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PubMed2006

Predictive and protective factors associated with colorectal cancer in ulcerative colitis: A case-control study.

BACKGROUND & AIMS: Predictive and protective factors associated with colorectal cancer in chronic ulcerative colitis are not well described. Surveillance colonoscopy and 5-aminosalicylic acid therapy may mitigate cancer risk, but there is debate because these variables have not been evaluated in the same study. The presence of postinflammatory pseudopolyps and use of other anti-inflammatory medications may be important variables that influence risk, but data are sparse. METHODS: Variables associated with colorectal cancer were registered in 188 patients with ulcerative colitis-related cancer and matched controls. Conditional logistic regression, adjusted for age at colitis diagnosis and colitis duration, identified a final set of variables independently associated with colorectal cancer. RESULTS: In the final multiple variable model, the most important factors associated with colorectal cancer were a history of pseudopolyps (OR, 2.5; 95% CI: 1.4-4.6), 1 or 2 surveillance colonoscopies (OR, 0.4; 95% CI: 0.2-0.7), smoking (OR, 0.5; 95% CI: 0.2-0.9) and use of corticosteroids (OR, 0.4; 95% CI: 0.2-0.8), aspirin (OR, 0.3; 95% CI: 0.1-0.8), nonsteroidal anti-inflammatory drugs (OR, 0.1; 95% CI: 0.03-0.5), and 5-aminosalicylic acid agents (OR, 0.4; 95% CI: 0.2-0.9), although the latter was not statistically significant after 5 years. Primary sclerosing cholangitis and immunosuppressive use were not statistically significant. CONCLUSIONS: These results suggest that, in a population matched for extent and duration of chronic ulcerative colitis, surveillance colonoscopy and use of anti-inflammatory medications may reduce the risk of colorectal cancer. A history of postinflammatory pseudopolyps appears to be a predictive factor for cancer.

Adolescent↗
PubMed1992

Neutrophil-mediated nitrosamine formation: role of nitric oxide in rats.

It is well known that chronic inflammation of the colon and rectum is associated with an increased risk of colorectal cancer, but the mechanisms by which inflammation promotes neoplasia remain undefined. The authors propose that inflammatory neutrophils may produce carcinogenic nitrosamines via the L-arginine-dependent formation of nitrogen oxides such as nitric oxide. Therefore, the objectives of the study were to characterize the L-arginine-dependent formation of nitrogen oxides by inflammatory (elicited) neutrophils using conditions that more closely mimic the extravascular (i.e., interstitial) compartment of the gut and to characterize the neutrophil-dependent N-nitrosation of a model amine to yield its nitrosamine derivative. In the absence of any metabolic activation, adherent, inflammatory neutrophils (2 x 10(6) cells) produced 12.8 +/- 1.4 mumol/L of nitrite during a 4-hour incubation period. Omission of L-arginine and/or inhibition of nitric oxide synthase by the addition of 1 mmol/L NG-nitro-L-arginine methyl ester (L-NAME) resulted in 35%-78% inhibition of nitrite production, suggesting that nitrite was derived from nitric oxide. By comparison, neither circulating rat neutrophils nor elicited rat macrophages produced significant amounts of nitrite under the same conditions. Furthermore, elicited neutrophils (2 x 10(6) cells) were capable of N-nitrosating 2,3-diaminonaphthalene to yield its nitrosamine derivative 1-naphtho-2,3-triazole (282 +/- 12 nmol/L) in a time- and cell-dependent pattern similar to that of nitrite production. Addition of a variety of antioxidants (e.g., ascorbic acid, reduced glutathione, alpha-tocopherol analog), 5-aminosalicylic acid, or L-NAME resulted in 80%-85% inhibition of neutrophil-mediated nitrosamine formation. Taken together, these data suggest that inflammatory neutrophils may represent an important metabolic source of endogenous carcinogens during times of active intestinal inflammation.

Aminosalicylic Acids↗
PubMed1988

Prospective, randomized, double-blind comparison of benzalazine and sulfasalazine in the treatment of active ulcerative colitis.

