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PubMed1992

The effect of sulfasalazine on bovine endothelial cell proliferation and cell cycle phase distribution. Comparison with olsalazine, 5-aminosalicylic acid, and sulfapyridine.

Sulfasalazine is used in the treatment of chronic inflammatory states, for example, in inflammatory bowel disease and to a lesser degree in rheumatoid arthritis. In chronic inflammation, the formation of new blood vessels may play a key role in maintaining the inflammatory state. This process is dependent on the activation and proliferation of the endothelial cells. To investigate the possible role of sulfasalazine and its metabolites, sulfapyridine and 5-aminosalicylic acid, we examined the effect of these drugs on vascular endothelial cell proliferation in vitro. Cultures of bovine aortic endothelial cells were incubated with sulfasalazine and its metabolites. At 24 hours of incubation, sulfasalazine inhibited tritiated thymidine incorporation and cell proliferation and had already slowed S-phase progression at a concentration greater than 0.125 mmol/L. After 3 hours of incubation, sulfasalazine inhibition of tritiated thymidine incorporation into the DNA of endothelial cells was observed. This inhibition was completely reversible 24 hours after the drug was removed. One of the possible mechanisms for the inhibition of endothelial cell proliferation is interference with the de novo synthesis of thymidine that depends on folate-dependent enzymes. The effect of deoxyuridine and tetrahydrofolate on tritiated thymidine incorporation into cellular DNA, as well as release of tritium to water by [5-3H]-labeled deoxyuridine on methylation to thymidine, were used as probes for the de novo synthesis of thymidine. Deoxyuridine and tetrahydrofolate, when added to cells either individually or together for 3 hours, suppressed incorporation of tritiated thymidine into DNA through an increase in de novo thymidine synthesis. Sulfasalazine, but not its metabolites, reduced this suppression.2+ culture is inhibited by sulfasalazine and olsalazine but not by their metabolites. This inhibition appears to depend partly on the reduction of de novo synthesis of thymidine that is folate dependent.

Aminosalicylic Acids↗
PubMed2002

In vitro evaluation of pectin-HPMC compression coated 5-aminosalicylic acid tablets for colonic delivery.

In this study, we report pectin-HPMC compression coated core tablets of 5-aminosalicylic acid (5-ASA) for colonic delivery. Each 100 mg core tablet contained 5-ASA and was compression coated at 20 kN or 30 kN using 100% pectin, 80% pectin-20% HPMC, or 60% pectin-40% HPMC, at two different coat weights as 400 or 500 mg. Drug dissolution/system erosion/degradation studies were carried out in pH 1.2 and 6.8 buffers using a pectinolytic enzyme. The system was designed based on the gastrointestinal transit time concept, under the assumption of colon arrival times of 6 h. It was found that pectin alone was not sufficient to protect the core tablets and HPMC addition was required to control the solubility of pectin. The optimum HPMC concentration was 20% and such system would protect the cores up to 6 h that corresponded to 25-35% erosion and after that under the influence of pectinase the system would degrade faster and delivering 5-ASA to the colon. The pectin-HPMC envelope was found to be a promising drug delivery system for those drugs to be delivered to the colon.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2006

5-aminosalicylic acid release from a new controlled-release mesalazine formulation during gastrointestinal transit in healthy volunteers.

BACKGROUND: Mesalazine (5-aminosalicylic acid, 5-ASA) containing formulations represent a cornerstone in the treatment of inflammatory bowel diseases. A novel formulation with an Eudragit L/S mixture coating has been developed to provide selective release of 5-ASA to the ileo-caecal region and the colon. AIM: To determine the release of 5-ASA during the gastrointestinal transit. METHODS: A single oral dose of mesalazine EC 500 mg gastroresistant tablets (Asamax) was administered to eight healthy male volunteers. Gastrointestinal transit and tablet disintegration were monitored by scintigraphy. 5-ASA release was verified by assessing plasma pharmacokinetics. RESULTS: Initial tablet disintegration was observed 5.65 +/- 0.86 h after dosing, corresponding to the detection of 5-ASA in plasma. This occurred in the ileo-caecal region in three subjects and the ascending colon in the remaining five. The relative percentage of 5-ASA absorption was more pronounced in the ascending colon (41 +/- 27.4%) than the ileo-caecal region (6.6 +/- 9.2%). CONCLUSION: This mesalazine EC gastroresistant tablets release locally active 5-ASA specifically in the ileo-caecal region and the ascending colon.

Administration, Oral↗
PubMed1986

Enhanced formation of sulfidopeptide-leukotrienes in ulcerative colitis and Crohn's disease: inhibition by sulfasalazine and 5-aminosalicylic acid.

