Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMINOSALICYLIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed1987

Inhibition of 5-lipoxygenase pathway of arachidonic acid metabolism in human neutrophils by sulfasalazine and 5-aminosalicylic acid.

The possible effect of sulfasalazine, 5-aminosalicylic acid, and acetyl-5-aminosalicylic acid on endogenous arachidonic acid release and metabolism was studied in human polymorphonuclear leukocytes (PMNs). A new in vitro assay was used by which [1-14C]arachidonic acid is incorporated by purified peripheral PMNs until steady state was obtained (5 hr). After preincubation with the test drugs prior to activation with calcium ionophore A23187, the released eicosanoids were isolated by extraction and thin-layer chromatography (TLC) and quantitated by autoradiography and laser densitometry. Median drug concentrations needed for 50% inhibition of leukotriene B4 and 5-hydroxyeicosatetraenoic acid (5-HETE) release was 4-5 mM (range 1-9 mM) for both sulfasalazine and 5-aminosalicylic acid. The acetylated derivative of 5-aminosalicylic acid was ineffective. The present data suggest that inhibition of arachidonic acid lipoxygenation may be an essential action of sulfasalazine and its active metabolite, 5-aminosalicylic acid. Interference with lipoxygenase enzymes, rather than a steroid-like inhibition of arachidonic acid release from intracellular phospholipids, seems to be the mode of action.

Aminosalicylic Acids↗
PubMed1992

PAF formation by human gastrointestinal mucosa/submucosa in-vitro: release by ricinoleic acid, and inhibition by 5-aminosalicylic acid.

Human isolated gastrointestinal mucosa/submucosa incubated with ricinoleic acid (12.5-100 micrograms mL-1) or the calcium ionophore A23187 (10 micrograms mL-1) released platelet-activating factor (PAF) as determined by a scintillation proximity assay after extraction and purification. 5-Aminosalicylic acid (25-100 micrograms mL-1) inhibited PAF release by ricinoleic acid in a concentration-dependent manner, and 50 micrograms mL-1 reduced the effect of A23187. We suggest that PAF may play a role in the laxation and mucosal damage by ricinoleic acid released from castor oil.

Aminosalicylic Acids↗
PubMed1989

Experience with topical administration of 4-aminosalicylic acid in ulcerative colitis.

4-Aminosalicylic acid was applied topically in a daily dose of 1.4 gm for two weeks in ten patients with ulcerative colitis. After favorable results, the therapeutic effects of 4-aminosalicylic acid and salazopyrin enemas were compared in a two-week cross-over open trial, in 20 patients suffering from recurrent ulcerative colitis involving the rectum and rectosigmoid. No significant difference was found in the changes of the endoscopic picture of the mucosa. The results did not show a significant difference between 4-aminosalicylic acid and salazopyrin enemas, either in the clinical activity or in the histologic picture. 4-Aminosalicylic acid seems to be a suitable drug for improving the clinical symptoms of ulcerative proctitis.

Administration, Topical↗
PubMed2002

On the antioxidant properties of therapeutic drugs: quenching of singlet molecular oxygen by aminosalicylic acids.

The ability of the widely employed therapeutic drugs 4-aminosalicylic acid and 5-aminosalicylic acid to act as singlet molecular oxygen (O(2)((1)delta(g))) scavengers was investigated at pH 7 and pH 12. The isomer 3-aminosalicylic acid was also included in the study for comparative purposes. All three compounds quench photochemically generated O(2)((1)delta(g)) with rate constants in the range of 10(7)-10(8) x M(-1)s(-1), depending on the experimental conditions. No chemical reaction (oxidation of the aminosalicylic acids) was detected at the neutral pH, whereas at pH 12 both chemical and physical interactions with O(2)((1)delta(g)) operated. The physical process implies the de-activation of the oxidant species without destruction of the aminosalicylic acid. The quotients between the overall and reactive rate constants for O(2)((1)delta(g)) quenching at pH 12 (k(r)/k(t) ratios), which account for the actual effectiveness of photodegradation, were relatively low (0.22, 0.04, and 0.06 for 3-, 4- and 5-aminosalicylic acids, respectively). This indicates that the drugs, particularly the 4- and 5-amino derivatives, de-activate the excited oxygen species, at both pH values studied, mainly in a physical fashion, preventing its photodegradation and providing an antioxidative protection for possible photo-oxidizable biological targets in the surroundings.

Aminosalicylic Acid↗
PubMed1991

Spectrofluorimetric determination of urinary p-aminobenzoic and p-aminosalicylic acids in the BT-PABA/PAS test of pancreatic function.