Benzalazine (salicylazobenzoic acid, SAB), a 5-azo derivative of 5-aminosalicylic acid, has been designed as a new therapeutic agent for the treatment of inflammatory bowel disease which might lack the frequent side effects caused by the sulfapyridine moiety of the sulfasalazine molecule (SASP). Here, we report on a prospective, randomized, double-blind comparison of SAB and SASP in patients with an acute relapse of ulcerative colitis. 43 patients with an acute relapse of ulcerative colitis proven by the pertinent endoscopic-macroscopic and histologic criteria were randomized to receive a 6-week course of either 1 g SASP (n = 21) or the equivalent dose of 0.72 g SAB (n = 22) three times a day. Both groups were comparable with respect to demographic data, previous duration and extension of the disease as well as clinical, endoscopic and histologic severity of the relapse. 1 patient on SASP had to be removed from the study due to side effects, while 3 patients on SAB were removed due to rapid worsening of the disease requiring either surgery (1 patient with toxic megacolon) or additional steroid treatment (2 patients). 2 SAB patients were lost to follow-up after substantial improvement had been observed within the first 3 weeks of treatment. In the remaining patients (20 SASP, 17 SAB), stool frequency, stool consistency and macroscopic appearance as well as histology of the diseased mucosa were improved within 6 weeks, with no significant difference between the two groups with respect to any of the parameters recorded. Side effects were recorded in 5 patients on SASP (3 with nausea, 1 with pruritus and 1 with a generalized exanthema) and in 3 patients on SAB (all nausea and vomiting; difference not statistically significant). We conclude that SAB and SASP in equivalent doses are of similar efficacy in the treatment of active ulcerative colitis.

Acute Disease↗
PubMed1984

Drug elimination function of rat small intestine: metabolism and intraluminal excretion.

The metabolic and excretory function of the small intestine was investigated after oral and intravenous administration of drugs having an aromatic amino group to rats. After administration of drugs into the intestinal loop at the initial concentration of 0.1 mM, significant excretion of their N-acetylated forms into the lumen was observed. The amount of N-acetyl forms excreted in the lumen were 39.3 +/- 3.5, 63.5 +/- 20.9 and 18.0 +/- 13.8% of disappeared drugs from the lumen for p-aminobenzoic acid (PABA), p-aminosalicylic acid and sulfanilic acid, respectively. The excretion of p-acetamidobenzoic acid (Ac-PABA) after the absorption of PABA was reduced by the coadministration with salicylic acid, benzoic acid and 2,4-dinitrophenol. Salicylic acid noncompetitively inhibited the acetylation of PABA by the intestinal N-acetyltransferase. A good correlation was found between the intestinal N-acetyltransferase activities for drugs and the intraluminal excretion of N-acetyl derivatives after intestinal absorption of drugs. These results indicate that a drug having a higher susceptibility to intestinal N-acetyltransferase would undergo a greater excretion into the lumen in its N-acetyl form after intestinal absorption. After intravenous administration of PABA at a dose of 100 mumole/kg, 4.02 +/- 0.51% of dose was excreted in the lumen as Ac-PABA in 30 min. On the other hand, a significantly smaller fraction (2.72 +/- 0.68% of dose) was excreted in the lumen after intravenous injection of 100 mumole/kg of Ac-PABA. The larger excretion of Ac-PABA after administration of PABA indicates the contribution of intestinal metabolism on the transfer of PABA not only after oral, but also after intravenous administration.

4-Aminobenzoic Acid↗
PubMed1989

Terbium chelate labels for fluorescence immunoassays.

Bovine serum albumin was labelled with a terbium complex by means of a reagent prepared from diethylenetriaminepentaacetic acid or diethylenetriaminepentaphosphonic acid and p-aminosalicylic acid. The ternary mixed ligand complexes showed strong fluorescence and were stable in very dilute solution (10(-10)M). The fluorescence of the conjugated products was compared with regard to their application in the fluoroimmunoassay of bovine serum albumin.

Chelating Agents↗
PubMed1958

The relative potencies of some substituted salicylic acids as metabolic stimulants in the intact rat.