Release of sulfidopeptide (SP)-leukotrienes (LT) in vitro from normal human colonic mucosa and from mucosal tissue obtained from patients with Crohn's disease (CD) and ulcerative colitis (UC) was investigated. It was found that inflamed mucosal tissue released significantly more SP-LT than normal colonic mucosa both under control conditions and after addition of calcium ionophore A23187. These results indicate the presence of endogenous stimuli as well as an increased responsiveness to an exogenous stimulus of LT formation in the inflamed mucosa. Sulfasalazine (SASP), a drug used in inflammatory bowel diseases, and its active metabolite 5-aminosalicylic acid (5-ASA) were found to inhibit colonic mucosal SP-LT formation, while only 5-ASA inhibited simultaneously synthesis of another arachidonic acid-derived inflammatory mediator, prostaglandin (PG) E2. The results suggest that SP-LT might be important mediators of inflammation in CD and UC.

Aminosalicylic Acids↗
PubMed1990

Prostaglandin catabolism and ulcerative colitis: effect of sulphasalazine, 5-aminosalicylic acid and other drugs.

1. Evidence is presented for the occurrence of type 1 prostaglandin 15-hydroxydehydrogenase in human rectal mucosa. No evidence of the presence of type 2 enzyme was found. 2. A 15-keto-prostaglandin reductase, responsible for the breakdown of 13,14-dihydro-15-keto prostaglandins to 13,14-dihydro prostaglandins, was also present in human rectal mucosa. 3. Ulcerative colitis patients catabolized prostaglandins to the same extent as the control group. PGE1 was catabolized significantly better than PGF2 alpha. 4. 5-Aminosalicylic acid and sulphapyridine did not affect prostaglandin catabolism. Sulphasalazine, methylsulphasalazine, indomethacin, flurbiprofen, disodium cromoglycate, sodium salicylate and carbenoxolone sodium inhibited prostaglandin catabolism to the same extent in both groups. Salicylazosulphadimidine was a more potent inhibitor of PGE1 catabolism than of PGF2 alpha. 5. The increased prostaglandin synthesis reported for ulcerative colitis patients was not paralleled by increased catabolism, a fact possibly contributing to the accumulation of such compounds in the diseased state.

Adult↗
PubMed1992

Lipogenesis from n-butyrate in colonocytes. Action of reducing agent and 5-aminosalicylic acid with relevance to ulcerative colitis.

Cell membranes of colonic epithelial cells (CEC) in ulcerative colitis show structural abnormalities which are specific to the disease and which suggest impaired lipogenesis in CECs. Lipogenesis from [1-14C]-n-butyrate, the chief oxidative fuel of colonic epithelial cells, was measured in isolated CECs under control conditions, with or without glucose and in the presence of mercaptoacetate, a major reducing agent in the colonic lumen. Glucose significantly (p < 0.01) stimulated lipogenesis from [1-14C]-butyrate which was reversed by 5 mM mercaptoacetate. Mercaptoacetate significantly diminished CEC thiolase activity (EC 2.3.1.9). 5-Aminosalicylic acid reversed the adverse effects of mercaptoacetate in the saponifiable fraction of extracted lipids. Changes in lipogenesis due to colonic luminal reducing agents would affect the barrier function of CECs a feature relevant to the disease process of ulcerative colitis.

Aminosalicylic Acids↗
PubMed1994

Intermittent therapy with high-dose 5-aminosalicylic acid enemas maintains remission in ulcerative proctitis and proctosigmoiditis.

PURPOSE: The aim of this study was to compare the efficacy of intermittent therapy with mesalazine enemas and continuous oral mesalazine to maintain remission of distal ulcerative colitis or proctitis. METHODS: Thirty-eight patients with distal ulcerative colitis (n = 17) or ulcerative proctitis (n = 21) in clinical, endoscopic, and histologic remission were randomly assigned to receive either oral mesalazine (0.5 g three times/day, Eudragit L coating, n = 19) or intermittent therapy with mesalazine enemas (4 g of 5-aminosalicylic acid enema every third night, n = 19). Both groups were comparable in regard to sex, age, age at disease onset, extent and duration of disease, number and mode of treatment of previous attacks, and time in remission. Patients were reviewed at the beginning of the study and, subsequently, at two-month intervals for 24 months or until a relapse occurred. At each visit, diaries were reviewed and clinical and laboratory assessments were performed. Sigmoidoscopy was carried out and biopsies were obtained by a blinded observer. Histology was assessed without knowledge of the patient's clinical state or treatment category. RESULTS: At the end of the study, 6 of 19 patients on oral mesalazine (32 percent) and 14 of 19 patients on mesalazine enemas (74 percent) were still in full remission (log rank test: 15.28, P < 0.001). Differences in relapse rates between groups were significant even when data were stratified by extent of disease (P < 0.01). In the oral group, six and seven patients relapsed at 12 and 24 months, respectively. In the enema group, three and two relapses occurred in the first and second year of the study, respectively. All patients complied with the treatment satisfactorily and there were no dropouts. CONCLUSION: These results suggest that intermittent therapy with mesalazine enemas is more effective than continuous oral mesalazine in maintaining remission in patients with distal ulcerative colitis and proctitis.

Administration, Oral↗
PubMedDate not supplied

Relationship between lipid composition and antibiotic-resistance to isoniazid, streptomycin, p-aminosalicylic acid, ethambutol, rifampicin in mycobacteria.