Spectrofluorimetry was investigated as an alternative to HPLC for determining p-aminobenzoic acid and p-aminosalicylic acid in the N-benzoyl-L-tyrosyl-p-aminobenzoic acid/p-aminosalicylic acid test of pancreatic exocrine function. Urine specimens were hydrolysed for 30 min in 4 M NaOH at 100 degrees C. The fluorescence of p-aminobenzoic acid was measured in dimethyl sulphoxide solution (lambda ex = 300 nm, lambda em = 340 nm) and that of p-aminosalicylic acid in sodium acetate buffer, pH 4.0 (lambda ex = 297 nm, lambda em = 394 nm). The linear range was 0.038-8 mM for p-aminobenzoic acid and 0.051-12 mM for p-aminosalicylic acid, within-batch precision was 2.2% and 5.5%, respectively, and the entire analysis could be completed within 40 min. Although not eliminated, drug interference was greatly reduced in comparison with colorimetry. In 23 consecutive pancreatic function tests there was an excellent correlation between the p-aminobenzoic acid/p-aminosalicylic acid excretion index obtained by fluorimetry and the results from HPLC analysis (y = 0.914x + 0.070, r = 0.987, p less than 0.001). The method is simple, cost-effective and may be particularly valuable in developing countries having a high incidence of chronic pancreatitis.

4-Aminobenzoic Acid↗
PubMed1985

[Successful acute treatment of chronic inflammatory intestinal diseases with oral 5-aminosalicylic acid].

The effectiveness of oral 5-aminosalicylic acid (0.5 g t.i.d.) and of salazosulfapyridine (1.0 g t.i.d.) was compared in a randomized controlled study in two groups with 30 patients each with ulcerative colitis and with Crohn's disease. Persistent complaints within the first 5 days were treated with additional methyl-prednisolone (40 mg/d initially). After treatment for 8 weeks patients with ulcerative colitis showed morphologic remissions in 60% of the 5-aminosalicylic acid group and in 53% of the salazosulfapyridine group. Clinical improvement was achieved in 86% in both groups. Clinical improvement in Crohn's disease was seen in 87% of patients of the 5-aminosalicylic acid group and in 80% of the salazosulfapyridine group. This was evidenced by the significant fall (P = 0,0001) of the mean activity index. Additional steroid medication was nearly equal in both treatment groups. There were no side effects during treatment with 5-aminosalicylic acid. In contrast, salazosulfapyridine had to be withdrawn in four patients due to signs of intolerance. 5-Aminosalicylic acid can thus be considered a valuable alternative to conventional treatment on the basis of equal effectiveness as salazosulfapyridine and lack of undesirable side effects.

Adolescent↗
PubMed1989

Colonic N-acetylation of 5-aminosalicylic acid in inflammatory bowel disease.

5-Aminosalicylic acid presently is believed to represent the therapeutically active moiety of the sulfasalazine molecule in the treatment of inflammatory bowel disease. The metabolism of this compound, however, has not been studied in detail. In this paper we provide evidence that 5-aminosalicylic acid is acetylated to N-acetyl-aminosalicylic acid in homogenates from colonic biopsy specimens (370 +/- 20 nmol/g wet wt or 2.9 +/- 0.9 nmol/mg.min, n = 10), whereas acetylation in fecal samples was only small (13.0 +/- 3.0 nmol/g). Mucosal N-acetylation was rapid, cofactor- and pH-dependent, and could be enriched in the cytosolic fraction. In contrast, fecal acetylation was slow and did not depend on the presence of acetyl-coenzyme A. There were neither significant differences of acetylation between patients and controls nor a significant correlation to the individual acetylation phenotype. From our results we believe that presystemic acetylation of 5-aminosalicylic acid may be mainly mediated by a colonic mucosal enzyme and only to a small extent by fecal (bacterial) processes.

Acetylation↗
PubMed1986

Stability of 5-aminosalicylic acid suspension.

The stability of 5-aminosalicylic acid in a suspension prepared extemporaneously for administration by enema was studied. The suspension was prepared (tragacanth was the suspending agent) and then placed in 3-ounce amber glass prescription bottles; five bottles were stored at room temperature and five were refrigerated for 90 days. Using samples from each bottle, concentrations of 5-aminosalicylic acid were determined in triplicate by high-performance liquid chromatography at 0, 30, 60, and 90 days. Throughout the study period, all samples retained more than 90% of the day 0 concentration of 5-aminosalicylic acid. At each storage time, concentrations in samples stored at either room temperature or under refrigeration were not significantly different. In this extemporaneously prepared suspension, 5-aminosalicylic acid was stable for 90 days at room temperature and under refrigeration.

Aminosalicylic Acids↗