The effects of eighteen substituted benzoic acids on the rate of oxygen consumption have been studied in rats. 2:3-Dihydroxybenzoic acid, phthalic acid and 6-methylsalicylic acid were, at the doses used, inactive; m- and p-hydroxybenzoic acid, 2:4-, 2:5-, 2:6-, 3:4-, and 3:5-dihydroxybenzoic acid, o-aminobenzoic acid, salicyluric acid, salicylamide and 5-aminosalicylic acid decreased the rate of oxygen consumption. Only salicylic acid and o-, m- and p-cresotic acid (3-, 4- and 5-methylsalicylic acid respectively) increased the rate of oxygen consumption. Molar potency ratios of the cresotic acids as metabolic stimulants relative to salicylic acid were determined; o-cresotic acid was the most powerful with a ratio of 2.61, m- and pcresotic acid had values of 1.78 and 1.89 respectively. Two possible explanations of the higher potencies of the cresotic acids were considered. No difference in the primary action of the drug was established by determining the effect on rate of oxygen consumption of a mixture of o-cresotic and salicylic acids. An alternative possibility was that the rates of detoxication and excretion of the cresotic acids differed among themselves and from salicylic acid. No such differences were found.

Animals↗
PubMed1994

Polymorphism of human acetyltransferases.

Acetylation by arylamine N-acetyltransferases (NATs) is a major route in the metabolism of numerous drugs and carcinogens. Recent studies suggest that the same enzymes also catalyze N,O-transacetylation and O-acetylation. A genetic polymorphism of clinical relevance divides the human population into slow and rapid acetylators of arylamines. Two human NATs, NAT1 and NAT2, have recently been characterized by protein purification, cloning, and functional expression of the respective genes; both were localized to chromosome 8. NAT1 codes for a protein with ubiquitous tissue distribution and a high affinity for p-aminobenzoic acid and p-aminosalicylic acid, so-called monomorphic substrates. NAT2 codes for a protein predominantly expressed in liver with a high affinity for sulfamethazine and other polymorphically metabolized drugs. NAT2 was analyzed at the level of protein, RNA and DNA derived from phenotyped slow and rapid acetylators. Two common (M1, M2) and one rare (M3) mutant allele were identified and their mutations characterized. A simple polymerase chain reaction-based DNA test can identify > 95% of mutant alleles and predict the phenotype.

Acetylation↗
PubMedDate not supplied

Review of drug interference with urine glucose tests.

Many drugs have been reported to interfere with copper-reduction or glucose oxidase tests used to measure urine glucose. However, only a few drugs or drug classes have been well documented to clinically interfere with these tests. The interfering drugs include ascorbic acid, beta-lactam antibiotics (e.g., cephalosporins and penicillins), levodopa, and salicylates. Several other drugs may also interfere with certain urine glucose tests, but the interactions are poorly documented. These drugs include chloral hydrate, hyaluronidase, nalidixic acid, nitrofurantoin, p-aminosalicylic acid, phenazopyridine, probenecid, and X-ray contrast media. Drugs or their metabolites that are strong reducing substances produce false-positive results by the copper-reduction method and false-negative results by the glucose oxidase method. The beta-lactam antibiotics interfere with copper-reduction tests by producing copper compounds of various colors that confuse interpretation of test results. Tables are provided that summarize the drug interferences discussed.

Anti-Bacterial Agents↗
PubMed2002

[Allergic reactions and hypopigmentation due to temporary tattooing with henna].

Skin tattooing with henna seems a safe alternative to permanent skin tattooing. Contact dermatitis due to henna is rare. Most of the reactions are due to additives, especially paraphenylenediamine, which is added to speed up the process of skin dyeing and to give a darker brown to black colour ('black' henna) instead of the otherwise reddish brown henna colour. Paraphenylenediamine is a well-known strong sensitizer, particularly due to its use as a hair dye. Three patients, two boys aged 8 and 10 years and a 30-year-old woman, developed allergic contact dermatitis after skin painting, after which hypopigmentation remained. Patch tests with paraphenylenediamine were strongly positive in all three patients. This positive reaction means that they will never be able to dye their hair and that they have an increased risk of cross-reactions with other dyes, but also with local anaesthetics, sulfonamides, para-aminoazobenzoic acid or para-aminosalicylic acid.

Adult↗
PubMed1989

The effects of repeated parenteral administration of chelating agents on the distribution and excretion of uranium.

The effects of repeated ip administration of gallic acid, 4,5-dihydroxy-1,3-benzenedisulfonic acid (Tiron), diethylenetriaminepentaacetic acid (DTPA), and 5-aminosalicylic acid (5-AS) on the distribution and excretion of uranium were assessed in male Swiss mice. Only Tiron significantly increased the amount of uranium excreted into urine and feces. A significant decrease in the concentration of uranium in liver, spleen and bone was observed after administration of Tiron, whereas injection of gallic acid or DTPA resulted in a significant decrease in the concentration of the metal in the liver. The results show that Tiron was consistently the most effective chelator of those tested in the treatment of uranium poisoning after repeated daily administration of the metal.

