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PubMed1975

Crohn's disease of the colon. II. Controversial aspects of hemorrhage, anemia and rectal involvement in granulomatous disease involving the colon.

In 160 cases with granulomatous colitis or ileocolitis, blood was found in the stool in 72 or 45%. Massive bleeding occurred in four patients (25%); overt bleeding in 51 (32%) and occult bleeding, repeated guaiac positive stools, in 17 (11%). Thus, clinically obvious bleeding occurred in about one patient in three. Of the four patients with massive hemorrhage one required subtotal colectomy, one right hemicolectomy and the other two were controlled by medical measures including blood transfusion. In each of the surgical cases, the massive bleeding originated in the region of the cecum. An additional patient, not in the series, required proctectomy as a life-saving measure following subtotal colectomy. Clinically obvious rectal bleeding in Crohn's colitis is approximately ten times as frequent as in regional enteritis but only one-third as frequent as in ulcerative colitis. There was no correlation between rectal bleeding and rectal involvement determined radiologically or by signoidoscopy, in the whole series but there was a strong association in the small group of Crohn's colitis with rectal involvement (86% with bleeding) and a significantly greater proportion of patients with colitis with rectal involvement and hemorrhage (P smaller than 0.02). Anemia is common in both groups but in Crohn's colitis it is almost always, 75%, associated with rectal blood loss, whereas in ileocolitis this association is much less marked, 40%, indicating other important causes of anemia when there is small bowel disease. The bleeding patient with Crohn's colitis should be managed medically initially. Uncontrollable, continuous, or massive hemorrhage may require angiography and early surgical intervention.

Adolescent↗
PubMed1992

Colonic proliferation and colon cancer risk. A review of clinical studies.

The purpose of this review is to discuss some of the recent hypotheses regarding the dietary etiology of colorectal cancer. We will review some of the epidemiological background and animal studies that were performed to test these hypotheses. The use of the rectal mucosal proliferation rate as measured by thymidine labelling index as an intermediate endpoint for clinical studies is discussed, including the results of testing these hypotheses using this marker. We believe that all hypotheses must eventually be tested in the human model and that carefully controlled, sequential analyses of each acceptable hypothesis is the most prudent road to understanding the environmental causes of colorectal cancer.

Biomarkers, Tumor↗
PubMed1986

Colonization of the nasal passages of calves with Pasteurella haemolytica serotype 1 and regeneration of colonization after experimentally induced viral infection of the respiratory tract.

Healthy nonstressed calves were inoculated intranasally with or subjected to aerosol exposure to Pasteurella haemolytica serotype 1. Only 4 of 28 calves harbored the bacterium in enough numbers to be isolated from the nasal passages for more than 7 days. After apparent clearing from the nasal passages, 8 calves were inoculated intranasally with infectious bovine rhinotracheitis virus; 2 of these calves shed the P haemolytica during clinical illness due to the virus. The remaining 20 calves were aerosol-exposed to parainfluenza-3 virus; 6 of these calves shed P haemolytica during clinical illness due to the parainfluenza-3 virus.

Animals↗
PubMed1981

Incidence of enteritis of Enterobacteriaceae isolates possessing human colonization factor antigen. New human colonization factors.

Of 462 Enterobacteriaceae strains including 435 Escherichia coli isolated from 250 patients, 298 haemagglutinating (HA) cultures were classified into 36 different HA groups. Sixteen of them belonged to Evan's I or II groups, although none possessed CF I or CF II antigen detectable by slide agglutination. Seventy-seven strains showed 4+ mannose resistant (MR) HA with human (53), bovine (2), chicken (6), guinea pig (7) or human and guinea pig (9) erythrocytes. These strains were significantly more frequent in patients under one year of age. Eighty-eight percent of the typable strains belonged to E. coli serogroups O1, O2, O4, O6, O18. HA positivity and fimbrial structures were correlated in 2 isolates (15/1, O18a, c:-K77: H-; 12/2/1 O1: K1: H .). Fimbriae of the two strains exhibited adhesive properties. Their fimbrial antigens differed serologically from each other and from those of the reference strains H 10407 and PB 176. Forty-nine of 4+ human MRHA strains showed variable reactions in the two sera for the new fimbrial antigens.

Antigens, Bacterial↗
PubMed1996

Tumor size and origin determine the antitumor activity of cisplatin or 5-fluorouracil and its modulation by leucovorin in murine colon carcinomas.

