaneous bowel evacuation (average 4-5 per day), and had normal bladder and sexual function. Sequential per rectal ileoscopies revealed loss of ileal folds and gradual transformation to a colonic type of mucosa. On barium studies, the anastomosed terminal ileum showed progressive ballooning and assumed a rectosigmoid appearance with complete disappearance of ileal characteristics. The histology showed a progressive transformation from ileal to colonic type of mucosa, with blunting and ultimate disappearance of villi, increasing goblet cell population, and increase in mononuclear cells in the lamina propria. Histochemical studies (high iron diamine and alcian blue stains) revealed a change from small intestinal to colonic mucin, progressing proximally from just above the anastomotic site. Two patients had a single recurrence with ileal histology resembling that of active ulcerative colitis; both responded to short term steroid therapy. The results of straight ileo-anal anastomosis compare well with Western reports of ileal reservoirs. Adaptative changes of 'colonisation' can be consistently demonstrated in the anastomosed ileum on follow-up; these start just above the anastomotic site and ascend proximally. The colonised ileum appears to be susceptible to the ulcerative disease.
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PMID:Adaptative changes in terminal ileum after total colectomy, mucosal proctectomy and straight ileo-anal anastomosis in chronic ulcerative colitis. 230 4


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