Animals↗
PubMed1986

Identification and inheritance of inbred hamster N-acetyltransferase isozymes in peripheral blood.

Acetyl CoA-dependent p-aminobenzoic acid and p-aminosalicylic acid N-acetyltransferase (NAT) activity was determined in peripheral blood and blood cells from homozygous rapid (RR) acetylator (Bio. 87.20) and homozygous slow (rr) acetylator (Bio. 82.73/H) inbred hamsters and in their F1, F2 and backcross progeny. NAT activity was localized primarily in erythrocytes and was acetylator genotype dependent, as highest levels were expressed in homozygous rapid acetylator hamsters, intermediate levels in heterozygous acetylator hamsters and lowest levels in homozygous slow acetylator hamsters. Bio. 87.20 X Bio. 82.73/H F1 progeny expressed a unimodal nonoverlapping distribution of NAT activity intermediate between the RR and rr parentals. F2 generation progeny segregated into three modes (low, intermediate and high) of 21, 42 and 11, which is not significantly different from 1, 2 and 1. Bio. 82.73/H X F1 backcross progeny segregated into two modes (low and intermediate) of 18 and 16, whereas Bio. 87.20 X F1 backcross progeny segregated into two modes (intermediate and high) of 17 and 14, neither of which is significantly different from 1 and 1. These data are consistent with simple autosomal Mendelian inheritance of blood NAT activity by two codominant alleles at a single genetic locus. Partial purification of peripheral blood NAT activity by ion-exchange chromatography yielded separation of two isozymes that both exhibited acetylator genotype-dependent expression with highest activity in RR, intermediate activity in Rr and nondetectable activity in rr genotypes, respectively.

4-Aminobenzoic Acid↗
PubMed1982

Prostanoid synthesis by cultured peripheral blood mononuclear cells in inflammatory diseases of the bowel.

Prostanoid synthesis by cultured peripheral blood mononuclear cells and monocytes in inflammatory bowel disease patients was determined because monocytosis was reported in inflammatory bowel diseases and prostanoids are synthesized by peripheral blood mononuclear cells in response to inflammatory stimuli. Prostaglandin E2 and thromboxane B2 accumulation in the medium of cultured peripheral blood mononuclear cells isolated from patients with active Crohn's disease was two and three times higher than their respective accumulation by peripheral blood mononuclear cells isolated from normal subjects or patients in remission. In ulcerative colitis, prostaglandin E2 and thromboxane B2 accumulation was not enhanced. 6-Keto-prostaglandin F1 alpha was not detected in any of the cultured medium. The absolute number of monocytes was determined according to their adherence to plastic surfaces, and the percent of phagocytic cells was significantly higher among peripheral blood mononuclear cells in patients with Crohn's disease and ulcerative colitis as compared with peripheral blood mononuclear cells isolated from normal subjects. However, prostaglandin E2 secretion, by the same number of cultured monocytes isolated from all groups of patients, was similar. Flufenamic acid, methylprednisolone, and 5-aminosalicylic acid significantly inhibited prostaglandin E2 and thromboxane B2 accumulation. These results suggest that in Crohn's disease enhanced prostanoid synthesis is probably due to the monocytosis, whereas in ulcerative colitis the monocytosis is not accompanied by a significant increase in prostanoid synthesis in vitro.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

A unique pharmacogenetic expression of the N-acetylation polymorphism in the inbred hamster.