The content of neutral lipids, peptido-glycolipids and phospholipids, separated by solvent extractions and TLC, was investigated and compared in various strains of Mycobacterium tuberculosis and in Mycobacterium avium. The examined strains could be divided into two groups: (i) those possessing a stable INH-resistance with a chromosomal location for the resistance genes, in which the content of total lipids and the distribution of lipid subfractions were modified with respect to the control strain H37Rv; (ii) those strains, such as the mutants resistant to streptomycin (Sm), ethambutol (EM), p-aminosalicylic acid (PAS) and rifampicin (R/AMP), uncorrelated drugs with different genetic location of the antibiotic-resistance, in which a disturbance of the lipid metabolism does not appeared to be significant. TLC and chemical analysis of INH-mutants suggested that the decrease of the cell lipids was associated with the peptidoglyco-phospholipid fraction, while the neutral lipids were characterized by a most elevated amount of both menaquinone-9 and free fatty acids, and by comparable levels of both glycerides and total fatty acids with respect to the sensitive strain. In the pattern of fatty acid shorter than C26 of all the fractions studied, no significant differences were observed between the H37Rv strain and the other resistant strains, including the M. avium. In the course of the lipid analysis no unusual phospholipids in addition to CL, PE and phosphatidylinositol-oligo-mannoside (PIM) were detected. Reasoning in a speculative way, the dramatic fall of the complex lipid elaboration in the INH-resistant mycobacteria, may underline a role for these substances in the envelope of the mycobacterial cell that defends itself from the selecting attack of the antibiotic molecule and that keeps this phenotypic expression of INH-resistance in the mutants.

Aminosalicylic Acids↗
PubMed1988

Determination of p-aminosalicylic acid and m-aminophenol by derivative UV-spectrophotometry.

A direct method for the simultaneous determination of p-aminosalicylic acid (PAS) and its major decomposition product, m-aminophenol (MAP), is described. The analysis is based on the use of derivative UV-spectrophotometry and is a rapid procedure which gives accurate and precise results. A simple purity test which utilizes the third derivative spectrum is also reported and compared with the USP XX spectrophotometric method for the estimation of MAP in PAS formulations.

Journal Article↗
PubMed2005

Properties of hot-melt extruded tablet formulations for the colonic delivery of 5-aminosalicylic acid.

Hot-melt extruded tablets were prepared using Eudragit S 100 as the polymeric carrier to target delivery of 5-aminosalicylic acid (5-ASA) to the colon. Scanning electron microscopy, modulated differential scanning calorimetry and X-ray diffraction analysis of the hot-melt tablet extrudates demonstrated that 5-ASA remained crystalline and was homogeneously dispersed throughout the polymer matrix. A pre-plasticization step was necessary when incorporating triethyl citrate (TEC) into the formulation in order to achieve uniform mixing of the polymer and plasticizer, effectively reduce the polymer glass transition temperature (T(g)), and to lower the processing temperatures. The concentration of TEC in the extrudates not only influenced the processing temperature, but also influenced the drug release rates from the extruded tablets due to leaching of the TEC during dissolution testing. Citric acid monohydrate was found to plasticize Eudragit S 100, and when combined with TEC in the powder blend, the temperatures required for processing were reduced. Tablets containing citric acid released drug at a slower rate as a result of the suppression of polymer ionization due to a decrease in the micro-environmental pH of the tablet. The drug release profiles of the extruded tablets were found to fit both diffusion and surface erosion models.

Chemistry, Pharmaceutical↗
PubMed2004

Systematic review: short-term adverse effects of 5-aminosalicylic acid agents in the treatment of ulcerative colitis.

AIM: To determine whether there is a difference in short-term adverse events in patients with ulcerative colitis treated with mesalazine, olsalazine or balsalazide. METHODS: MEDLINE was searched for articles published until 2002. Randomized trials of oral mesalazine, olsalazine or balsalazide for the treatment of active disease or the maintenance of remission were included. Outcomes of interest were the frequencies of patients experiencing adverse events and those withdrawn due to adverse events. RESULTS: Forty-six trials were included. One study of mesalazine vs. sulfasalazine for active colitis showed significantly fewer patients with adverse events with mesalazine. Both balsalazide vs. sulfasalazine studies for active disease showed significantly fewer withdrawals with balsalazide. One trial of balsalazide vs. sulfasalazine for maintenance showed significantly fewer patients with adverse events with balsalazide. Otherwise, no significant differences in safety outcomes were noted. CONCLUSION: All three 5-aminosalicylic acid agents are safe in the short term. In mesalazine-treated patients, the frequencies of adverse events or withdrawals due to adverse events were comparable with those in placebo-treated patients and lower than those in sulfasalazine-treated patients. Overall, adverse events or withdrawals were not significantly more frequent with olsalazine than with placebo or sulfasalazine. Adverse events and study withdrawals on balsalazide were less frequent than those on sulfasalazine.

Administration, Oral↗