5-Fluorouracil (FUra) is one of the few effective agents in the treatment of patients with colorectal cancer. Its effects on the target enzyme thymidylate synthase (TS) can be modulated by leucovorin (LV) or cisplatin (CDDP). Tumor size and differentiation of tumor characteristics can influence therapeutic efficacy. We therefore studied the relationship between tumor size (cutoff point 200 mm3) and the antitumor activity of FUra and its modulation by LV in murine Colon 26 and Colon 38 tumors. The doubling time of tumors measuring > 200 mm3 was about 160% longer. The antitumor effect of FUra in these large tumors was decreased and could not be modulated by LV. In addition, three subtypes of Colon 26 (Colon 26-A, Colon 26-B, and Colon 26-10) were identified and characterized for tumor-induced weight loss, TS activity, response to chemotherapy, and histological features. Mice bearing Colon 38 and Colon 26-10 did not lose weight as a result of tumor growth. Colon 26-A caused a weight loss of up to 19%, whereas mice with Colon 26-B tumors remained within 10% of their initial weight and tolerated at least 2.5 times more tumor load than did mice bearing Colon 26-A, which induces cachexia. Among untreated tumors, TS catalytic activity was highest in Colon 26-B (5536 pmol mg protein(-1) h(-1)) and lowest in Colon 38 (799 pmol mg protein(-1) h(-1)); Colon 26-A and Colon 26-10 had intermediate activities (about 2500 pmol mg protein(-1) h(-1)). 5-Fluoro-2'-deoxyuridine monophosphate (FdUMP) binding was comparable in the three Colon 26 subtypes but was lower in Colon 38. The antitumor activity of FUra could be modulated by LV in Colon 38, Colon 26-10, and Colon 26-A but could not in Colon 26-B, with complete responses (CR) being obtained in Colon 26-10 and Colon 38. The latter two were highly sensitive to CDDP, followed by Colon 26-A and Colon 26-B (CRs: 50%, 40%, 25%, and 0, respectively). Furthermore, necrosis was noted in Colon 26-B and Colon 38 but not in Colon 26-A. In conclusion, (1) the antitumor activity of FUra in large tumors is decreased and cannot be modulated by LV and (2) characteristics and sensitivity to chemotherapeutics can vary substantially in closely related tumors of the same origin.

Adenocarcinoma↗
PubMedDate not supplied

Pharmaceutical approaches to colon targeted drug delivery systems.

PURPOSE: Although oral delivery has become a widely accepted route of administration of therapeutic drugs, the gastrointestinal tract presents several formidable barriers to drug delivery. Colonic drug delivery has gained increased importance not just for the delivery of the drugs for the treatment of local diseases associated with the colon but also for its potential for the delivery of proteins and therapeutic peptides. To achieve successful colonic delivery, a drug needs to be protected from absorption and /or the environment of the upper gastrointestinal tract (GIT) and then be abruptly released into the proximal colon, which is considered the optimum site for colon-targeted delivery of drugs. Colon targeting is naturally of value for the topical treatment of diseases of colon such as Chron's diseases, ulcerative colitis, colorectal cancer and amebiasis. Peptides, proteins, oligonucleotides and vaccines pose potential candidature for colon targeted drug delivery. METHODS: The various strategies for targeting orally administered drugs to the colon include covalent linkage of a drug with a carrier, coating with pH-sensitive polymers, formulation of timed released systems, exploitation of carriers that are degraded specifically by colonic bacteria, bioadhesive systems and osmotic controlled drug delivery systems. Various prodrugs (sulfasalazine, ipsalazine, balsalazine and olsalazine) have been developed that are aimed to deliver 5-amino salicylic acid (5-ASA) for localized chemotherapy of inflammatory bowl disease (IBD). Microbially degradable polymers especially azo crosslinked polymers have been investigated for use in targeting of drugs to colon. Certain plant polysaccharides such as amylose, inulin, pectin and guar gum remains unaffected in the presence of gastrointestinal enzymes and pave the way for the formulation of colon targeted drug delivery systems. The concept of using pH as a rigger to release a drug in the colon is based on the pH conditions that vary continuously down the gastrointestinal tract. Times dependent drug delivery systems have been developed that are based on the principle to prevent release of drug until 3-4 h after leaving the stomach. Redox sensitive polymers and bioadhesive systems have also been exploited to deliver the drugs into the colon. RESULTS: The approach that is based on the formation of prodrug involves covalent linkage between drug and carrier. The type of linkage that is formed between drug and carrier would decide the triggering mechanism for the release of drug in colon. The presence of azo reductase enzymes play pivotal role in the release of drug from azo bond prodrugs while glycosidase activity of the colonic microflora is responsible for liberation of drugs from glycosidic prodrugs. Release of drugs from azo polymer coated dosage forms is supposed to take place after reduction and thus cleavage of the azo bonds by the azoreductase enzymes present in the colonic microflora. Natural polysaccharides have been used as tools to deliver the drugs specifically to the colon. These polysaccharides remain intact in the physiological environment of stomach and small intestine but once the dosage form enters into colon, it is acted upon by polysaccharidases, which degrades the polysaccharide and releases the drug into the vicinity of bioenvironment of colon. However, they should be protected while gaining entry into stomach and small intestine due to enormous swelling and hydrophilic properties of polysaccharides. This has been achieved either by chemical crosslinking or by addition of a protective coat. Formulation coated with enteric polymers releases drug when pH move towards alkaline range while as the multicoated formulation passes the stomach, the drug is released after a lag time of 3-5 h that is equivalent to small intestinal transit time. Drug coated with a bioadhesive polymer that selectively provides adhesion to the colonic mucosa may release drug in the colon. CONCLUSIONS: Improved drug delivery systems are required for drugs currently in use to treat localized diseases of the colon. The advantages of targeting drugs specifically to the diseased colon are reduced incidence of systemic side effects, lower dose of drug, supply of the drug to the biophase only when it is required and maintenance of the drug in its intact form as close as possible to the target site.

Animals↗