Liver N-acetyltransferase (NAT) preparations (105,000 x g cytosol) were obtained from both sexes of 26 strains of inbred hamsters. Liver NAT activity levels were determined for six arylamine substrates; isoniazid, p-aminobenzoic acid (PABA), p-aminosalicylic acid (PAS), sulfamethazine (SMZ), procainamide and 2-aminofluorene. The N-acetylation of isoniazid, SMZ, procainamide and 2-aminofluorene exhibited a monomorphic expression in the hamster as the genetic variation in NAT activity levels between hamster strains was only about 2-fold for each substrate. In contrast, the N-acetylation of PABA and PAS showed a polymorphic expression in the hamster. Two inbred hamster lines (Bio 1.5 and Bio 82.73) had over 400-fold lower PABA NAT and over 20-fold lower PAS NAT activity levels than did the other inbred strains. In addition, the genetically determined N-acetylation differences between the rapid and slow acetylator hamster strains were also demonstrated in vivo for PABA but not for SMZ. Comparison of Michaelis-Menten kinetic constants of PABA NAT activity in a rapid and slow acetylator strain showed a 20-fold lower Km in the rapid acetylator strain suggesting an intrinsic structural difference in rapid and slow acetylator hamster liver NAT. Thus, the pharmacogenetic expression of the N-acetylation polymorphism is quite unique in the inbred hamster, in that PABA and PAS are genetically polymorphic substrates, whereas isoniazid, SMZ, procainamide and 2-aminofluorene are monomorphic, in direct contrast to man and rabbit.

Acetylation↗
PubMed1980

Nitrosation of orally administered drugs under simulated stomach conditions.

Of a total of 61 drugs considered to be potentially nitrosatable on the basis of their chemical structure, 7 have indeed been nitrosated in gastric juice at pH 2 and under simulated human stomach conditions, where the pH was varied from about 7 to 2 within 60 min. The 7 nitrosatable drugs were ethambutole, despiramine hydrochloride, clomipramine hydrochloride, phenoxymethyl penicillin, aminophenazone, piperazine diadipate and analgine. Inhibition of nitrosation under simulated stomach conditions was also investigated using ascorbic acid, sulfanilamide, p-aminosalicylic acid and sulfamic acid. The first three agents were effective inhibitors, whereas sulfamic acid stimulated nitrosation within a distinct pH range.

Animals↗
PubMed1978

The correlation of bacteriophage types of Mycobacterium tuberculosis with guinea-pig virulence and in vitro-indicators of virulence.

Among 58 isoniazid-sensitive strains of Mycobacterium tuberculosis from India, Burma and East Africa, 23 were of phage type A, 31 of type I (intermediate), 4 of type B and none of type C. Type I strains differed from type A strains in being attenuated in the guinea-pig, susceptible to H2O2, sensitive to thiophen-2-carboxylic acid hydrazide and resistant to thiacetazone and p-aminosalicylic acid; the content of strongly acidic lipids and of sulphatide lipids was low and the attenuation indicator lipid was present. The pattern of results with the type B strains did not correspond to the patterns for types A or I. Strains of type I appear to be a distinct group within the species M. tuberculosis.

Aminosalicylic Acid↗
PubMed2006

Anti-tryptase treatment using nafamostat mesilate has a therapeutic effect on experimental colitis.

OBJECTIVE: Mast cell tryptase has been proposed to be involved in the pathogenesis of human inflammatory bowel disease (IBD). Recently, it was reported that a low dose of nafamostat mesilate (NM), a serine protease inhibitor that is widely used to treat disseminated intravascular coagulation (DIC) and acute pancreatitis, can selectively inhibit human tryptase activity. The aim of this study was to investigate the anti-inflammatory effects of NM on experimental colitis in rats. MATERIAL AND METHODS: Colitis was induced in male Wistar rats using an enema of trinitrobenzene sulfonic acid (TNBS) dissolved in 50% ethanol. NM or 5-aminosalicylic acid (5-ASA), foundation therapy for mild-to-moderate IBD, was administered via the anus once a day on each of the 6 days after administration of TNBS. Colonic inflammation was assessed 1 week after TNBS administration. RESULTS: Intracolonic administration of TNBS resulted in the infiltration of numerous tryptase-positive cells in the colonic mucosa. The colonic mucosal injury induced by TNBS was significantly decreased by treatment with NM or 5-ASA. The increases in thiobarbituric acid-reactive substances (TBA-RS), myeloperoxidase (MPO) activity, tumor necrosis factor (TNF)-alpha and cytokine-induced neutrophil chemoattractants-1 (CINC-1) in the colonic mucosa were inhibited in the NM group and the 5-ASA group, without significant differences between them. CONCLUSIONS: These results indicate that a low dose of NM can inhibit the colonic mucosal inflammation induced by TNBS in rats, which suggests that anti-tryptase therapy using low doses of NM has excellent potential to become a new therapeutic strategy for IBD.

Aminosalicylic Acids↗